MVMA 2020 Convention Proceedings Book by movma

Missouri Veterinary Medical Association Annual Convention January 23-26, 2020 Holiday Inn Executive Center â&#x20AC;˘ 2200 I-70 Drive Southwest, Columbia, Mo. 65203

p U p e e K

ll with n the ba edicine. o y a t s and inary m in veter t s e t la e

Kick Ba

relax, ha ve

fun and You des make friends. erve it.

PROCEEDINGS

Table of Contents Note: Abstracts received as of 12-20-19. Some speakers will use handouts at their lecture.

Companion Animal Presentations Valerie V. Tynes, DVM, DACVB, DACAW

Introduction to The Fear Free™ Initiative..................................................................................................11 Using Pharmaceuticals to Prevent Fear, Anxiety and Stress in the Veterinary Clinic................................15 Preventing Behavior Problems in Your Practice .........................................................................................21 Reading Canine and Feline Body Language ...............................................................................................27 Understanding and Managing Fear and Anxiety in Companion Animals ................................................33

Anne Barger, DVM

A Case Based Approach to Cytology...........................................................................................................39 Common Cutaneous Masses . .....................................................................................................................45 Lymph Node Aspiration, It’s Really Useful ................................................................................................49 Urine-Luck: A Thorough Review of Urine Sediment.................................................................................55

Gary Norsworthy, DVM, DABVP

Two Feline Enigmas: Chronic Vomiting and Diabetes Mellitus..................................................................66

Amber Ihrke, DVM, DACVSM

Introduction to Rehabilitation– Improving Mobility…..............................................................................95 Rehabilitation and Osteoarthritis in Canines – a Multimodal Approach to Patient Care.........................99 Neurologic Rehabilitation: Common Conditions Treated in a Rehab Practice . .....................................105 Rehabilitation for the Geriatric Patient: You can teach an old dog new tricks! ......................................109

Richard Meadows, DVM, DABVP

CCUS/CUPS and Feline Stomatitis/Caudal Mucositis.............................................................................115 Dental Equipment for Fun and Profit........................................................................................................121 Dental Radiography - Image Acquisition and Interpretation ..................................................................131

Food Animal Presentations Bill Pittenger

A Review of the National Poultry Improvement Plan...............................................................................139 Biosecurity Guidelines ..............................................................................................................................141 Recommendations for Collecting Specimens from Poultry for Viral Diagnostic Testing .........................145 Testing For Pullorum-Typhoid Disease .....................................................................................................149

Daniel Shaw, DVM, PhD, DACVP, DACPV

Diseases of Poultry.....................................................................................................................................159

Bob Weaber, PhD 1

Beef Cattle Selection Tools: EPDs and Beyond.........................................................................................179 Beef Sire Relacement Selection Strategies ...............................................................................................191

Dietrich Volkmann, DVM, DACT

Bull Breeding Soundness Examinations....................................................................................................203

David R Smith, DVM, PhD, DACVPM (Epidemiology)

Systems Approach to Bovine Respiratory Disease....................................................................................213 What Does Antimicrobial Stewardship in Cattle Practice Look Like? . ..................................................219 I’m Not Positive That’s a Positive -The Art and Science of Making a Better Diagnosis . ......................................................................................................................223

John T. Groves, DVM

The Challenges and Rewards of Working with Stocker/Backgrounders...................................................231

Lourens J Havenga, BVSc

Trace Minerals in Cattle: Maternal Transfer, Fluctuations and Production Cycle Changes.....................239

David Pugh, MS, DVM, DACT, ACVN, ACVM

Ruminant Nutrition...................................................................................................................................245 Internal Nematode Parasites in Cattle .....................................................................................................259 Tips for Fly Control . .................................................................................................................................267

Equine Presentations Fairfield Bain, MBA, DVM, ACVIM, ACVP, ACVEC

A Review of the Equine Colic Examination – Is there anything new? ....................................................277

Earl Michael Gaughan, DVM, DACVS

Wounds Near Synovial Structures . ..........................................................................................................289

Bo Brock, DVM

The Horse in Motion ................................................................................................................................295

Peter Morresey, DVM, DACT, DAVIM

Peripartum Mare and Foal: What to look for, what to do ........................................................................313 Care of the Neonate: The First 48 Hours..................................................................................................317 Diarrhea And Respiratory Conditions In the Growing Foal.....................................................................327

Basic Science Review Christopher Baines, PhD and Brian Flesner, DVM, MS, DACVIM

Dr. Jekyll and Mr. Hyde: Cancer vs. Cardiac Cell Killing By Anthracyclines...........................................345

Lane Clark, DVM, PhD and Philip Johnson , DVM, DACVIM

Gastrointestinal Complications Of Phenylbutazone Treatment In Horses: Pathophysiological and Clinical Considerations.......................................................................................................................349

Nicole Nichols, PhD and Matthew Hull, DVM

Mineralocorticoids and a Clinical Review of Hydroadrenocortic.............................................................355 2

Leah Cohn, DVM, PhD, DACVIM

Cytauxzoonosis and Other Vector Borne Diseases . .................................................................................369

Alison LaCarruba, DVM, ABVP (Equine)

Equine Endocrine Dysfunction . ...............................................................................................................381

Soft Skills Presentations Brian Patrick, DVM

Building Trust With Clients.......................................................................................................................393 Making a Clear Recommendation.............................................................................................................411 Empathy: What’s the big deal?..................................................................................................................421 Elephant In the Room - Money Talk In the Veterinarian-Client Relationship........................................427

Rebecca Johnson, PhD, RN, FAAN, FNAP

The Client-Animal-Veterinarian Bond: Imperative for Health................................................................449 Expanding Small Animal Practice: TigerPlace, A Pet Encouraging Retirement Residence . ..................451

Zoe Agnew-Svoboda

Breaking the Cycle: Animal Abuse and Human Violence........................................................................455

Practice Management Presentations David Galloway, DVM, DACVS-SA

Army Veterinary Corps: Update/VC Internship Program.........................................................................463

Elizabeth Johnson, DVM

The Life of An Item: NAVLE Demystified...............................................................................................479

Rob Bertman, CFA, CFB

Best Repayment Strategies for Veterinarians with Six-Figure Student Debt............................................485

Tom Lenz, DVM, MS, DACT and Jean Schmidt, DVM

The Veterinarian’s Role in Suspected Equine Neglect, Abuse and Mistreatment....................................489

Special Interest Presentations Michael Boeger

Missouri Bureau of Narcotics & Dangerous Drugs...................................................................................499

Carol Ryan, DVM

Standards for Missouri Veterinary Medical Records..................................................................................507

MU-CVM 25-Minute Lectures Karen Campbell-Motsinger, DVM, DACVIM, DACVD

Help For the Bald Cat................................................................................................................................521

Pamela Adkins, MS, DVM, PhD, DACVIM

The Impact of Heat Stress on Cattle.........................................................................................................535

Tim Evans, DVM, MS, PhD, DACT, DABVT

Free Toxicology Information Resources for Veterinarians.........................................................................541

Martha Scharf, DVM, AVBP (Equine)

Equine Fecal Egg Counts...........................................................................................................................545

Leon Tu, DVM

Current Practices in Spay/Neuter of Dogs and Cats.................................................................................553

Partners for Progress Presentations Keith VanHoy, MS, CPA

Questions You Wished Your CPA Would Ask You and Five Tax Ideas to Discuss With Your CPA This Year . ..............................................................................561

Companion Animal

Valerie V. Tynes, DVM, DACVB, DACAW Veterinary Services Specialist Ceva Animal Health Sweetwater, Texas

Introduction to The Fear Free™ Initiative Valarie V. Tynes, DVM, DACVB, DACAW Ceva Animal Health Valarie.tynes@ceva.com While every visit to the veterinary hospital may never be completely fear free, by paying close attention to the visual cues that our patients are sending us and working to make the visit as low stress as possible, we can still make a huge improvement upon the typical experience that patients have in the veterinary hospital. “Why is that even important?” you may ask. There are actually a variety of reasons, one of the most important being the learning experience that every animal has when they come to the clinic and discover that scary things are going to happen to them and there is nothing, they can do about it. In these situations, we must be aware that it does not matter that we do not think the experience is scary or we are trying to not behave in a scary fashion. All that matters is how the pet perceives the experience! If they perceive it as scary, then they will have a memory of the experience as scary and next time they return to the clinic, they will be prepared to defend themselves, possibly in a more aggressive manner against the threat that they remember well. Allowing this unpleasant learning experience to occur ensures that our job of providing health care for this patient will become increasingly difficult with every subsequent visit. A second reason it is important to improve the experience animals are having in our clinic is due to the fact that fear and anxiety are the underlying cause for a huge number of the behavior problems we see in pets. When you see a pet in the clinic that is fearful or anxious, there is a high likelihood that the pet has fear and anxiety related problems in other contexts. Taking the opportunity to discuss them with the owner, sooner than later, increases the chance these problems can be identified and treated appropriately. Since these problems always worsen with time (all that varies is the degree to which they do so) it is critical that they be dealt with before they become a problem that results in a broken human animal bond and a relinquished pet. Behavior problems are still a leading cause of owner relinquishment to shelters so is a completely unnecessary loss of patients and income to the practice. There are so many reasons to take a lower stress approach to handling your patients but ultimately the most important is probably the oath that every veterinarian has taken to prevent animal suffering. We cannot continue to treat animals’ physical health at the expense of their emotional health! There is a growing awareness that physical and mental health issues can be very intricately related so you cannot successfully treat physical conditions while ignoring the behavioral issues that may be influencing them and physical problems leading to pain or discomfort is a commonly overlooked cause of behavioral change in many pets. Reading Body Language In order to be most successful at maintaining a pet friendly practice, you must begin by learning to read animal body language and respond to it appropriately. There are many excellent resources in text books and on line for helping you learn to read body language, but the single most important thing you can begin doing is being more observant of your patients’ body language. If you can recognize the signs of fear anxiety and stress before it becomes severe, you will be able to prevent it from worsening. Our body language is equally important if we are to keep our patients from being uncomfortable about our approach. Animals should always be greeted with a quiet voice and a slow approach. Avoid making eye contact and stand sideways to the animal, looking at them using your peripheral vision. Never bend over them at the waist and reach your hand over their heads. Allow dogs to step forward and sniff you but do not immediately reach to pet them. If the dog remains standing near you and acts as if it is enjoying the interaction, then you can gently bring your hand up and rub or scratch their neck. You can also reach up 1

from below and rub or scratch the ears as long as the dog is not being presented for an ear infection! A similar approach should be made to the cat, avoiding direct eye contact or reaching for them suddenly. Using Pheromones in The Clinic Appropriate use of pheromones is an easy way to aid in keeping your practice pet friendly. Pheromones are semiochemicals that evolved as a signal between organisms of the same species that elicit a particular reaction from the receiver. The term semiochemical simply refers to any of the chemicals used by animals for communication. The word “semio” taken from the Latin means “sign”. Semiochemicals have evolved over thousands of years to enable animals to communicate within their species and between species. Olfactory cues, or odors may also serve as semiochemicals but in many cases, they did not evolve to serve the function of communication between species. One of the most important differences to be aware of when thinking about semiochemicals and the pheromones is that pheromones are innate cues which do not require learning. When an animal is born, it is born having the genetically predetermined, physiological capability of responding to the semiochemicals that are appropriate to its species. When a puppy is born and it snuggles against its dam’s teats and perceives the canine appeasing pheromone for the first time, it immediately begins to feel calm and relaxed. Conversely, olfactory cues are cues that are affected by our experiences. For example, if your favorite grandmother wore a particular perfume, every time you smell that perfume, you might experience a sense of well‐being, as you remember pleasant times with your grandmother. However, if you had an irritable, demanding school teacher that wore that identical perfume and frequently gave you bad grades or complained about your school work or behavior, then the smell of that very same perfume, might make you feel very uncomfortable whenever you smelled it. This is a very important difference between pheromones and olfactory cues! The puppy will never feel differently when exposed to appeasing pheromone, regardless of the experiences it might have in its presence and regardless of its age of weaning or whether or not it was even reared by its own mother. An animal’s responses to the pheromones specific to its species are innate or “hard wired”. Olfactory cues, or odors, require learning. Semiochemicals, as opposed to olfactory cues are perceived primarily through the vomeronasal organ or VNO (also more commonly referred to as the Jacobson’s organ). When animals perform the behavior known as flehmen, they are helping to open the duct to the VNO and to increase movement of molecules into the organ. The VNO is a hollow, bi‐lobed structure which lies above the oral cavity and has a duct that opens into the roof of the mouth in most mammals (it opens into the nostrils in horses). The inside of the organ is lined with sensory epithelium. When a semiochemical reaches this epithelium, it triggers a nervous transmission to the accessory olfactory bulb via the vomeronasal nerve. From the olfactory bulb, messages are then sent directly to the amygdala, the area of the brain primarily responsible for emotions such as fear and anxiety. Feliway Classic®, Feliway Multicat® and Adaptil ®are synthetic analogues of naturally occurring pheromones. Feliway Classic® is an analogue of the F3 fraction of the feline facial pheromone. This is one of the pheromones cats leave behind when they rub their face on items in the environment. It is best described as a territorial safety cue, likely helping them feel more comfortable about their surroundings. Adaptil® and Feliway Multicat® are appeasing pheromones. These pheromones are produced by the lactating bitch and queen respectively during the period shortly after birth until weaning and likely helps with the bonding process. Several different studies have demonstrated that Adaptil® and Feliway Classic® can decrease signs associated with fear and anxiety in the veterinary and kennel setting. Thus far, the feline appeasing pheromone has only been studied in multicat households with inter cat conflict but hopefully, continuing research will demonstrate other potential uses. Pheromones are species specific so can be used at the same time in the same locations. Diffusers can be used in exam rooms, waiting areas, kennels, treatment and recovery areas. Pheromone sprays can be applied to mats for use on tables and scales, towels for handling, bedding for recovery and even muzzles, 2

e‐collars, and the scrubs and lab coats of the staff. These sprays are in an alcohol base so it is critically important that you allow the alcohol to dissipate prior to exposing it to the pet. This can take anywhere from 3‐5 minutes. The sprays last 4‐5 hours once applied to fabrics and other surfaces so I recommend that staff routinely spray items they suspect they may need twice daily (first thing in the morning and again at lunch time) so that the items are ready for immediate use. Bear in mind that the goal is to keep the pheromone in front of the animal as much as possible. Pheromone perception is an "all or nothing" type of response, similar to triggering the firing of any nerve, so keeping the pheromones in front of the animal ensures that they are constantly receiving that calming message. The sensory systems of the animal in the clinic are being bombarded with hundreds of other messages telling them they are in trouble; they are in a dangerous place! In order to increase the chance that the calming signal will over ride all of those other messages, the pheromones need to be constantly available. Ideally, you want to keep anxiety levels from climbing rather than ever be forced to have to bring them down after they have climbed to very high levels. As you can imagine, this is a big job and it is more difficult for some animals than others, depending on their personality, their age and their prior experiences in veterinary hospitals. Use Food to Change the Way the Pet Feels About the Visit Recognizing the earliest stages of anxiety in your patients is the first step, but changing the way they feel about the visit is the next step and the easiest way to do that is with food. An animal that is extremely distressed will not eat and conversely, when an animal is eating, they are in a mental state that is incompatible with fear and anxiety. By offering food to an animal the entire time they are in the clinic situation, you can change their feelings about the clinic from one of fear and trepidation to one of pleasure. In order to be prepared for every animal’s needs and preferences, you must have a variety of foods available. These must be primarily chewy, meaty and soft items. Consider, chewy liver treats, turkey hot dogs, canned tuna, anchovy paste, low fat deli meats and beef, lamb, beef or chicken baby foods. You also need items that can be easily licked because many animals will lick when they will not chew. These items may include cream cheese, canned whipping cream, peanut butter, canned cheese and semi-frozen chicken broth. For animals with allergies, you can keep some chopped apples and carrots handy or fruit baby foods. Mini marshmallows are another excellent treat for animals with allergies because they are pure sugar! Throughout every step of the procedure, small bites of food should be placed in front of the animal so that it stays busy eating and somewhat distracted during any procedures being performed. Once the food favored by the animal is identified, it should be offered immediately before and during every procedure. Note that we are not rewarding or reinforcing the animal for good behavior! We are classically conditioning the animal to view the veterinary visit as a wonderful thing. To do this we simply have to associate every aspect of the visit with wonderful food! This may take a few minutes longer but when you are finished, your patient will be far more likely to allow a blood draw next time it visits the clinic, then it would if you simply restrained the animal with it struggling and fighting. Improving the Sensory Experience One way to decrease stress in your practice is to be aware of all of the other sensory stimuli that may be distressing. Sound should be kept as low as possible in the clinic so staff may need to be reminded occasionally to keep their voices as low as possible. This may take some time to become a habit but many people seem to forget how loud a veterinary clinic can be, especially in treatment or ICU, and of course in kennel areas. Much of the diagnostic equipment in a veterinary clinic can produce noise and frequently it is in the higher range that dogs can hear while seeming relatively benign to us. Care should be taken to keep diagnostic equipment as far from the ICU cages as possible. Lights should be kept as low as reasonably possible as well, especially in exam rooms. Once animals are 3 13

removed to a cage in the ICU/treatment area, you can give them bedding that they can snuggle down into and place a towel or blanket over the front of the cage. For cats, especially, it is critical that they have a place to hide. A deep bed, or most ideally a cardboard box can be provided to help them feel safe. Studies have demonstrated that when cats are unable to hide, their stress level and subsequently their sensitivity to infectious disease increases. It is an established fact that safety and security are the most important basic needs of all living things. When you place an animal on a slippery table, you immediately take away any feelings of safety or security. Whether the animal freezes or struggles due to its discomfort does not matter; it is still learning that the veterinary clinic is a scary place. There are a variety of different, easy, safe and inexpensive ways to provide animals with a non‐slip surface on your exam table. For small animas a towel may be all that is necessary. A number of small, non‐slip bathmats can also be acquired from discount stores and a different one used for each pet. These can then be washed and re‐used as needed. There is also a commercially available non-slip mat for use in veterinary clinics called the Pet Vet Mat™. This mat has a non‐slip backing and is made of a heavy plasticized material that can be cleaned between patients using your standard germicidal agents. These are relatively inexpensive and available online at PetVetMat.com. Putting in the effort today to ensure that your patient has a pleasant visit should be seen as an investment in the future of that pet’s health care. Every pleasant visit increases the chance that on the next visit the animal will be tractable and a pleasure to handle rather than a patient you dread seeing. Every tractable, happy patient is likely attached to a happy owner who will be loyal to your clinic because you cared enough to treat their pet with kindness and respect. Every happy, loyal owner is likely to give their pet the best quality health care; the type that you are providing! Non-slip mats on the exam table are a “must” if you and your practice are trying to practice in a Fear Free™ manner. Many people like the response that most animals have when put on a slippery stainless-steel table; they freeze. However, as you have learned, freezing may make our job easier but the pet is still having a traumatic experience and learning that the veterinary clinic is a frightening place to be. Next time the animal is put on that table its response may be different. It may escalate its aggression based on the learning experience it had. Conclusion Putting in the effort today to ensure that your patient has a pleasant visit should be seen as an investment in the future of that pet’s health care. Every pleasant visit increases the chance that on the next visit the animal will be tractable and a pleasure to handle rather than a patient you dread seeing. Every tractable, happy patient is likely attached to a happy owner who will be loyal to your clinic because you cared enough to treat their pet with kindness and respect. Every happy, loyal owner is likely to give their pet the best quality health care; the type that you are providing! Useful Resources Fear Free℠ Certification program‐ www.fearfreepets.com Herron ME, Shreyer T. The Pet Friendly Veterinary Practice: A Guide for Practitioners. Vet Clinics of North America Small Anim 44 (2014) 451‐481. Horwitz D. The Blackwell Five Minute Behavior Consult. Yin, Sophia. Low Stress Handling, Restraint and Behavior Modification of Dogs and Cats. Cattle Dog Publishing.

Using Pharmaceuticals to Prevent Fear, Anxiety and Stress in the Veterinary Clinic Valarie V. Tynes, DVM, DACVB Ceva Animal Health Valarie.tynes@ceva.com Psychotropic drugs can be excellent tools for treating many behavior problems. The main reason for using these medications to treat behavior problems is twofold; to prevent suffering, as in many cases of separation anxiety or severe phobias, and to aid with behavior modification. The primary reason for using pharmaceuticals to prevent fear, anxiety and stress (FAS) in the veterinary clinic is to prevent suffering. In addition, by preventing a pet from experiencing FAS during the veterinary visit, you prevent them from learning to associate the veterinary visit with FAS. It is this learned association that causes the majority of handling problems in the clinic. Fractious, aggressive and difficult to handle animals are almost always behaving this way as a result of having learned to fear what happens in the veterinary clinic. Using medications in this way can require a major “culture change” in the practice and a lot of client education. Everyone in the practice must agree that preventing emotional pain and distress is equally important in most cases as preventing physical pain and distress. What this means is that when a patient is presented for anything other than an emergency, and is showing high FAS either before or during the procedure, the staff and veterinarians need to be prepared to discuss with owners the options for giving the pet the best care. These may include: returning home and giving pre visit pharmaceuticals prior to returning for a rescheduled visit or using some sedative or anxiolytic medications at the present appointment and being able to wait until they take effect. These conversations will be critical to helping the pet owner understand why this is important and how it is in the best interest of their pet to not continue with a procedure that is going to cause increasing FAS. Generally speaking, I like to separate the psychotropic drugs into two groups; “event” medications and “daily use” medications. Event medications are those that act rapidly and are typically short lived. The most common example of these are the benzodiazepines but recently, trazodone, gabapentin and clonidine are also receiving use as event medications. These medications can readily be used on an as needed basis and only when the animal is expected to need medication to help it deal with a particular stimulus or situation. These medications can also be given regularly, but they do not have to be, in order to be effective or useful. The daily use medications are the medications that typically take several weeks to take effect. Because of that, they will be ineffective if people try to give them only “as needed” and will not be covered here in depth because they will not be that useful for dealing with FAS in the clinic. When using these drugs in practice it is important to be aware of the different neurotransmitters that they target. Which neurotransmitter is targeted helps to explain what the common side effects and contraindications are for each particular drug. As a general rule of thumb, when it is necessary to use multiple medications to achieve a satisfactory level of anxiolysis or sedation, using drugs that target different neurotransmitters is likely to be safer and more effective than using multiple drugs that target a single neurotransmitter. Serotonin 2A Antagonist/reuptake Inhibitor Trazodone is structurally unrelated to the other SSRIs (selective serotonin reuptake inhibitors) but is a weak inhibitor of serotonin reuptake and a potent antagonist of some serotonin receptors. In humans it has been used primarily to treat depression, anxiety and insomnia. Similar to clonidine, trazadone has been used in veterinary medicine as an adjunctive agent to treat anxiety related problems, when benzodiazepines have been ineffective or not tolerated by the patient. Trazodone potentiates the effects of 1

The most common side effects associated with trazodone use are sedation, hypotension and nausea. Compared to other antidepressants, it is the one with the lowest risk of seizures. In several different studies, trazodone has been evaluated for its ability to decrease signs of stress in hospitalized dogs, to facilitate post-surgical confinement in dogs and to sedate cats for veterinary examination. In all studies the drug has been shown to be very helpful and while much more research is needed, this medication probably receives more use as a pre veterinary medication than any other. The needed dose may vary from 4-14 mg/kg and anecdotally, some animals may benefit from being given a dose the evening before a veterinary visit as well as the morning of the visit. In the one study of cats (Orlando JM, et al. 2015) 50, 75 and 100 mg tablets were given per cat and no negative side effects were noted. The best effects of trazodone are seen at about 1 ½ to 2 hours after dosing. Benzodiazepines Benzodiazepines work by facilitating the transmission of alpha aminobutyric acid (GABA) in the central nervous system. GABA is the major inhibitory neurotransmitter in the brain. GABAergic neurons are widely distributed throughout the brain where they serve important regulatory functions such as vigilance, anxiety, muscle tension, memory and epileptogenic activity. The primary functions for which we use benzodiazepines in veterinary medicine are: reducing muscle movement and anxiety and controlling seizure activity. Generally speaking, benzodiazepines have a rapid onset of action with effects that can last for a few to several hours. At low doses benzodiazepines have calming, anti-anxiety affects and at higher doses they may be sedating. Paradoxical excitation seems to be a relatively common problem noted with the benzodiazepines so pet owners should always be instructed to give a “test dose” when they can be home to observe the pet but before the pet is likely to experience exposure to what it fears. So, if giving a benzodiazepine for a veterinary visit, the client should be encouraged to give a dose a day or two before when they are home to observe the dog and be able to report exactly how the dog responds to the drug. Benzodiazepines should be avoided in animals that have a history of aggression due to the possibility of the drug disinhibiting aggression and increasing the likelihood that the animal will behave aggressively when frightened. Benzodiazepines are metabolized in the liver and excreted by the kidneys so their use should be avoided if liver or kidney disease exists. Idiopathic hepatic necrosis has been documented in cats receiving diazepam so when prescribing diazepam to cats, blood work should be rechecked after 3-5 days of treatment but there are so many other, safer benzodiazepines that can be used in cats, you may want to simply avoid the use of diazepam. Other side-effects include, ataxia, muscle relaxation, increased appetite, anxiety, hallucinations, muscle spasticity and insomnia. Contraindications for the use of most benzodiazepines also include glaucoma, pregnancy and lactation. All benzodiazepines have the potential for human abuse so care should be taken when prescribing and refilling prescriptions for benzodiazepines. Benzodiazepines are an excellent first choice of medication when dealing with any suspected fear or anxiety related problem but with their propensity to cause paradoxical excitation and the risk of human abuse, many veterinarians prefer to use other drugs first. The other challenge you will face with the benzodiazepines is the large individual response that animals may have to the exact same drug when given at the exact same dosage rate. They do not have long term effects and different benzodiazepines last for different periods of time so for all of these reasons’ practitioners should become familiar with several 2

different benzodiazepines that may be useful for treating FAS; alprazolam, clonazepam, oxazepam and lorazepam, to mention a few. Gabapentin Gabapentin is an anticonvulsant that has been used as adjunctive therapy in the treatment of seizures in dogs and cats. It is structurally similar to GABA so it acts as an inhibitory neurotransmitter, but it does not appear to interact with GABA receptors. Its actual mechanism of action is not entirely clear but it has bene found to have the following therapeutic effects: anxiolytic, analgesic, sedative and/or anticonvulsant activities, tranquilization, or skeletal muscle relaxation dependent on the dosage used. In studies, 50-100 mg of gabapentin have been used to decrease FAS in cats during a veterinary visit. Again, doses should be administered about 90 minutes prior to the fear inducing stimuli. Anecdotally, much higher doses are often used as a part of a pre-visit dose to decrease FAS. Alpha 2-adrenergic Agonists Clonidine is a presynaptic alpha 2-adrenergic agonist. Its original use in humans was as a hypertensive agent but because of its widespread actions on the noradrenergic system, it has gained popularity as a psychopharmacologic agent. In veterinary medicine it has been used primarily in the dog to treat fear or anxiety-based problems such as noise phobias, separation anxiety and fear of car travel. It may be especially useful when paradoxical excitation prevents the use of benzodiazepines. Clonidine can be given regularly (2 times daily) but is most commonly used for situational anxieties and/or as an adjunct to other longer lasting medications such as SSRIs or TCAs. If used for situational anxiety, clonidine should be given about 2 hours prior to the fear inducing event. Side effects are uncommon but may include sedation, dry mouth, nausea or constipation. Clonidine can enhance the CNS effects of other CNS antidepressants such as trazodone, barbiturates and other sedativehypnotics. If needed, the effects of clonidine can be reversed using yohimbine or atipamazole. Sileo® is dexmedetomidine in an oromucosal gel for transdermal use. Another alpha 2 agonist, it has been shown in this form to alleviate acute fear and anxiety associated with noise in some dogs while used at sub sedative doses. Side effects are similar to those of other alpha 2 adrenergic drugs. Some veterinarians have tried using Sileo® off label as a pre-visit pharmaceutical or to further decrease FAS after an animal arrives at the clinic and the PVPs it has already been given prove inadequate. Anecdotally, some have found this helpful. Phenothiazine Tranquilizers Acepromazine is the only drug in this family that is commonly used in companion animal medicine. These agents block the action of dopamine leading to sedation and tranquilization. While this also results in behavioral quieting and depression it does not decrease fear or anxiety; it simply decreases the ability to respond to environmental stimuli. In addition, the blockade of dopamine receptors effects brain regions responsible for controlling thermoregulation, basal metabolic rate, emesis, vasomotor tone and hormonal balance. Antipsychotics also produce a state of decreased emotional arousal and a relative indifference to stressful situations. Therefore, acepromazine should never be used alone in an animal that is exhibiting FAS. It may be a very helpful adjunct in an animal that has been given other anxiolytics but remains so fractious or aggressive that additional sedation is required. Summary When using pharmaceuticals to decrease FAS in the clinic, one must always be prepared to add another medication if an appropriately high dose of one does not adequately relieve an animals FAS. It is common for multiple drugs to be required and it is common for multiple repeat visits to be required in the beginning to determine exactly which combination of drugs at which dosages are going to be required for 3

nay given medication. Many animals may need complete sedation after arriving at the vet in order for their procedures to be completed safely and effectively. This should not be avoided if it means a less stressful visit for the pet. Again, if the procedure is performed more completely and safely, and more accurate data is collected from the physical exam, then it is worth the trouble. An animal that has been given a pre-visit pharmaceutical should be able to be injected more quickly and safely with a sedative than one that was not given a PVP and the procedure should not increase the patients FAS. The charts below give some examples of PVPs as well as “in hospital” medications for decreasing FAS. Ultimately, remember there is no “one size fits all”! Finding the most effective protocol for every given individual will take some patience but once a protocol for a given patient is determined and recorded in its record, then every subsequent visit will go more quickly and be less stressful for everyone involved; the exact opposite of what will happen if you do not take the time to find the protocol that will work for the individual. Examples of Some Pre-Visit Pharmaceuticals for Preventing FAS (Courtesy of Fear Free℠) Medication

Dog dose

Cat dose

Alprazolam

0.02-0.1 mg/kg dose PO

0.125-0.25 mg/CAT (Not per kg) PO

Diazepam

0.5-2.0 mg/kg/dose PO

Do not give to cats PO

Clonidine

Dog: 0.01-0.05 mg/kg/dose PO

DOSE/EFFICACY NOT ESTABLISHED IN CATS

Gabapentin

10.0-40.0 mg/kg/dose PO

Cat: 10.0-20.0 mg/kg/dose or 50.0100.0 mg/CAT (NOT /kg) PO

Trazodone

Dog: 3.0-8.0 mg/kg/dose PO

Cat: 50.0 mg/CAT (NOT /kg)

Acepromazine

0.05-2.0 mg/kg PO

Useful information Administer 30-60 minutes before need Test dose in advance! Minimal active metabolites Rapid onset of action Administer 30-60 minutes before need Metabolized rapidly Variable response among individuals; test dose! Can be used in combination with other anxiolytic drugs Administer 1 ½ hours before need Good for combining with other drugs when needed Give 1-2 hours before need For max sedation, give a loading dose the night before For dogs, may give a loading dose the night before May combine with other drugs Administer 1-2 hours before need Dosage will depend on other drugs in combination! Use only in combination with anxiolytics for additional sedation May increase aggression and noise sensitivity

Examples of Some In-Hospital Pharmaceuticals for Preventing FAS (Courtesy of Fear Freeയ

Class & Action: Alpha-2 agonists; Sedative-analgesics Medication Dosage Advantages Dexmedetomidine

for light to moderate sedation: Dog- 1.0-3.0 microg/kg IV or 3.010.0 microg/kg IM; Cat-1.0-5.0 microg/kg IV or 5.0-15.0 microg/kg IM; for profound sedation: Dog- 8.0-28.0 microg/kg IV or 12-40 microg/kg IM; Cat-20-40 microg/kg IM; DECREASE DOSAGES IF USED WITH OPIOIDS; use low end of dosing range for older patients, low level of FAS, & when used with opioid; high end range for younger patients, higher level of FAS or when used solo

Rapid onset Can be given IM Titratable sedation Reversable

Diazepam

Dog or Cat- 0.1 0.2 mg/kg IM or IV Dog or Cat - 0.10.2 mg/kg IV only

Cardiovascular effects Patient can react to painful stimulus even when deeply sedated

Useful Information Generally, the best drug for patients exhibiting high FAS and/or aggression Do not use in patients with cardiovascular disease Most predictable effects when used in combination with other drugs to avoid arousal

Class & Action: Benzodiazepines; Anxiolytic Medication Dosage Advantages Midazolam

Disadvantages

Fast acting Minimal adverse physiological effects Enhances calming when used with true sedative

Disadvantages Reversal may cause arousal in some May not be effective if patient is already exhibiting high levels of FAS Paradoxical excitation possible

Useful Information Use in combination with true sedative if patient is already exhibiting aggression or high FAS

Class & Action: Opioids; Analgesics Medication Dosage Butorphanol; Buprenorphine

Hydromorphone; Methadone; Morphine

Low Pain butorphanol Dog & Cat- 0.20.4 mg/kg IM or IV; buprenorphine Dog & Cat- 0.020.03 mg/kg IM or IV High Pain hydromorphone: Dog- 0.1-0.2 mg/kg IM or IV; Cat- 0.1 mg/kg IM or IV; methadone: Dog0.3-0.5 mg/kg IM or IV; Cat- 0.3 mg/kg IM or IV; morphine: Dog0.3-1.0 mg/kg IM; Cat- 0.1-0.3 mg/kg IM

Advantages

Disadvantages

Mild to potent analgesia Wide safety margin Fast onset of action except buprenorphine Synergistic with sedatives Reversible Variety of routes of administration

May cause vomiting and slow GI motility and decrease reparatory function More potent opioids may cause excitement in cats

Class & Action: Dissociative anesthetic drugs; Immobilizers Medication Dosage Advantages Disadvantages Ketamine

Dog & Cat- 1.0-2.0 mg/kg IM when used in combination with a sedative may provide dissociation without anesthesia while the same dose IV will provide light anesthesia; 5.0-10.0 mg/kg IM for true anesthesia; IM good route for cats; volume at this dose may be too high for large sized dogs

Decrease CNS response to circulating neurotransmitters in those already exhibiting FAS and/or aggression; decreases incidence of sudden arousal to stimulus

Can produce anesthesia so patients must be monitored Duration may be longer than desired Not reversible Painful injection

Useful Information Combine with sedatives in cats to avoid excitement Use with caution in patients in which vomiting could be detrimental or patients with existing respiratory depression

Useful Information Use with caution in patients with sympathetically driven cardiac arrythmias or seizures Use with caution in patients with known liver or kidney disease.

Preventing Behavior Problems in Your Practice Valarie V. Tynes, DVM, DACVB, DACAW Ceva Animal Health Valarie.tynes@ceva.com Behavior problems remain a leading cause of pet relinquishment in spite of the fact that many pet behavior problems can be managed successfully. The frustration that pet owners feel when faced with a behavior problem is worsened when they do not know where to go for good advice and when they are given inappropriate advice by well-meaning friends and acquaintances. Although the internet can be an excellent source of information, it also contains a lot of bad information and clients who go there seeking help don’t know how to tell the difference. Veterinarians are still considered the most reliable source of pet related information by most pet owners, however, the failure of most veterinary schools to educate veterinary students about animal behavior, results in veterinarians who don’t know how, and are often not interested in helping pet owners with their pet’s behavior problems. It is understandable that many veterinarians do not feel equipped to treat pet behavior problems and do not feel that they have the time to invest in the lengthy consultations that treatment requires. However, giving clients the information needed to prevent behavior problems from developing does not take any more time than educating clients about the importance of vaccinations, parasite prevention or any other preventive health subject and is just as critical to the pet’s long-term health. In addition, most behavior problems that are ignored, worsen with time and become more resistant to treatment so early intervention is another important role that the general practitioner must take on in order to save pets lives and keep clients. Educating clients starts at the first puppy or kitten visit and should involve the entire staff. Staff can and should be trained to cover some of the basic aspects of raising and training the new pet much as they do other preventive health care subjects. In addition, having prepared handouts available can also minimize the amount of time it takes to share this important information with clients. Good handouts on raising puppies and preventing behavior problems are available from a variety of sources. (See below) Developmental Periods and Socialization of the Dog Understanding the important developmental periods that puppies and kittens go through may not be critical to the pet owner but veterinarians should have a passing familiarity with these critical periods. The neonatal period begins with the birth of the puppy and ends at about 13 days of age. During this time, the puppy is completely dependent upon its mother and mainly exhibits basic reflexes associated with acquiring food and comfort. The transitional period- begins when the eyes open (about day 13) and ends when the startle response to sounds appears (about day 20). New visual and auditory capacities develop during this time; puppies begin to lap and chew food, eliminate without stimulation, stand, walk and wag their tails. The socialization period begins after the startle response appears and extends to approximately 14-16 weeks of age. This is a period of rapid behavioral and especially social, development. Weaning begins at 5 weeks and ends at about 7-10 weeks and this period is critical for the dog to learn about proper social behavior with other dogs. By 8-9 weeks, pups are attracted by odors of urine and feces as areas for elimination. During the socialization period, pups begin exploring novel objects and exhibiting social play, social following and the ability to form strong attachments to others. The juvenile period begins when the primary socialization period ends and extends to sexual maturity (about 6 months). During this time, behavioral skills are refined and while adult learning capabilities appear, attention spans are short. With sexual maturity, sexually dimorphic behaviors such as urine marking, aggression, roaming, mounting also appear One must always remember that these periods are "windows" not brick walls! They aren't written in stone; puppies can and should continue to be "socialized" after 16 weeks of age. 1

The socialization period is likely one of the most important periods that the puppy will go through while in the pet owners’ home. When owners acquire puppies after this important period of development has passed, the challenge of helping the puppy to adapt and grow into a well-adjusted individual can be huge. Lack of proper socialization is a likely root cause of many behavior problems seen in dogs so proper socialization cannot be over emphasized to the pet owner! While shyness/fearfulness is highly heritable and fearful puppies should never be forced into a situation when they are exhibiting signs of fear or anxiety, proper socialization can dramatically increase the chance of a puppy developing into a good pet. Socialization is an active process. Owners must go out of their way to expose puppies to a variety of novel places, objects, people, animals and situations. In order for socialization to be successful, experiences with these novel stimuli must be positive ones. In some cases, such as meeting new people, it may be beneficial to have the stranger offer the puppy small, tasty treats so that the puppy learns to associate strangers with good things happening. Puppies that have good positive experiences with novelty during the socialization period are more likely to make good pets as adults. They will be less fearful, more confident and more capable of dealing with novel stimuli later in life. Socialization must also be a safe process. Puppies should not be taken to areas where unvaccinated dogs may congregate, such as dog parks. However, play time can be arranged with the dogs of friends and family members that are known to be well vaccinated. Puppy socialization classes can be invaluable! A good class will require that all puppies have at least one vaccination, that puppies not be allowed to come to class showing any signs of illness, and the class location should have a substrate that is easily cleaned and sanitized. More dogs will end up euthanized in shelters due to unacceptable behavior than will die from contagious disease so there is absolutely no excuse for telling clients to wait until their puppy has been completely vaccinated before beginning the socialization process. By then, it may be too late! At least one study has demonstrated no higher risk of disease in puppy’s that attended puppy socialization classes than puppies that do not and there have been no documented cases of outbreaks of infectious disease associated with properly managed puppy classes. Developmental Periods and Socialization of the Cat The cat has been shown to go through developmental periods similar to the dog although they may be less clearly defined. The variation between individuals can be due to genetic factors, environmental factors such as handling, and maternal factors such as maternal stress and nutrition or a combination of these things. The first two weeks of a kitten’s life, when it is entirely dependent upon the queen, is considered the neonatal period. The transitional period is that period between the second and third week of life when locomotor skills begin to improve and sensory capabilities begin dramatic improvement. The socialization period begins in week 3 and extends through approximately the seventh week of life. This is the critical period when kittens are most able to form social attachments. This is the time when kittens should be exposed to as many people, other species and other cats as possible, in a very positive and nonthreatening way. Several studies have shown that human handling plays a very important role in the developing kitten, making it friendlier to humans, so adopting kittens with a known history of gentle handling by humans can be valuable if you want to increase the chance of getting a cat with a friendly personality. Kittens that are separated from their mother completely prior to two weeks of age have been shown to be more fearful and display a variety of developmental deficits. Studies of cat personality have identified at least two personality types: 1.) sociable or confident; 2.) timid and nervous. Again, many different factors probably play a role in the development of the personality type including early socialization, genetics and social or observational effects. It is important to be aware that approximately 15% of kittens will appear to be completely resistant to socialization.

Playful behavior is one feature of the cat that many people find very appealing, so the clinician should understand the development of play behavior in the cat so that they can educate their clients about the different types of play in the cat and how to appropriately shape the behavior. Social play in the kitten appears first at about 3-4 weeks of age, is well developed by 7 weeks and begins to decline at about 12-14 weeks of age. Kittens usually engage their litter mates in this type of play, by pawing, chasing, rolling, biting, wrestling and pouncing. Kittens may direct this behavior at the human hand unless taught otherwise. Object play begins a little later, along with predatory play, at about 7-8 weeks of age and peaks at around 18 weeks of age before beginning to decline. The juvenile period of kitten development begins at around the time the socialization period ends and lasts until sexual maturity. Sexual maturity usually occurs at around 5-9 months of age but some male cats are not fully sexually mature until 9-12 months of age. Social maturity is not reached until 2-4 years of age. Five Easy Steps to Behavioral Health Generally speaking, all pet behavior problems could be prevented if you could teach pet owners to follow these 5 basic guidelines: 1.) Elicit and reinforce appropriate behavior Teach pet owners to “catch their pet doing something good!” Every time they walk by the puppy and it is lying quietly and chewing on its own toys, stop and praise it and give it a treat. Rewarding cats for scratching on the scratching post has been shown to be associated with more frequent use of the scratching post. Teach owners to keep food treats handy when people come to the door so they can reward the puppy for sitting quietly. You can teach owners about basic training with positive reinforcement techniques as well as how to use food rewards appropriately. 2.) Prevent or minimize inappropriate behavior Teach pet owners how to “set their pets up to succeed”. Teach them to manage the pet’s environment so that he/she is not put into a position where he can practice inappropriate behavior. This is why crate training is so critical for puppies! A pet that is crated or confined to a pet proof space cannot chew on shoes and furniture or get into the trash or eliminate in the house. Similarly, a new kitten should probably not be allowed to roam freely in a large home. They should be confined to a single room and provided with their needs when no one is home to supervise. Preventing the practice of the inappropriate behavior is the owner’s responsibility. The pet doesn’t automatically know what is expected of it! 3.) Meet the pet’s behavioral and developmental needs. Many times, owners think their pet is “being bad” when in fact the pet’s behavioral needs are not being met. A certain amount of physical and mental stimulation is necessary for the normal development of all animals. Dogs need some social play each day as well as object play with toys. For example, chewing is a normal and necessary part of a puppy’s development. The pet owner must be instructed of the importance of providing the puppy with appropriate items to chew and keeping inappropriate items away from the puppy. The puppy also needs plenty of exercise, not just leash walks, but walks where the puppy can sniff and investigate. A variety of toys (different sizes, shapes and textures) should be available and rotated regularly to keep them “novel” to the puppy. Kittens must be provided with appropriate litter boxes and surfaces for scratching so that they are able to make acceptable choices. 4.) Use the “take away” method (negative punishment) to discourage inappropriate behavior. This method works by removing something that the animal values as soon as the animal begins displaying unwanted behaviors. For example, if a puppy or kitten begins biting or playing too roughly, the owner should be instructed to immediately get up and walk away rather than pushing the pet away or yelling at it. Responding consistently this way teaches the pet that these types of behaviors “make the fun stop”. 3

Puppies should be taught to sit before they are greeted by people. If they begin jumping and pawing, everyone should be instructed to ignore the puppy until it calms down and sits. The puppy learns that jumping and pawing cause it to be ignored. At the same time, you should also encourage owners to teach alternative behaviors that are incompatible with behaviors they don’t like. For example, a puppy that is sitting cannot be jumping on someone at the same time, so “sit” is an important cue to teach. A puppy cannot be barking if it has something in its mouth so teaching a dog to retrieve a toy when visitors come to the house can help decrease barking. These are just a few examples. Encourage owners to always look for alternative behaviors rather than just focus on stopping behaviors they don’t like.

  

5.) Minimize discipline (positive punishment) and use it correctly when necessary. If the first four steps are followed, then punishment will be unnecessary. For a variety of reasons, punishment is inappropriate as the first response for dealing with unwanted behaviors. In order for punishment to be effective it must: Occur within a second or two of the inappropriate behavior It must occur every time the inappropriate behavior occurs It must be of an appropriate intensity that results in the behavior stopping without causing undo fear or anxiety If any punishment is to be used at all, remote punishment is best. Remote punishment prevents the animal from associating punishment with the owners, thus preventing some of the more common punishment associated problems such as fear of the owner and avoidance behaviors. This is most easily accomplished using commercially available devices that can be effective in the owner’s absence. These include motion activated devices that shoot a blast of air, mats that emit a slight electric shock when stepped on and startling devices such as Snappy Trainers®, to name a few. If remote punishment can be used so that it meets all of the above criteria it can be helpful in preventing the development of some problems. In order for the pet owner to have lasting success though, it will still be necessary for them to first apply all of the four steps described above. Punishment does not teach the pet what we want it to do and since most behaviors exist for a reason (in other words they serve a purpose for the pet) attempting to stop them without teaching a suitable alternative for the pet, will either result in complete failure or the development of some other, often more annoying problem. Food Bowl Manners Many puppy owners are aware of the existence of food-related aggression, so they may take steps on their own to avoid or eliminate this problem. However, many of these steps can actually make the situation worse. Techniques such as taking the bowl from the puppy while he is eating (and possibly not returning it if the puppy "protests") or repeatedly touching the puppy or bowl while she is eating, or feeding by hand one piece at a time, may make the puppy more anxious or aggressive about food. Start by teaching the puppy to sit calmly and wait to be fed, however, make sure owners don't overdo this by requesting multiple behaviors before allowing the dog to eat. Next, teach the puppy that disturbance while eating equals "good things". Do this by having the owners walk by the bowl and toss in a special treat (e.g. pieces of cheese or hot dog) while the puppy is eating. After a couple of weeks of this they can also occasionally reach for the bowl or pick the bowl up and return it with a special treat. Only disturb the dog once during a meal, on occasion, so training doesn't cross the line into teasing or annoying. Owners can use a similar technique (trading for something good) to teach the dog to happily relinquish rawhides, pig's ears, etc. Make sure owners know that if they have problems with this (e.g. dog growls, lifts a lip, etc.) they should STOP what they have been doing and talk to you. The situation has gone from preventative 4

puppy training to dealing with a real and potentially dangerous behavior problem and should be addressed as such. Scratching and Destructive Behavior Destructive scratching is another behavior that can be prevented if the new kitten or cat is initially confined to one cat proofed room. Cats need to scratch just as puppies need to chew and just like puppies, they can be taught what is acceptable to scratch and what is not. Scratching helps to maintain the claw by removing the outer layers of nail but it also leaves a visual marker and an olfactory marker due to the digital glands so it serves several purposes. Several appropriate scratching surfaces should be provided for the cat, initially in the cat proofed room and later throughout the house. Cats seem to prefer loosely woven material, sisal or even real logs. These materials should be on vertical surfaces that are long enough for the cat to stretch out completely and claw, and stable so that the cat can scratch without the structure wobbling or falling. Once several of these devices are provided, owners should pay attention to the cat and reward them with small treats or play whenever they approach the scratching posts. If the cat is seen using the posts, they should be rewarded with an even bigger, better treat immediately after they finish scratching. Cat nip and toys can also be placed on or around the posts to further attract the cat. Feliscratch®, a synthetic analogue of the feline interdigital pheromone can also be applied to scratching posts. The product has been clinically proven to attract cats to the scratching post when applied properly and to decrease scratching of other, inappropriate items. In addition to providing appropriate scratching posts and rewarding appropriate behaviors, surfaces that the owners don’t want scratched should be made inaccessible or booby trapped. Booby traps can consist of double sided tape, inflated balloons attached to fabric surfaces, upside down mouse traps, etc. Frequent nail trims should also be included as one important step in the prevention of destructive scratching behavior. Preventing most behavior problems is far easier than correcting them once they become established. Once problems become established, they tend to become worse with time. Many people believe that what appears as a minor problem in a young puppy is “just a phase” and will pass, but this is rarely the case. Few behavior problems spontaneously go away. Most will become worse and more difficult to correct. You can decrease the chance of a pet losing its home, or worse, its life by demonstrating your interest in the pet’s behavior from the very first visit. With this approach, your clients become used to talking to you about behavior, giving you the opportunity to intervene early when a problem appears, even if that intervention just involves a referral! Useful Resources for clients, staff and veterinarians Decoding Your Dog by the American College of Veterinary Behaviorists, edited by Debbie Horwitz and John Ciribassi with Steve Dale. Twelve Terrible Dog Training Mistakes by Suzanne Hetts Family Friendly Dog Training by Patricia McConnell and Aimee Moore FearFreehappyhomes.com Useful Resources for Client Handouts Blackwell's Five-Minute Veterinary Consult Clinical Companion: Canine and Feline Behavior, 2nd Edition, 2017. Behavior Advice for Clients, Horwitz and Landsberg, Published by Lifelearn, 2016

Reading Canine and Feline Body Language Valarie V. Tynes, DVM, DACVB, DACAW Ceva Animal Health Valarie.tynes@ceva.com Learning to read body language is critical if you wish to be able to work with animals safely. When interacting with dogs and cats, keep in mind that visual cues are the only way they have of communicating with us and we ignore those messages at our peril. Most aggression in the veterinary clinic is a result of fear and anxiety. Recognizing those emotional states before the pet becomes extremely aggressively aroused enables the handler to adjust their techniques, or in some cases stop what they are doing completely, in order to decrease fear and anxiety. Staying calm ourselves and recognizing aggression for what it is; a distance-increasing form of communication can help to increase our empathy and understanding. Then we can approach restraint with the dog’s mental, as well as physical, welfare in mind. Fear and anxiety are two differing emotions that share similar physiological attributes. The most important thing to remember however is that they both lead to physiological changes and the animal has no control over these changes. That is why it is so critical that everyone be taught the importance of avoiding the use of any type of aversive response, or punishment of any type, in response to an animal that is behaving aggressively. Doing so not only increases the likelihood that the animal will increase its aggressive behavior but it teaches the animal to associate pain or discomfort with the source of its fear and anxiety which increases the chance that it will use aggression next time it is in a similar situation. These responses have been well documented in the scientific literature. The physiological signs of fear and anxiety are usually somewhat obvious to you: they may include a slightly elevated heart rate, followed by an increase in respiration and then blood pressure. Pretty quickly the anxious or fearful dog will begin panting and salivating. As the emotional state intensifies, the dog may begin to tremble, their pupils may dilate and if possible, they may begin to pace and show avoidance behaviors. Cats can be harder to “read” because they may “freeze” and the most obvious physiological sign you may see are their dilated pupils. However, if you observe closely, you may often see their rapid respirations by looking closely for the obviously movement of their thorax. Cats that are panting are obviously extremely distressed. If an animal remains uncomfortable with the situation, and whatever is causing it concern does not go away, then the visual cues that most people commonly associate with fear will begin to appear; the head and neck will be lowered, the ears will be pulled back closer to the head, the tail will be tucked and in dogs, the avoidance of eye contact will continue to the point that the whites of the eyes are often seen (what many people refer to as “whale eye”). If the dog is not being restrained, it may even attempt to turn sideways to the threat or roll over on its side or back. Some dogs will lift a front foot while doing this. If none of the visual demonstrations previously described succeeds in stopping the approach of a threat, whether the threat is an approaching dog or person, then what happens next will vary depending on the animals’ individual personality and experiences. Some animals will try very hard to escape before resorting to more aggressive threats while others may progress immediately to snarling, growling and attempting to bite. The “ladder of aggression” which is attached here will be discussed in more detail during the presentation but what is most important to keep in mind is that every individual will “climb the ladder” at their own pace; not every individual will necessarily go straight to the top and some individuals will move up and down. It is not necessarily always a linear process!

The” Ladder” does not apply to cats so much, not because they are incapable of using such subtlety,( you would see many of these visual cues if you could watch cats interact with each other in a natural environment) but probably because cats in the clinic are already so distressed when they arrive. What is certain is that every time an animal has a scary experience that necessitates it using a high level of aggression, it “discovers” how effective that is and we should be concerned about that making it more likely that the animal will use that method in the future when put in a scary situation. Similarly, if we repeatedly ignore those low-level messages that an animal sends us, we “teach” it that its subtle methods of communicating with us are useless, increasing the chance that it will go straight to the higher levels of aggression. Lastly, one of the worst things we can do is punish a dog for growling at us, because by doing so, we teach it that growling is a waste of its time, so it may simply move straight to the biting. Another visual cue that we should pay attention to in dogs is their overall degree of tension in their body. For example, a dog with a loose jaw and open mouth is likely to be relaxed. A tightly closed mouth indicates a certain amount of tension. A relaxed dog that is “happy to see you” will have squinty eyes that wrinkle at the corners. A startled, alert or frightened dog will have wide open rounded eyes. It should be kept in mind that a wagging tail only indicates a dogs desire to interact! It does not suggest that the dog is either friendly or aggressive. An upright, stiff, wagging tail is common in a confident aggressive dog but is likely to be seen along with a stiffened body posture. A friendly dog will have a loose, relaxed tail that wags the entire hindquarters with it. A slightly lowered wagging tail is commonly seen when a dog is attempting to initiate play. The tail that is much lower and wagging slowly, if at all, suggests that the dog is unsure about the interaction. A fearful dog will tuck its tail between its legs and hold it relatively still. The degree of body tension can be useful to note when a dog rolls over in response to your approach. Many humans believe that when a dog rolls over, this is an invitation for you to swoop in for a belly rub. However, you may note from the ladder of aggression that lying down with the leg up is mid-way up the ladder. Many dogs roll over as a part of their appeasement display when they feel threatened. An appeasement display is a behavior demonstrated by an animal in an attempt to ”turn off” an aggressive threat so when a dog rolls over and offers you its belly it is just as likely to be saying “Stop, I am no threat to you! Back off!” as they are to be saying, “Come on! I love a good belly rub!” So, how do you tell the difference? Mainly by the tension in their body and their facial expression. The dog that is fearful will likely have their tail tucked and their ears lowered. They may avoid eye contact and their entire body and upraised paw will likely be held very stiffly. The dog that is truly wanting to interact with you should be completely relaxed from head to toe! Other behaviors that humans find perfectly normal but dogs find threatening include hugging. Many people hug their dogs without ever really noting if the dog enjoys the behavior very much. Sadly, many bites to children occur because they try to hug dogs or they approach them at eye level. Due to their stature, children are frequently bitten on the face and seriously injured by dogs simply due to this inability to speak the same language.

When trying to read the visual cues cats send it is critical to observe the entire body, not just the posture, not just the eyes or ears and not just the tail. All of these cues need to be observed simultaneously. In the graphic below, the cat on the upper left is alert and as you view the images from left to right across the top, you see the cat becoming increasingly threatening.

As you may note, this offensively aggressive cat walks on tiptoe with its head down. The cat’s hind legs are longer than its fore legs so the cat will appear to be slanting downward from rump to head. The tail is held down but slightly arched away from the hocks and partially piloerected. As you view the pictures from top upper left to the bottom left, you see the cat becoming increasingly fearful. This fearful cat is attempting to appear small so as to avoid a perceived threat. This cat may freeze but if it feels that the threat is not going away, this freezing behavior can change to a more defensively aggressive behavior and the cat may roll over on its back and use all four feet to keep the threat away. Regardless of how scary this cat may look keep in mind that these behaviors are motivated by fear. The picture on the lower right depicts a cat that is likely feeling threatened but is willing to use overt physical aggression if needed. This cat presents the classic picture of the “halloween cat”. All four feet will be drawn underneath the body and the cat will stand erect with an arched back and tail piloerected. While the tail in this diagram is upright, it has been suggested by others that cats in this position are just as likely to have their tail in an inverted “U” position. Other aspects of tail position that should be noted: the tail of the relaxed cat will hang down straight and the tip may be wagged when the cat is stalking. As the cat’s attention is attracted the tail will go up. A cat that is interested in interacting will usually approach with an upright tail and the tail may curl over slightly at the top. Kittens, in particular, when interested in play often approach another cat with their tail 4

curled up and over their back. A cat with a rapidly twitching tail is at the very least, agitated and should be handled cautiously.

In this second diagram, depicting the facial expressions of the cat, we again see that the cat in the upper left-hand corner is the “neutral” cat. This cats’ ears are up and the pinna rotated forward. As you move from the upper left to the upper right, you see the cat becoming increasingly alert and threatening. The ears of this more threatening cat are up and the pinna are rotated to the side. From the upper left moving down to the lower left you see a cat becoming more fearful. This defensively aggressive cats’ ears are flattened back on its head. On the lower right is a cat demonstrating some mixed signals. This cat displays some features of the fearful cat with its ears being partially lowered, but they are also similar to the offensively aggressive cats’ ears since the openings are turned slightly sideways. This most likely represents a threatened cat that is simply not afraid to fight if necessary. Staring in cats, just as in dogs, is a threat. Cats that are trying to avoid a threat from another individual will try hard to avoid eye contact by pointing their head away or to the side. The pupils are important although you may not always be able to or want to get close enough to see them. Dilated pupils are more typical of a fearful animal that is more physiologically aroused. Constricted pupils are reflective of less arousal. The fearful, aggressive cat is more likely to have its mouth open in a snarl and hiss or spit. The offensively aggressive cat is likely to be silent. Whiskers are another feature that may not be easily or readily apparent but an offensively threatening cat’s whiskers are more likely to be directed forward. The whiskers of the more fearful cat will be drawn back closer to its face. 5

As part of the medical community, letâ&#x20AC;&#x2122;s include not only excellent self- education and self- awareness on the subject of how animals communicate, but improved public education as well. Every time we place a pet in a position where it must use aggression, we have given it a learning experience, possibly a rather traumatic experience, that it will never forget, and we have increased the chance that next time it is afraid it will call upon the memory of that coping mechanism first and be much more willing to use aggression to defend itself. The knowledge of dog body language and how dogs communicate must be spread to more pet owners as well since this miscommunication results in many dog bites as well as many of the problem behaviors and broken human-animal bonds that lead people to euthanize or abandon their pet.

6Â Â

Understanding and Managing Fear and Anxiety in Companion Animals Valarie V. Tynes, DVM, DACVB, DACAW Ceva Animal Health Valarie.tynes@ceva.com Anxiety and fear are some of the most common contributing factors to behavior problems in dogs and cats. Anxiety and/or fear can manifest in several different ways, including: destruction, vocalization, house soiling and aggression. In fact, fear and anxiety are at the root of most aggression problems in dogs. Dogs and cats may also experience anxiety or fear associated with thunderstorms or other loud noises, traveling in the car, strange people or animals, as well as separation from their owners. Chronic anxiety can also result in stress related illnesses such as gastrointestinal upset, decreased resistance to disease and urinary tract problems in cats (FIC). As is the case with most behavior problems, fear and anxiety typically worsen with time. They also become more resistant to successful treatment, so the veterinary staff needs to be attentive to signs of fear and anxiety in their patients and pay attention when clients mention any behavior problem. Informing the client of the danger of ignoring the problem is an important responsibility, as is seeing that they are given appropriate advice regarding referral. In addition, it is incumbent upon the healthcare team to “do no harm” and not do or suggest things that can make the behavior worse. Some important definitions Fear is an emotion that induces an animal to avoid situations and activities that may be dangerous. The emotional response occurs when an animal perceives that something or someone is dangerous. The key word here is “perceives”. It is critical that veterinarians and pet owners understand that just because they do not believe that the person or thing is to be feared, does not mean that the fear is not real to the pet. The pets’ “perception” is their “reality” and that is what the pet will act on. Normally fear is an adaptive response. It results in the animal showing an avoidance response that would, in the natural world, serve to keep it safe. However, in the home environment, it can lead to behavior that is unacceptable to the pet owner, such as aggression, destruction or excessive vocalization. Phobias are persistent and excessive fears of certain things or situations that are usually out of proportion to the actual threat that they present. Animals anticipating exposure to these stimuli will often display anxiety. An animal’s response to actual exposure to the stimuli can result in a range of responses from relatively mild symptoms of anxiety to extreme panic and even catatonia. Serious injury may occur when animals exhibit such a severe panic response that they chew or tear through doors or windows in an apparent attempt to escape from the frightening stimuli. Anxiety is the anticipation of future danger that may be unknown, imagined or real. It results in physiological responses that are similar to those associated with fear. The animal may begin to pace, pant, tremble and salivate. Pupils dilate and heart rate, blood pressure and respiratory rate may increase. Anxious or fearful animals may exhibit avoidance behaviors such as hiding and may be hyper vigilant; i.e. Constantly on alert and possibly even startling at the slightest sudden stimuli. In the case of intense fear, an animal may lose bladder and bowel control and may express its anal sacs. Stress can be defined as any physical, chemical or emotional force that threatens homeostasis.. While a certain amount of anxiety or fear may be adaptive in some situations, an animal that experiences fear or anxiety frequently, especially if unable to safely escape from fear inducing stimuli, will begin to suffer from stress and its effects. Since the initial result of fear and anxiety is a physiologic one involving autonomic arousal and stimulation of the hypothalamic-pituitary-adrenal axis (and accompanying release of stress hormones), eventually the animal can suffer physical harm such as an increased susceptibility to disease secondary to suppression of the immune system. 1

No one knows exactly why some animals develop fear or anxiety related problems but it is likely that numerous possible factors contribute to making an animal susceptible to developing them. They include: 1.A lack of, or inappropriate socialization.  



The first 3-16 weeks of a puppy’s life compose a critical period of development in where it can best benefit from exposure to varied stimuli, such as other animals, people, environments, etc. Instructing a client to keep their puppy at home until it has had all of its shots sets them up for failure and can have extreme and lasting consequences on the animal’s suitability as a pet. Dogs that have no (or limited) exposure to people or other dogs during this period tend to be fearful and may be aggressive when exposed to strange dogs and people. The young pup’s experiences with people and other dogs must be primarily positive ones during this time. Taking a puppy to a puppy class and forcing it to interact with other dogs while it is shaking, cringing and trying to escape is not “socialization”! This is essentially teaching a dog that other dogs and strangers are indeed scary things to be feared. While the socialization period of the cat is much shorter than that of the dog (lasting from about 2 to 7 weeks of age) exposing them to a variety of novelty in their early months of life is still likely to help them cope with novelty as adults. This early and brief socialization period is just one reason why feral cats can be so hard to tame. Ideally, kittens should be handled by people regularly between 2 and six weeks of age so as to increase the chances that they will be friendly towards people.

2. Genetics  



Numerous studies have shown that several different behavioral traits associated with a dogs’ personality are heritable. In particular, shyness or fearfulness is a highly heritable trait. Clients interested in acquiring purebred dogs should be informed of the important role that genetics plays in a dog’s temperament and choose the breed and individual puppy carefully. The dam, and preferably the sire as well, should be available when looking at a litter of puppies since their behavior is probably the best predictor of the puppies’ future behavior. Genetics have also been shown to be important in determining the personality of cats. Studies have shown that kittens whose fathers are friendly are more likely to be friendly than kittens born of unfriendly fathers.

3. Pre-natal and peri-natal effects 

Chronic glucocorticoid exposure such as due to maternal stress, can facilitate fear conditioning (contributes to phobia development?) and may impair learning and memory.

4. Early traumatic events 

A particular traumatic event may lead to an animal developing a fear or phobic response to a particular stimulus. Some individuals, for reasons that we don’t fully understand, develop profound fears or phobias based on a single traumatic event; this is often referred to as “one trial “or “single trial learning”. It appears to be more likely to occur in a young animal, but can feasibly occur at any age.

5. Pain or discomfort, in particular if it is chronic may lead to increased anxiety. 

Pain is one of the most commonly and easily overlooked causes of fear and anxiety in pets. Since our patients can’t tell us when they are uncomfortable, it is easy to overlook problems until they become severe and cause extreme pain. Often times, radiographs, blood work and even ultrasound do not reveal problems in their very early stages so an animal may suffer from chronic, low levels of pain or discomfort that can lead to changes in behavior.



Any animal over 5-6 years of age that suddenly develops a fear or anxiety related behavior problem should be evaluated very thoroughly for an underlying medical condition.

6. Unpredictable environments or interactions with people   

Examples are ill timed or harsh punishment. Underground fences may be another example. A certain amount of choice and control over the environment are crucial for good mental health.

7. Animals that are not given appropriate outlets for normal behaviors 

Both dogs and cats need physical exercise and environmental enrichment appropriate to their age and breed.

8. Cognitive decline 

Cognitive decline is sometimes accompanied by increased anxiety.. Animals experiencing cognitive decline are often disoriented and may appear confused at times. Individuals experiencing this confusion may be more sensitive to changes in their routine, loud unexpected noises, and separation from their owners; things that previously may not have appeared to concern them. When presented with a pet over the age of 7 that has recently begun to show signs of anxiety, cognitive decline should be considered.

What can the veterinary healthcare team do to prevent or treat anxiety related problems? 1. Recommend proper socialization. This will be covered in more detail in the presentation on problem prevention 2. Teach clients the importance of not using punishment since it can easily worsen the pet’s behavior. 3. Teach clients the basics of reward-based training and how a consistent cue-response-reward type of interaction can help to decrease anxiety. 4. Teach the importance of avoiding stimuli that lead to fear or anxiety and not forcing fearful animals into situations that they are clearly worried about. Many clients mistakenly believe that constantly exposing an animal to the stimulus that it is afraid of will result in the pet eventually losing their fear of that stimulus. However, in most cases, this actually serves to worsen the problem by further sensitizing the animal to the stimuli. Complete avoidance of the fearful stimuli can at least stop or slow the progression of the problem until further behavior modification can be started. 5. Be familiar with the concepts of desensitization and counter conditioning - When the particular stimuli that cause fear and anxiety can be identified, then the animal can be desensitized to those stimuli so that they no longer cause fear or anxiety. Desensitization is the process where an individual is exposed to the stimulus that causes fear or anxiety at such a low level that the fear or anxiety is not triggered. The exposure is repeated with the stimuli being increased very slowly until eventually the animal does not respond to it. Desensitization alone can be a very time consuming and slow process but it does work when performed correctly. Adding counter conditioning to the process of desensitization can help the process to move much faster. Counter conditioning is simply the part of the process where small food treats are constantly fed to the animal while the stimulus is presented. Eating is a pleasant, relaxing behavior that is inconsistent with fear or anxiety so the animal learns over time to associate the stimulus with a comfortable emotional state rather than a fearful or anxious one.

6. Medication can play a critical role in the treatment of fear and anxiety related behavior problems. However, they are only one tool and they rarely lead to long term success on their own. Medication is most effective when combined with a complete behavior modification protocol. Medications for fear and anxiety related problems can be divided into two primary groups: event medications and daily use medications. Event medications include benzodiazepines, trazodone and clonidine to name a few. These are drugs that are most useful when the fear or anxiety related problem is limited to a few, very predictable circumstances. Thunderstorms, car rides and trips to the vet or groomer are just some examples. The efficacy of these drugs is very dose related and vary by individual so clients should always be instructed to try a “test dose” of the medication before the actual event. This allows for the opportunity to be sure that the animal has no paradoxical reactions and to determine exactly what dose will allow the animal to best tolerate the frightening experience. The most commonly used daily use medications include the SSRIs and the TCAs. These are all drugs that do not work when given on an as needed basis. They require 6-8 weeks to take effect. It is not at all uncommon for these drugs to be used in conjunction with event medications for the best results. In addition, pheromones products such as Adaptil and Feliway can be helpful in preventing or treating mild anxiety related problems. They are excellent choices for difficult to medicate animals or geriatric patients o patients on other medications that make adding pharmaceuticals riskier. They may also be excellent adjuncts when treating more serious problems with medications. Anxitane and Zylkene are two nutraceuticals that can also be useful in dealing with mild anxiety related problems. The palatability of Anxitane and the ease of dosing with Zylkene make them both especially useful for cats that may be difficult to medicate. All of these products have performed well in studies looking at their use and are excellent first choices when faced with clients who are hesitant to give their pets psychotropic drugs. At some point however, one of the most important reasons for treating a patient with severe anxiety fear or phobias may be to improve their welfare or quality of life. Helping pet owners to recognize when their pet’s emotional health is suffering maybe another challenge that the veterinarian faces. References Araujo J, Rivera C, Ethier J, et al. (2010) “Anxitane tablets reduce fear of human beings in a laboratory model of anxiety-related behavior.” Journal of Veterinary Behavior, 5, pp 268-275. Beata C, Cordel J, Marlois N. (2007) “Effect of alpha-casozepine (Zylkene) on anxiety in cats.” Journal of Veterinary Behavior, 2, pp. 40-46. Beata C, Cordel J, Marlois N. (2007) “Effects of alpha-casozepine (Zylkene) versus selegiline hydrochloride (Selgian, Anipryl) on anxiety disorders in dogs.” Journal of Veterinary Behavior, 2, pp175-183. Duxbury, M.M., Jackson, J.A., Line, S.W., et al. (2003), “Evaluation of Association Between Retention in the Home and Attendance at Puppy Socialization Classes”, Journal of the American Veterinary Medical Association, 233, pp. 61-66. Landsberg, G., Hunthausen, W., Ackerman, L. (2003), Handbook of Behavior Problems of the Dog and Cat, 2nd Ed. Philadelphia, PA, Saunders. Mackenzie, S.A, Oltenacu, E.A.B., and Houpt, K.A. (1986),” Canine Behavioral Genetics – A review”, Applied Animal Behaviour Science, 15, pp. 365-393. Mills D, Ramos D, Estelles M, Hargrave C. (2006) “A triple blind placebo-controlled investigation into the assessment of the effect of Dog Appeasing Pheromone (DAP) on anxiety related behaviour of problem dogs in the veterinary clinic.” Applied Animal Behaviour Science, 98, pp 114-116. Scott, J.P. and Fuller, J.L. (1965), Dog behavior, the genetic basis, Chicago, University of Chicago Press. Serpell, J. and Jagoe, J.A. (1995), “Early Experience and the Development of Behavior”, in The Domestic Dog, J. Serpell, ed. Cambridge, England, Cambridge University Press. Tod E, Brander D, Wran N. ( 2005) “Efficacy of a dog appeasing pheromone in reducing stress and fear related behaviour in shelter dogs. “ Applied Animal Behaviour Science, 93, pp 295-308.

Companion Animal

Anne Barger, DVM

Clinical Professor & Section Head University of Illinois Urbana, Illinois

10/21/2019

• Start at 10x • Low power evaluation can help guide the overall process • Diagnostic quality sample • Adequate cellularity • Identifying the best area to evaluate • Inflammatory vs. neoplastic • Arrangement of cells

A Case Based Approach to Cytology Anne Barger University of Illinois College of Veterinary Medicine

Microscopic Evaluation 2

Inflammation • Diagnosis • Septic suppurative inflammation • Degenerative neutrophils • Mixed population of bacteria

• Two year old mixed breed dog, history of vomiting for three days. • PE: Fever of 103, distended and painful abdomen

Inflammation 3

• Suppurative inflammation • 90% neutrophils • Condition of neutrophils • Causes • Bacterial infection • Immune‐mediated disease • Foreign body reaction

Inflammation At surgery, an area of dead intestine was observed and was likely leaking into the abdomen

Inflammation 5

10/21/2019

Inflammation • Diagnosis: Pyogranulomatous inflammation with Blastomyces dermatitidis • Organisms have a double contoured wall and broad based bud

• 5 year old, shepherd mix, neutered male • History of lameness for last 3 days and a soft cough • PE: Febrile, painful on left front leg, harsh lung sounds, few draining lesions

Inflammation 7

• Pyogranulomatous inflammation • Mixed inflammatory population, predominated by neutrophil • Multinucleated giant cells and macrophages noted • Dimorphic fungus • Foreign body reaction

• 4 year old Boxer dog, spayed female • Small dermal mass on ear, has been there for 2 weeks, scabs on and off • PE unremarkable other than mass

Inflammation

• Granulomatous inflammation • Macrophages, multinucleated giant cells and few other cells • Causes: • Atypical bacterial infections • Fungal infection • Foreign body • Sterile

• Cytology revealed a mixed inflammatory population, predominated by macrophages with few multinucleated giant cells and low numbers of neutrophils. • Diagnosis: Granulomatous inflammation with Mycobacteria sp.

Inflammation 11

Inflammation 12

10/21/2019

• Characterized by the tissue of origin • Epithelial • Mesenchymal • Round cell

• 7 year old, golden retriever, neutered male • Received vaccinations, presented with swollen face and small mass at the site of vaccination

Inflammation

Neoplasia

• Malignant vs. Benign • Criteria of malignancy • How do the cells look different from one another • Location • Are there cells in the lymph node or spleen that do not belong • Regrowth

Round Cell neoplasia

• Eosinophilic inflammation • High percentage of eosinophils with lesser numbers of other inflammatory cells • Causes: • Hypersensitivity reaction • Parasite infection • Paraneoplastic

• 8 year old, spayed female mixed breed dog • Large mass on hind foot • Raised, hairless, rapid growth

Inflammation 15

• Gross features are often similar • Red, raised, round masses • Cytologically • Population of individualized round cells, each with slightly different features

• Mast cell neoplasia • Round cells, containing metachromatic granules within the cytoplasm • Round nuclei • Often accompanied by eosinophils

Round Cell Neoplasia 17

Round Cell Neoplasia

• Tumor types: • Lymphoma • Mast cell tumor • Plasma cell tumor • Histiocytoma • Transmissible venereal tumor

10/21/2019

• Transmissible Venereal tumor • Cytoplasm contains cytoplasmic vacuoles • Samples are very cellular

• 6 year old, intact female golden retriever • Several week history of vaginal bleeding

Neoplasia

Round cell neoplasia

Round Cell Neoplasia

Neoplasia

• Each round cell tumor has a unique feature • Histiocytoma: Peripheral clearing of the cytoplasm • Plasma cell tumor: Perinuclear clearing • Mast cell tumor: Metachromatic granules • Lymphoma: Prominent nucleoli and scant rim of cytoplasm • TVT: Punctate vacuoles in the cytoplasm

• 12 year old, neutered male cat • History of retching and gagging • Oral exam revealed a painful mass

• Squamous cell carcinoma • Clusters of neoplastic epithelial cells, occasionally with keratinized cytoplasm • These tumors are often accompanied by a suppurative inflammatory response

• These cells are commonly arranged in clusters, most notable at low power • Tight cell to cell junctions can be observed • The cells are round with round nuclei and exfoliate well

Epithelial Neoplasia 23

Epithelial Neoplasia 24

10/21/2019

Epithelial Neoplasia • 10 year old, collie‐mix, spayed female • Difficulty defecating for 2 weeks • Mass palpated in anal region

• Apocrine Anal Sac Adenocarcinoma • Uniform population of epithelial cells but behaving malignantly

Epithelial neoplasia 25

Mesenchymal Neoplasia • Anal Neoplasms • Apocrine gland adenocarcinoma • Perianal gland neoplasia • The majority of these tumors are benign and appear hepatoid in appearence

• 14 year old Lab mix • History of mass on tarsus for 2 months • Recently, has become lame

Epithelial Neoplasia 27

• Soft tissue sarcoma • Population of individualized mesenchymal cells • Spindle shaped with long cytoplasmic projections

• Connective Tissue • If malignant, sarcoma • Cellular appearance • Individualized cells • Often spindle shaped, some round • Round to oval nuclei

Mesenchymal Neoplasia 29

Mesenchymal Neoplasia 30

10/21/2019

Mesenchymal Neoplasia • Osteosarcoma • Highly cellular sample, prominent criteria of malignancy • Many of the cells are round with eccentrically placed nuclei

• 8 year old Labrador, neutered male • Limping for last 3 weeks • Swelling and pain, distal front leg

Mesenchymal Neoplasia 31

Cytology is simple, inexpensive and can be very useful

• Protein • Blood

Conclusion

• Bare nuclei • Granules • Microorganisms

Background Material 33

If you do not feel comfortable interpreting an in‐house cytology preparation, no worries, send it out!

Questions???

Lumps

and bumps Dermal vs. Subcutaneous

Anne Barger, DVM, DACVP University of Illinois

Inflammation

Granuloma, pyogranuloma, abscess

Neoplasia

| |

mass ma asssss o orr draining dr d rai aini aini ning ng tract tra racctt

Neutrophils Ne N Neut eu uttro oph phiills

Bacteria, Ba B acctter ter eria ia, often o te of ten n iintrain nttrra- and a d an extracellular e ex ttrrac acel e lu el lula la ar

Epithelial Mesenchymal Round cell

Tr True T ru rue ue e

Ab Abscess bsscces e s

and cysts

Benign vs. malignant Tissue type |

Foreign Fo F ore reig eig ign n body body bo dy Fungus Fu F un un ng gu uss SSterile ter eril ille

Impact diagnosis Differential list

Degenerate De D ege gene ne era ratte te

C Cytology Cy yto tollo og gyy

Macrophages M Ma acr crop oph ha ag ge es Multinucleated Mu M ulti llttiin nucle uccle u lea attted ed ed giant gi g ian ant cells cell ce cel lls lls Few Fe F e ew w neutrophils, ne n eu eut uttro rop ph hiillss,, llymphocytes, ly ym mp pho hocy cytte ess,, pl p la assma ma ccells ellls e ls plasma

A Atypical At tyyp piicca all

bacterial bac acte teri rial al iin nffe ect ctiio ons ns infections Fu Fungus F u un ngus ng us

Ep Epithelial E piitth he eli liial all a

llined iin ne ed d structures sst tru ruct ctures es M Many Ma any ny different difffere r ntt re tty yp pe es types

cell tumor

Can Ca C a be dermal or subcutaneous Often O Of f observed at mucocutaneous junctions Highly Hig Hi g cellular | | |

Round cells R Moderate amount of cytoplasm M Filled with metachromatic granules F

Se SSebaceous

adenoma or epithelioma

Dermal mass Benign Clusters of vacuolated epithelial cells C SSmall condensed nucleus

| | |

Dermal mass Most common in dogs <3 years of age Benign neoplasm, will resolve on its own Cytologically y Round cell population y Pale basophilic cytoplasm y Centrally placed nucleus y Peripheral clearing of the cytoplasm

Pl Plasma P las asma ma

C Cell ell Tu el T Tumor um mo or

Common Co C omm mmon on o on n he h head, ead, ad, face ad fac fa ace ce and and nd feet fee ee t Dermal De D errm ma all mass ma asss Cellular C Ce ellllul ula arr Cells Ce C ell lls ls are arrre a e round rou ro un nd with wiith w th eccentrically ecc ccentr en e ntr trica ica ic allly ly placed pla lace ced nuclei nucl nu nucl clei ei an nd p pe erriiin nuccllea nu ear clearing cle cl ea arriing ng and perinuclear Binucleation Bi B inu nucl clea eattiio on n is is a common comm co mmon on feature fe ea atu ture re

Ba Basal B s l sa

Cell Cellll Tumor Ce Tumo um mo orr

Co mon Common Comm o h head ead ea d an a and nd ne eck c ttumor um mor or o ats neck off ca cats R Recategorized Re ecca ec a ate t go te gori rizze ed for fo or d do dog ogs gs a dogs ass trichoblastoma ttr ric icho ho oblas bllas a to toma a Cy Cytology yto tolo logy log gy

cell tumors

Histiocytoma |

SSebaceous Se ebaceo e ous Follicular F Fo llicul ularr Apocrine

M Mast Ma as

Round

Clusters Clu Cl C lusst lu ste te te ers rs of rs of uniform u ffo uni un for orrm o epithelial e ep epi pitheli pi tthe th he helia liia al cells cells ellllls ell e Small Sma SSm m ma all ll and an a nd round nd ro ound nd wi nd w with ith th sca cant ca can nt rim rriim im of of b ba aso ssop op o ph hil i iicc scant basophilic ccytoplasm cy cyt y op opl pla pl asssm asm m Condensed C Con de den ens en nsed sed se ed chromatin chrom ch chr ro ati attiin pa pat p attter te te errn pattern

Squamous

Cell Carcinoma

Common locations | | | |

Mouth Eyes Ears Mucocutaneous junctions

Sq Squamous quam ua u am mo ou uss

Li Lipoma L ip ip po oma ma

Beni Benign Be nig gn nn neoplasm eopl pllas asm More M Mo ore re common co om mmo mmo on in in dogs do og gs than tth han an cats ca atttss Can C Ca an have ha h ave ve multiple mul ulti tip plle lipomas lliip po om ma as Cytologically C Cy ytto olo log giicca all lly | | |

L Lo ow cellularity ce ce ell llul ll ula arritty Low Many M Ma an nyy o only nly sse nl see ee fe ffew ew lli lipid ip piid d dr droplets ro op ple lets ts Aggregates A Ag gg grreg ega atte ess of of large larrg la larg ge adipocytes ad a dip dip ipoc ocyytte ess

Soft

| | |

Tissue Sarcoma

Vaccine Associated Sarcoma

Spindle shaped cells Wispy cytoplasmic borders

Behavior | | |

Aggressive Fast growing Locally Invasive

Usually locally invasive though higher grade Grading is only done on histopathology so cytology for diagnosis only

Feline

Samples vary greatly in cellularity Cytologically they look fairly similar |

Hemangiopericytoma Neurofibroma Schwannoma Fibrosarcoma

Behavior |

Soft

tissue sarcoma

Inclusive term |

cell ce elll carcinoma cca arc rcin rci inom oma

Cellular Ce C ellllu ulla arr sample sam ampl ple commonly ple comm co mmon onlyy w with ith se it ssecondary eco cond nda arry ssuppurative su upp ppu urrat ativ ive inflammation in nflam fflla am mma mati tio on n Clusters Cl C lu lus usstte ers rs of of epithelial epiitth ep theli helliial he ial al cells cell ells el ls with wit ith some sso ome me differentiation di d iff ffer eren enttiia attio ion to to mature mat atur urre e squamous s qu sq ua am mo ou uss epithelial epi p the tth hel elia al cells cce ellls Perinuclear Pe P eri rinu nucllea ar vacuolization vva acu cuo olliz izat atio on Nuclei Nu N Nuc uccllei ei a are re large re lar ar g ge e and an nd d round ro ou und nd w with ith p ith it pr prominent rom ominen in ne en nt n nu ucclleo eoli li nucleoli

Fibrosarcoma Histiocytic Sarcoma Osteosarcoma Chondrosarcoma Rhabdomyosarcoma

Vaccine

Associated Sarcoma

Cytology | |

| |

Usually low cellularity Cells exhibit obvious criteria of malignancy Spindle shaped cells May have extracellular matrix May have lymphoid infiltrate or secondary inflammation

Many

diagnoses can be made with cytology the common masses have very distinct cytologic features that can be differentiated from one another If you ever have a question about a cytology, consult a clinical pathologist Often

y Diagnostic Tool y Neoplasia y Primary or metastatic y Staging and prognosis

Anne Barger University of Illinois

y Inflammation y Identification of inflammatory processes y Organisms y Immune-stimulation y Supportive evidence for localized or systemic disease

y Histology y Encapsulated with subcapsular sinuses y Cortex, paracortex, medulla y Cortex y Spherical follicles y B cell areas y When activated a germinal center is formed

y Paracortex y Primarily T cell areas

y Medulla y Lymphatic and blood vessels Willard-Mack CL. Toxicol Pathol 2006

y Normal Node y Primarily small lymphocytes y Round cells, scant rim of basophilic cytoplasm, large nucleus y <10% intermediate and large lymphocytes y Equal in size or larger than a neutrophils y Open chromatin pattern y <1% other cell types y Macrophages, neutrophils, plasma cells, mast cells, melanocytes y Background structures y Red blood cells y Lymphoglandular bodies

y Reactive lymph node y Antigenic exposure resulting in immune stimulation

y Lymphadenitis y Lymph node draining an inflammatory lesion

y Neoplasia y Lymphoma y Metastatic neoplasia

y Probably the most common diagnosis y Submandibular lymph nodes are often reactive y Generalized lymphadenomegaly, systemic disease

should be considered

y Tick-borne diseases such as E. canis

y Immune Stimulation y Lymphoid expansion and division y Increased intermediate and large lymphocytes y Small lymphocytes still predominate y Increased (>1%) plasma cells y Mott cells y Still only few inflammatory cells

y Characterized based on the type of inflammatory cell y Suppurative lymphadenitis y >5% neutrophils y Lymphoid population may appear reactive or mixed with

increased large or intermediate lymphocytes

y Suppurative lymphadenitis y Causes y Bacterial infection or abscess y Immune-mediated disease y Neoplasia y Tumor is ulcerated or inflamed

y Pyogranulomatous lymphadenitis y Mixed lymphoid population y >5% neutrophils, macrophages and multinucleated

giant cells

y Causes y Fungal infection y Foreign body response y Salmon poisoning

y Granulomatous y >5% macrophages with multinucleated giant cells y Reactive lymphoid population y Causes y Mycobacterium y Fungus

y Eosinophilic lymphadenitis y >3% eosinophils y Reactive lymphoid population y Causes y Allergic or hypersensitivity response y Paraneoplastic y Parasitic infestation

y Lymphoma y Primary neoplasia of the lymph node y Generally the lymph node is enlarged y Lymphoid population described by size y Red blood cell can be used to evaluate size y Pure population of lymphocytes y Large y Intermediate y Small

y Cytology y Cell size based on comparison to RBC y Determine the nuclear shape y Also the location of the nucleus within the cell y Eccentric, central etc.

y Identify and quantify nucleoli y Also examine the shape of the nucleolus y Evaluate the cytoplasm y Quantity and color y Describe any mitotic figures

y Additional testing y Histopathology y Wedge or excisional biopsy y Phenotyping: T vs. B cell lymphoma y Immunocytochemistry y Flow Cytometry y PCR y TCR and BCR gene rearrangement y Excellent diagnostic test in conjunction with cytology

y Metastatic Neoplasia y Lymphoid population often reactive or inflammatory y Identification of non-lymphoid cells in the node y Metastatic carcinoma y Clusters of epithelial cells

y Metastatic mast cell neoplasia y Increased numbers or aggregates of mast cells

y Metastatic melanoma y Melanin containing cells exhibit obvious criteria of malignancy

y Identification of the residual lymphoid population y Primary tumor vs. lymph node

y Important to aspirate the draining lymph node y Tumor behavior y Prognosis y May change therapeutic options

y P Perinodal Pe eeri rriin no od daal Fat Fat Fa y T The Th he majority maajjo orriity ty of of the tth he lymph lymp ly mph nodes no n ode des are aarre embedded eem mb beed dd ded d iin n de deep eep ep

maatss of m of fat fat mats

y Un Unless U Unle nlleess ss tthe h lymph he lym mph p node nod ode iiss significantly siig gni nif ifi fica cant ntly ly enlarged, enl nlaarrge rg geed d,, it it may maay

bee challenging b cha hallllen engi g ng gi g to to aspirate aassp piira rate te

y Salivary gland y Neighboring structure y Palpates similarly to lymph node y Clusters of epithelial cells y Mucin in the background

y Lymph node aspiration is an inexpensive, noninvasive

diagnostic tool

y Important prognostic and diagnostic information can

be obtained

Urine Collection Free catch/voided sample

Urine-Luck: A Thorough Review of Urine Sediment

Urinary catheterization Cystocentesis

Dr. Anne Barger University of Illinois

Gross Examination

Color

Normal color is yellow

Clarity

Red urine

Odor

Red blood cells or hemoglobin

Dark yellow to brown

Bilirubin

Reddish brown

Clarity Normal urine should be clear Cloudy urine may indicate an “active

sediment

Hemoglobin Myoglobin

Urine concentration Specific gravity Rough assessment of functioning capacity of tubules and collecting ducts Normal, wide range 1.001-1.065 Up to 1.080 in the cat

Urine Concentration Factors affecting specific gravity

Increases of 0.001 by the addition of a substrate to 1L of urine

2.7 g/dl glucose 4.0 g/dl protein 1.47 g/dl sodium 3.6 g/dl urea

Interpretation of Urine Concentration Remember, any specific gravity at one point

in time may be “normal” for that patient. Hydration status, presence or absence of azotemia and clinical signs must all be considered.

Interpretation of Urine Concentration Hydration status of patient must be considered If an animal is >3% dehydrated, ADH should have an effect on the renal tubules to concentrate the urine Hyposthenuria Specific gravity: 1.001-1.007 Isosthenuria Specific gravity: 1.008-1.014

Urine Chemistry Measured via reagent strip

Glucose

H+ concentration

Normal urine is negative for glucose

pH of urine varies with diet

Renal threshold for glucose

Carnivores: acidic Herbivores: alkalotic

Abnormal pH

Therapy Cystitis

Dog: 180 mg/dl Cat: 280 mg/dl Ruminant: <100 mg/dl

Glucosuria

pH Glucose Ketones Bilirubin Blood Protein

Fear- primarily cat Diabetes mellitus Glucocorticoid release

Ketones

Bilirubin

Normal urine is negative Positive result Starvation Diabetes mellitus Bovine ketosis Ovine pregnancy toxemia High fat diet Severe vomiting and diarrhea Ketonuria present before ketonemia Ketones Acetone Acetoacetone E-hydroxybutyric acid: Reagent strip is insensitive

Unconjugated bilirubin is bound to albumin

Blood

Test based on pseudoperoxidase activity of

Renal threshold for bilirubin is lower in the dog Any amount of bilirubin in the urine of cats is significant

Tests detect primarily conjugated bilirubin

Causes of hematuria

erythrocytes UA strips sensitive to RBCs, hemoglobin and myoglobin Hematuria vs. Hemoglobin vs. Myoglobin Hematuria: Intact red cells in sediment, red color of urine will clear when spun Hemoglobin: hemolyzed plasma Myoglobin: colorless plasma with concurrent increase in CPK, LDH and AST

Results from injury or disease of the urogenital tract Causes of hemoglobinuria Observed with intravascular hemolysis Lysis of red cells within the urine can also result in hemoglobinuria Vaden et al, Vet Clin Pathol 2004 showed that hematuria may not affect urine protein until macroscopic and 81% of dogs with pyuria had a normal UPC (<0.4)

Mechanisms of proteinuria

Definitions

Damage to the glomerulus

Loss of negative charge on basement membrane People, many hereditary diseases result from podocyte abnormalities Nephrin Podocin Damage to Tubules Tubulointerstitial disease prevents proximal tubules from reabsorbin low molecular weight proteins from the glomerular ultrafiltrate Over flow proteins Bence-Jones proteinuria

and does not pass through the glomerulus Conjugated bilirubin passes freely through the glomerulus

Proteinuria

>300 mg/l

Microalbuminuria

30-300mg/day or 20-200 mg/l Dog: 10-300 mg/L in urine normalized to a specific gravity of 1.010 (JAVMA 2006)

Proteinuria

National Kidney Foundation recommends that

Historically, 24 hour urine considered gold

an increase in protein excretion be used as a screening tool in patients at risk of developing renal disease (Am J Kidney Dis, 2002)

standard in assessment of protein excretion

Preeclampsia Diabetic nephropathy Drug toxicity

Variation of protein excretion throughout the day Use of creatinine can lessen this variability

Urine luck

Urine dipstick Urine protein to creatinine ratio (UPC) Urine albumin/creatinine ratio Microalbuminuria

Protein:Creatinine can be just as useful as 24 urine (Clin Chem 2005)

Whittemore et al, JAVMA 2004 Prospective study, evaluated 600 dogs Measured

UAC, UPC, and semiquantitative and quantitative Evaluated 408 dogs with a negative urine dipstick

48 healthy dogs Dogs with systemic disease were more likely to have a positive microalbuminuria The semiquantitative test was the most sensitive for detection of systemic disease 4% of healthy dogs had microalbuminuria

Urine Sediment

Epithelial cells

Cells in urine sediment

Squamous epithelial cells No clinical significance Distal urethra and urogenital tract Transitional epithelial cells Proximal urethra, urinary bladder, ureter, renal pelvis No significance unless neoplastic Catheterized samples may have clusters of transitional cells Renal tubular epithelium

Constant throughout the day GFR must be stable

Epithelial cells Red blood cells White blood cells

Sqames

TCC

Transitional epithelial cells

Red blood cells RBCs can be round or crenated Important to differentiate from fat droplets >4-5 RBCs/hpf considered significant

RBCs

Important to consider how sample was taken.

Lipid Droplets

White Blood cells

WBCs

WBCs are larger than RBCs and can lyse in

hypotonic or alkaline urine >5 WBCs/hpf are considered significant in the absence of blood contamination

Casts

Cast formation

Formed in the distal tubules The turds of the renal tubules Types of casts Hyaline casts Granular cast Epithelial cast Waxy cast

Indicate chronicity

RBC cast WBC cast

Granular G ranular aand nd w waxy axy ccasts asts

Hyaline cast

Waxy cast

Microorganisms Bacteria Sample collection very important for interpretation of bacteria If true pathogen, and not just contaminant, should see inflammation Fungi Generally considered a contaminant Parasites Stephanurus dentatus Capillaria plica Dioctophyma renale Microfilaria

Capillaria

Dioctophema renale

Capillaria

Fungal F ungal hhyphae yphae

Bacteria

Crystals Crystal formation affected by:

Crystals

Characteristics of Individual crystals

Crystals found in acidic urine

Ammonium biurate Liver disease, PSS Calcium oxalate Dihydrate Can be seen in normal urine and associated with urolithiasis Monohydrate Ethylene glycol toxicity Triple phosphate crystals One of the most common uroliths in cats Cystine Defect in amino acid transport of proximal renal tubule Calcium Carbonate Considered “normal” in horse and rabbit

Calcium oxalate Cystine Hippuric acid Sulfonamide

Crystals found in alkaline urine

Triple phosphate Ammonium biurate Calcium carbonate

Ammonium urates

Urine pH Temperature Medications given

Ammonium Urate

Calcium Oxalate

Triple T riple pphosphate hosphate

Cystine

Bilirubin Crystals

Calcium C alcium C Carbonate arbonate

Uric Acid

Other Structures Fat droplets Sperm Plant material or pollen grains

Questions

Companion Animal

Gary D. Norsworthy, DVM, DABVP (Feline) Alamo Feline Health Center San Antonio, Texas

Two Feline Enigmas Chronic Vomiting Diabetes Mellitus

Gary D. Norsworthy, DVM Diplomate, ABVP (Feline) Alamo Feline Health Center San Antonio, Texas January 25, 2020 Missouri Veterinary Medical Association Copyright 2020, Gary D. Norsworthy, DVM. Duplication of this material is prohibited without the written consent of Gary D. Norsworthy, DVM. Due to severe time limitations, Dr. Norsworthy is not able to offer telephone consultation services except for those who live in his geographic area and send referral cases to him. He apologizes that he must enforce this policy.

The Vomiting Cat

aka: Chronic Small Bowel Disease Gary D. Norsworthy, DVM, DABVP (Feline) Alamo Feline Health Center ♦ San Antonio, Texas

A. Overview a. Chronic vomiting is very common in cats, but we (veterinarians and owners) have either made excuses for it or accept it as normal using the following excuses: i. My cat eats too fast. ii. My cat has a nervous stomach. iii. It is just hairballs and they are normal. iv. “He’s just a puker,” i.e., it is normal for this cat. b. Most chronic vomiting and chronic diarrhea in cats originate in the small bowel, not in the stomach. c. Small bowel disease is segmental in over ¾ of cats. Areas of normal and abnormal alternate. It is important to examine the entire bowel to make proper biopsy site choices. d. Endoscopic biopsies are a poor way to diagnose most cases because: i. Location: You can access the stomach + 1-2 cm of duodenum OR colon (if you are really proficient with an endoscope. The ileum is very difficult to access, and most cases of lymphoma begin in the ileum. The cat’s small bowel is about 4 feet long. 1. Small bowel disease may be in any part of the small bowel, and it is usually segmental. In many cats only the jejunum is involved, and it is inaccessible by an endoscope. ii. Sample Size: about 1 mm piece of tissue; not full thickness. The pathologist is hindered by getting to only read small fragments of the mucosa. e. Chronic small bowel disease is manifested as chronic vomiting, chronic diarrhea, or both. B. What we are not talking about a. Vomiting of whole dry food is not due to eating too fast. Cats typically swallow 80% of the dry food they consume. b. Cats that eat grass vomit because grass is irritating to the stomach. They eat it because they like it. C. Typical history a. “My cat has vomited all of its life. The vomiting was occasional for months to years. Then it became 1-2 times per month. Now it is daily. Otherwise, he/she feels good and eats good.” i. Think small bowel, not stomach. b. “My cat has vomited hairballs all of its life. The vomiting was occasional for months to years. Then it became 1-2 times per month. Now it is several times per week. Otherwise, he/she feels good and eats good.” c. Alternative: “has been losing weight” “losing weight but has a tremendous appetite.” d. Differential list 1. Chronic Enteritis or Chronic Inflammatory Disease a. Due to known causes b. Inflammatory Bowel Disease 2. Neoplasia without mass formation a. Small cell lymphoma b. Large cell lymphoma c. Mast cell tumor d. Note: Mast cell tumor, adenocarcinoma, and large cell lymphoma can cause chronic small bowel signs, but a mass forms resulting in rapid weight loss and vomiting (partial to full obstruction). The mass is found by palpation, ultrasound, or surgery. 3. Food intolerance (less than 10%) D. Diagnostics a. When the clinical picture is presented to me I recommend: i. Small intestinal ultrasound looking for thickening of the small bowel wall. Use of a linear probe is highly recommended to get needed detail. ii. If the walls are thick (0.28 cm or more), I recommend a full-thickness biopsy of the small bowel via laparotomy. 67

iii. Possible exception: food trial first, but 6+ weeks are lost so you must consider the consequences of that. In some cats that is not a problem. In cats losing weight rapidly, that can be disastrous. b. Objections to this approach i. Cannot do ultrasound. ii. What an ultrasound study does: 1. Allow you to document small bowel thickening. 2. Allows the owner to see it. 3. Makes a laparotomy much easier to sell. 4. The laparotomy and biopsies get a diagnosis leading to specific treatment. 5. Pays for the ultrasound machine. c. Why palpation fails to get a diagnosis i. Mild to moderate small bowel thickening is not palpable. ii. Heavy cats are hard to palpate. iii. Segmental disease occurs. Small bowel biopsy technique a. You need a full-thickness sample. b. Cut out a wedge beginning on the antemesenteric side of the bowel. c. Alternate: 6 mm biopsy punch (***Much better sample than a wedge made with a scalpel.) d. Trim away excess mucosa so you suture muscle and serosa to muscle and serosa. e. Use simple interrupted through-and-through sutures of 4-0 PDS placed 1 mm apart. f. When the bowel is closed, test with a saline injection. g. Consider biopsy of the mesenteric lymph node if it is enlarged, but not a part of my current protocol. It is often misleading as LN may be inflammatory with lymphoma in small bowel. Triad disease (concurrent inflammation in the small bowel, liver, and pancreas) is reported to be common in the cat. During this laparotomy, get samples of the pancreas and liver. a. Pancreas: Examine both limbs of the pancreas. Biopsy an area that appears grossly abnormal. If there are no abnormal areas (likely), use a 4-mm biopsy punch to take a sample on the edge of the organ to avoid the centrally located exocrine duct; bleeding unlikely. b. Alternative Technique: Use a 4-mm biopsy punch to â&#x20AC;&#x153;scoopâ&#x20AC;? pancreatic tissue from the surface or edge of the organ. As above, avoid the exocrine duct. i. If bleeding occurs, use a clotting powder (HemaBlock [formerly Bleed-X] Vet Clotting Powder, DVM Solutions) ii. Because this is a very small sample, put it in a separate tube so it does not get lost during tissue processing. c. Liver: Cut a wedge of liver with scissors then close with (usually) one 4-0 PDS suture. Choose an area that appears grossly abnormal, but most cats with liver disease have diffuse disease so the location is usually chosen based on accessibility. Do not crush this tissue during the biopsy process or when handling the tissue. Biopsy sequence a. Remove the falciform ligament. b. Biopsy the liver. c. Biopsy the pancreas. d. Biopsy the duodenum. e. Examine the jejunum and the ileum from one end to the other. f. Biopsy 2+ sites but at least one each of the jejunum and the ileum. g. Check the pancreas and liver for bleeding. h. Close the abdomen. Miscellaneous observations and comments a. Enlargement of the mesenteric lymph node is not diagnostic or prognostic. i. A biopsy of the LN will not substitute for a full-thickness biopsy of the small bowel. Sometimes the LN will be inflammatory and the bowel wall neoplastic. ii. Biopsy of the LN rarely adds to the diagnosis; it is an optional procedure. iii. It is a friable organ; close it with mattress sutures. iv. Do not cut the mesenteric artery. Take a superficial biopsy. b. Mesenteric LN aspiration 3

e. f. g.

i. Enlarged mesenteric LNs are often found on ultrasound and often palpable. ii. They may be aspirated with or without ultrasound guidance in lieu of surgical biopsy of the small bowel. iii. Mesenteric lymph nodes were aspirated in 8 cats during surgery to determine correlation with LN cytology and histopath of the small bowel. iv. Expected finding: poor correlation with T-cell (small cell) lymphoma. 1. 85% of the cats with lymphoma in the study had small cell lymphoma. v. Total correlation: 1/8 correct. The two cats with lymphoma did not have lymphoma in the lymph nodes. vi. Unexpected findings 1. 6/8 had either very poor appetite or anorexia for 7-14 days post-op. a. Cause not determined but compromise of the mesenteric artery is suspected. Will result in compromised blood flow to the small bowel. 2. Concerning amount of bleeding in 2/8 cats. Norsworthy and Estep believe that this is one disease with a continuum. i. Mild inflammation – severe inflammation (IBD) – small cell lymphoma – intermediate cell lymphoma – large cell lymphoma. ii. The big question is: What starts the mild inflammation? 1. No firm answer at this time. 2. Considered: Dry cat food, grains in cat food, too many carbohydrates in cat foods, genetics. iii. Evidence 1. Age: The youngest cats we have diagnosed with small cell lymphoma are 6 years. The youngest cats with chronic enteritis are 2 years old. (N = 500) 2. The youngest cats we have diagnosed with small cell lymphoma are 6 years. 3. Cats are found with inflammation in the pancreas and/or liver but lymphoma in the small bowel. Was it Triad Disease that transformed in the small bowel? 4. Enteritis and lymphoma have been found in different parts of the same cat’s small bowel. 5. PARR testing is needed to differentiate enteritis from lymphoma in some cats. 6. Large cell lymphoma has been found at necropsy in cats histologically diagnosed with small cell lymphoma and treated. Treatment is often successful for several months then fails. Case Schedule i. Day 1: Surgery. ii. Day 2: Remove IV and offer food. iii. Day 3: Discharge if doing well. iv. Day 5-7: Get HP report and call owner. Send the appropriate handout regarding the disease and the treatment protocol. v. Day 10-14: Remove sutures; begin treatment. vi. Modifications for fractious cats 1. Induce with chamber (Wild Child, Veterinary Concepts). 2. Place IV catheter and begin fluids at 100 ml/hr. 3. Give IV fluids through the end of surgery. 4. Before extubation, remove IV catheter and give 150 ml fluids SC. 5. Offer food the next morning. 6. If doing well, discharge that afternoon. Small masses may accompany thickened loops and be very hard to find with palpation or ultrasound. If found, resect them. Take more than one biopsy as the disease is segmental. Often, some samples will be normal and some abnormal. Frequently, there will be enteritis in one or two and lymphoma in the others. This is more evidence that the disease has transformed from IBD to lymphoma. Hairball obstruction i. Chronic small bowel disease (IBD or lymphoma) can cause reduced small bowel motility. ii. This results in slower movement of hair through the GI tract. iii. This results in more vomiting of hairballs or hairball obstruction. 4

iv. When removing a hairball, biopsy the bowel about 3-4 inches aboral (downstream). 1. Expect to find that the cat has either chronic enteritis or lymphoma. h. Norsworthy’s thoughts regarding hairballs i. Hairballs can be normal due to normal shedding and the cat’s grooming behavior. ii. However, most chronic cases are a sign of chronic small bowel disease. iii. Therefore, ultrasound the small bowel. 1. If the US is normal, treat for hairballs – hairball diet, GI lubricants. a. If the response decreases over time, US the SI again. 2. If the US is abnormal, recommend surgery for small bowel biopsy. iv. Treating hairballs symptomatically can mask the signs of chronic small bowel disease. Our concern is allowing IBD to transform to lymphoma. v. Treatment options 1. Shave the cat’s hair every 3 months 2. Mineral oil – ONLY use it by putting it in the food. 3. Lubricants: Laxatone, etc. 4. Hairball diets 5. Capilex: www.bockvetpharma.com; Chewable; Not available on the Internet. i. Loss of layering of the bowel wall i. There is a strong correlation with neoplasia. ii. Occurs most commonly in large cell lymphoma and when a GI mass occurs. iii. Cats with GI infiltrative disease (especially small cell lymphoma) have normal layering. j. The stomach i. Can be the site of tumors and IBD and can be the source of vomiting. ii. When doing an ultrasound of the small bowel, look at the stomach also. k. Transformation i. There have been multiple publications that support the transformation of IBD to lymphoma. ii. Evidence is mounting that this happens. iii. However, it has never been definitely documented in the cat – yet. l. Acute on Chronic Vomiting i. Some cats will be presented for multiple vomiting events per day for 2-5 days. ii. Ask about the vomiting history for the past six months. iii. Acute on chronic vomiting is common in cats with chronic small bowel disease. iv. Don’t miss the bigger picture by treating an acute event. I. Histopathology Service a. J Scot Estep, DVM, DACVP (co-author on the JAVMA papers). b. Texas Veterinary Pathology c. (830) 237-2955 d. texvetpath.com e. 3-4 small bowel samples: $75; 3-4 small bowel samples + liver + pancreas = $125; includes FedEx. f. Ambiguous cases: an additional $70. J. JAVMA, Nov. 15, 2013: Diagnosis of chronic small bowel disease in cats: 100 cases (2008-2012); Norsworthy, Estep, Kiupel, Olson, Gassler. a. Findings i. Clinical signs 1. Vomiting only 61% 2. Diarrhea only 11% 3. Vom & Diarr 13% 4. Weight loss* 70% a. Most with vomiting or diarrhea. b. Many without vomiting OR diarrhea. ii. Diagnoses 1. Normal 1% 2. Chronic enteritis 49% 3. Adenocarcinoma 1% | 4. Mast cell tumor 3% | --- Neoplasia 50% 5. Lymphoma 46% | 70

a. Large cell = 15% b. Small cell = 85%

K. Client Response a. “Let’s go to surgery.” b. Rejection due to: i. Cat is too sick. ii. Cat is too old. (Oldest cat we have operated is 19 yrs.) iii. Cost: Either cannot afford or will not spend this much money on a cat. iv. Must check with spouse. (Real or excuse?) v. Disbelief. This is different than they have heard in the past, including from other veterinarians. vi. Will not spend this much money on this cat. c. Rejection rate 30%. i. Owner’s decision. ii. My decision or a joint decision. 1. Not a good surgical candidate. Recall that 50% have neoplasia, they are usually over 12 years of age, they have BCS of 1-3/9, and often have concurrent geriatric diseases. d. If rejection occurs. i. Caution: too much pressure can cause you to lose a client even though you are convinced that you are recommending the correct course of action for the cat. ii. Give handout material about chronic small bowel disease. 1. https://dl.dropboxusercontent.com/u/69563616/Intestinal%20Disease.pub iii. Do a food trial. 1. It might work although the chances of success are about 10%. 2. It keeps the owner focused on the problem for 6 weeks. If the food trial fails, there is a better chance surgery will be reconsidered. iv. Treat without a diagnosis. v. Do not bring it up next year. They may reconsider but let them take the initiative. L. Main messages a. Chronic vomiting usually originates in the small bowel. b. A full thickness biopsy is needed for diagnosis. c. Quit treating these cats for hairballs and get a real diagnosis. d. Untreated IBD probably has the ability to progress to lymphoma. M. Anesthesia and Surgery on Geriatric Cats a. Pre-Anesthetic Workup i. Good physical examination ii. Chemistry panel with electrolytes (and TT4) iii. CBC (or PCV) iv. Careful cardiac auscultation v. Single-lead ECG b. Anesthetic Induction i. Isoflurane (or sevoflurane) by face mask 1. In my practice, we do this 5-10 times per day. ii. Problems with face mask induction are due to 1. Wrong size mask (Jorgensen; 5.5” diameter). 2. Improper restraint. 3. Lack of cleanliness of the mask (smell of dogs). c. Medications i. Pre-op 1. Buprenorphine-SR (120 mcg/kg IM or SC) (www.srvet.net) or buprenorphine mucosal: 0.02 mg/kg IM or SC See Footnote. 2. Antibiotics: Convenia OR Baytril + ampicillin injectables 3. Fluids: IV ii. Intra-op 1. Atropine PRN for bradycardia (HR <90 bpm) iii. Post-op 1. Acepromazine for rough recovery 71

a. Dilute 1:10; 1 mg/kg concentration b. Give 0.05 mg/# IM or SC

d. Surgical Monitoring i. Parameters 1. Respiration rate * 2. Heart rate * 3. Temperature * 4. ECG tracing 5. Blood pressure 6. Pulse Ox 7. End Tidal CO2 ii. Equipment 1. VetGard (DVM Solutions; 1-866-373-9627) e. Temperature Control during Surgery: For Prevention of Hypothermia i. Warm IV fluids ii. IV Fluid wrap: Kennaâ&#x20AC;&#x2122;s Kreations; Small (fits 500 ml bag) - $45.00 plus shipping; Large (fits 1000 ml) - $50.00 plus shipping. kenna.mckenney@yahoo.com iii. Run the IV line between two beanies on its way to the cat. iv. Surgery table worming pad: ChillBusterVet (ThermoGear, Inc.; 1-503-697-1900) v. Beanies laterally to the cat. Caution: if too hot will burn the catâ&#x20AC;&#x2122;s skin. vi. Booties (for 6-12 month baby) on each foot to prevent heat loss from the pads. vii. Multiparameter surgical monitor that includes core body temperature. (VetGard; DVMSolutions.com) viii. Abdominal infusion of 100 ml of warm (100 F) saline for cats with end-surgery temperature below 97 F. Leave in the abdomen at closure. Caution: Some of the fluid will leak through the incision and be blood tinged from the bleeding of the liver biopsy. This is not active hemorrhage so do not re-operate the cat. ix. Warming pad (ChillBusterVet) in the recovery cage. x. Note: Extended surgery time will directly contribute to hypothermia. Our laparotomies are 1 hour from induction to extubation with 20 minutes from skin to skin. f. Body Wall Closure i. Needs to be secure and fast ii. Muscle 1. 2-0 PDS 2. Simple interrupted pattern about 1.0 cm apart 3. Simple interrupted (1.5 cm apart) + continuous pattern on top of simple interrupted. iii. Subcutaneous tissue 1. 4-0 PDS in continuous pattern iv. Skin 1. 4-0 Braunamid/Polymid 2. Ford interlocking pattern. g. Recovery i. Very rapid due to the anesthetic protocol used. ii. Wrap in warm bath towel iii. Beanies (if needed) and Chillbuster for warmth OR heating pad below the cage rack iv. Watch brachycephalic cats for airway obstruction during recovery. h. Post-op Protocol i. Continue IV fluids for 24 hours post-op and keep the cat NPO. ii. Then, offer food and keep the cat another night. iii. If the cat eats and does not spike a fever, it goes home on the second post-op day (after two nights in the hospital). N. Advanced Testing a. Immunophenotyping i. To differentiate B-cell and T-cell lymphoma. ii. Options 1. Immunohistochemistry 72

2. Flow Cytometry iii. Therapeutic Implications 1. Dogs have significantly better response to therapy if it is B-cell. 2. There is minimal to no difference in response for cats. 3. In our study, only 4% of the lymphoma cases were B-cell. (2/46) 4. Lymphoma caused by the FeLV is B-cell. (Once very common but not now.) b. PARR Testing (PCR for Antigen Receptor Rearrangement); Michigan State University; Dr. Matti Kiupel’s lab; he is the creator of this test. i. Differentiates small cell lymphoma from chronic enteritis. ii. Performed on “ambiguous” cases; these are defined by Dr. Estep in the JAVMA paper. iii. Definite therapeutic implications on how to treat and outcome. iv. Your pathologist should determine when this testing is needed; about 10% of the time. O. Therapy a. General prognoses a. Good: food reaction, inflammatory bowel disease, small cell lymphoma, mast cell tumor. b. Less Good: large cell lymphoma c. Bad: adenocarcinoma. b. Food reaction a. There is a technical difference in food allergy vs. food intolerance, but it is not clinically feasible to make the distinction. This distinction is skirted by using the term ‘food reaction.’ b. The HP will usually state “eosinophilic enteritis.” a. If the HP says that and the cat does not respond to a food trial, eosinophilic enteritis is more difficult to treat than other types. See below. c. As a rule, anti-inflammatories are not effective or may be effective for only a few days to weeks. d. Food trials based on novel protein diets (rabbit [Royal Canin], d/d duck [Hill’s], d/d venison [Hill’s]) or hydrolyzed protein diets (HA [Purina], z/d [Hill’s], HF [Blue Buffalo], HP [Royal Canin]). e. The food trial should go 6+ weeks before deeming it to be a failure. The cats MUST eat one or more of these diets EXCLUSIVELY for the food trial to be valid. c. “Chronic Enteritis” a. IBD is a diagnosis of exclusion. We must rule out known cause of chronic enteritis to justify a diagnosis of IBD. The histopath will be the same for the following. Eliminate each with therapy. a. Food allergy/intolerance: food trial (see above) b. GI Parasitism (Tapeworms, Physaloptera, Ollulanus, and Giardia): Droncit injection + oral fenbendazole 1. The quantity when using liquid Panacur liquid is too great 2. Compounded capsules or liquid: 50 mg/kg q24h PO 3. Roadrunner Pharmacy: recommended chicken marshmallow flavor. a. Very bitter drug; the marshmallow masks the bitter taste. c. Dysbiosis (formerly, bacterial overgrowth) 1. Metronidazole a. Compounded tabs: 50 mg q24h PO 2. Probiotic: FortiFlora (Purina) or Proviable (Nutramax) a. DO NOT USE DURING A FOOD TRIAL. d. Therapeutic trial schedule 1. Day 1-42+: Food trial 2. Day 1-5: Fenbendazole 3. Day 6-36: Metronidazole + probiotic 4. Recheck at 6+ weeks to assess success or failure. 5. Do not use steroids or do not use them past Day 30. b. Cobalamin (B12) a. Testing can be done (GI Lab, Texas A&M) OR treat every cat. 1. 1000 mcg/dose 2. Give SC 2X per week for 6 weeks then 3. Give SC 1X per week for 6 weeks. 4. Video on giving SC injections: https://www.youtube.com/watch?v=fKKxgXm3Fp8 73

b. Advantage of treating all is that vitamin B12 is a good appetite stimulant, which is a plus when changing a cat’s diet. c. Check list for therapeutic trials a. Hypoallergenic diet 1. Dry: RC Hydrolyzed Protein (HP), RC Select Protein Rabbit, Blue Buffalo NP, Blue Buffalo HF, Purina HA, Hill’s d/d duck, Hill’s d/d venison 2. Canned: RC Select Protein Rabbit, Blue Buffalo NP, Blue Buffalo HF, Hill’s d/d duck, Hill’s z/d b. Fenbendazole c. Metronidazole d. Vitamin B12 d. Inflammatory Bowel Disease a. Diagnosis made by eliminating the above causes of chronic enteritis. b. Diet: Change to a low-carb, high-protein diet and feed long-term 1. My preference: EN or DM. 2. Fancy Feast alternatives: https://dl.dropboxusercontent.com/u/69563616/Fancy%20Feast%20CHO%20DM.doc c. Cerenia: Can be given PRN to control episodes of vomiting. d. Immune suppressants 1. One of more of the following needed to suppress the over-reaction of the immune system. The goal is control not cure; therefore, treatment is needed long-term. 2. Corticosteroids: prednisolone 2 mg/kg q24h PO or Depo-Medrol at 20 mg q30d. a. Oral prednisolone preferred; less chance of inducing diabetes. 3. Alternatives if prednisolone not effective. a. Cyclosporine (Atopica): 25 mg q24h PO for 15-30 days then 25 mg q48h PO. May change to prednisolone for long-term control. b. Lomustine (CCNU): i. 6, 9, and12 mg capsules q28d PO. See below. ii. Monitor for neutropenia. iii. I use this if the wall thickening is great or there are eosinophils in the inflammation. iv. Give 2-3 doses with prednisolone or Depo-Medrol then continue with the steroid only. c. Apoquel i. 0.5-1.0 mg/kg BID ii. If not treating skin, this drug must be given BID. 4. Probiotic: FortiFlora (Purina) or Proviable (Nutramax) e. Laser therapy: Artemis by Epica Medical; greg@epicamed.com 1. Caution: Do not use in the presence of neoplasia; rule out lymphoma first. e. Lymphoma a. Success is remission, not cure. Remission is defined as lack of clinical signs. These cats will stop vomiting, eat well, regain their lost weight, and become very active. The small bowel walls should return to normal or near normal as documented by ultrasound. b. Short-term 1. Vitamin B12: 1000 mcg/dose a. SC 2X per week for 6 weeks then SC 1X per week for 6 weeks b. May be given long-term if it increases the appetite and make the cat feel better. c. Video on giving SC injections: https://www.youtube.com/watch?v=fKKxgXm3Fp8 2. Probiotic (FortiFlora or Proviable) for 30-90 days or long-term. 3. Vomiting control: Cerenia** or transdermal metoclopramide. c. Diet 1. Low-carb, high-protein diet preferred a. EN or DM (Purina) b. Should be fed long-term. 74

d. Chemotherapy Options 1. Prednisolone: 2 mg/kg q12h PO for +7-10 days then reduce slowly to 5-10 mg/cat q24h PO. Least expensive approach with fewest side effects; however, the least effective approach. If given alone for several weeks, the response to other chemo protocols may be reduced significantly. 2. Modified Wisconsin protocol: 15 treatments in 24 weeks using Modified CHOP) (Lasparaginase, vincristine, cyclophosphamide, chlorambucil, doxorubicin, prednisolone); first remission rate 68%; median survival time 225 days. See The Feline Patient editions 2-5 for specific protocol. The protocol of choice for most veterinary oncologists. 3. Chlorambucil + prednisolone: Chlorambucil (0.1 mg/kg q24h PO or 6-8 mg/m2 PO. The tablets should never be split so cats must take 2 mg q24h PO to q3d depending on the weight of the cat; Prednisolone (1-2 mg/kg q24h PO) a. Note that chlorambucil has been shown to cause Fanconiâ&#x20AC;&#x2122;s Syndrome in cats: glucosuria without hyperglycemia. This is considered a contraindication. 4. Lomustine + prednisolone a. Generally, not considered a first-line chemotherapy agent. It is usually given as a rescue drug to dying cats so its efficacy is considered poor. b. My treatment of choice for lymphoma (both) and mast cell tumors. c. Lomustine: (CCNU): See dosing chart below d. Depo-Medrol q4w (or oral prednisolone at 1-2 mg/kg q24h PO) e. Monitor for neutropenia. If it occurs, use the next lower dose of lomustine If neutrophil count falls below 1.0, delay the next treatment until neutrophil count is at least 1.5 (~ 2 weeks). In Norsworthyâ&#x20AC;&#x2122;s experience neutropenia occurs about 40% of the time, and the prognosis seems to be better in these cats. f. Dosing of lomustine Body Weight in Kg 2.0-3.0 3.1-4.5 4.6-5.9 6 or more

Mg of Lomustine 6 9 12 15

g. Other side effects i. Focal hair loss ii. Very slow regrowth of hair from surgery. (Very common) iii. Focal alopecia; any location. (Uncommon) h. Protocol: iv. Visit 1: CBC + administer lomustine + give Depo-Medrol at the time of stitch removal = 10-14 days post-op. 1. Also start vitamin B12, probiotic, LCHP diet. v. Visits 2-6: Recheck, CBC, & lomustine 4 weeks later. vi. Visit 6: Repeat ultrasound: measure small bowel wall thickness. i. Success is remission, not cure. vii. Vomiting stops viii. Good appetite ix. Weight gain (if weight loss initially) x. Good quality of life xi. Small bowel walls normal or greatly improved. j. At 6th dose xii. Explain that discontinuing lomustine will eventually result in relapse and that cats do not respond after relapse occurs. However, continuing long term results in permanent damage to the intestinal wall lining resulting in malabsorption. 75

xiii. Measure the small bowel wall. 1. If improved or normal and clinical signs are gone or much improved: 2. Give 2-4 more doses at 6 week intervals + Depo-Medrol then stop. Alternatively, continue prednisolone orally long-term. k. The capsule becomes very sticky when moist. xiv. Use a Pill Popper if needed for clean administration. xv. Give water with two 2X2 gauze squares (soaked in water) to prevent the capsule from sticking to the esophageal wall and causing an esophageal stricture. xvi. If pill becomes sticky, roll it in Corn Starch. l. Sources of lomustine xvii. Local pharmacies or veterinary distributors 1. CCNU 2. 10 mg capsules; bottle of 20 3. ~$200 per bottle/~$10 per capsule 4. When available xviii. Roadrunner Pharmacy (Phoenix) 1. Phone: (877) 518-4589 2. 6, 9, and 12 mg capsules available 3. ~$8.00 each (either size) m. Treating the fractious cat xix. Induce with isoflurane or sevoflurane using induction chamber (or face mask). xx. Draw blood and perform CBC. xxi. Pass a 12 Fr. red rubber catheter into the stomach. xxii. Put the contents of a lomustine capsule in 5 ml of water in a 6 cc syringe; shake well. Flush through the stomach tube. xxiii. Administer Depo-Medrol. xxiv. Cat will recover in 15 minutes and can be discharged immediately. e. Treatment without a confirmed diagnosis 1. The cat has the correct clinical signs, especially significant weight loss. 2. The small bowel walls are thickened according to U/S. a. Or, U/S not available. 3. Owner will not agree to a laparotomy for biopsies OR 4. The cat is not a good candidate for a laparotomy. 5. The odds are 95+% that the cat has either chronic enteritis or lymphoma. 6. I prefer to treat for lymphoma because both will respond to the lomustine + steroid protocol. 7. It is ESSENTIAL that you receive informed consent from the owner and document it in your records.

P. Take Home a. Chronic vomiting is VERY common in cats. b. It is so common that we have made excuses for it. c. Therefore, clients usually do not report it. d. You must ask about it. e. Chronic vomiting is not normal. f. Chronic vomiting originates from the small bowel, not the stomach 98% of the time. g. Chronic small bowel disease is segmental in most (about Âž) of cats. h. Proper biopsies need to be made in the proper locations, as determined by full bowel inspection (run the bowel). i. Proper biopsies need to be full-thickness. j. You can do it, and you should do it. These do not have to be referral cases. k. You can treat these cats, and you should treat these cats. They do not have to be referrals. l. You clients and your bottom line will appreciate it. 76

Q. Vaccinations during chemotherapy a. No veterinary reference available b. CDC: Recommendations of the Advisory Committee on Immunization (ACIP): Use of vaccines and Immune Globulins in Persons with Altered Immunocompetence. i. “Killed or inactivated vaccines do not represent a danger to immunocompromised persons and generally should be administered as recommended for healthy persons.” ii. “Frequently, the immune response of immunocompromised persons to these vaccine antigens is not as good as that of immunocompetent persons; higher doses or more frequent boosters may be required, although even with these modifications, the immune response may be suboptimal.” iii. “When cancer therapy or immunosuppressive therapy is being considered, vaccination ideally should precede the initiation of chemotherapy or immunosuppression by greater than or equal to 2 weeks.” iv. “Vaccination during chemotherapy or radiation therapy should be avoided because antibody responses are suboptimal.” a. What if long-term (maintenance) chemotherapy is used? c. Our dilemma i. Chemotherapy patients will be in our hospitals monthly. ii. Exposure to respiratory viruses is likely to occur. iii. FHV-1 is a very poor antigen. iv. It does not produce sterilizing immunity. v. Exposure results in infection and illness. vi. It has the shorted DOI of all of our major vaccines. d. My Plan i. Herpesvirus vaccine is the most important because it is the most common hospital pathogen. ii. Infection in an immunocompromised patient can be deadly. iii. Ideal: Give FVRCP > 2 weeks before starting and repeat every 6 months. iv. When boosters are due: a) Give FVRCP one week before the next dose: the best compromise of immunocompromise and immune response. b) Use a killed product. c) Do not give with other vaccines. Footnote: Buprenorphine SR by ZooPharm (www.zoopharm.net) Key Features of Buprenorphine SR™ - Provides sustained release delivery of Buprenorphine in a fully biodegradable liquid polymer matrix - Provides a consistent 72‐hour release profile with consistent drug absorption - Provides blood levels greater than 1 nanogram/mL for post-operative analgesia - Formulation can be injected subcutaneously through a 22‐gauge needle Pharmacokinetics Buprenorphine is metabolized by the liver, via CYP3A4 (also CYP2C8 seems to be involved) isozymes of the cytochrome P450 enzyme system, into norbuprenorphine (by N‐dealkylation). The glucuronidation of buprenorphine is primarily carried out by UGT1A1 and UGT2B7, and that of norbuprenorphine by UGT1A1 and UGT1A3. These glucuronides are then eliminated mainly through excretion into the bile. The elimination half‐life of buprenorphine is 20–73 hours (mean 37). Due to the mainly hepatic elimination, there is no risk of accumulation in patients with renal impairment.5 Buprenorphine's main active metabolite, norbuprenorphine, is a μ‐opioid, δ‐opioid, and nociception receptor full agonist, with a κ‐opioid receptor partial agonist. Buprenorphine antagonizes its effects. In an unpublished study, three dogs administered 270 ug/kg subcutaneously had plasma concentrations that rose rapidly reaching average Cmax of

2.14 ng/mL at an average Tmax of 1 hour. Notably average plasma concentration remained over 1.0 ng/mL from under 1 hour to over 72 hours post injection. A recently published study in the Journal of the American Association for Laboratory Animal Science, tested this sustained‐release formulation of buprenorphine in rats for analgesic efficacy and plasma concentration over a 72‐h time period. Rats were injected subcutaneously with either 1.2 mg/kg sustained‐release formulation (Bup‐SR), 0.2 mL/kg buprenorphine HCl (Bup‐HCl) and tested in a thermal nociception model or a surgical postoperative pain model. In both models, Buprenorphine‐SR showed evidence of providing analgesia for 2 to 3 d, reporting plasma concentrations of buprenorphine remaining over 1 ng/mL for 72 h after a single dose.6 A pilot study conducted in domestic cats was designed to determine if the sustained release Buprenorphine SR™ formulation was equivalent to repeated doses of transmucosal administration of the commercial preparation Buprenex™ over a period of 72 hours. Animals received either a single, subcutaneous injection of Buprenorphine SR at a dose rate of 120 mcg/kg, or a transmucosal dose of buprenorphine HCl [Buprenex™] every 12 hours for 72 hours. Results from analysis of blood samples [obtained at 1, 4, 8, 12, 18, 24, 36, 48 and 72 hours], reported data showing that only the single‐dosed Buprenorphine SR cats maintained therapeutic blood levels for 72 hours.7 No visible injection site irritations or clinical side effects were reported within both test groups.7 5. Moody DE, Fang Lin SN, Weyant DM, Strom SC, Omiecinski CJ. Effect of Rifampin and Nelfinavir on the Metabolism of Methadone and Buprenorphine in Primary Cultures of Human Hepatocytes. Drug Metab Dispos December 2009 37:2323-29. 6. Foley PL, LiangH, Crichlow AR. Evaluation of a sustained release formulation of buprenorphine for analgesia in rats. JAALAS Vol 50, No 2, March 2011, 198–204. 7. Pilot Study: Comparison of sustained release buprenorphine and transmucosal buprenorphine in cats.

Recommended Fancy Feast Products

Fancy Feast Can Cat Savory Salmon Fancy Feast Can Cat Creamy Delights Salmon Pate with Real Milk Fancy Feast Gourmet Salmon and Shrimp Feast Fancy Feast Can Cat Cod, Sole, & Shrimp Fancy Feast Can Cat Seafood Feast Fancy Feast Can Cat Beef & Liver Fancy Feast Can Cat Beef Pate Canada Fancy Feast Can Cat Ocean Whitefish & Tuna Fancy Feast Can Cat Tender Liver & Chicken Fancy Feast Can Cat Turkey & Giblets Fancy Feast Kitten Turkey Fancy Feast Can Cat Gourmet Chicken Fancy Feast Kitten Ocean Whitefish Fancy Feast Can Cat Beef & Chicken Fancy Feast Can Cat Chopped Grill Fancy Feast Can Cat Tender Beef Fancy Feast Can Cat Chunky Chicken Feast Fancy Feast Can Cat Medleys Pate White Meat Chicken Primavera with Garden Veggies and Greens Fancy Feast Can Cat Medleys Pate Salmon Primavera with Garden Veggies and Greens Fancy Feast Can Cat Medleys Pate White Meat Chicken Florentine with Cheese and Garden Greens Fancy Feast Can Cat Salmon & Cheddar Cheese Fancy Feast Can Cat Chunky Chopped Grill 55.4 % 6.1 % Fancy Feast Can Cat Medleys Pate Ocean Whitefish & Tuna Florentine with Cheese and Garden Greens Fancy Feast Can Cat Flaked Trout Fancy Feast Can Cat Chunky Turkey Feast Fancy Feast Can Cat Flaked Salmon & Ocean Whitefish Fancy Feast Can Cat Flaked Chicken & Tuna Fancy Feast Can Cat Medleys Souffle White Meat Chicken & Whipped Egg Fancy Feast Can Cat Flaked Tuna Fancy Feast Can Cat Medleys Souffle Wild Salmon & Whipped Egg Fancy Feast Can Cat Flaked Tuna & Mackerel Fancy Feast Can Cat Medleys Souffle White Meat Chicken & Cheddar Cheese Fancy Feast Can Cat Roasted Turkey Fancy Feast Can Cat Roasted Beef Fancy Feast Can Cat Mornings Souffle Wild Salmon Garden Veggies & Egg Fancy Feast Can Cat Mornings Souffle White Meat Chicken Garden Veggies & Egg Fancy Feast Can Cat Mornings Souffle Turkey Garden Veggies & Egg Fancy Feast Can Cat Roasted Chicken *Percentages are on a dry matter basis Revised 12-18

Protein* Carbs* 54.1 % 1.7 % 54.2 % 2.3 % 54.3 % 2.4 % 61.1 % 2.5 % 58.4 % 3.2 % 52.0 % 3.3 % 53.8 % 3.4 % 59.9 % 3.5 % 55.0 % 3.6 % 53.3 % 3.9 % 51.8 % 4.1 % 53.0 % 4.1 % 54.5 % 4.2 % 51.4 % 4.3 % 52.9 % 4.7 % 54.5 % 4.9 % 57.8 % 5.3 % 52.1 % 5.4 % 53.3 % 5.4 % 50.0 % 5.7 % 51.4 % 6.0 % 55.7 % 60.8 % 56.3 % 60.5 % 62.3 % 57.4 % 62.4 % 58.5 % 65.1 % 56.4 % 65.2 % 62.7 % 55.8 % 56.5 % 57.1 % 62.8 %

6.1 % 6.1 % 6.2 % 6.3 % 6.7 % 7.4 % 7.4 % 7.5 % 7.6 % 7.7 % 8.2 % 8.6 % 8.8 % 8.8 % 8.9 % 9.4 %

Increasing Acceptance of Laparotomies Gary D. Norsworthy, DVM, DABVP (Feline) Alamo Feline Health Center We averaged 2.1 laparotomies per week during 2012 through 2016. However, it took us four years to get to that level. See Figure 1. It took most of those four years to make the connection between “normal vomiting” and small bowel disease. After a few laparotomies with histopathologic confirmation of our suspicions, we became more and more confident that we would get an answer if we could just do the biopsies. During those four years, we also learned to appreciate the segmentality of chronic small bowel disease (CSBD) and appreciate how important it is to have access to the entire small bowel so biopsies could be taken at the correct locations. Although endoscopic biopsies had been my primary approach to the vomiting cat, I realized the limitations (and folly) of getting a biopsy from 1-2 inches of duodenum when the small bowel in the cat is about four feet long. How to Get Consent to do a Laparotomy 1. After nine years and 600 laparotomies we are absolutely convinced that a laparotomy to do multiple full-thickness biopsies of the small bowel and to biopsy the liver and pancreas is the correct way to diagnose cats with chronic small bowel disease and its associated diseases. That is the first step in getting clients to let me do surgery. I can speak with authority because the data is there. See references 1 and 2. Note that in the second paper we looked at ways, other than surgery, to differentiate chronic enteritis and lymphoma. We could not find a single way short of laparotomy that is reliable. 2. After the client admits that the cat vomits twice per month to daily, he or she will have one or more of four excuses: 1) The cat eats too fast. 2) The cat has a sensitive stomach. 3) The cat vomits hairballs and that is normal. 4) The cat is “just a puker.,” i.e., it is normal for this cat. Without being confrontational, do not agree with these excuses. If you do, the discussion stops. 3. Owners are more likely to permit a laparotomy if they have visual evidence that a problem in the small bowel really exists. Watching performance of the ultrasound study is the best way to do this. Find a clearly visible loop of bowel and point out the lumen and the four wall layers. Note that the wall should be 0.25 cm or less in thickness. Also note that most cats have some normal measurements and some abnormal measurements (segmentality) so finding normal measurements does not rule out the presence of disease. 4. As the abnormal ultrasound findings become apparent, explain that thickened small bowel loops have two differentials: chronic inflammation (call it IBD) and lymphoma. IBD is much like Crohn’s Disease, and we do not know the cause of it or IBD. (What we are saying is, “If MDs do not know the cause of Crohn’s Disease, it is OK if DVMs do not know the cause of IBD.”) Both look the same on ultrasound, and both produce the same clinical signs. 5. State that if chronic enteritis is present, the walls will be packed with inflammatory cells. (This statement sets you up for needing to have the cells examined by a pathologist.) However, if lymphoma is present, the walls will be packed with lymphoma cells. (Don’t use the term ‘cancer’ at this point in the discussion.) 6. State that differentiation requires a microscopic examination of the small bowel walls by a pathologist, and the segmental nature of the disease requires that we get samples from the correct locations. These are determined after inspection of the entire intestinal tract. 7. State that knowing the exact diagnosis directs the treatment approach. 8. State that both diseases have very good treatment protocols, and even many cats with lymphoma can survive many years after just a few months of treatment.

9. State that we have mounting evidence that cats with IBD may transition to lymphoma as some people with Crohn’s Disease later develop lymphoma. Failure to act increases the likelihood that this will occur. Also state that many cats with IBD will go years before this transition. If you do not state this, the owner may jump to the conclusion that an older cat has lymphoma and request treatment without biopsies or even euthanasia. 10. State that the lymphoma protocol using lomustine has minimal, if any, side effects. Many owners know the side effects of chemotherapy and will reject chemotherapy prematurely. State that the treatment is given only every four weeks and given orally and that the cat is not hospitalized for the treatments. 11. Avoid using three terms too often or prematurely. A) Chemotherapy. Rather, refer to having a “drug” or a “treatment” for lymphoma. After getting across the positives (lack of side effects, only given monthly, an oral treatment, no hospitalization needed) should you use the C word, if at all. B) Surgery. The invasiveness of this can be scary. As much as possible, talk about “collecting tissues,” “doing biopsies of the organs,” a rapid recovery with the cat going home after surgery as if nothing happened. However, do not leave them the false impression this is not surgery or is non-invasive. C) Cancer. This word often denotes hopelessness or a very hard struggle associated with treatment. Instead of using this term, say lymphoma. To us, there is not difference, but to many clients there is a big difference. We do not want our clients to let negative thoughts stop communication. 12. As they begin to seriously consider surgery, state that cats handle this kind of surgery MUCH better than we would. Note that they appear virtually normal the day they are discharged from the hospital. 13. Reiterate that we will have a comprehensive treatment plan because we are biopsying the small bowel, liver, and pancreas. 14. Schedule the ultrasound study and surgery as soon as possible. If we do the exam and ultrasound study in the morning (before our surgery time) and the schedules permits, we tell the owner that we can do surgery TODAY. If we must delay it until tomorrow, we recommend admitting the cat to the hospital now so we will be ready to go tomorrow morning. Buyer’s remorse is a very powerful force. If the cat goes home and is to return for surgery, the chances of a No Show are significant. 15. Dr. Todd Tams says: “Offer Plan A and keep your mouth shut.” This is a powerful selling technique. After offering Plan A, the course of action will be determined by the one (you or the client) who speaks first. If you speak first and offer Plan B, the client will take that. If the client speaks first, Plan A will be accepted. Objections to Surgery & Treating Without a Diagnosis The most common objections to surgery are 1) the cat is not a good surgical candidate, 2) the owner has financial limitations, and 3) it is too invasive for the owner. One or more of these often lead to a request for treatment without biopsies. Usually the owner asks to treat for IBD to see what happens. The problem with this approach is that putting a cat with lymphoma on a course of steroids will usually achieve response to both diseases so you cannot use response to differentiate them. In addition, and more importantly, lymphoma cats will have a temporary response followed by drug resistance. Subsequently, these cats do not respond well to the chemotherapy drugs. If the client refuses surgery or if the cat is really not a good surgical candidate, treatment should still be considered. Although no veterinarian really wants to do this, it has its place. A food trial with a hypoallergenic diet is a reasonable approach unless spending six to eight weeks could be detrimental to the cat. If the cat has lost significant weight, this may not be a good approach. If a food trial is not performed or fails, medical treatment is still feasible with informed consent. My preference is to treat for lymphoma knowing that cats with IBD will respond to that approach. However, the problem comes in knowing when to stop treatment. I strongly prefer to stop after eight doses of lomustine, and I do not continue using steroids after that. If the cat has IBD, the clinical signs will return when treatment is discontinued. One could argue that if that occurs, putting the cat on steroids would be appropriate, and I would agree with that in most cases. It should control IBD, and it would not be harmful to the cat with lymphoma.

References 1. Norsworthy, GD, Estep JS, Kiupel K, Olson JC, Gassler LN. Diagnosis of chronic small bowel disease in cats: 100 cases (2008â&#x20AC;&#x201C;2012). JAVMA, 243(10): 1455-1461. 2. Norsworthy GD, Estep JS, Hollinger C, Steiner JM, Lavallee JO, Gassler LN, Restine LM, Kiupel M. Prevalence and underlying causes of histologic abnormalities in cats suspected to have chronic small bowel disease: 300 cases (2008-2013). JAVMA. 247(6): 629-635.

Laparotomies by year from 2008 through 2017 performed at Alamo Feline Health Center for cats with suspected chronic small bowel disease. Average 2012-2017: 111 per year or 2.2 per week.

The Diabetic Cat: Don’t Let it Get the Best of You Gary D. Norsworthy, DVM, DABVP (Feline) Alamo Feline Health Center ♦ San Antonio, Texas

1) The Big Picture a) Diabetes often occurs in the presence of other diseases, most of which cause insulin resistance. b) We need to deal with them, so we can manage diabetes well. c) Diabetes is due to i) Lack of insulin production ii) Insulin resistance d) To be successful we must treat both aspects of this disease. e) To do that we must look for and resolve causes of insulin resistance. i) Obesity (1) RX: low carb high protein weight control diet with measured portions ii) Chronic pancreatitis. (50% of newly diagnosed diabetics have an elevated fPL.) (1) Antibiotics? (2) Anti-inflammatories (a) Cerenia: 6 mg/d (b) Denamarin: 1/d (c) Prednisolone: 2.5-5 mg/d (d) Cyclosporine: 25 mg/d iii) Periodontal disease. (1) RX: Teeth cleaning; after 2-3 weeks of treatment but before regulation occurs. iv) Bacturia (1) Incidence: Norsworthy study = 6%; ABVP Diplomates = 6% (2) RX: Antibiotics – Convenia a very good choice. v) Other infections (1) RX: Antibiotics – Convenia or oral fluoroquinolone 2) Tight Control Approach a) Ref: Roomp & Rand; J Feline Medicine & Surgery, August 2009 b) Why needed? i) In Germany and Australia (authors’ homes) a veterinary product must be used first is one is available. ii) Veterinary insulin available: Caninsulin (same as Vetsulin); has a DOA of 8 hours. iii) The authors felt the need for a longer acting product because of the short DOA of Caninsulin. iv) The only choice available: glargine (Lantus) v) There was no protamine zinc insulin available in those countries. c) Protocol i) 55 diabetic cats were treated with a tight glucose control protocol (1) 209 owners of diabetic cats that were in the German Diabetes-Katzen Forum were solicited to participate. (2) 117 were eligible and began the study (3) 62 (53%) dropped out in less than 10 weeks for non-compliance (4) 55 completed the study (26% of those solicited to participate and 47% of those that were eligible and began the study). (5) Home glucose testing daily (6) Glargine (7) Ultra-low, carbohydrate diet; not dry. d) Results i) 84% went into diabetic remission if the protocol was started less than 6 months after the diagnosis was made or they had been on steroids prior to the onset of diabetes. (Note: This is misleading because many cats with steroid-induced DM will go into remission when steroids are withdrawn even if they are not put on insulin.) e) Details of the protocol i) Diet: ultra-low carbohydrate diet (1) Less than 10% metabolizable energy from carbs (2) Canned only (3) Most were commercial diets (4) Some were home-made or raw meat diets. ii) Insulin (1) Glargine (a) The only long-acting insulin available in Germany (site of study).

iii) Glucose Testing (1) Glucose values were determined daily by the owner using a human glucometer (2) An algorithm was given to the owners to direct dose changes. (3) Acceptable BG = 80-200 mg/dl. (4) The average number of glucose tests performed per days was 5. (a) Range of 3-7. (b) At least 3 times per day was required to remain in the study. f) My assessment i) This study shows that diabetes in cats can be well controlled or eliminated (remission) under ideal circumstances of an ultra-low carbohydrate diet, a long-acting insulin, and a rigid protocol. iii. My assessment: 1) Interesting, 2) Not sustainable, 3) Risky (hypoglycemia) iv. Gostelow, Forcada, Graves, et al. Systematic review of feline diabetic remission: Separating fact from fiction. The Veterinary Journal, 2014; 202: 208-221. i. This study has a serious selection bias. ii. 56% of the cats were steroid-associated and accounted for 47% of all remission cases. ii) Perspectives from Boarded Feline Practitioners (1) On September 18, 2014 ten ABVP Feline Diplomates participated in a Diabetes Roundtable Discussion held in conjunction with the AAFP meeting. It was convened by Dr. Elaine Wexler-Mitchell who sent the following email: “I don't know about you, but I feel frustrated about treating feline diabetes, and when I go to CE seminars and look up information on VIN, I don't agree with a lot of the recommendations. I have asked several other feline specialists about their experiences with feline diabetes, and I think others are frustrated too and not seeing the type of responses being presented in academia. At my practice, we have been reviewing our feline diabetic patients over the past few years and were surprised to see that more than 50% were not well regulated based on currently "accepted criteria." i. Many ABVP Diplomates responded. Here are two: i. “I also think ‘tight control’ measures are great for the unemployed...But, one trip to the ER with a hypoglycemic cat is $1500.00 overnight in my area.” ii. “My remission rates are also not that high. Did try a tight aggressive regulation right at diagnosis. Patient in remission and in hypoglycemic crisis in 5 days. So not as aggressive initially now.” 3) Traditional Approach a) Diagnosis i) Diagnostic triad: hyperglycemia, glucosuria, and appropriate clinical signs ii) Confirmed with fructosamine. b) Management i) Insulin (glargine) and a low carbohydrate diet are started, and the cat is discharged for home treatment. (1) Some hospitalize the cat to get it regulated. ii) The owner monitors the cat’s blood glucose 2-14 times per week per your instructions. iii) The owner calls for recommendations on dosage changes based on numbers gathered at home (home glucose testing). iv) The cat is checked by you: (1) 1-4 times during regulation. (2) Every 3-6 months thereafter. (3) Anytime the home glucose numbers are outside 100-300 mg/dl (5.5-16.5 mmol/L). (4) Each recheck includes a glucose curve and possibly a fructosamine. The average cost is $300-500 for the recheck. v) The Goal: Remission vi) The Expectation: bG 100-300 mg/dl vii) The cat lives happily ever after. 4) Loose Control Approach a) Why I searched for an alternative: i) Too many euthanasias due to the financial and personal commitment required of owners, hypoglycemic episodes, and home monitoring demands on the owner and the cat. ii) I was frustrated because I had patients that seemed to be doing well but had terrible blood glucose values. iii) Owners fed on my feelings and got discouraged, leading to more euthanasias. iv) I saw a disconnect between clinical signs and blood glucose values. (1) Cats with “unacceptable” numbers (bG=400-500) were doing great and owners were happy. v) I became frustrated with glucose curves. (1) Many/most were not “curves.” vi) I had been using PZI since I graduated in 1972. I tried other insulins but saw no improvement in glucose numbers. I always went back to PZI.

vii) Then I read this quote from Feldman and Nelson: “Glycemic control is attained when clinical signs of diabetes have resolved, the cat is healthy and interactive in the home, its body weight is stable, the owner is satisfied with the progress of therapy, and, if possible, the blood glucose concentrations range between 100 and 300 mg/dl throughout the day.” Veterinary Endocrinology, Feldman and Nelson, 1996, p.363 viii) My Response (1) I continue to use PZI. (2) I discontinued the use of glucose curves. (3) I paid more attention to the cat if there was a conflict between the cat and the blood glucose levels. (4) Data from the ABVP Diabetes Roundtable

Remission Became diabetic post remission Longevity for Survivors (days) Home Glucose Testing Became Hypoglycemic (% of treatment days) Ate LCHP Diet Insulin

Loose Control (GDN) N=76; 27% of total 30% 18% 472 2.8% 0.06 74% PZI = 92%

Traditional Approach N=206; 73% of total 25% 41% 438 26.7% 0.13% 43% Glargine = 77%

b) Restine-Norsworthy-Kass Study Canadian Veterinary Journal. 2019;60(4);399-404. i) Loose-control of diabetes mellitus with protamine zinc insulin in cats: 185 cases (2005-2015) (1) The published DM study with the highest N. (2) The published DM study with the longest duration. (3) All cats on protamine zinc insulin (ProZinc). ii) Remission Rate 56.2% (1) Including 20 cats that were euthanized or died in the first 3 days after diagnosis (20 cats; 10.8% of the N); with the 20 cats excluded, the rate was 63%. iii) Hypoglycemia during treatment: 10/185 (5.4%) (1) This is about 50% of the rate of all others in the ABVP Roundtable Discussion. (2) This is expected since we are keeping BG levels higher than other treatment approaches. iv) Rate of DKA (1) 18/185 (9.7%); 11 (5.4%) at time of DM diagnosis (2) DKA during treatment: 7/185 during treatment (3.8%) (3) This low level was not expected since we are keeping BG levels higher than other treatment approaches. (4) Cats tolerate hyperglycemia much better than other species. v) Survival: 0-3,808 days; median = 1,488 days; Includes the 20 cats that died or were euthanized in the first 3 days. vi) Survival (1) Factors favoring longer survival (a) Low carb diet (b) Occurrence of remission (c) Lack of DKA at diagnosis (d) Lower mean BG during treatment (e) Lower BG at diagnosis vii) Remission (1) Factors favoring remission (a) Lower mean BG during treatment (b) Lower mean insulin dose during treatment (c) Steroid-induced diabetes viii) Other Findings (1) 15 cats had diabetic neuropathy at diagnosis – all resolved. (2) Bacturia at diagnosis: 3.7% (3) DKA occurred in 15 cats (a) 10 at diagnosis (5.4%) and 5 during treatment (2.7%) (b) Conclusions (i) The occurrence of DKA during treatment was expected to be much higher due to the higher tolerated blood glucose levels.

(ii) Cats tolerate hyperglycemia much better than dogs (don’t go into DKA as readily) (iii) Do cats really have glucose toxicity? c) Diagnosis using Loose Control (1) Diagnostic Triad: hyperglycemia, glucosuria, clinical signs of PU/PD/PP/WL (2) If questionable: Fructosamine OR Repeat labs in 1-2 weeks. (3) Reveals Two Groups (a) Borderline Diabetics: bG < 400 + clinical signs + glucosuria (about 10%) (b) Overt Diabetics: bG > 400 + clinical signs + glucosuria (about 90%) d) Regulation: Borderline Diabetics i) Address insulin resistance (1) Convenia (2) Treat pancreatitis PRN (3) Correct periodontal disease ii) Low carb high protein diet iii) No insulin iv) Recheck q2-4-6w to determine remission, continuance, or overt diabetes (1) In all three situations, continue LCHP diet. e) Regulation: Overt Diabetics i) Address insulin resistance. (1) Convenia (2) Treat pancreatitis PRN (3) Correct periodontal disease ii) LCHP diet iii) Protamine zinc insulin (ProZinc): ~ 2 units per cat q12h SC (1) Video on giving SC injections: https://www.youtube.com/watch?v=fKKxgXm3Fp8 iv) Recheck in 5-10 days (1) Weight – compared to last weight taken (1 week ago) (2) Thirst, urine output, appetite – compared to last and to normal (3) “How is the cat feeling?” Subjective answers but very important (4) Check bG at 6 or 12 hrs. post insulin without fasting.

6 hrs. Post Insulin Nadir Predicts Hypoglycemia Better Less Predictable Clients Less Available Considered the Ideal Time

12 hrs. Post Insulin Peak Predicts Hyperglycemia Better More Predictable Clients More Available 95% of Our Rechecks

(a) How rigid is 12 hours? (i) 10-14 hours is acceptable but extrapolate if not 12 hrs. (ii) One solution: Have the owner give the last dose 12 hours before the recheck even if that is not exactly the time insulin is normally given. v) Rechecks during regulation process (1) Every 5-14 days (a) It takes about 5 days of a constant dose to get repeatable numbers. (2) Same questions as above (3) bG at 12 (or 6) hours (4) Adjust insulin dose PRN vi) Rechecks: Long term (1) ~ every 4-6 weeks (2) ~ 1-2 weeks if dose is changed (3) Same questions (4) bG at 12 (or 6) hours (5) Adjust insulin dose PRN. Insulin Adjustments (General Rules!) i) Remember that General Rules always have exceptions. Don’t turn your brain off when using General Rules. ii) Consider and factor in the Stress Factor. (1) How long was the drive to get to my office? (2) How did the cat act during the drive? (3) Did it urinate or defecate? 21

(4) Is it showing aggression to me and my staff? (5) Look at the heart rate, respiration rate, and for dilation of the pupils. iii) It is always better to underdose than to overdose. iv) Adjust the dose slowly and conservatively. v) Cats tolerate bG of 400-500 mg/dl much better than you were taught and better than dogs or humans. vi) Adjustments are largely based on clinical signs. vii) If the clinical signs conflict: (1) Weight trumps others (2) Don’t ignore marked PU/PD. (3) Exception: If glucose is < 300 mg/dl viii) Caution: You do not always get correct information from clients (1) 3 reasons client give unreliable answers (a) They don’t know the answer due to lack of effort; they won’t admit it or they will appear to be irresponsible cat owners. (b) They don’t understand how to get the answer but don’t want to admit it. (c) They don’t want to be scolded by the veterinarian for the cat not doing well. (2) Therefore … (i) Weigh the answers carefully (ii) Weigh the cat. 1. WL trumps the other clinical signs because it is measured objectively. 2. It is specific to this cat. 3. Note: WL can be due to other situations: hyperthyroidism, WL diet, etc. ix) Be aware of Pancreatic Rebound (1) As the insulin dose increases, more beta cells become functional again. (2) Increasing the dose too rapidly can result in hypoglycemia. (a) Due to return in pancreatic function. (b) Due to onset of remission. x) Dose changes (1) Based on 12 hour rechecks. (2) Consider clinical signs when interpreting the BG level. (3) Ideal: 300-350 mg/dl. (4) Good: 350-400 mg/dl (5) Usually good: 400-450 mg/dl xi) If the blood glucose is below the ideal (1) 250-300 mg/dl (a) Clinical signs will be very well controlled (i) If not, check the glucometer (b) Reduce by 50%. (c) Recheck in 1-2 weeks. (2) 180-250 mg/dl (a) Clinical signs will be gone, and the owner will be extremely happy. (i) If not, check the glucometer. (b) Reduce the dose by 50% (c) Recheck in 1 week: remission is possible. (3) < 180 mg/dl (a) Stop insulin for 2-4 days then recheck bG to see if the cat is still diabetic. (i) Any time of day is acceptable because the cat is not getting insulin (ii) If bG < 200: No insulin; remission is present. (iii) If bG 200-300: Cat has not decided yet. No insulin; recheck in 1-2 weeks. (iv) If bG > 300: Resume insulin at 50% of prior dose. (b) Diet: If bG is stopped, continue the LCHP diet to reduce or delay recurrence. xii) If the blood glucose is above the ideal (1) 400-500 mg/dl and the clinical signs are controlled. (a) No dose change. (b) Consider stress hyperglycemia (i) Fructosamine OR (ii) Recheck in 2 weeks. (2) 400-500 mg/dl and the clinical signs are not controlled (especially weight). (a) If dose is 1-3 units: increase by 0.5 units per dose. (b) If dose is 3.5+ units: increase by 1.0 unit per dose. (3) 400-500 mg/dl

(a) Always increase the dose conservatively. (b) Recheck in 1-2 weeks. (c) Adjust again conservatively. (4) 500-600 mg/dl (a) Do not panic. (b) Is the cat stable? (i) Eating well, hydrated, bright and alert, interactive with the family? (ii) If you are nervous, check for ketonuria (DKA) or a bG at About 6 hrs. (Somogyi). (c) Continue as prior instruction above based on clinical signs. (d) Do not over-react by raising the insulin dose too much. (i) You may induce hypoglycemia. (e) Go up slowly and down rapidly! Review of studies on diabetic remission: Systemic review of feline diabetic remission: Separating fact from opinion. Gostelow R, Forcada Y, Graves T, Church D, Niessen S. The Veterinary Journal, 2015. a) “Twenty-two studies were included in the review.” b) “The current level of evidence was found to be moderate to poor.” c) “No single factor predicts remission and successful remission has been documented with a variety of insulin types and protocols.” d) “Dietary carbohydrate reduction might be beneficial but requires further study.” e) “A lack of well-designed trials prevents reliable remission rate comparison.” Remission bottom lines a) Remission is desirable; it results in longer survival. b) However, it is not essential for long survival with very good quality of life for the cat and the owner. c) Not achieving remission is not failure. The glucose curve a) JAVMA 2/1/03: “Although the serial blood glucose curve appears to be a useful test for distinguishing levels of glycemic control in a group of diabetic dogs, it seems to be an unreliable clinical tool for evaluation of insulin dose in individual diabetic dogs. There was marked disparity between the theoretical recommendations for dose adjustment based on the curves obtained on consecutive days, particularly in dogs with lower minimum blood glucose concentrations, which represented those with better glycemic control.” b) JAVMA 4/1/07: There was high variation in nadir, time to nadir, maximum bG, and mean bG. There was no difference in home and clinic results. Paired home curves were in agreement in 6/14 cats (43%). c) Five Minute Veterinary Consult, Diabetes Mellitus without Complications, Cats; 3rd, 4th, and 5th editions. (D. Greco): “Glucose curve – not helpful in cats.” Insulin Choices a) Lente (Vetsulin® – United States; Caninsulin® – Canada, Europe, New Zealand, and Australia) i) 100% pork; therefore, best for dogs. (1) Approved in dogs first, but has been approved in cats. ii) U-40 concentration iii) Intermediate acting: ~8 hour duration of action b) NPH (Humulin N®) i) Also intermediate acting: ~8 hour duration of action ii) Human origin; possibility some antibody reactions that inactivate the insulin. c) Protamine Zinc (ProZinc®) i) Made by Boehringer-Ingelheim ii) U-40 concentration iii) A recombinant product – no antibody formation. iv) My insulin of choice for 40 years. v) Our cost: $82.60 per bottle vi) Our retail: $118 per bottle (1) Permits sale to most clients; we sell about 25 bottles per month (X $35 = $875/mo.). vii) Gives excellent results permitting me to treat many diabetics for many years and to address the other health issues as they age. viii) Compounded PZI: JAVMA 3/1/12 (1) Problems found in 11/12 compounded products: lack of expiration date or lot number on the vial, lack of identification of the species of origin, unacceptably high endotoxin concentration, pH above or below the recommended range, low total insulin concentration, zinc concentrations below or above acceptable limits, variability in insulin concentration, unacceptably high concentrations of insulin in the supernatant. d) Glargine (Lantus®) i) Initial interest based in Europe and Australia where the law requires the use of a veterinary product if one is available. The only one was Caninsulin, a lente product with a duration of action of about 8 hours. 23

ii) When a longer acting insulin was needed, the only one available was glargine; there was no PZI product available. iii) Many cats have a good response so it is widely used. iv) U100 product v) Do not dilute it because any change in pH inactivates the product. vi) Currently sells for ~$250-300 per bottle. vii) A recombinant product: no antibody formation. viii) Observations by Jacquie Rand (website) (1) “For many cats, the time at which the nadir (lowest) glucose concentration occurs is often not consistent from day to day, or between cats. Sometimes it occurs between the two doses, but sometimes the nadir occurs around the time of the next dose.” (2) “Most commonly the highest glucose concentrations occur in the morning and the lowest in the evening.” (3) “Some cats consistently have their nadir glucose concentration in the evening just before the next insulin injection, and less commonly, it occurs around the time of their morning injection.” ix) What does a BG tell you? (1) The peak and the nadir are not predictable like PZI. (2) When do you test and how do you interpret the results? (3) What is the most meaningful test for a cat on glargine? Ans: Fructosamine x) Pharmacodynamics of Insulin Detemir and Insulin Glargine Assessed by an Isoglycemic Clamp Method J Vet Intern Med 2010;24:870-874. (1) “The average time-action curve (Fig. 1K) suggests that both analogs are relatively flat curves. Considering the individual time action curves, however, it is clearly not safe to assume that either insulin detemir or insulin glargine is long-acting and flat in any given patient. Fig. 1A-J.” (2) The duration of action in 50% of the cats in this study was less than 12 hours. (3) The duration of action of 30% was equal to or less than lente. xi) Glargine in humans (1) Used as a background insulin. (2) Short-acting and intermediate-acting insulins are given several times per day on a PRN basis. (3) It was not designed to be the sole insulin product for diabetic humans. (4) About 3% of humans experience significant pain at the injection sites because it has a pH of 4. e) Detemir (Levemir®) i) A “cousin” drug to glargine. Works in much the same way. ii) Hoelmkjaer, Spodsberg, Bjornvad. Insulin detemir treatment in diabetic cats in a practice setting. JFMS, 2015; 17(2): 144-151. (1) Fourteen cats were treated for at least 3 months. (2) 13/14 achieved moderate or excellent control of symptoms in 3 months. (3) 3 achieved remission in 3 months; 1 more at 13 months. (4) The remission rate was 29%. (5) “Improvements in clinical symptoms were markedly better than indicated by blood glucose and serum fructosamine concentrations.” (a) “Controlled” based on BG levels: 11% (b) “Controlled” based on clinical signs: 57% (6) Based on these results detemir can be recommended for the treatment of diabetic cats.” (7) These cats were essentially treated using a loose control approach. The assessment of remission was based on clinical signs and not on BG levels. 9) Report from the ABVP Roundtable on Feline Diabetes; AAFP Newsletter, Feb. 2015 “Unfortunately, we don’t know as much as we’d like about what goes on metabolically and physiologically with our diabetic cats. Insulin and a consistent diet best control the disease, but some cats actually survive reasonably well with minimal care. We thought the studies from academia were giving us hope for better control using glargine insulin and obtaining diabetic remission, but in reality the majority of cats need loose regulation of their blood sugar and more attention to their weights, water consumption, and urination. Based on our findings we believe that veterinarians and owners need to rethink and focus on the diabetic cat’s quality of life and not just his blood sugar values.” Elaine Wexler-Mitchell, DVM, DABVP (Feline) 10) Feline Diabetes Roundtable Discussion: J Fel Med Surg. 2015;17(11):967-969. “This is the first published discussion of treatment outcomes managed in primary care settings by ABVP boarded practitioners. All of the participants were well informed on the ‘gold standard’ approach to feline diabetes. The realities of primary care practice were imposed on the individual treatment protocols, and the participants believe the outcomes represent what is commonly found in primary care practice. The roundtable was created in response to a survey of all ABVP feline diplomates regarding treatment of feline diabetes. The consensus of those who responded was that we are not achieving

expected remission rates; nor are we finding the reported good control of hyperglycemia with insulin glargine. The participants wanted to share their own clinical experiences with feline diabetes and allay the sense of incompetence that was felt when their feline diabetic remission rates were only 25-30%. The practice identified as P3 [Norsworthy’s] was notable because with its loose control protocol it achieved as good or better results in all categories monitored. It placed more emphasis on clinical signs than on BG values. The insulin of choice in this practice was PZIR, and home BG testing was not employed. The rate of clinical hypoglycemia was 50% that of the rest of the participating practices.” 11) Summary a) Tell the Owner i) This is a marathon, not a sprint. Be patient. ii) It is always better to underdose than overdose. iii) We will not attain a stable long-term dose. Rechecks are necessary. iv) Consistency is the key to success. (1) … without quitting your job. (2) But, it will take dedication. This is not a casual disease. b) Key Points i) Realize that DM is due to: (1) Lack of insulin production. (2) Insulin resistance. ii) Diagnose and treat underlying diseases that cause insulin resistance. iii) Put dual emphasis on: (1) Clinical signs (UP/PD/PP/WL) (2) Glucose levels iv) Tolerate reasonable hyperglycemia if the clinical signs are controlled. (1) Clinical signs are more important than glucose levels. v) No glucose curves. vi) No home BG testing by owner. vii) No glargine or lente; all ProZinc viii) Infrequent use of fructosamine ix) Owners feed, inject, and observe. x) I decide on changes based on patient exams. xi) There is more than one right way to treat this disease. xii) Be open-minded to the loose control approach. (1) Try it on a few newly-diagnosed diabetic cats. (2) You might be surprised how well it works.

June 17, 2014

To the Diabetes Management Roundtable:

I am writing to share my positive experience using Dr. Norsworthy’s loose control. Let me first give background on myself. I am 5 years out of veterinary school and have completed a small animal rotating internship at Alameda East in Denver and have since been in private practice and emergency medicine for four years, the last two years of which were in feline specialty at Dr. Norsworthy’s Alamo Feline Health Center in San Antonio. Prior to working with Dr. Norsworthy at AFHC, I managed diabetic cats with more traditional approaches: inhospital and at-home glucose curves, fructosamine, and with patients on either glargine or ProZinc. I had owners discouraged by costs of glucose curves or costs of phone consults about curve results, as well as frustration with the frequency of re-checks. I had some owners take the reins with at-home glucose testing and start dose-adjusting at home without my consult. On emergency, I saw hypoglycemic and DKA kitties. Let me first say, there are many similarities between the traditional and loose approaches: emphasis on diabetic diet, monitoring water intake and urination at home, monitoring appetite and energy level, monitoring body weight, and controlling clinical signs. Using loose control, I find that I see my patients on a semi-regular basis - tolerable to both me and the owner but that we are managing the whole cat, rather than just the glucose. This sounds so common sense – of course we want to manage the whole cat – but I feel that with at-home or in-hospital glucose curves, we found the client’s and my attention shifting to the “numbers.” With loose control, cats come in weekly during regulation and when dosage changes are made, but then every 4-6wks weeks when clinical signs are well controlled. These re-checks are timed to be about 12 hours after a dose of insulin which is when the cat is just coming due for the next dose. We run an inhouse glucose; we collect a sample from the median saphenous vein and have the tech run the number on a glucometer out of the exam room (to keep client’s from getting ideas about taking the reins). We discuss diet, appetite, body weight, and clinical signs, each as much as the glucose number, and put all of it together. I feel that by using ProZinc in this protocol we have achieved repeatable positive results. Being a microbiology major in undergrad, I was skeptical of using a short course of empirical antibiotics in newly diagnosed diabetics, but I must convey that in doing so, patients seem to respond well. Another important point is that we proactively look for concurrent treatable conditions (e.g. dental disease, UTI, pancreatitis) and address as needed. I have had several patients go into remission or be much easier to regulate after a professional dental cleaning. Based on my emergency experience, I feel strongly that avoiding a hypoglycemic crisis, as this can lead owners to a euthanasia decision. This protocol is very good at preventing hypoglycemia – woohoo! On the flip side, the complications associated with hyperglycemia are uncommon. For example, I have had patients that had diabetic neuropathy and plantigrade stance at the time of diagnosis, and then improved and resolved with treatment – which I was told would be attributable to good regulation! As I set my sights on owning and running my own feline specialty hospital, I will continue to use the loose approach as I see it as win-win-win-win: good for the cat, good for the owner, good for my sanity, and good for the hospital! Jen Olson Lavallee, DVM Castle Rock, CO

Companion Animal

Amber Ihrke, DVM, DACVSM

Integrative Pet Care of Homer Glen â&#x20AC;&#x201C; Medical Director Homer Glen, Illinois

Introduction to Rehabilitation– Improving Mobility Amber Ihrke, DVM American College of Veterinary Sports Medicine and Rehabilitation - Resident Integrative Pet Care of Homer Glen – Medical Director Introduction: Veterinary rehabilitation is a rapidly growing and exciting field. The recognition of how rehabilitation benefits our patients is becoming more widespread and if we think of this specialty as the science of improving mobility, it can be argued that rehabilitation can benefit most every patient. Pet owners are seeking out this benefit on their own and learning the indications for rehabilitation is a win for the patient, the client and the practitioner. Goals of Rehabilitation: The goal of rehabilitation is primarily to decrease pain and restore function to injured or maladapted tissues. These goals are as follows: 1. Decrease pain and restore function 2. Improve Range of motion 3. Improve strength and endurance 4. Conditioning and weight loss 5. Improve and prolong quality of life. These goals are achieved by collaborating with the clients, the primary care veterinarians, and specialty veterinarians to achieve the best outcome for the patient. The rehabilitation team: The rehabilitation team can consist of a combination of veterinarian, veterinary technician and/or physical therapist. The veterinarian is the leader of the team and ideally each member of the rehabilitation team has post-graduate training and certification in veterinary rehabilitation. Each practitioner must check with their state practice acts to determine what type of training and licensing is needed to practice on animals. The training can be pursued at one of the various programs: 1. The Healing Oasis – www.thehealingoasis.edu 2. The Canine Rehabilitation Institute – www.caninerehabinstitute.com 3. Northeast Seminars – www.neseminars.com Additionally, both veterinarians and veterinary technicians have a pathway to achieve specialist designations. 1. American College of Veterinary Sports Medicine and Rehabilitation – www.vsmr.org 2. Academy of Physical Rehabilitation Veterinary Technicians – www.aprvt.com

Types of rehab patients: All patients can potentially benefit from rehabilitation; the scope and intensity of the treatment will differ dramatically depending on your patient. There is something for everyone! • puppies, • seniors, • athletes • working dogs • pre-operative, post-operative and non-operative patients • neurologic patients • obese patients The Rehabilitation Exam: As with all aspects of veterinary medicine the findings of your physical exam and the resulting diagnosis form the basis for your treatment approach and plan. The rehabilitation exam focuses heavily on the musculoskeletal and neurologic systems. Tools used during the rehabilitation exam can be had for a minimal investment: 1. Goniometer 2. Gulick Tape measurer 3. Reflex Hammer 4. Pen Light Advanced diagnostics that can be utilized: 1. Stance Analyzer 2. Force plate gait analysis 3. Digital Thermal imaging 4. Musculoskeletal Ultrasound Primary Therapeutic Modalities The primary modality of therapy for the rehabilitation practitioner is your brain and hands. Advanced modalities are ALWAYS based on acuity and are employed to PREPARE the patient for the primary plan components of manual therapy and therapeutic exercises, NOT to replace the primary components. 1. Pharmacologic Management a. Multimodal management of different pharmacological classes to address pain. 2. Nutrition a. Assist with weight loss b. Supplements 3. Manual therapy a. Massage b. Advanced manual techniques c. Dry needling techniques for trigger points 4. Therapeutic exercises

a. Tailored exercise program for the patient that allow for strength training, weight shifting and proper return to function. Advanced Therapeutic Modalities 1. Therapeutic Laser a. Specific light wavelengths that can work on a cellular level to aid in healing and provide analgesia 2. Thermotherapy b. Cold packs, hot packs, cold compression c. Benefits of heat – Vasodilation, pain relief, warm up tissues prior to stretching d. Benefits of cold – Vasoconstriction, pain relief, anti-inflammatory 3. Electrical Stimulation a. TENS – mostly for short term pain relief b. NMES – creates a muscle contraction to address muscle atrophy 4. Pulse Electromagnetic Field Therapy a. Pain relief modality used mostly as an at-home therapy 5. Therapeutic ultrasound a. Use of sound waves to heat deeper tissues to allow for manual therapies 6. Hydrotherapy a. Underwater treadmill or a therapy pool 7. Extracorporeal Shockwave Therapy a. Use of shockwaves to induce biological responses that produce therapeutic effect in clinical application 8. Regenerative medicine a. Platelet Rich Plasma b. Stem Cells 9. Assistive devices a. Carts b. Orthotics and Prosthetics In summary, learning the art and science of veterinary rehabilitation and sports medicine can be a rewarding and beneficial addition to your practice. Pursuing post-graduate training in rehabilitation or building a relationship with a rehabilitation trained veterinarian in your area can be a major benefit to your patients.1-6

1. Zink C, VanDyke, J. B. Canine Sports Medicine and Rehabilitation: Wiley Blackwell, 2013. 2. Millis DL, Levine, D. Canine Rehabilitation and Physical Therapy: Elsevier, 2014. 3. Brunke M. Non-Walking to Walking: Introduction to Rehab. VMX 2019;762-764. 4. LoGiudice RJ. Starting to Practice Rehabilitation Veterinary Medicine - Itâ&#x20AC;&#x2122;s more than an underwater treadmill. Southwest Veterinary Symposium 2018 2018. 5. Brunke M. Treadmills and the Latest Rehab Tools. VMX 2019;765-768. 6. Dycus DL. Back to the Basics: What is Rehabilittion and How can it Benefit Your Patients? Pacific Veterinary Conference 2018 2018.

Rehabilitation and Osteoarthritis in Canines – a Multimodal Approach to Patient Care. Amber Ihrke, DVM American College of Veterinary Sports Medicine and Rehabilitation - Resident Integrative Pet Care of Homer Glen – Medical Director Introduction Osteoarthritis is the most common cause of chronic pain in dogs, affecting up to 20% of adult canines. This progressive and degenerative condition mostly affects diarthrodial joints and as the degenerative process continues, this can lead to joint failure. The consequences of this failure can limit activity, decrease performance, cause pain and discomfort and decrease the quality of life for the patient. Recognizing early signs of osteoarthritis combined with a multimodal treatment approach that includes a comprehensive rehabilitation plan can lead to improved outcomes for your patient. Normal Joint Anatomy and the Pathophysiology of Osteoarthritis1 The main components of a diarthrodial joint are as follows 1. Joint capsule – the fibrous tissue that surrounds the joint and contributes to the stabilization of the joint 2. Synovial membrane – this forms the capsular enclosure of the joint and is made up of Type A synoviocyte that are primarily responsible for immune surveillance within the joint and type B synoviocyte that are primarily responsible for production of hyaluronic acid, proteoglycans etc. The synovial membrane is where the pain of OA begins. 3. Articular Cartilage – Hyaline cartilage that receives nutrients and cleans waste products by movement of fluid under the influence of weight bearing. 4. Synovial fluid – This fluid is similar in makeup to plasma and the exchange of fluid between the articular cartilage and synovial fluid is the major route by which nutrients are delivered to chondrocytes 5. Subchondral Bone – A thin layer of bone that joins the hyaline cartilage with cancellous bone supporting the bony plate. This bone plays a major role in the distribution of forces across the joint. Once there is an injury to the joint a cascade begins of mechanical and biochemical events that lead to cartilage destruction, subchondral bone sclerosis, synovial membrane inflammation and periarticular osteophyte formation. The Lameness Evaluation2 In order to have a complete picture of the patient, a thorough and systematic lameness evaluation must be performed to arrive at diagnosis. This evaluation consists of 5 parts: 1. Signalment – The signalment includes breed, age, weight, gender and neuter status (and age of time of neuter). These factors can be helpful due to the prevalence of certain orthopedic diseases associated with particular ages and breeds of dogs.

2. History – A complete history is vital. An owner questionnaire prior to the visit can be useful in gathering information about the pet and help in determining client goals. If the case is a referral, previous records can give important information that the client may not recall. Other important information such as medication history and efficacy, previous activity level vs. current activity level, and how the patient performs routine activities today vs. prior to injury/illness should be included in your history. 3. Gait analysis – Watch the patient walk around the room in a relaxed state (this is usually done while I’m talking over the history with the client). Watch the patient at a walk and at a trot if possible. Evaluate transitions and how the patient performs a stand to sit to down to stand transition. Use a lameness scale to quantify any lameness. (See Table 1)3 4. Physical and Orthopedic exam – A general physical exam should not be overlooked and can help determine if something other than orthopedic disease (i.e. neurologic dysfunction) is the primary cause of the problem or perhaps a contributing factor. Decide where you would like to perform your exam – on the table or on the floor. Initially assess for muscle atrophy, asymmetry, joint swelling, muscle tenderness and areas of heat. Use the CREPI system to evaluate joints: Crepitus, Range of motion, Effusion, Pain, Instability. Most importantly, go slow, avoid causing pain and if the patient is painful, use a pain scale (See Table 2). 5. Diagnostics – Once the evaluation is complete, diagnostics can be chosen based on your exam finding. Radiographs are the primary diagnostic tests related to orthopedic disease, however musculoskeletal ultrasound, advanced imaging (CT, MRI), joint taps, bloodwork can also be important in reaching a diagnosis. If osteoarthritis is diagnosed, document the stage. (See Table 3) Table 1: Lameness scale4,5

100

Grade

Description

No detectable lameness

Barely perceptible lameness

Mild or inconsistently apparent, weight bearing lameness

Moderate, obviously apparent, weight bearing lameness

Severe, predominantly weight bearing lameness

Severe, predominantly non-weight bearing lameness

Table 2: Pain scale for OA6 Pain Score

Description

Mild behavior changes, mild discomfort, possible lameness/gait changes

Behavior changes noted, mild lameness/gait change. Pain response on joint manipulation.

Overt behavior changes noted. Reluctance to move. Obvious lame/gait changes. Moderate pain on joint manipulation

Significant behavior changes. Significant lame/gait changes. Guarded or reactive to handling. Overt pain on joint manipulation. Sedation may be needed.

Depressed. Significantly lame, Reactive to handling/touch. Severe pain with joint and region. Sedation required.

Table 3: Stages of Osteoarthritis â&#x20AC;&#x201C; COAST7

101

Stage

Description

0 1 2

No risk factors At-Risk dogs; may detect subtle clinical signs Intermittent, obvious sign; obvious impairment of ability to perform certain daily activities; consistent, obvious alterations in body carriage and the beginning of apparent muscle loss

Consistent impairment of form and diminished capacity to engage in activities of daily living

Mobility impairment; clearly diminished ability to move or jump relative to previous normal activity

Treatment Plan – A multimodal approach A multimodal approach is key when treating a patient with osteoarthritis. Depending on the diagnosis and severity of the disease, the treatment plan may include any or all of the following components: 1. Pharmaceutical management8,9 a. NSAIDS are the cornerstone of treatment for osteoarthritis and the front-line defense for alleviating pain. b. Adjuvant medications (i.e. gabapentin, amantadine) c. Disease modifying osteoarthritis medications (i.e. Adequan) 2. Dietary modifications10 a. Weight optimization is crucial for our OA patients and adjusting their caloric intake is an important first step. b. EPA-rich diets c. Glycosaminoglycans supplements and omega-3 fatty acid supplements have been shown to be helpful in reducing inflammatory mediators in the joint. 3. Rehabilitation2,11 a. The rehabilitation plan’s primary components will always consist of i. Environmental modifications, ii. Cryotherapy and/or thermotherapy iii. Manual therapy and iv. Therapeutic exercise. b. Advanced modalities i. Photobiomodulation (therapeutic laser) ii. Hydrotherapy iii. Therapeutic ultrasound iv. Extracorporeal shockwave therapy v. Pulse electromagnetic field therapy (PEMF) REMEMBER: Advanced modalities are ALWAYS based on acuity and are employed to PREPARE the patient for the primary plan components of manual therapy and therapeutic exercises, NOT to replace the primary components. 4. Intraarticular Therapies – used to decrease pain and inflammation, promote cartilage function and assist healing in osteoarthritis patients. 12 a. Regenerative Medicine i. Platelet rich plasma (PRP) ii. Stem Cells b. Hyaluronic Acid c. Corticosteroids

102

References: 1. Fox SM. Multimodal Management of Canine Osteoarthrits: CRC Press, 2017. 2. Zink C, VanDyke, J. B. Canine Sports Medicine and Rehabilitation: Wiley Blackwell, 2013. 3. Lane D. Where Does it hurt? A Case-Based Approach to Lameness Diagnosis. VMX 2019. 4. Palmer RH. The Art & Science of the Canine Lameness Exam. VMX 2019;687-690. 5. Huntingford JL. Where is the pain? How to improve your orthopedic and lameness examinations and find out where they hurt. VMX 2019;728-731. 6. Caninearthritis.co.uk. 2019. 7. Canine Osteoarthritis: Optimizing Diagnosis and Disease Management: Clinicianâ&#x20AC;&#x2122;s Forum, 2017. 8. Papich MG. The Changing Toolbox ofr Canine OA Pain Management. VMX 2019;747-750. 9. Epstein M, Rodan I, Griffenhagen G, et al. 2015 AAHA/AAFP Pain Management Guidelines for Dogs and Cats. Journal of the American Animal Hospital Association 2015;51:67-84. 10. Wynn SG. Diet Therapy for Osteoarthritis. VMX 2019;553-554. 11. Millis DL, Levine, D. Canine Rehabilitation and Physical Therapy: Elsevier, 2014. 12. Brunke M. Is PRP Magic Pixie Dust? VMX 2019;759-761 .

103

104

Neurologic rehabilitation – Common Conditions treated in a rehab practice Amber Ihrke, DVM American College of Veterinary Sports Medicine and Rehabilitation - Resident Integrative Pet Care of Homer Glen – Medical Director

Introduction Rehabilitation of the patient with neurological disease works toward the goal of independent function. This is achieved by addressing pain, reestablishing normal neural pathways and preventing secondary complications. Success with neurological rehabilitation begins with adequate analgesia, as a comfortable patient is relaxed, cooperative and can have a faster and more complete recovery. A multimodal approach to pain management that includes analgesic and anti-inflammatory medication in conjunction with rehabilitation modalities are often utilized for the best results. Restoring function is primarily accomplished via a combination of therapeutic exercises and manual therapies. Exercises can include assisted standing, walking, and hydrotherapy. Manual therapies can relieve some of the secondary complications including shortening of ligaments and tendons, muscle atrophy and contracture, and pressure sores that may occur secondary to immobility, recumbency and altered biomechanical stresses. Intervertebral Disc Disease Intervertebral disc disease (IVDD) is an extrusion (Hanson Type 1) or protrusion (Hanson Type 2) of the intervertebral disc that can occur in all breeds of dogs. Hanson Type 1 is a chondroid metaplasia and occurs in chondrodystrophic breeds. Hyaline cartilage replaces the nucleus and further degeneration leads to calcification. This leads the disc to loss of the disc to absorb normal compressive forces. The increased rigidity in the nuclear leads to tears in the annulus and extrusion of the nuclear material into the IVDD space. Hanson Type 2 is a fibrous metaplasia that occurs in nonchondrodysplastic breeds. This begins around age 4-5 and slowly progresses. This is most commonly seen in large dogs. The fibroid degeneration and weakening of the dorsal anulus produces a domeshaped mass that can compress the spinal cord and /or irritate the meninges. The lifetime prevalence of IVDD in all dogs is 3.5% with a mortality rate of 1%. Dachshunds have the highest risk of IVDD with a 20% chance of exhibiting signs in their lifetime. Clinical Signs Symptoms of Intervertebral disc disease will depend on the location of the injury and is commonly seen in small breed dogs in their middle to older years with Beagles and Dachshunds being most at risk. C2-C3 is the most common site, but any disk can be affected. Cervical disease can present as: • Neck pain • +/- lameness on one or both thoracic limbs • Ataxia, paresis or paralysis in all limbs • Normal to exaggerated spinal reflexes Thoracolumbar intervertebral disease is overrepresented in Dachshunds, Cocker Spaniels and Beagles and can have a sudden or gradual onset. The most affected areas are T12-13 and L1-2 with approximately 10% exhibiting back pain but no neurological defects. Thoracolumbar disease can present as: • Reluctance to run, jump or climb stairs

105

• • • •

Kyphotic posture Mild ataxia of the pelvic limbs to paraplegia with absent deep pan +/- urinary and fecal incontinence Normal to exaggerated spinal reflexes but can be weak to absent caudal to L3.

Rehabilitation plan Depending on the severity of the clinical signs and with discussion with the client, IVDD can be managed medically or surgically. Some patients may start with medical management, but if the symptoms cannot be improved may move to a surgical treatment plan. Medical management is usually reserved for the patients that have little to no neurologic deficits and is can include: • Pain management • Restricted activity • Harness recommendation instead of leash • Environmental modifications at home (i.e. no stairs) • Manual therapy • Thermotherapy • Therapeutic exercises • Electrical stimulation • PEMF • Photobiomodulation • Hydrotherapy Post-operative rehabilitation is staged based on the neurologic presentation during the initial exam. Managing expectations and communicating the prognosis with the client is extremely important when rehabbing the post-operative IVDD patient. Post-operative rehabilitation can begin immediately to help with muscle spasm and pain and a conversation about nursing care (discussed later in these proceedings) of a paralyzed dog is imperative to the overall health of the patient. The post-operative patient can receive all the same modalities, when appropriate, as the medical management patient. If, however, the patient will be unable to achieve independent mobility, the practitioner can discuss carting options with the client. Degenerative Myelopathy Degenerative myelopathy (DM) is a progressive, general proprioceptive ataxia and upper motor neuro and lower motor neuron spastic paresis of the pelvic limbs that ultimately leads to paraplegia and euthanasia. If affects middle aged to older dogs with no sex predilection. It is considered a multisystem disease involving central and peripheral motor and sensory axons. DM is a heartbreaking progressive disease that is over represented in German shepherds, Corgis, Boxers and Chesapeake Bay Retrievers. Most of the affected patients progress to nonambulatory paraparesis within 6-9 months. Clinical Signs The early stage of the disease is characterized by generalized proprioceptive ataxia/paresis in the pelvic limbs which is usually asymmetrical. There is no paraspinal hyperesthesia but there is usually abnormal toenail wear in the rear feet. The spinal reflexes are consistent with UMN abnormalities. In the late stage of the disease, there in LMN paraplegia that will ascend to the thoracic limbs. There is widespread neurogenic atrophy, urinary and fecal incontinence and in very late stages cranial nerve abnormalities. Degenerative Myelopathy will present as: • Stage 1 - Asymmetrical spastic paraparesis and general proprioceptive ataxia

106

• • •

Stage 2 - Progressing to nonambulatory paraparesis/paraplegia with pelvic limb lower motor neuron (LMN) signs Stage 3 – Neurologic deficits progress to include thoracic limb weakness Stage 4 – Flaccid tetraplegia, generalized muscle atrophy, and brainstem dysfunction1

Rehabilitation Plan: The goal of rehabilitation in the DM patient is to keep them independently mobile for as long as possible and then successfully transition them to a cart if that is an option for the client for the remainder of the patient’s life. The rehabilitation treatment plan may include: • NMES • Therapeutic exercise • Manual therapy • Environmental modification • Weight management • Hydrotherapy • Carts Managing the client’s expectations about the long-term poor prognosis and having constant dialogue about the progression of the disease is helpful when working with DM patients. Geriatric Onset Laryngeal Paralysis and Paresis (GOLPP)2 GOLPP is a condition the affects mostly medium to large breed dogs with Labrador Retrievers overrepresented. The age distribution is 8-13 years of age with the average being 11 years old. This disease is the loss of large caliber nerve fibers and axonal degeneration that is thought to be part of a generalized polyneuropathy. This type of degeneration is not painful, and the affected dogs are still bright, alert and happy when presented. Clinical Signs • Increase in noisy breathing, most noticeable when panting • Distressed breathing when excited or stressed • Exercise intolerance • Bark changes • Hind end weakness and unsteady gait • Loss of muscle mass Rehabilitation Plan: Rehabilitation has been found to help maintain a superior quality of life with patients with polyneuropathy. The cornerstone of the rehabilitation plan is a therapeutic program that aims to maintain and/or improve muscle strength, endurance and generalized proprioception and may include: • Manual therapy • Therapeutic exercises • NMES • Environmental modification • Hydrotherapy • Weight management3-5 Nursing Care of the down dog6-8

107

Dogs that are neurologically impaired can present as recumbent, non-ambulatory or minimally ambulatory. There are many consequences to being “down” as these patients will require some special attention and nursing care. There are several basic aspects to providing optimum care that can lead to a positive outcome for the patient: • Pain Management: A quiet patient does not equal a pain-free patient. Recognizing a painful patient and employing a multimodal approach to analgesia is key when addressing pain. • Turning the patient: recumbent patients should be turned to sternal or the opposite lateral position every 4-6 hours. • Appropriate bedding: clean, dry, well-padded bedding with absorbent pads is imperative to preventing urine/fecal scalding and decubital ulcers. • Bladder care: Dogs with thoracolumbar and lumbosacral diseases are prone to the inability to urinate and urinary incontinence. Without proper bladder care, the bladder itself can become damaged and these dogs can be prone to UTI’s, pyelonephritis, urine scald and bed sores. The Bladder should be emptied several times/day either by manual expression or urethral catheterization • Hydration & Nutrition: Care should be taken to ensure adequate access to water and food.

1. Wininger FA, Zeng R, Johnson GS, et al. Degenerative myelopathy in a Bernese Mountain Dog with a novel SOD1 missense mutation. Journal of veterinary internal medicine 2011;25:1166-1170. 2. Thieman KM, Krahwinkel DJ, Sims MH, et al. Histopathological confirmation of polyneuropathy in 11 dogs with laryngeal paralysis. Journal of the American Animal Hospital Association 2010;46:161-167. 3. cvm.msu.edu. Geriatric Onset Laryngeal Paralysis and Paresis, 2019. 4. Millis DL, Levine, D. Canine Rehabilitation and Physical Therapy: Elsevier, 2014. 5. Zink C, VanDyke, J. B. Canine Sports Medicine and Rehabilitation: Wiley Blackwell, 2013. 6. Cook L. Caring for the Down Patient. American College of Veterinary Internal Medicine Forum 2017. 7. Hughston L. Down, Not out: Nursing Care of the recumbant patient. Southwest Veterinary Symposium 2016. 8. Gillespe T. Get Moving! Caring for the recumbant patient. International Veterinary Emergency & Critical Care Symposium 2018.

108

Rehabilitation for the Geriatric Patient – You can teach an old dog new tricks! Amber Ihrke, DVM American College of Veterinary Sports Medicine and Rehabilitation – Resident Integrative Pet Care of Homer Glen – Medical Director Introduction Geriatric patients can comprise a large quantity of a rehabilitation’s practice patient population. Although aging is not a disease, these patients have specific medical and rehabilitation needs that coincide with increasing age that can manifest as decreased mobility and chronic conditions. The rehabilitation practitioner needs to understand the process and effects of aging in general and help to manage the factors that may contribute to the aging process. When prescribing rehabilitation plans it is important to consider all factors physiologic as well as cognitive in the aging dog. Managing quality of life issues, pain management and nutritional considerations are also integral to success when working with these patients. In addition, understanding the concerns and goals of the owner is important when developing a rehabilitation plan. The rehabilitation therapist, the owner and the patient must all work together to improve the quality of life for the patient and improve functional ability in the home environment. Incorporating a multimodal approach has been shown to be the best way to serve our clients and our geriatric patients. Who is a Geriatric Patient? The number of years considered to be a geriatric patient varies, however according to the American Animal Hospital Associations’ Senior Guidelines Senior Task a dog is considered geriatric when they are in the last 25% of their predicted life expectancy for their breed. 1 It is generally accepted that smaller breeds of dogs have longer life expectancies than large/giant breeds of dogs. Table 1. Typical Ages at which May be considered Geriatric2 Weight Small Dogs Medium Dogs Large Dogs Giant Dogs

0-20 pounds 21-50 pounds 51-90 pounds >90 pounds

Age (Mean + Standard Deviation 11.48 + 1.86 10.19 + 1.56 8.85 + 1.38 7.46 + 1.27

Common age-related changes seen in the Geriatric Patient2 Owners of geriatric pets seek out rehabilitation for many reasons but usually have one goal – How to make their pet’s remaining years quality years. A dog’s ability to maintain homeostasis and respond to stress decreases with age and leaves them more susceptible to disease. Common effects of aging include: • Decreased metabolic rate • Decreased immune competence

109

• Decreased phagocytosis and chemotaxis • Changes in haircoat and sin • Loss of muscle, bone and cartilage mass • Decrease in number of nervous system cells • Decrease in pulmonary vital capacity Prior to starting a rehabilitation program, it is good medicine to have a minimum laboratory database such as CBC, Chemistry and Urinalysis to understand the health of your patient. Initial patient assessment focuses on all underlying musculoskeletal, physiologic, neurologic and metabolic disorders.3 Common Medical Problems seen in the rehabilitation practice:4,5 • Intervertebral Disc Disease • Muscle Atrophy • Lumbosacral disease • Degenerative myelopathies • Neoplasia • Osteoarthritis • Metabolic diseases • Obesity • Cognitive changes and sensory system disorders • Immune-mediated diseases • Urinary/fecal incontinence The therapeutic options for geriatric patients Therapy options for the geriatric patient are numerous and should be based on presenting clinical signs, physical exam and goals of the client. The objectives include managing pain, improving mobility and strength, and promoting independent ambulation.5 These patients may have numerous comorbidities and the patient’s tolerance of your interventions as well at the clients ability to implement the plan must be taken into account. A multimodal approach works best with the geriatric population and may include: • Pain management6 • Dietary changes including nutraceuticals and supplements7 • Physical modalities • Manual therapies • Therapeutic exercises • Hydrotherapy • Regenerative Medicine • Assistive Devices • Acupuncture • Chiropractic End of life Issues

110

Veterinary hospice is defined as “giving clients time to make decisions regarding a terminal companion animal and to prepare for its pending death. The comfort of the animal must always be considered.”8 Rehabilitation can be utilized for end of life care in our geriatric population in order to make the transition from therapeutic to palliative to hospice care. Providing guidance and resources for clients to make the best decisions when dealing with end of life decisions is just as important as the care given at previous life stages.1,8 A quality of life assessment scale can also be utilized to help guide clients with decisions.9 Palliative and Hospice rehabilitation options include: • Pain management • Nutritional support • Environmental modifications • Hygiene needs • Manual therapies Conclusion Working with geriatric patients can be extremely rewarding and small interventions in their lives can have a huge impact on their quality of life as well as their owner’s. Taking into account the special needs of the geriatric population allows for the rehabilitation practitioner to customize the most effective therapeutic plan to maximize results. A well planned and implemeted rehabilitation strategy can be effective tool to allow for these patients to get the most out of their golden years.

1. Epstein M, Kuehn NF, Landsberg G, et al. AAHA senior care guidelines for dogs and cats. Journal of the American Animal Hospital Association 2005;41:81-91. 2. Millis DL, Levine, D. Canine Rehabilitation and Physical Therapy: Elsevier, 2014. 3. Gleason D. Geriatric Rehablitation. Wild West Veterinary Conference 2013. 4. Zink C, VanDyke, J. B. Canine Sports Medicine and Rehabilitation: Wiley Blackwell, 2013. 5. LoGiudice RJ. Age is Not a Diagnosis - Rehabilitation Therapy for Geriatric Patients. Southwest Veterinary Symposium 2018. 6. Epstein M, Rodan I, Griffenhagen G, et al. 2015 AAHA/AAFP Pain Management Guidelines for Dogs and Cats. Journal of the American Animal Hospital Association 2015;51:67-84. 7. Wynn SG. Diet Therapy for Osteoarthritis. VMX 2019;553-554. 8. Bishop G, Cooney K, Cox S, et al. 2016 AAHA/IAAHPC End-of-Life Care Guidelines. Journal of the American Animal Hospital Association 2016;52:341-356. 9. Villalobos A. The HHHHHMM Quality of Life Scale. Ontario VMA Conference 2008.

111

112

Companion Animal

Richard Meadows, DVM

MU-College of Veterinary Medicine Columbia, Missouri

113

blank page

114

CCUS/CUPS and Feline Stomatitis/Caudal Mucositis MVMA 2020 NOTES Richard Meadows, DVM, DABVP Curators’ Distingusihed Teaching Professor William T. Kemper Fellow for Teaching Excellence University of Missouri College of Veterinary Medicine

Some generalities for you about Chronic Contact Ulcerative Stomatitis (CCUS) CUPS – Chronic, ulcerative paradental stomatitis is a name that many veterinarians use and will continue to use for awhile to come although it is technically not correct according to the latest studies because mucosal ulceration was present opposite edentulous areas in 40% Maltese are predisposed (“poster child breed”) for this disorder. The hallmark lesion is a "kissing" ulcer. The chief complaint from the owner is usually fetid halitosis and drooling and it is a painful condition for dogs. On awake oral exam, They may paw at their mouth and/or chatter their jaw. Frequently these dogs do not have much calculus accumulated and may or may not have obvious periodontitis by an awake oral exam This is a nasty disease – highlights of some clinical findings • 20% with weight loss • 20% suffering • 90% > 6 oral ulcers • 80% ulcer on attached gingiva • 70% tongue and palate ulcers • 60% glossopalatine arch ulcer The basic issue appears to be a dysregulation of the mucosal immune system – again, Mucosal ulceration opposite edentulous areas in 40% Clinical Approach: •

115

First thing to do: Use pain medications. • Acetaminophen at 15-25 mg/kg BID or TID is safe and helpful in dogs; also synergistic with tramadol, etc. • Normal NSAIDS may help the pain but not very good at treating inflammation. • Coating oral rinses - can help with pain (and maybe healing?) – see more below. • Decaffinated tea rinses (tannins) can help – deadener and anti-oxidant effect • Pulsed antibiotic therapy (antimicrobials administered the first five days of each month) is not recommended. Not even by Dr. Bellows who used to argue for it in some cases.

•

• • • • •

•

The use of corticosteroids to control CUPS is controversial. Personally, if I use them, I use triamcinolone at 0.2 mg/kg q24h for no more than about 10-14 days. They are, however, not a magic bullet and they will cause more problems than they are worth over time. Second thing: Do whole mouth, intra-oral dental radiography as well as whole mouth periodontal staging/charting/cleaning/polishing. Be sure to clean and polish above and BELOW the gum line and irrigate well after polishing. Third – remove any teeth (especially non-strategic ones) with significant periodontal disease Fourth: Biopsy representative lesions NOTE: Antibiotics will NOT be the answer, period!! After the dental work you need to do some type of immunosuppressive therapy – see details below - AND get the owners to do as much home care as possible.The more home care they can do the better off the dog will be and the more likely the dog will be to keep his/her teeth. NOTE: Whole mouth extractions (unlike the case in cats) is RARELY indicated in dogs.

Antibiotics approved for dental infections are indicated to help treat severe presentations where osteomyelitis is also present. For me that is 11 mg/kg BID Clindamycin usually with periodontal disease/osteomyelitis but there are some boarded veterinary dentists that claim Baytril helps – I personally hate Baytril so wouldn’t know/and wouldn’t go there. DON’T use Cipro!!! PLEASE. Metronidazole – 22 mg/kg BID for no more than 14 days and no more than 500 mg/dose regardless of dog’s weight; good for Spirochetes and inflammation.The antiinflammatory effect is probably more important than the antibiotic effect. TO REPEAT: Antibiotics will NOT be the answer, period!! Specifics of a recent Trial: 5 mg/kg Atopica (micronized cyclosporine) PO SID – can cause emesis 15 mg/kg metronidazole PO SID Regarding emesis from Atopica…. For me, it is standard procedure to give maropitant (Cerenia) at label dose of 1 mg/kg SQ at least 1 hour before starting cyclosporine I then send home 4 days of oral Cerenia (2 mg/kg/day – again, label dose) This protocol greatly reduces the frequency of emesis from cyclosporine administration Daily, long term metronidazole scares me I am not comfortable giving metronidazole (at least BID) for more than 14 days without a break but I have a few patients on longer term q24h PO metronidazole without noted issues to date. Drugs for Vasculitis/Immune mediated conditions often help; for example; Pentoxifylline with Niacinamide and a member of the tetracycline antibiotic family (doxycycline or minocycline typically).

116

NOTE: This protocol (below) has become quite popular with bard-certified veterinary dentists Pentoxifylline (trade name – Trental but available as a generic for a long time now (patient < 7 kg: 100 mg t.i.d.; 7 to 16 kg: 200 mg t.i.d.; > 16 kg: 400 mg t.i.d.) can be prescribed to decrease inflammation. This is an anti-vasculitis drug used in dermatology a lot. 15-25 mg/kg preferably TID and the trade name Trental is superior to the generics for tough cases in some dermatology studies of, for instance, Dermatomyositis. Niacinamide with equal dosages of tetracycline (patient < 20 kg: 250 mg t.i.d.; > 20 kg: 500 mg t.i.d.) may also be helpful. We substitute doxycycline/minocycline for tetracycline and use them q12 h. Start at 10 mg/kg BID and see if they tolerate that – decrease to as low as 5 mg/kg q24h PO if still beneficial. NOTE: BID can be tried but, at least at first, TID is just palin better if the owner can be motivated to do it. MAGIC MOUTHWASH: DIPHENHYDRAMINE/MAALOX/LIDOCAINE MOUTHWASH (1:1:1) COMPOUNDING PROCESS 1) Measure all ingredients 2) Place in appropriately sized amber bottle 3) EXP: 2 WEEKS 4) LABEL: Shake well, Use as a rinse and do not swallow • We use the diphenhydramine oral solution (12.5 mg/5 mL), Maalox antacid and lidocaine HCl oral topical solution USP, 2% (viscous). • We generally make 60 mL total volume so use 20 mL of each ingredient. The label shown above is what goes on the bottle and we will generally send home an oral dosing syringe with it. Courtesy of Carrie Duran, DVM, PharmD Home Care • Brushing the pet’s teeth up to twice daily • Applying a gel or an oral rinse containing zinc • Applying plaque prevention gel (OraVet Plaque Prevention Gel—Merial) • t/d diet or a coated diet (sodium hexametaphosphate, etc) • Healthy Mouth rinses • Virbac VeggieDents • Etc • I frequently send clients to www.VOHC.org for a list of approved products • I tell owners the more thoroughly they do home care the more likely we are to be able to keep their dog’s teeth

117

Feline Chronic Stomatitis +/- Caudal Mucositis: Caudal Mucosisits is inflammation caudal/distal to the teeth – lateral to the palatoglossal folds Old name for cadual mucositis was Faucitis – Faucitis would, correctly, only refer to the palatoglossal folds themselves and not to the tissues around that area. My understanding – hypersensitivity to the bacteria in plaque – this sticky plaque adhering to the teeth and gums makes for “innocent bystander” attacks on the oral tissues is the primary cause Chronic Calici Viral infections tend to have made their “last stand” in the caudal oral tissues – in the lymphoid accumulations in the area lateral to the palatoglossal folds and back to the tonsils Calici Virus infections DO NOT appear to cause this syndrome BUT do exacerbate it! Juvenile Gingivitis/Eruption Gingivitis: Some young cats get dramatically red, inflammed gums early in life. These cats (or kittens) should have a THOROUGH dental cleaning and vigorous home care to prevent possible progression to Gingivostomatitis – this is my belief but I can’t prove they are related. My personal treatment plans for stomatitis cats: Clean the teeth very well and do whole mouth intra-oral dental radiographs at the VERY LEAST – many have healthy teeth but a significant % also have tooth resorptions and/or periodontal disease. Tartar is quite often mild or absent. Extracting all unhealthy teeth OR all caudal teeth – may need to pull all 30 teeth – is THE TREATMENT OF CHOICE The sooner this is done the more likely it is to work well Of course, treat the pain as best you can. NOTE about Mouth gags, particularly if used for an extended period, can cause blindness in cats – there is one blood vessel supply blood to the brain that is constricted in cats when their mouth is held open too long or too wide. NOTE: Cats (and dogs for that matter) do well with NO teeth and even eat dry food and Caudal extraction of teeth “cures” at least 60% of these cats; 20% are significantly improved after this surgery; 13% had little improvement and 7% are not improved at all; from a classic study I believe is still the best data we have. A more recent study from Penn said caudal extractions were as good as whole mouth extractions but I do not think the study was done as well as the older study was. Of the 7 % not helped AT ALL – the ones with significant inflammation mostly or strictly in the caudal part of the mouth (behind the teeth) are the ones most likely to be in this group. In the process of extracting the teeth you must be 100% sure you get ALL the roots. That means doing pre and post extraction dental radiographs!!!! Debriding the sockets with a fine or medium grit, diamond bur is in vogue and probably helpful Filling sockets with a bone grafting material like Synergy may help??? We don’t commonly do that.

118

Testing/Treating for Bartonella – most likely useless and I don’t think there are any boardcertifiec veterinary dentists that do this currently. Treatment post extractions – if needed: Cyclosporine +/- methyl prednisolone or triamcinolone (my favorite) – very helpful primarily in cases where extractions were not helpful or not helpful enough and where the inflammation was limited primarily to the caudal part of the mouth – I have not had as much luck in cases where the mouth was not cleaned up with thorough dental surgery NEW “HOT” TREATMENT Recombinant feline interferon omega A major Pain to get imported into the USA NOT EFFECTIVE without first cleaning up the mouth thoroughly!!!!!!!!!!!! I have it and it works more often than not – but not always of course. We mix it up, aliqout it out into 10,00 IU/ml, freeze it (once only) and use it as a 1ml dose for 100 days – per the European Veterianry Dentists Concensus statement on it’s use. Chloambucil and/or surgery laser ablation are last ditch alternatives. Unofrtunatley, Chlroambucil is quite expensive these days. For that 7% of patients with deep pocket owners they can consider going to the veterinary School at UC Davis for stem cell therapy. This study uses the cat’s own stem cells grown out several generations and then injected. Working on about 50% of the 7 % of hard core non-responders to date.

119

120

Dental Equipment for Fun and Profit Richard Meadows, DVM, DABVP Curator’s Distinguished Teaching Professor William T. Kemper Fellow for Teaching Excellence Section Leader, Primary Care, Dermatology, Dentistry and Shelter Medicine University of Missouri College of Veterinary Medicine Veterinary Health Center

Current Veterinary Dentistry If you don’t have a high speed unit, a good ultrasonic scaler and a quick way to get quality dental radiographic images you are not practicing current veterinary dentistry and it is costing you money not to have these tools. And, more and more clients are tuned into this reality. I know because they seek us out to get what their local practice doesn’t offer. For veterinary dentists the next “holy grail” is Cone Beam CT. There is at least one Cone Beam CT in a more general practice here in Missouri. These compact DISCLAIMER: There are many good sources of veterinary dentistry equipment and we frequently buy things from the human dental world. The MU CVM has considerable equipment but I have experience with a limited number of the companies so my presentation will focus on what I know and my opinions/experiences are not meant to slight any of our corporate partners. I am not paid a penny by any dentistry company. I am happy to share my good (and perhaps more importantly) bad experiences with you person to person. You can contact me at: meadowsr@missouri.edu or by phone – main number (573)-882-7821 or by cell at (573)-8239377. Talking to other veterinarians is considered part of my job at MU and I do it essentially daily. A few companies I have had good experiences with include: iM3 USA - https://www.im3vet.com/ I “own” considerable iM3 teaching equipment and it has served me well. Their dental units (high speed/low speed, etc) units are rugged and reliable. When they break we have found a quick phone call often diagnoses the issue for us and the parts are usually something my tech and I can install ourselves. You can buy cheaper, more compact units but then you have to use them. I am also a major fan of their CR-7 computed radiography unit and it is the “go to” unit for my entire dental team. The software is not the best in class but it serves us well. I am less of a fan of their ultrasonic cleaners, periotome, swivel handpieces and hand instruments.

121

Cislak or Zoll dental - https://cislak.com/ or http://www.zolldental.com/ This is a small, family owned business near Chicago. They make world class hand instruments and most of them can be resharpened (by them or you) and retipped/repaired. Again, not the least expensive choice but good equipment can make your life easier (save time and decrease cursing). DENTALAIRE: https://www.dentalaireproducts.com/ I have only started interacting with this company recently but my experience to date is great. I recently purchased 8 very compact teaching units from them and they were quite inexpensive but appear to be of great quality. I can not speak to their customer service or long term durability yet. And I have purchased tow “Biox” hand held Xray generators from them. My technicians basically refuse to use my wall mount unit now because the Biox is so portable, quick and easy. It is also less expensive than the other alternatives I have used/found. Dental Focus: https://dentalfocus.biz/ I have known the owner, Jim Merritt for nearly 20 years and he has treated me well. We have had his digital sensor (Sopix) for a long time and it provides no fuss service with excellent images and free updates. We like our Sopix sensor. Supposedly it is the only digital sensor on the market that never overexposes with the highest detail available every time. These days Dental Focus is really into cone beam CTs and Pieziotomes, neither of which are likely to interest most practitioners. We recently bought a pieziotome from him for our mandibulectomies/maxillectomies but, since we have 2 big CTs already a Cone Beam is not a likely purchase for us. I think they start at $175,000.00 and go up from there? Categories to Discuss Dental Power Equipment Dental Radiography Generators and Image Processors Hand Instruments Burs High Speed handpieces Two basic types of high-speed, water cooled handpieces; Push Button and Latch: Push button cheaper; latch type more rugged but quite a bit more expensive typically. They cut with speed, not torque – float them and let them do the work – you pushing down will break them and/or harm the teeth/hard tissues. They need a good, fine water mist shooting onto them to help prevent burning the bone and dulling them. Make sure they are WELL lubricated; they spin 300,000-500,00 rpm so they need lubrication. Make sure never to run a high speed handpiece without a bur.

122

The turbines can be replaced but they are often not cheap Using the bend of your thumb can help you push this button hard enough to release the friction grip the handpiece has on the bur. The spring has to be strong to last and prevent the bur from flying out. When you put a bur in and turn it on point it away from anything important (like your eyes) at first in case it goes flying like a missile There is a wide array of options on high speeds that companies will try to sell you – swivel bases, LED lights etc. I prefer pediatric heads and do not personally think the swivel or LED lights are something you should spend money on. A fair number of people disagree with me about that. Price: You can get a 10 pack online for a little over $200.00. They are not pediatric heads and I know at least two of our Missouri colleagues that use them and when one breaks they throw it away. I recently bought some of these to see if they will work for my student dental labs. On the other end of the spectrum, you can easily spend $1,000.00 or more for a swivel head, LED light, latch type high speed. For most medium range ($200-400.00), pediatric sized high speeds you can replace the turbines for $80.00 or a bit more. Low Speed handpieces: Again, two basic types – polishing heads (classically have a green insert but colors can vary) and Surgical heads (typically blue, but again colors can vary). Surgical heads spin about 2,000 rpm, have more torque and have no water cooling – I rarely use one personally. Polishing heads – have a 4:1 reduction so they spin about 500 rpm. After cleaning teeth polishing is VERY IMPORTANT and we greatly prefer the disposable, oscillating heads to the 360 degree spinners. Oscillating heads don’t wind up hair like the 360s do. Hand instruments Instruments stored away (and organized) in a pack is a GOOD idea (instead of loose in a drawer somewhere). The mouth is far from sterile so why sterilize the packs? It helps take care of them It is our responsibility to prevent iatrogenic disease And learning how to sharpen instruments can make the instruments work FAR better – and put a smile on your face instead of a grimace. More on sharpening below.

123

Particular Instruments I love. Cislak EX-9 Periosteal Elevator – the Cat’s Meow – many board-certified veterinary denstists use this instrument daily and for many more uses than it was made for. Keyes 3/16” straight periosteal elevator – Cislak calls them EX-60s and they make them much less expensively than Miltex, etc does. They also put a dental handle on them for you (called an RHT-1 handle) Winged tip elevators – designed by the legendary (deceased) veterinary dentist Dr. Bob Wiggs. They are great invention he dreamed up when he was a 3rd year veterinary student. Most kits will include sizes 1-4 but 5, 6 and 8 are available. Dr. Wiggs, to my knowledge rarely ever used anything larger than a size 3 but he was a grand master. Elevators/Luxators – especially the small one (LT-2S) for getting started widening out/cutting the periodontal space with medium to large teeth in dogs and cats. Technically luxators are not the same as elevators but these names get interchanged frequently. For cats, Cislak makes a LT-1.3S and even a LT-1.0S. I use these for cat incisors and in whole mouth extractions in cats. They are sharp and fragile so careful use is required. I rarely use larger elevators larger than the 2 mm one. They are also made in all kinds of crazy crooks but I have never seen a need for them personally. Excavators and cavity curettes (aka, Miller’s bone Curettes) I keep a small and medium sized one in each extraction pack to debride (scrape the crud out of sockets). This will reduce the time required for healing. The numbers of them always confuse me but the two we carry in our extraction packs are: Medium - EX-2 112 Small – EXC-18 Serrated edge, gingival scissors I would be lost without them! The serrations give you the ability to precisely remove unhealthy/excess gingival tissue before suturing up flaps. There are multiple varieties but the one we use the most frequently is: LaGrange double curved 11.5 cm premium – Cislka number is Z-4015 Another one I like is called Z 3519. These are straight tipped with a 45-degree curve at the start of the scissors.

124

University of Minnesota Retractor (CIS R6). This instrument can be very handy for retracting the lips without trauma. Works like a third hand for me. Root tip forceps – CIS Z6481 – Root tip forcep premium. I do not use/condone use of root tip picks but these will do a similar thing for you when you have a small root tip fragment in a hole. I use them a few times per year but they are great in those rare cases. Beaver scalpel handle – not sure of the Cislak number but they will know what Ophthalmologists use these regularly and I use them commonly. The blade I use (I call my fancy blade) cuts pushing and pulling and on top – see picture in PowerPoint. It is called a Beaver6900. It seems sharper than the average scalpel blade to me. Burs We use FG (friction grip) burs – only held in by friction so the springs holding them in are strong. In general we use…. Round burs for erasing alveolar bone Cross cut burs to section teeth into single root fragments Diamond burs to smooth off sharp bony edges (called alveoplasty) and reduce bone height around a retained root tip 12 Fluted carbide burs to reduce excess gingiva Arkansas White stones for minor enamel shaping and to reduce unsupported enamel ledges on uncomplicated crown fractures Some burs have longer shafts than the others – those are called surgical length burs and can be very handy in rare cases. Round burs - Again, used mostly to “erase” bone over tooth roots – use parallel to tooth root, not perpendicular. We carry a range from ¼ round to 8 round. ¼ and ½ rounds are used to moat around root remnants and to make a thin opening to get luxators/elevators in socket to remove a root tip fragment. These tiny burs are also used to Also used to make a thin line through the area of the periodontal ligament; NOTE: You do not want to make a wide gap because, if you do, you may remove the hard tissues you wedge against (i.e., the cementum and/or the lamina dura) # 2 and # 4 round burs are used to erase buccal bone, etc -

125

Cross Cut Burs700 L (for long) – this is a nice bur that has grown on me over the years. Very thin at tip and gives you precise control. If you want to sound stuffy you can call them by their correct name – cross cut, fissure taper burs. 701L (my long term, previous favorite one) 557 (a very aggressive bur that I only use for mandibulectomies/maxillectomies in large dogs) Diamond burs Diamond burs come in a dizzying array of grits (fine, medium, course, etc), sizes and shapes The one we use the most is a football shaped, medium or coarse grit diamond bur I find the football shaped diamond bur to be very versatile so that is what is in all of our bur blocks.

Fluted carbide burs At least two styles of 12 fluted carbide burs for high speed dental hand pieces. Used primarily for gingival reduction where it is causing pseudo-pockets (supragingival pockets – e.g., like in Boxers) that predispose that tooth/those teeth to periodontitis; Use plenty of water and move around from place to place to prevent heat and trauma that can harm gingival and bony tissues; these burs cause very little bleeding. I prefer the gold colored version. Arkansas White Stone burs Used primarily to smooth out unsupported enamel ledges on uncomplicated crown fractures In practice you will (commonly) see chipped enamel in dogs as many of them are “abusive” chewers. Rounding off these sharp edges reduces the probability of further enamel loss and it is a valid thing to charge owners for.

126

331 bur This is a nice bur I use mostly to start root canals but it is very versatile. It has a rounded end and can also function like a short cross cut bur. This bur could easily be used to remove the buccal alveolar bone over tooth roots instead of a round bur. Sharpening instruments An extensive discussion of sharpening all dental instruments (curettes and scalers, etc) would take the entire hour so, below, are some videos you can access… •

www.youtube.com/iM3 Sharpening Dental Elevators – very short and to the point; <1 min.

•

www.youtube.com/Hu-Friedy’s It’s about time... This is a classic, time honored method and system

•

https://www.youtube.com/watch?v=ijbeN2HEB9g – Kimberly Wehrmann. This video is very detailed – key points: bevel the side that doesn’t touch the tooth, “4S” pattern and sanding. Note that her touch is very light.

Gleason Glide System- great for scalers and curetteshttps://www.youtube.com/watch?v=P5OS1pX2TsU Conical Sharpening Stones or Small Steels – good to keep in your packs. # 299 Arkansas Conical, Super Fine Grit Patterson Dental www.youtube.com/iM3 Sharpening Dental Elevators; again worth watching https://www.youtube.com/watch?v=y-lZ2jKQBnU – using a miniature steel; also < 1min. I got one from my Local Ace Hardware Store. I keep it handy in the dental room Sharpening Stones and Accessories – Summary Clean the stone/sterilize; dirty stones can spread disease and don’t work as well. India or Ceramic stones work better for sterilizing. Can use sterile water. Sharpen during a procedure? – I do! Elevators and luxators will be much more effective for the wedge technique (the major technique we use) if they have a back side bevel and a sharp edge. Ultrasonic Scalers: Our Favorite Ultrasonic Scaler is a Piezo unit for which the movement is parallel to tooth!!!

127

Movement of others is perpendicular and so they pound the tooth. It is called a Newtron Booster by Aceton. It is sold by some distributors like Patterson I believe. The two subgingival tips we prefer (and you have to specifically order to get) are the 10P and the 10Z. The best rated one by AAHA is made by iM3 and called a 42-12. I own two of them and my techs hate them. Lighting and Magnification Many things look different when taken out of the dark and looked at in detail (but enough about politics ☺). Good lighting is IMPERATIVE and magnification may take a while to get comfortable with but, once you adapt you can’t live without it. And, as you age, you MUST have magnification and good light to do dentistry well. You can spend a lot of money on lighted surgical loupes (and I have) but, at my age I couldn’t do precise, tedious procedures without them. Here is what I use for student teaching; claims to be 3,500 to 6,000 lumens. I seriously doubt that - but it is VERY bright. Less than $20.00 on eBay, Amazon, etc.The batteries are cheap as is the charger; may work fine but I bought better batteries and chargers (Batteries Plus Store) and they are even brighter and the batteries last longer. Has 4 modes but I tell students to only use the central light so the batteries last longer (first mode). Uses 18650 batteries – same as a vaping device apparently. •

https://www.amazon.com/Boruit-Lumens-Headlamp-HeadlightCharger/dp/B016O8ON2C

My personal preference for a head lamp and loupe is Perioptix by DenMat. Hogie frames with a Solaris lamp and extended working range 2.5 mag loupes (Panoramic) work well and can be used with or without glasses and can potentially be shared amongst all the doctors in a practice With that said, there are a dizzying array of options and I suggest you buy one at a trade show where you can listen to their spiel and try them on before buying. Ergonomic chairs Saddle Chairs: There are many types of dental chairs available. My favorite is from a company called RGP. My own chair is called a HAG (Swedish name pronounced Hog) - partly because I wait for a woman to sit in it before I point out the name of the chair. But that’s just me. HAG Quickship Capisco H8106 Saddle Seat w/ Back. About $800.00 so not for everyone but it helps my back after a long procedure so it is worth it to me. We also recently bought a second RGP chair called – 400D Hybrid stool. My techs prefer it. Also about $800.00 so you would need to use it frequently to justify but we do.

128

Below is an invoice from Cislak for one of my surgical extraction packs.

129

blank page

130

Dental Radiography - Image Acquisition and Interpretation. Richard Meadows, DVM, DABVP Curators’ Teaching Professor University of Missouri College of Veterinary Medicine Intra-oral, digital dental radiology is vital for diagnosis, treatment planning, follow-up evaluation, and legal medical record information. Without quality radiographs, you will be treating patients while only guessing at the diagnosis and quality of treatment. And experience has taught me, and many others, that you miss A LOT of things without good, intra-oral dental radiographic images. That is bad for your patient, your client and even your reputation and bottom line. Dental radiography also offers the technician/assistant the opportunity to play a very important role in veterinary dentistry. They generate income, do most of the work for you – and generally feel more satisfied with their job as a result. WIN, WIN!! I am reminded of the old saying – “Work fascinates me, I could watch it for hours.” This is not uncommonly the case for me in my dental procedure room. Intra-oral radiology is essential – skull films are basically unreadable by everyone I know – and I know a lot of veterinary radiologists and veterinary dentists. The disadvantages of the intra-oral radiograph are the mouth size in the smaller breeds of dogs and cats and the restrictive confines of the mouth structures. The shallow dome of the hard palate necessitates the angling of the film to accommodate these confines. Intra-oral technique must take into account the angle of x-ray tube with respect to the film for obtaining an anatomically correct radiograph. Many of these issues can be dealt with by purchasing a computed radiographic image processor rather than a size 2 digital sensor. DENTAL X-RAY UNITS A dental x-ray unit is recommended for optimum ease of use. Dental x-ray units are small in comparison regular veterinary tabletop units. They can be stored against an operatory wall, taking up very little space and available for immediate radiographic diagnosis. Most dental x-ray units have a fixed mA (7-10) and a fixed kVp (~70). The only parameter that is changed is the exposure time (seconds).Wall Mounted or mobile units designed specifically for veterinary use are available. These units enable the veterinary dental team to produce dental x-rays quickly and accurately. Now there is a proliferation of hand held X-ray generators. One down side to them is that they appear to have a shorter life (5 years of so I am told) and you need to make sure they have good radiation protection. The two main units I am aware of are the Nomad and the Biox generators. I have owned both and my team prefers the Biox unit

131

Image processing Intra-oral film is basically a thing best left to history. There are two basic options now â&#x20AC;&#x201C; direct digital sensors (usually only available as stiff, thick size 2 sensors) and computed radiography processors. The direct, digital sensors are, by far and away, what most practitioners purchase and that befuddles me personally. The primary reasons are â&#x20AC;&#x201C; that is what the companies push and they cost a bit less money. That is becoming less true over time. A number 2 digital sensor is quite handy but you will not be able to get it into the back of a small cat or tiny dog very well. It also takes several more views to get whole mouth images. Computed radiographic image processors have a variety of reusable phosphor plates (the size of old conventional dental films). These range from rabbit plates and size 0 to 6. One new unit even allows you to use several large films together for things like small dog/cat, bird, etc extremities with fantastic detail (better than any screened film can possibly provide). These films are relatively inexpensive but do eventually wear out and must be replaced. INTRA-ORAL TECHNIQUE: POSITIONING ANGLES Intra-oral dental radiology makes use of two basic techniques to attain accurate film images: THE PARALLEL TECHNIQUE The film is placed behind (parallel to) the tooth and the x-ray beam is directed at right angles (90 degrees) to the tooth and film. It is used for the posterior mandibular teeth (premolars and molars). THE BISECTING ANGLE TECHNIQUE The film is placed a right angle to the tooth. The x-ray beam is placed at right angle to an imaginary line that bisects the angle formed by the film and the long axis of the tooth. It is used for the majority of teeth in the mouth including all maxillary teeth as well as the anterior mandibular teeth (incisors, canines and anterior premolars). The bisecting angle technique is the technique of choice for most of the teeth in the mouth. It allows for the limited confines of the intra-oral structures. Because of the irregularities in the oral anatomy, the film cannot always be placed parallel to many of the teeth being imaged. When the teeth and the film are not parallel with one another, the x-ray will produce a shadow on the film that can be either shorter or longer that the teeth themselves. To obtain a shadow equal in length to the teeth the bisecting angle technique is used. People freak out about this and

132

overthink it. I will show/describe the simple method I use to this day. I call it the Goldilocks method. There is also a confusing technique called the SLOB rule – basically it is doing cranial and caudal oblique angles on top of the bisecting angle. Also made way too difficult by many people. Indications for Dental Radiographs 1. Periodontal Disease 2. Survey films during routine professional prophylaxis – this is now the norm for AAHA clinics and for us at the MU VHC. 3. Missing teeth 4. Injured / fractured teeth 5. Pre- and post-extraction 6. Resorptive lesions 7. Carious lesions 8. Endodontic disease and treatment (root canals) 9. Discolored teeth 10. Evaluation of missing teeth 11. Swellings, lumps, tumors of the mouth or jaw 12. Evaluation of oral pain Viewing and interpreting dental films Classically dental films have no markers except for a raised dot (dimple) that can be felt on the film. The dot can also be seen and felt on the outside of the film packet prior to developing the film. This dot can be used to correctly orient the film for viewing, by following three basic steps. 1. Place the convex (raised) side of the dot toward you. This orients the film as if you were outside the animal’s mouth looking at the patient. Imagine your eye being in the same position that the X-ray tube was in when the film was taken. Once the dot is toward your eye, do not flip the film over. This orientation is the accepted standard in veterinary dentistry. This step (and only this step) is automatically done for you when using a digital dental film system. 2. Determine if the film is of the maxillary or mandibular quadrants. If needed, rotate the film so upper teeth (maxillary) have the roots point up, just as if you were looking at the patient’s mouth from outside the mouth. Mandibular quadrants are rotated so that the roots point down, again just as if you were outside the patient’s mouth looking in. We do not want to evaluate the patient upside down, so we rotate as needed to position the patient in a normal standing position (not upside down). Specific things to look for to help decide which quadrant you are looking at are listed below. After a little practice, it is very easy to tell maxillary and mandibular films apart. 3. Determine if the film is from the right or left side. The simplest method is to identify which end of the radiograph is towards the front of the patient and which is toward the back. Imagine the patient standing in front of you with the nose in one direction and the back of the head in the other direction. Then, simply imagine the whole patient standing in front of you facing that direction. If the patient’s nose is pointed to the right, you are

133

looking at the right side of the patient. If the patient’s nose is pointed left, you are looking at the left side of the patient’s mouth. When positioned as described above, views of incisors have right and left swapped, similar to looking at AP abdominal films. For example, the left side of the correctly positioned film is actually the right side of the patient. Initially, you can use a skull or dental model to help you decide which side you are looking at. Very soon, it becomes second nature. Pay attention to increasing size of teeth in the premolar region, as well as unique anatomy in the carnassial teeth areas to help you out. Currently, with computed radiography phosphor plates, some of them have dots or small marks on one corner. By convention we use this as a marker of the right side – i.e., we place the dot/mark closer to the right side of the mouth. Identifying abnormalities on dental images Just like your anatomy training preceded pathology training you must learn normal before you learn abnormal. And remember abnormal doesn’t always mean important – dogs and cat “Gee whiz” lesions are not uncommon. Some common examples include: Supernumerary teeth – especially supernumerary first maxillary incisors (105S and 205S). Supernumerary roots – especially third roots on third maxillary premolars (107 and 207). Actually this one predisposes that tooth/teeth (often symmetrical) to periodontal disease on the extra (palatal) root because the gingival seal around the root isn’t always tight. Gemination crowns – two crowns attempt to form on one tooth with (usually) normal root formation. This is most common in maxillary incisors in my own experience. Many more examples exist. To find the proper names (and pictures) of many such issues you can go to this link: https://avdc.org/avdc-nomenclature/ One veterinary dental radiography textbook is head and shoulders above the others out there. It is a 2009 text but has 837 quality images. Atlas of Dental Radiography in Dogs and Cats. Gregg A. DuPont and Linda J. DeBowes Saunders Elsevier. ISBN 978-1-4160-3386-8 The lecture will be image heavy and include case types we see commonly.

134

Food Animal

135

136

Food Animal

Bill Pittenger

Poultry Health Program Manager - Missouri Department of Agriculture Jefferson City, Missouri

137

138

History of the NPIP

A Review of the National Poultry Improvement Plan January 2020 By Bill Pittenger

• Started in the early 1900’s as the Bacillary White Diarrhea (BWD) Program. • In the 1930’s the BWD Program was renamed the National Poultry Improvement Plan. • The NPIP was to focus on eradicating pullorum and typhoid salmonellas from the commercial poultry industry. • Pullorum Disease caused on average 80% mortality in hatching eggs and chicks.

The NPIP is comprised of 4 main parts. • Since then several disease programs have been added to the NPIP to meet various needs of the poultry industry. • These disease programs include: • Mycoplasma • Avian influenza • Salmonella (SE Clean, Sanitation Monitored and Salmonella Monitored)

• • • •

Part 145 Breeding Poultry Part 146 Commercial Poultry Part 147 Lab Testing Procedures Part 56 Program Standards

Part 145 is comprised of 9 subparts • Subpart A. General provisions. • Subpart B. Egg-Type .Chicken Breeding Flocks and products. • Subpart C. Meat-Type. Chicken Breeding Flocks and products. • Subpart D. Turkey Breeding Flocks and products.

139

• Subpart E. Hobbyist and exhibition water fowl, Exhibition poulty, and Game Bird breeding flocks and products. • Subpart F. Ostrich, Emu, Rhea, and Cassowary. • Subpart G. Primary egg-type chicken breeding flocks and products. • Subpart H. Primary meat-type chicken breeding flocks and products.

Part 146 is comprised of 5 Subparts • Subpart I. Meat-type waterfowl breeding flocks and products.

Three points of the National Poultry Improvement Plan • Bio-security. Practice and Teach bio-security protocols. • Surveillance. Disease Testing Programs (parts 145 & 146). • Education. Outreach programs and daily interactions with poultry producers.

140

• Subpart A. General Provisions • Subpart B. Commercial Table-Egg Layer Flocks • Subpart C. Meat-Type Chicken Slaughter Plants. • Subpart D. Meat-Type Turkey Slaughter Plants. • Subpart E. Commercial Upland Game Birds, Waterfowl, Raise-for-Release Upland Game Birds and Waterfowl.

Biosecurity Guidelines: KEEP YOUR DISTANCE: • • • • •

Restrict access to your birds Use barriers to prevent contact between your birds and wildlife, especially wild waterfowl Keep pets out of barns Allow no visitors into your barns or areas close to your barns Don’t visit places that have poultry

KEEP IT CLEAN: Person: • • • •

Have a dedicated pair of shoes and clothing to wear when working around your birds Foot bath or some form of disinfection should be at entrances of your barns Wash hands with soap and water or hand sanitizer before entering your barn, then repeat process upon exiting and before entering the next barn Take care of sick or quarantined birds last

Barn: • • • • • • •

Clean and disinfect equipment that comes in contact with the birds and/or their dropping Try to clean feeders and waterers daily, keep them clean from debris Remove manure to prevent buildup Manure and debris needs to be removed prior to cleaning and disinfecting Dispose of dead birds properly so not to spread disease Any death loss that occurs need to be removed daily Keep the housing area clean and dry best as possible

Rodent Control: • • • • •

141

Rodent spread diseases and parasites Keep feed in a protected area or storage container away from rodents Clean up spilled or old feed around feeders. Keep debris/trash away from outside barn Keep inside storage area clean and free from a food sources for the rodents

KEEP IT CLEAN: Rodent Control: • • • •

Clean up feed spills after they occur so not to attract rodents Use some form of traps or bait stations around barns/outbuildings Switch rodenticide every 6 months Keep weeds/grass trimmed around barns

Insect Control: • • • •

Don’t allow manure to buildup Keep coop area and nesting area clean and dry as much as possible Remove or prevent standing water from occurring Use some form of traps, stripes, or baits to control flies and other insects

Wildlife Control: • • • • •

Reduce food source for the wild birds along with other wild animals Remove standing water Avoid using pond water Remove perches, ledges, or any other area where wild birds could potentially use for a nesting area. Fix holes in roofs, roof lines, screens and walls

DON’T HAUL DISEASE HOME: • • • •

142

Don’t borrow or loan equipment , tools, coops/cages out without first properly cleaning and disinfecting them before they return to your property Don’t share birds Clean and disinfect all wheels, on vehicles, wagons, trailers, etc if visiting an area or a farm where poultry is located Don’t share porous materials or cardboard egg cartons because they cannot be disinfected.

References: “Avian Influenza Finding Emphasize the Need for Good Biosecurity”, United States Department of Agriculture, Animal and Plant Inspection Service, Veterinary Services, APHIS 91-55-099, April 2016 “Backyard Biosecurity Practices to Keep Your Birds Healthy”, United States Department of Agriculture, Animal and Plant Health Inspection Services, Program Aid No 1765, March 2015 “Prevent Avian Influenza at Your Farm, Improve Your Biosecurity with Simple Wildlife Management Practices”, United States Department of Agriculture, Animal and Plant Health Inspection Services, July 2015

Bill Pittenger Poultry Health Program Manager Missouri Department of Agriculture Animal Health Division 573-644-4732 Bill.Pittenger@mda.mo.gov

143

144

145

146

147

blank page

148

TESTING FOR PULLORUM-TYPHOID DISEASE The most common test used to detect pullorum-typhoid disease is the rapid whole-blood plate test. Three other tests— the rapid serum plate test, the tube agglutination test, and the microagglutination test—can also be used but must be performed in an authorized laboratory. A negative test result— either from an authorized lab or a certified blood tester— is required for all birds that will be exhibited. Infected birds that don’t die of pullorum-typhoid disease may grow to maturity and remain lifetime carriers. The rapid whole-blood plate test, like the other three methods, tests birds for immune substances called antibodies, which are proteins that are carried in the bloodstream following exposure to the disease. To detect antibodies in the blood, a solution called an antigen is used. The antigen is made from pullorum-typhoid bacteria that have been chemically killed and suspended in a salt solution. When this antigen is mixed with the blood of a disease bird, the antibodies agglutinate. Simply put, this means that the pullorum-typhoid antibodies clump together with the antigen. A bird showing this type of result is labeled as being a reactor. Since the blood of a healthy bird does not contain pullorum-typhoid antibodies, no clumps form when its blood is mixed with the antigen. Much of the success in preventing the spread of pullorum-typhoid disease in chickens and other birds can be directly attributed to the rapid whole-blood plate test. This simple procedure, when properly done, accurately detects birds carrying pullorum-typhoid antibodies in their blood. This test can be easily done by anyone who has been trained in the proper techniques.

MATERIALS NEEDED FOR TESTING Materials needed to conduct the rapid whole-blood plate test include:

149

•

Bottle of properly stored antigen

•

Portable table

•

Glass, porcelain or opaque plastic testing plate(s)

•

Light box (optional)

•

Bleeding needle and standardized blood loop. Note: Although there are different kinds of blood loops, for this test they must all be:

20-gauge wire

2 1/2 inches in length

3/16 inch diameter loop

•

Container of fresh water (for rinsing the bleeding needle and blood loop)

•

Bucket of fresh water (for rinsing the testing plates)

•

Identification bands for birds showing a positive reaction In addition, you will need the following:

•

Clean coveralls and headgear

•

Rubber boots, (disinfected)

•

Holding pen for the birds being tested

•

Separate coop/pen for isolating any birds that test positive

SAFE HANDLING PROCEDURES 1. Antigen Proper handling of the antigen is important for obtaining accurate test results. •

150

When not being used, the antigen should be stored in a refrigerator at approximately 45 degrees Fahrenheit.

•

Before testing, remove the antigen from the refrigerator and allow it to warm up to room temperature (65–75 degrees Fahrenheit).

•

Refrigerate the antigen again immediately after testing to keep it fresh. Using past-date or improperly stored antigen increases the possibility of unreliable results.

•

If a large number of positive results are observed, these may be false reactions caused by using old antigen that becomes too sensitive. 2. Birds When performing the rapid whole-blood plate test, it is extremely important to handle the birds properly so that none are harmed.

•

When testing a large number of birds, the testing procedure should involve a minimum of three to four people: one or two to catch the bird to be tested, one to position and hold the bird during testing, and another to draw the blood and test it.

•

Two people can manage the procedure if only a few birds are tested.

•

Everyone involved in the testing must practice safe biosecurity techniques.

•

This means wearing clean coveralls, headgear, and rubber boots. Each person should carefully scrub his or her boots with a disinfectant before coming into contact with the flock.

BEFORE YOU BEGIN THE TEST To achieve the most reliable testing results, everyone involved in the testing must practice good biosecurity techniques. •

Each person should wear clean coveralls, headgear, and rubber boots.

•

All participants should carefully scrub their boots with a disinfectant before coming into contact with the flock. It is important to gather all materials before you begin testing, so you do not have to leave the poultry area.

151

•

Set up your portable table and testing materials close to the area for catching birds.

•

Only after checking to make sure you have all of the testing materials needed to perform the tests, you may begin Step 1.

•

Do not begin Step 1 until you have all of the testing materials properly prepared.

STEPS FOR CONDUCTING A WHOLE-BLOOD PLATE TEST Step 1. Apply antigen to the test slide. •

Ideally, the testing plate needs to be somewhere between 70 and 80 degrees Fahrenheit.

At this temperature, the plate should feel warm to the touch.

•

If the testing area is cold, place the light box under the testing plate to warm it.

•

Hold the dropper straight up and down, close to the glass surface, to keep the antigen from splattering.

•

Allow normal-size drops to fall one at a time onto the testing plate.

•

If the antigen should accidentally spill during handling, there is no danger of spreading the disease, since the organisms are dead. While some testing plates are plain, many have a large number of squares printed or etched on them. This allows for groups of up to 60 birds to be tested with 10 grams of antigen being applied in a row at one time. Make sure that the drops of antigen don’t dry up on the plate before being mixed with blood. Step 2. Position the bird’s wing. Be sure to handle the birds with care.

•

152

Gently turn the bird on its back with a grip on their legs to prevent the bird from clawing.

•

Tuck one wing close to the body so the bird will not flap when blood is drawn. Larger birds may require two people to position.

•

With the assistance of another person, extend the bird’s wing and spread it out flat on the table so the underside is exposed. This uncovers the wing vein, or brachial vein, which is the large blue vein from where the blood sample is taken.

•

Keep in mind that feathers may need to be plucked from this elbow area to expose this vein.

•

Have a paper towel ready to place on the inside of wing to clot birds that may be excessively bleeding. Step 3. Use the bleeding needle to puncture the wing vein and draw the blood sample.

•

After the testing plate is prepared with the antigen, hold the bleeding needle like a pencil and gently puncture the wing vein.

•

Keep in mind that the needle needs to be sharp so this can be done easily.

•

To help make the procedure as simple as possible, a commonly used type of bleeding needle also has a blood loop attached.

•

Using a blood loop with the correct diameter provides the exact amount of blood needed to perform the test. Step 4. Mix the collected blood with the antigen on the testing plate.

•

When the blood loop is full, without any gaps, the blood contained in it should be mixed with one of the drops of antigen on the testing plate.

•

The loop is used to combine the bird’s blood with the antigen on the testing plate.

•

When doing this, it is necessary to mix the blood and antigen together so they form a smear about the size of a dime to a nickel. Step 5. Clean the bleeding needle and blood loop.

153

•

After combining the sample of blood with the antigen, you must clean the needle and loop before drawing the next blood sample.

•

Rinse them in a container of fresh water, then wipe them with a clean cloth. (Repeat steps 2-5 until the testing plate is full). Step 6. Rotate the testing plate and watch for a reaction.

•

With the blood and antigen mixed together, the testing plate needs to be tilted in a rocking motion for about two minutes, so any reactions can be observed.

•

Sometimes a positive result will be evident after only 15 to 30 seconds.

•

Place the light box under the testing plate to make results easier to see. Step 7. Evaluate your test results. Negative Test Result

•

No clumping of sample within 2 minutes.

•

Bird may be returned to the flock. Positive Test Result

154

•

Clumping occurs in sample within 2 minutes.

•

If clumping occurs, re-test the bird to make sure that clumping is within 2 minutes, it only indicates a possible positive test result. This result must be verified by further testing conducted by an authorized laboratory.

•

Do not panic! It is possible this is a false positive. Follow-up testing is required of serum by tube-agglutination test, or microagglutination test, and/or internal organ Salmonella culture test.

•

Attach identification band to mark the bird as a positive reactor.

•

Isolate the bird immediately from the rest of the flock until further testing can be completed.

•

Contact the Missouri Department of Agriculture, Poultry Health Program immediately at 573-751-3377. A determination of a positive reaction is made by looking for clumps that form after mixing the bird’s blood with the antigen. This happens when the antibodies in the blood combine with the killed bacteria. For the rapid whole-blood plate test, a blue dye is added to the antigen so the bacteria becomes stained, making it easier to interpret the results. If the reaction is positive, blue clumps can be seen in the mixture following an interval of between fifteen seconds and two minutes. Remember, there are various degrees to which this reaction, called agglutination, takes place. If the results are negative, meaning that the tested bird does not have pullorumtyphoid disease, no clumping will be evident. But a true positive reaction shows a definite clumping, or agglutination, while causing the blood and antigen mixture to become clearer, or more transparent, where there are no clumps. Sometimes dust on the testing plate may look like a positive reaction. To tell the difference, remember that clumping caused by dirt takes place only in one or two spots. To help avoid possible dust and to make sure that the smears don’t dry up following a test, clean the plate as soon as possible after the results have been determined. To do this, dip the testing plate in a bucket of clean water, use a large scrub brush to remove all residue, then wipe it dry with a squeegee and clean cloth. A positive test result, however, does not always mean that a bird is infected with pullorumtyphoid disease. Sometimes a reaction is caused by what is called cross agglutination. This happens when other antibodies are present—ones that are produced by an antigen closely related to those of pullorum-typhoid bacteria.

155

156

Food Animal

Daniel Shaw, DVM, PhD, DACVP, DACPV MU-College of Veterinary Medicine - Retired Columbia, Missouri

157

158

Diseases of Poultry

Poultry Practice To help 4-legged practitioners think about it: Broilers are analogous to beef cattle. Turkeys are analogous to hog production. Layers are analogous to dairy cattle. Game birds (and etc.) are analogous to small ruminants.

Daniel Shaw, DVM, PhD, DACVP, DACPV Veterinary Medical Diagnostic Laboratory University of Missouri

Wing Vein

Jugular Vein

159

Serum

Serum Rest blood samples at angle to maximize serum yield. 6 to 8 hours at room temperature for good clot retraction.

Pharyngeal Swab

Coccidiosis Requires warmth and moistureâ&#x20AC;&#x201D;6-8 day life cycle Takes 3 cycles before signs Pasting of vents Blood in feces Thickened and hemorrhagic wall of intestine Intestinal cores

160

Pull off clot. Send serum overnight.

Enteric Disease

9 wk. old Chukar

Chicken Hen

9 wk. old Chukar

Pheasant Chick 4-weeks-old

Diagnosis of Coccidiosis 4X

20X

161

Prevention, Treatment, and Control of Coccidiosis Prevent exposure. Raise on wire Vaccinationâ&#x20AC;&#x201D;Chickens & turkeys. Amprolium, sulfa, ionophores. Feed or water Immune to a species once they survive the infection. Lasts 4 weeks without re-exposure

Salmonellosis Salmonella spp. Depression and high mortality most commonly in young poultry (under 2 weeks of age). Vertical transmission for S. pullorum, S. gallinarum, and S. enteritidis (group D). Horizontal transmission for most of the paratyphoids. S. typhimurium can be transmitted vertically.

Omphalitis

Cecal cores

Hepatitis

Diagnosis and Treatment of Salmonellosis Bacterial culture. Treat with appropriate antibiotic. Prevention: NPIP source chicks for group D Salmonella spp. Appropriate sanitation and rodent control for paratyphoids. Human infection possible.

162

Blackhead Histomoniasis. Caused by the protozoan Histomonas meleagridis. Turkeys, chukar partridge, peafowl. Chickens can get it but usually don’t get sick. Typhlitis and hepatitis--caseous cecal cores and round pale spots on liver. Carried by cecal worm which is harbored by earthworms.

Treatment and Prevention No approved treatment for food animals. Metronidazole under veterinary supervision for “pets” not food animals. Treat flock for cecal worms. Control earthworms.

163

Ulcerative Enteritis Quail Disease-- Clostridium colinum. May be secondary to coccidiosis. Birds become emaciated and weak and die. Multiple areas of necrosis and ulceration in the intestines—ulcers may perforate and cause peritonitis.

Treatment and Control Treat coccidiosis if present. Antibiotics in water. Enhance sanitation. Raise on wire floors. Monensin in feed.

Respiratory

164

Gasping Chicken

Swollen Head & Conjunctivitis

Exudate partially occludes larynx.

Exudate in Trachea In larynx, mouth, or esophagus; thick caseous plaques may occlude the larynx. May have high mortality.

Hemorrhage in Tracheas

Causes of Tracheitis Infectious laryngotracheitis virus--Herpesvirus. Chickens, pheasants, peafowl of any age. Wet form of fowl pox--Pox virus. All species

165

ILT

Fowl Pox

Intracytoplasmic inclusions.

Proliferation of epithelial lining.

Intranuclear inclusions

Prevention and Control of ILT & Fowl Pox Must differentiate ILT from wet form of fowl pox. ILT virus very delicate and does not survive long. Shed when stressed Reportable in Missouri. Pox is durable in environment. Requires abrasions for entry Cleaning and disinfection between flocks Control vectors Vaccination.

Airsacculitis

166

Pneumonia

Septicemia

Foci of necrosis and inflammation in liver. May see swollen liver and spleen.

Causes Colisepticemia: E. Coli Fowl cholera: Pasteurella multocida Infectious coryza: Avibacterium (Hemophilus) paragallinarum MG: Mycoplasma gallisepticum

Prevention and Treatment Provide optimal environmental conditions. Keep free ranging animals and birds away. Water sanitation. Buy from NPIP accredited sources—MG Vaccination: Bacterins--injection Modified live vaccines—spray, eye-drop, wing web Antibiotics: May develop resistance.

167

Diagnosis Culture to identify cause: Liver Lung Trachea Swab of air sac PCR assay of trachea for MG, AI, NCD.

Antibiotics for Use in Poultry Tetracyclines Water and feed labels—requires prescription. Aureomycin brand of chlortetracycline can go in feed for laying hens—requires VFD. Bacitracin Sulfa—requires prescription Neomycin—requires prescription Penicillin—requires prescription Tylan—VFD Others

Parasites

Lice Common in free range and wild. Insect: 6 legs. Uncommon in commercial operations. Bird species specific. On the host all the time.

Louse Nits

Chicken Louse

Northern Fowl Mite (Ornithonyssus sylviarum) Bloodsucking. On host all the time. 8 legs. Only stays on birds but is not bird species specific. May harbor other disease agents.

168

Northern Fowl Mite (Ornithonyssus sylviarum)

NFM by Vent

NFM Nits on Feather

Northern Fowl Mite

Control of NFM and Lice

Chicken Mite (Dermanyssus gallinae)

Prevent contact with wild birds. Spray with approved insecticides at 5 to 7 day intervals. Keep facility empty and above freezing for 10 days.

169

Dermanyssus gallinae Bloodsucker--Causes anemia; can kill young birds. Uncommon in US commercial operations. Live in cracks and crevices. Feed on host at nightâ&#x20AC;&#x201D;examine a few hours after have gone to roost. Survives up to 34 weeks without a blood meal. Can be problem for mammalian species.

Chicken Mite

Control of Chicken Mite

Blackflies

(Buffalo Gnats)

Survives for several months off host. Thoroughly clean buildings and apply approved insecticide (Tempo by Bayer, malathion, etc.). APPROVED IN EUROPE: Fluralaner via drinking water 0.5 mg/kg body weight twice at 1-week interval. Roost paint.

Scaly Leg Mite

Scaly leg mite (Knimidocoptes mutans)

Knemidocoptes sp. Life cycle on host. Direct transmission. Unfeathered portions of body. Burrow in skin. Raises scale on legs and causes a rough appearance of leg and occasionally on bare skin of head.

170

Scaly Leg Mite

Treatment and Control of Scaly Leg Mite Dip legs in mineral oil or approved insecticide. Ivermectin not approved. Clean up of facility. Clean up environment. Cull old birds if possible.

Round Worms (Ascaridia sp.)

Tapeworms

Insects such as flies and darkling beetles serve as intermediate hosts. Not usually harmful. Can get into eggs occasionally.

Cecal Worm

Heterakis gallinarum Carries Histomonas meleagridis. Carried by earthworms.

171

Gapeworms

Syngamus trachea located in trachea. Carried by earthworms. More severe in young birds.

Gapeworms in Chukar

Threadworms Capillaria sp. have wide host range. Cause unthriftiness. Direct transmission but can be carried by invertebrates (earthworms and copepods). Upper digestive tract and intestine. Scrapings, fecal smears, histopath. Not prolific egg layers.

Capillaria sp. embedded in crop mucosa

172

Capillaria sp.

Fecal Exam

Treatment and Prevention of Nematode Infestations Treatment with appropriate anthelmintic: Fenbendazole--broad spectrum. Licensed for feed in turkeys. Licensed for water in laying chickens. Piperazine in water for roundworms. Levasole in waterâ&#x20AC;&#x201D;broad spectrum but not licensed for use in poultry. Control earthworms. No approved treatment for tapeworms in birds.

Miscellaneous

Broiler Ascites Syndrome Right ventricular heart failure. Seen primarily in broilers 2 to 5 weeks of age. Can be seen in turkeys. May have dyspnea, weakness, or are found dead. Enlarged cardiac silhouette, right ventricular dilation and hypertrophy, and ascites.

Ascites

Causes of Broiler Ascites Syndrome High altitude Chilling in brooding Excessive salt in ration Other

173

Leukosis Complex Tumors in any internal organ Marek's diseaseâ&#x20AC;&#x201D;herpesvirus (DNA) Lymphoid leukosisâ&#x20AC;&#x201D;retrovirus (RNA)

Marek's Disease

Peripheral nerves and CNS. Virus shed from feather follicles in dander. All ages affected. 174

Marek's Disease

Lymphoid Leukosis Tumors in bursa are common. Rarely in nerves. Seen in sexually mature birds. Egg transmitted.

Sciatic nerve infiltrated by neoplastic lymphocytes. HE 10X and 40X

Control of Leukosis Differentiate MD from LL. MD controlled vaccination at day of age. Cell associated vaccine is best. Lyophilized available. Cleaning and disinfection of brooder house. Single age brooding. LL controlled by testing and elimination of infected breeders.

175

176

Food Animal

Bob Weaber, PhD

Professor - Department of Animal Sciences and Industry Kansas State University Manhattan, Kansas

177

178

“The native cattle are extinct, but the island is full of artificial breeds. The agriculturalist Bakewell created sheep and cows and horses to order, and breeds in which everything is omitted but what is economical. The cow is sacrificed to her bag; the ox to his sirloin.” Ralph Waldo Emerson Bob Weaber, Ph.D.

2020

MVMA Convention - Columbia, MO

Cow-calf Ext. Specialist Kansas State University 785-532-1460 bweaber@k-state.edu

 Set Goals  Assess Cow Herd  Assess Resources  Breed Selection  Bull Selection  Reproduction  Structure  Performance  Visual Appraisal http://www.nbcec.org/producers/sire.html 2020

MVMA Convention - Columbia, MO

2020

MVMA Convention - Columbia, MO

Phenotype Genetic Merit

2020

179

MVMA Convention - Columbia, MO

2020

MVMA Convention - Columbia, MO

Contemporary Group and Other Effects

ď&#x201A;&#x2014; Animal to animal variation

ď&#x201A; Genetics ď&#x201A; Additive (the stuff for which we select) ď&#x201A; Non-additive (heterosis)

ď&#x201A; Environment ď&#x201A; Forage resources ď&#x201A; Dam milk production

ď&#x201A; Effects A = Breeding value (Additive gene effects)

ď&#x201A; Sex

D = Dominance effects (pairing of genes effects)

ď&#x201A; Age of calf

I = Epistatic (interactions among genes)

ď&#x201A; Age of dam

2020

MVMA Convention - Columbia, MO

2020

MVMA Convention - Columbia, MO

ď&#x201A;&#x2014; Examine variation to build models

Pedigree Estimate EPD

ď&#x201A;&#x2014; Exploit the genetic contribution to phenotypic

variation via selection

TRUE Progeny Difference

ď&#x201A;&#x2014; Non-genetic variation can be modeled ď&#x201A; Contemporary group, sex of calf, age of dam, breed composition, heterosis ď&#x201A;&#x2014; Adjust records to equalize animals for non-genetic

Sire EPD

Dam EPD

effects which cause variation in phenotypes

Mendelian Sampling Effect 2020

MVMA Convention - Columbia, MO

â&#x201E;&#x17D;ďż˝ =

đ?&#x153;&#x17D;đ?&#x153;&#x17D;ďż˝ďż˝

2020

180

đ?&#x153;&#x17D;đ?&#x153;&#x17D;ďż˝ďż˝

đ?&#x153;&#x17D;ďż˝ďż˝ đ?&#x153;&#x17D;ďż˝ďż˝

2020

MVMA Convention - Columbia, MO

= 40%

h2 is the proportion of variation between individuals that is under genetic control.

MVMA Convention - Columbia, MO

 A way of comparing animals

DNA Markers EPD Ratios Adjusted weights Raw Weights

group

Ability to generate response to selection

 Contemporary group average = 500  Animal = 550  Ratio = 110  (550/500)*100

 Why not outside of that group?

Cost

 Different environmental influences  Group averages may not be equal

Visual Appraisal 2020

MVMA Convention - Columbia, MO

within a contemporary

2020

MVMA Convention - Columbia, MO

 Separates the ‘wheat from the chaff’  What information is included?

 Pedigree information  (Parents, grand-parents, half –sibs, etc.)

    

2020

MVMA Convention - Columbia, MO

Individuals’ own record (very important) Progeny information Correlated traits (BW, WW, YW) REMOVES ENVIRONMENTAL EFFECTS Can be used across herds but only within a breed

2020

MVMA Convention - Columbia, MO

Expected

SIRE (1/2 EPD )

 Future, average, mean

Progeny

CALF

 Offspring

Difference

 Implies comparison between animals  NOT phenotypic performance

DAM (1/2 EPD)

Measure of relative merit among individuals  Estimate of average effect of animal as parent  Estimate of average gamete genetic merit 

2020

181

MVMA Convention - Columbia, MO

Pedigree Est. EPD = 1/2 Sire EPD + 1/2 Dam EPD 17

2020

MVMA Convention - Columbia, MO

+30 lb EPDI = (0.5*EPDS) + (0.5*EPDD) + (0.5 *Mendelian Sampling Effect)

-10 lb

Mendelian sampling (MS) is the difference between an individual's EPD and its parent average or pedigree estimate (PE-EPD). In other words, how different is the progeny’s genetic sampling from the average mating of these parents. See Beef Improvement Federation Guidelines 2020

+15 lb

MVMA Convention - Columbia, MO

Sire

+ 5 lb

Offspring of one sire exhibit more than ¾ diversity of the entire population

+10 lb

2020

Progeny +10 lb

MVMA Convention - Columbia, MO

0 .0 6 0 .0 5

+30 lb

Garrick, 2013

0 .0 4

+15 lb

0 .0 3 0 .0 2

-10 lb

0 .0 1

+ 5 lb

Sire (EPD is “shrunk”)

Sire EPD +8-9 lb 2020

+10 lb 21

Average value of gametes EPD = 40

Progeny +10 lb

MVMA Convention - Columbia, MO

2020

MVMA Convention - Columbia, MO

0.06 0.05

 Consists of animals that are:

0.04

 Given equal opportunity to perform  Of similar age and sex

0.03

 Identify fair competition

0.02

 Formed from management information

0.01 0

 The basis of all genetic comparisons 20

10 lb. Difference in EPD of Two Bulls 2020

182

MVMA Convention - Columbia, MO

2020

MVMA Convention - Columbia, MO

 Consists of animals that are:  Given equal opportunity to perform  Of similar age and sex

 Identify fair competition  Formed from management information  The basis of all genetic comparisons

Phenotype = CG + Genetics Genetics = Phenotype - CG MVMA Convention - Columbia, MO

 Much more effective generating response to

1200 Bulls Adjusted YW (lb)

selection than phenotypic selection  Can be used to:  Increase performance  Decrease performance  Optimize performance

 Do not select for maximum genetic expression w/o

100

1150

1100

1050 1000

950

900

850 800

regard to other factors

1970

 Nutritional conditions

YW EPD

2020

1975

1980

1985 1990 1995 Year of Birth YW-Bulls

2000

2005

-20 2010

YW EPD

Data Source: 2009 Am. Angus Sire Evaluation Report; Phenotypic and Genetic Trends MVMA Convention - Columbia, MO

2020

YWPheno = 910 + 3.38*YWEPD R2 = 0.96

-20

20 YW-Bulls

40 YW EPD

Adjusted BW - Bulls

YW-Bulls

YW Line Fit Plot 1250 1200 1150 1100 1050 1000 950 900 850 800

100

85 83 81 79 77 75 73 71 69 67 65 1970

Predicted YW-Bulls

183

MVMA Convention - Columbia, MO

3 2 1 0 -1 -2 1975

1980

1985

1990 1995 Year of Birth

BW-Bulls

Data Source: 2009 Am. Angus Sire Evaluation Report; Phenotypic and Genetic Trends 2020

MVMA Convention - Columbia, MO

BW EPD

2020

2000

2005

-3 2010

BW EPD

Data Source: 2009 Am. Angus Sire Evaluation Report; Phenotypic and Genetic Trends 29

2020

MVMA Convention - Columbia, MO

BW Line Fit Plot 85

BWPheno = 75 + 2.68*BWEPD R2 = 0.95

BW-Bulls

80 75 70 65 -3

-2

-1 BW-Bulls

0 BW EPD

Predicted BW-Bulls

Data Source: 2009 Am. Angus Sire Evaluation Report; Phenotypic and Genetic Trends 2020

MVMA Convention - Columbia, MO

2020

MVMA Convention - Columbia, MO

 Selection is challenging  Not all economically

important traits have EPD

    

Fertility Disease resistance Fescue fitness Conformation traits Mature weight

 Use the right tool for job!  Multiple trait selection 2020

MVMA Convention - Columbia, MO

0.12

0.1

 Measure of reliability of EPD

0.08

 How much data was included in making the EPD  0.05

Pedigree estimate

 0.30

Own performance plus pedigree info.

 0.90

Lots of progeny data

0.06

0.04

 As Prediction Error Variance goes to zero accuracy

0.02

goes to 1.00

Difference in EPD Accuracy Acc = 0.30, SEP = 11.4 2020

184

MVMA Convention - Columbia, MO

2020

Acc = 0.8, SEP = 3.3

MVMA Convention - Columbia, MO

BIF Accuracy

 Mitigation of risk

0.90 0.80 0.70 0.60 0.50 0.40 0.30 0.20 0.10 0.00

 Faster genetic progress

 BV / t 

rBV , EBV i BV L

 Increased accuracy does not mean higher or lower EPDs!  Increased information can make EPDs go up or down

2020

MVMA Convention - Columbia, MO

2020

MVMA Convention - Columbia, MO

2020

MVMA Convention - Columbia, MO

G/T SNP

1 BTA-6

2 BTA-6 •

2020

185

MVMA Convention - Columbia, MO

…ATCGTAGATATTGGCC… …TAGCATCTATAACCGG… …ATCGTATATATTGGCC… …TAGCATATATAACCGG…

Mutation may be in exon (coding sequence; possibly causal) or in intron (non-coding sequence) of gene

2020

MVMA Convention - Columbia, MO

McClure et al., 2011

BTA-6 Marker 1

Quantitative Trait Nucleotide (QTN) = Favorable Allele = Unfavorable Allele 2020

MVMA Convention - Columbia, MO

2020

Cattle usually have 30 pairs of chromosomes (29 autosomes and 1 sex) Half of the pair from sire and half of the pair from dam Each chromosome has about 100 million base pairs (A, G, T or C) ~ 3 billion base pairs per animal

MVMA Convention - Columbia, MO

-2

-4

-3

-2

-5

-2

-3

-5

-4

-5

EBV=10 EPD= 5 EBV= -6 EPD= -3

EBV= 2 EPD= 1

Blue base pairs represent genes

Yellow represents the strand inherited from the sire Orange represents the strand inherited from the dam 2020

MVMA Convention - Columbia, MO

2020

Below-average bulls have- some above-average alleles and vice46versa! MVMAwill Convention Columbia, MO

The expected (averaged across loci) relationship between individuals.

Imputation

â&#x20AC;˘All animals imputed to common SNP density

NCE 2020

186

MVMA Convention - Columbia, MO

1 2 3 4 5 6 7 8 9 10 11

â&#x20AC;˘Includes pedigree, phenotypes, genotypes 47

2020

0 1

0 0

0.5 0.5

0 0

0.25 0.25

0 0

0 1

0 0 1

0 0 0 1

0 0 0 0 1

0 0 0.5 0.5 0 1

0.5 0.25 0.25 0.5 0.25 0.25 0 0 0.25 0 0 0.25 0 0.5 0 0 0 0.5 1

MVMA Convention - Columbia, MO

0.5 0.5 1 0.25 1

The realized (averaged across loci) relationship between individuals. 1 2 3 4 5 6 7 8 9 10 11 1 0.99 0.01 0.01 -0.13 0.12 -0.04 0.49 0.01 -0.09 0.2 -0.04 0.81 0.00 -0.18 0.09 0.08 0.41 0.1 -0.03 0.11 0.06 2 0.8 0.16 -0.03 -0.01 -0.09 -0.06 0.46 0.14 0.24 3 1.03 -0.09 0.13 -0.12 0.05 0.57 0.25 0.27 4 0.95 -0.04 0.09 0.5 -0.1 -0.05 0.41 5 0.85 0.00 0.43 0.11 0.16 0.09 6 0.95 0.09 -0.08 0.44 0.04 7 1.11 0.06 0.13 0.58 8 1.04 0.52 0.51 9 0.99 0.23 10 1.03 11

2020

MVMA Convention - Columbia, MO

2020

from Theta Solutions, LLC a priori ď&#x201A;&#x2014; American Hereford Association (AHA) ď&#x201A;&#x2014; International Genetic Solutions (IGS) ď&#x201A; Multi-breed ď&#x201A; 15 breed organizations

MVMA Convention - Columbia, MO

ď&#x201A;&#x2014; BOLT software

ď&#x201A;&#x2014; Marker subset (~2,500) identified

2020

MVMA Convention - Columbia, MO

187

đ?&#x153;&#x17D;đ?&#x153;&#x17D;ďż˝ďż˝

2020

MVMA Convention - Columbia, MO

2020

MVMA Convention - Columbia, MO

â&#x201E;&#x17D;ďż˝ =40%

%GV= 80%

2020

â&#x201E;&#x17D;ďż˝ =40%

%GV= 33%

đ?&#x153;&#x17D;đ?&#x153;&#x17D;ďż˝ďż˝

MVMA Convention - Columbia, MO

BIF Accuracy

0.90 0.80 0.70 0.60 0.50 0.40 0.30 0.20 0.10 0.00

Spangler, 2011 2020

MVMA Convention - Columbia, MO

TRAIT CED BWT WWT YWT MCE Milk STAY Marbling 2020

AAA 28 21 26 21 18 33 No EPD 9

AHA 17 8 12 9 ---------3

MVMA Convention - Columbia, MO

2020

MVMA Convention - Columbia, MO

 Mitigation of risk

IGS 15 21 22 24 3 18 25 5

 Faster genetic progress

 BV / t 

rBV , EBV i BV L

 Increased accuracy does not mean higher or lower

EBV!

 Increased information can make EPDs go up or down 57

2020

MVMA Convention - Columbia, MO

 Calf survival  Male fertility  Disease susceptibility  Calving ease direct  Growth rate  Feed efficiency  Carcass quality/composition 2020

188

MVMA Convention - Columbia, MO

“There is no easily accessible, objective way for breeders, particularly breeders in the beef and sheep industries where ownership is diverse and production environments vary a great deal, to use these predictions intelligently.”

 Female fertility  Maternal

calving ease  Maintenance requirements*  Longevity  Maternal weaning weight (Milk)*  Disease susceptibility  Adaptation  Temperament 2020

MVMA Convention - Columbia, MO

-- R. M. Bourdon, 1998 61

 Independent Culling Levels

2020

 List of traits that influence “satisfaction”  Relative Economic Value (REV) of each trait

 Increase in satisfaction with one unit change in a trait, all others held constant

 Selection Indexes

 Objective  Easy to use and interpret ($)  Economically driven

 List of characteristics to be measured on animal  Relationships between characteristics (phenotypes)

and traits (genotypes)

 REVs from bio-economic simulation

 Links ERTs and Indicator Traits  Customizable (Site/user specific) MVMA Convention - Columbia, MO

H i  a1BVi1  a2 BVi 2    an BVin 63

 $W - One number to use in selection that

summarizes five  Appropriately weights each trait for its influence of profit  Selection on ‘aggregate merit’ (Hazel, 1943)  Value of each trait - increase in satisfaction with one unit change in a trait, all others held constant  Selection index is formal statement of trade-offs among traits used to evaluate selection candidates (MacNeil et al., 1997) 2020

189

MVMA Convention - Columbia, MO

 Selection on ‘aggregate merit’ (Hazel, 1943)

 Too cumbersome  Inefficient in generating response to selection  Economics sketchy—’seat of pants’ approach

2020

MVMA Convention - Columbia, MO

2020

MVMA Convention - Columbia, MO

Maternal Terminal • $W, $M, $EN (Angus) $B, $F, $G (Angus) • API (Simmental) TI (Simmental) CHB$ (Hereford) • BMI$, BII$ (Hereford) MTI (Limousin) • HerdBuilder (Red Angus) EPI and FPI (Gelbvieh) • $Cow (Gelbvieh) TSI (Charolais) • $M (Beefmaster) GridMaster (Red Angus) $T (Beefmaster)

• • • • • • • •

2020

MVMA Convention - Columbia, MO

 Profitability

per exposure

 Profitability

 HerdBuilder

 Bull A: 134  Bull B: 110

 30 cows/yr. over 4 yrs. = 120 exposures

 120 exposures X (134-110) =

 $2,880 profit difference

 If you follow the assumptions of the

index!

2020

190

per exposure

MVMA Convention - Columbia, MO

index!

2020

MVMA Convention - Columbia, MO

 Set Goals  Assess Cow Herd  Assess Resources  Breed Selection  Bull Selection  Reproduction  Structure  Performance  Visual Appraisal Bob Weaber, Ph.D.

http://www.nbcec.org/producers/sire.html

Cow-calf Ext. Specialist Kansas State University 785-532-1460 bweaber@k-state.edu

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

Pick the right breed(s) PLANNED Crossbreeding Breeding objectives Considerations

Chose right individual in that breed EPDs Genetic risk management Selection indexes

2019

191

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

Our objective is to breed cattle that breed as yearlings, calve unassisted and rear a good calf for sale at weaning every year. We aim to breed functional cattle that flesh easily and can forage on the hills over winter but must have the temperament and soundness to be farmed intensively during calving and the breeding season.

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

Production Environment

 Many

definitions, but here are the musts:

Traits

Feed Stress Milk Mature Ability Resistance Calving Lean Availability Size to to stress ease yield store energy High Low

Low

M-H

L-M

M-H

High

L-H

M-H

Low

L-M

M-H

High

L-M

 Has minimal maintenance requirements, but carries enough body condition to withstand feed shortages  Produces enough milk to raise a good, healthy calf  Gets pregnant  On Time, Every Time  Has excellent maternal characteristics

Adapted from Gosey

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

2019

Don’t forget…she’s a grass harvester first and foremost!

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

1,400 1,350 1,300 1,250 1,200 1,150 1,100 1,050 1,000

322 lb

1975

2005 (McMurray, 2008)

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 16% Milk

2019

192

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

Average Calf Weaning Weight

 27% Wt.

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

Efficiency has to be viewed from an operation standpoint and not from a per cow or per steer basis. – Steve Radakovich at Beef Cow Efficiency Forum, 1984

WW / Exposed Cow

2019

Mature Weight of Cows KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

A. B.

2019

Change environment to fit the cows? Change the cows to fit the environment? KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

Profit = Revenue – Costs Revenue – easy to measure Costs – hard to measure 2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

Seedstock Cattle

2019

193

Communicate Value??

Cow-calf Feeder Packer Consumer

Information

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

ERT EPD

 A trait that has a direct cost or return associated

with it is an Economically Relevant Trait (ERT).

 Traits that are correlated to ERTs are indicator traits.  Example:

INDICATORS

 Sale Wt.

Is Birth Weight or Calving Ease the ERT?

Why??  Weaning Weight or Yearling Weight?

 205 d Weight

Weaning Direct

 365 d Weight

Weaning Maternal (MILK)

 Carcass Weight

600 d. Direct

 Birth Weight

Carcass Weight Direct

 Fat Thickness

Salvage Cow Weight

 Cull Cow Weight

 Probability of Calving Ease

 CE Score, BW, Gest. Length

 Cow Maintenance Feed Requirement

 Mature Cow Wt., BCS, Milk, Gut Wt.

 Days to Target Finish (Fat Th., Weight, Marbling Sc)

 BF and Age at Sl., Wt and Age at Sl., Grade and Age at Sl.

Adapted from Golden et al. 2000 2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

2019

Reproduction:Growth:End Product

2:1:1

(Melton, 1995) KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

(Melton, 1995) 22

 Sell calves at weaning and …  purchase crossbred replacement heifers  think ‘Terminal Sire’, moderate calving ease, high growth  raise your own replacements  think ‘Balance’, calving ease, easy fleshing, moderate milk and moderate growth

2019

194

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 Retain ownership

beef and …

and sell calves in the

 purchase crossbred replacement heifers  think ‘Terminal Sire’, high growth (carcass wt), balance of quality and yield traits  raise your own replacements  think ‘Balance’, calving ease, easy fleshing, moderate milk and moderate growth, balance of quality and yield.

MANAGE MARKET RISK WITH BALANCED CARCASS TRAITS !!

AVOID CARCASS TRAIT LOSERS!! 2019

Reproduction:Growth:End Product

10:5:1

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 If you use terminal trait EPD or terminal indexes in

selection, what do you get? You get response in terminal traits!  If maternal traits are important to you, put pressure on maternal traits  Think ‘optimization’  Traits: CE, CEM, DOC, HP, Stay (rebreeding), MW, ME, replacement indexes

 Align traits used in selection with marketing

endpoint/breeding objective

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 Calf survival

 Female fertility

 Male fertility

 Maternal

calving ease  Maintenance requirements*  Longevity  Maternal weaning weight (Milk)*  Disease susceptibility  Adaptation  Temperament

 Disease susceptibility  Calving ease direct  Growth rate  Feed efficiency  Carcass quality/composition

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

Antagonisms Retained Heterosis

Breed Complementarity Selection tools/trait focus

195

 Heavier calves and more product from smaller

cows

 Benefit of terminal producer  Reduce industry-wide feed intake by smaller cows

 Less calving difficulty industry-wide  Maternal producers are the only ones calving heifers

Do the benefits of selection for economically important/convenience traits within breed (straight-breeding) outweigh the improvement of lowly heritable traits via heterosis (especially maternal)?

 Increased uniformity industry-wide  Common objectives

Selection should be for BOTH additive and nonadditive genetic merit.

 Focus objectives  Only trying to do one thing

 Optimality of stocking rate and profit risk… 2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

SHOULD care about BOTH additive and non-additive effects.

compared to the average of its straightbred parents  More divergent parental lines = more heterosis  NOT available from within breed matings

 Seedstock

producers SHOULD focus on additive genetic merit, and putting it in a package that helps clientele exploit nonadditive effects.

Trait Reproduction (fertility) Production (growth) Product (carcass)

Heritability Low

Moderate

High

 Superiority of a crossbred animal as

 Selection index/EPDs  Hybrid vigor or heterosis

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 Hybrid Vigor

 Commercial cattlemen

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

Heterosis High

Trait

Moderate

Low

Observed Improvement

% Heterosis

Calving rate

3.2

4.4

Survival to weaning

1.4

1.9

Birth weight

1.7

2.4

Weaning weight

16.3

3.9

ADG

0.08

2.6

Yearling weight

29.1

3.8

Adapted from Cundiff and Gregory, 1999 2019

196

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

Trait

% Heterosis

1.36

16.2

Longevity Cow Lifetime Production: No. Calves

0.97

17.0

Cumulative Wean. Wt., lb.

600

25.3



Heterosis increases production 20 to 25% per cow in Bos taurus x Bos taurus crosses; 50% in Bos indicus x Bos taurus crosses in subtropical regions More than half of this effect is dependent on use of crossbred cows

Adapted from Cundiff and Gregory, 1999. 2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 [Dam Weight*Lean Value of Dam + No.

Progeny*Progeny Weight*Lean Value of Progeny] [Dam Feed*Value of Feed for Dam + No. Progeny*Progeny Feed*Value of Feed for Progeny].

 By simply increasing number of progeny per dam

through either selection, heterosis from crossing, or better management, we will increase efficiency of production.

2019

25% % Improvement in Weaning Weight per Cow Exposed



Observed Improvement

20% 15% 10% 5% 0% -5%

Jenkins, MARC

Straightbred Straightbred Cows Cows Straightbred Crossbred Calves Calves

Crossbred Cows Crossbred Calves

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 Two breed terminal  Three breed terminal  Two breed rotation  Three breed rotation  These systems are dependent on:  Production goals  Herd size  Available resources (land and labor)

Adapted from Dickerson 1970 2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 Seedstock production…all the tools all the time!  Genotype is what we build and sell

 Commercial production    

197

Phenotype pays the bills P=G+E What’s the role of ‘E’ proportionally? What genetics technologies should we use?

Sire

 Most of improvement is not from selection of

heifers per se.

 Heritability of fertility/repro traits is low  Maternal trait heritability is low  In commercial herds little to no genetic predictions on candidates

 Sire selection contributes >87% of gene flow in herd

50% Replacement Heifer

over time…make it count!

25% Dam

Maternal Grand Sire Maternal Great Grand Sire 12.5% Maternal Grand Dam

 Leverage sire selection

 “Maternal” is more than “I didn’t select for carcass”

 Select sires of replacements for traits of economic

 Culling open cows is not selecting for fertility

importance for maternal performance

 Improvement comes primarily from bull selection

 Optimal growth, mature size, milk, etc.  Desirable levels of CED, MCE, HP, STAY, $EN, ME

 Presumably larger ranches

 Breeding system-build and maintain optimal levels of

maternal heterosis  Build environmentally adapted cows; breed them to market targeted bulls

 Preferably composite cows  Produce bred cows (2nd or later parity).  F1 cows bred to terminal bulls

2019

 A small number of replacements makes managing

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 Fact is these herds produce a large fraction of all

heifers as a separate group challenging  Night calving—Is it worth it to spend hours looking over a few heifers?

calves in the U.S.

 It seems logical that these herds could increase

profit if they purchased replacement females  Females bred for 2nd (or later) calf

 Bulls selected for terminal traits and cows selected

for maternal traits

 True complementarity

2019

198

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

“The customary approach…has been to select and develop heifers calves on the ranch. However, certain factors have led many managers to re-evaluate their replacement female programs. 1. The inability to… incorporate the advantages of maternal and terminal heterosis… 2. The desire to reduce the number of enterprises they are required to manage… 3. Maternal supplier enterprises that make high quality replacement females more accessible and often more affordable than “home-raised” replacement heifers.” Jack Whittier

 Environmental Effects?

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 Age at breeding  When were they born in calving distribution  Body condition score at calving and breeding

 Genetic Effects  Heritability of traits important to maternal performance? LOW .1.2  Heterosis (value ~$250/cow/year)

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

Calving periods, 21 day intervals 1

651 (64)

304 (30)

64 (6)

Birth date

77a

93b

113c

<0.01

Weaning Weight

482a

469b

433c

<0.03

Prebreeding Weight

651a

642b

607c

0.01

Cycling @ breeding, %

70a

58b

39c

<0.01

Pregnancy rate, %

90a

86b

78c

0.02

Precalving weight

944

946

920

0.06

Calved in 1st 21 days, %

81a

69b

65b

0.01

Calf weaning weight

425

416

409

0.10

8 7 6 Years in herd

n (%)

P-Value

600

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

2 1 1st 21 d

2019

2nd 21 d Time of first calving

later Cushman et al., 2013

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

1 to 21 22 to 42

500

SDSU MARC

Funston et al., 2012 2019

5 4

43 and after

400

 Select heifers born early in calving season (first 30

days) 50% or heifers

 Select heifers from the middle 50% for adjusted

weaning weight to prevent run up in mature weight lactation.  Half of half is a quarter. How many replacements do you need?

300 200 100

 Many breeders will breed enough to replace ~20-25% of herd EACH YEAR.

0 Calf 1

Calf 2

Calf 3

Calf 4

Calf 5

Calf 6

Calf 7

Calf 8

Calf 9

Cushman et al., 2013 2019

199

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 Preferentially select crossbred heifers or AI sired

heifers  Is there any room left to use genomics?  How do you value the genetic merit of traits in your breeding objective to offset the above factors?

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 Do DNA tests work in commercial cattle?  Yes,  if the breed(s) match the panel  Account for ~1/3 to 1/2 of additive genetic variation in traits  Is there a positive ROI?  I don’t know…depends on lots of things

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 Estrus Sync and AI to breed early calved cows to

high merit maternal sires

 Gender sort semen to target female production  reduces proportion of the cows bred ‘maternally’ in herd  Increases cows mated to ‘terminal’ bulls-enhanced calf revenue

 Easier implementation of crossbreeding system

 Genomics to confirm parentage of AI calves if

necessary

 Assume you test 80% of your heifer calves as

‘potential replacements’ and have a 20% replacement rate.  How much does each retained heifer have to return to cover all testing costs?  You retain ¼ of candidates so each retained heifer has to return 4X test cost to break even. $40 test => $160 value capture to be par money

2019

Don’t invest in knowledge you won’t

use to:

 Must inform a selection or management decision and have value you can capture  Market a product (bred replacements)

2019

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

 Genetic progress is gene flow from bull selection

(80% over time)

 Use DNA parentage to preferentially select

daughters of specific sires:

 Maternal focus  AI calves (simplify subsequent breedings)

 DNA parentage/paternity assignment is low cost

($13-15/test)

2019

200

KRIRM Lectureship--Application of Advanced Genetic Technology in Beef Cattle--Centennial, CO

Food Animal

Dietrich Volkmann, DVM, DACT

Professor - MU- College of Veterinary Medicine Columbia, Missouri

201

202

Bull Breeding Soundness Examinations Dietrich Volkmann, BVSc, MMedVet(Gyn), Diplomate ACT Dept. of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri

In 2019 the Society of Theriogenology, whose template and certificate for bull breeding soundness is widely used in North America , issued revised guidelines for this important veterinary contribution to the optimal management of cattle breeding herds. Using the format of the SFT is, however, neither law nor is it the only approach to verifying that a bull is optimally suited to perform his anticipated use in a breeding program. Many practitioners have developed their own methods for the examination of bulls and reporting their findings in the forms of more or less comprehensive certificates/reports. The author uses the SFT format with minor adjustments. 1. Establish the purpose of the BSE: Not all bulls are subjected to a BSE for the same reason. Keeping the purpose of the bull in mind is extremely relevant when interpreting the findings of a breeding soundness examination. Certain purposes require additional tests that are not necessarily included in a “standard” examination. Also, some deficiencies that are commonly held against a bull may not be significant in particular breeding operations. 2. Appropriate signalment: how is the bull identified?; breed and age of bull 3. Relevant anamnestic information: is the bull a virgin?; was the bull recently ill or lame? how did he perform in the most recent breeding season? 4. Evaluate the eyes: can the bull see out of both eyes?; are there any corneal scars (usually caused by pink eye, but can also be the consequence of intra-uterine exposure to BVD)? Any ocular lesions that impair the bull’s ability to find his way or recognize other animals? Squamous cell carcinoma will limit the bull’s functional life span. 5. Body condition: Many state that a bull needs to be in good body condition to perform the “hard work” of breeding during the breeding season, but the author values body condition more as an indicator of general health of the animal. Bulls need to be extremely underconditioned before they stop breeding or suffer from subfertility. Keeping older bulls in lean condition also reduces their weight and hence the stress on their joints and reduces the risk of breeding injuries that result from an excessively heavy bulls breeding smaller females. 6. Locomotor system: In today’s cattle industry the selection of bulls has shifted from a traditional evaluation of the bull’s phenotype to his genotype (in the form of EPDs). Therefore, more emphasis is placed on the animal’s performance traits than on the evaluation of his physical traits. The recognition of screw claw remains important as this condition will most certainly impair the bull’s ability to do his work without significant risk of lameness and will increase the risk of locomotor disease in his offspring (male and female) retained for breeding.

203

The legs are best evaluated visually for symmetry, comparing left and right limbs from the bottom to the top. Any sign of asymmetry should raise an alarm, regardless of whether or not the exact cause for the asymmetry is apparent. Most text books suggest that bulls be observed for lameness prior to being restrained in a chute for the remainder of the BSE, but this is hardly ever practical or even safe. Therefore it may be more practical to visually inspect the locomotor system in the chute and search for evidence of lameness as the bull leaves the chute at the conclusion of the BSE. 7. External genitalia: In the hands of many practitioners this facet of a bull BSE has unfortunately deteriorated into the measurement of the bullâ&#x20AC;&#x2122;s scrotal circumference only. Testes, epididymedes (head, body and tail), and spermatic cords should be palpated for symmetry with regard to size, shape and texture in every single bull that is examined. In addition, the unimpaired mobility of the testes within the vaginal cavity must be confirmed. The skin of the scrotum should be examined for any lesions that may interfere with the normal dissipation of heat from its surface, the primary element of the complex cooling system of the testes. Measuring the widest circumference of the scrotum is a measure of testis size and is not only correlated with the number of spermatozoa produced by the bull, but has also been associated with increased growth of bulls until puberty and earlier age at puberty in the bullâ&#x20AC;&#x2122;s female offspring. Examination of the penis and prepuce is usually accomplished by palpation of the sheath from the scrotum to the preputial opening, paying careful attention to any lumps and/or swellings. The author will also palpate the sigmoid flexure of the penis of every bull. This structure is most commonly not located between the scrotum and the preputial orifice, but rather dorsal and caudal to the neck of the scrotum. In most cases the actual penis is best examined during semen collection when the penis is likely to protrude from the preputial orifice. 8. Internal genitalia: If it were not for seminal vesiculitis, this part of the traditional BSE would probably not ever be performed. The seminal vesicles should be assessed for palpable differences in size, shape and consistency. Immediately after the palpation of the seminal vesicles it is useful to gently handle the ejaculatory ducts (terminal portions of vasa deferentes or ampulli). This stimulates smooth muscle activity and lowers the emission threshold. Experienced clinicians will frequently follow the stimulation of the ampulli with firm transrectal massage of the pelvic urethra (from about 5 cm cranial to 5 cm caudal of the prostate), thus collecting a semen sample without the need for electro-stimulation. Even if no semen is obtained in this manner, trans-rectal massage will dramatically reduce the extent of electro-stimulation required for the successful collection of a semen sample.

204

9. Semen collection: Semen is easier to collect from young bulls than from mature bulls. Transrectal massage is the authorâ&#x20AC;&#x2122;s method of choice in all cases, but is certainly more successful in virgin bulls (about 80%) than in mature bulls (about 60%). Electro-stimulation is most commonly accomplished using the automatic setting of any modern electro-ejaculator. Manual control of the electro-stimulation process requires extensive experience and is hardly ever more successful than the automatic mode which requires no more than pushing a few buttons on the control unit. Collecting semen from bulls that are running with cows is particularly difficult in many cases. On the other hand, semen collected from mature bulls after protracted sexual rest frequently yields aged spermatozoa that are either non-motile and/or affected by morphological defects associated with ageing (detached heads and distal midpiece reflexes). Particularly for electro-ejaculation it is important to ensure that the bull is adequately restrained in a sturdy chute that will withstand the sometimes massive forces exerted by a bull during electro-stimulation. Many bulls involuntarily extend one or both hind legs during electrostimulation. It is important that they do not slip, causing them to fall with hyper-extended limbs. Slipping can be prevented by placing a solid wooden bar near ground level behind the bullâ&#x20AC;&#x2122;s feet or by closing the tail gate of the chute. Placing a butt bar behind the bull at some distance above the ground can be very dangerous if the bull falls during stimulation and the electro-ejaculator probe gets caught on the bar. Semen should be collected into a single use plastic tube. The latter is usually connected to a disposable plastic cone that is suspended in a collection handle. It should be borne in mind that the collection cone cannot be warmed up inside the collection cup. However, the semen tube can be warmed up in the collectorâ&#x20AC;&#x2122;s hand or by suspending it in a warm water jacket. When a single semen sample is judged inadequate for the evaluation of a bull it is strongly advised that a subsequent semen collection attempt be made by an alternative method (massage, followed by electro-stimulation or visa versa). In extremely rare cases we have resorted to collection of semen by artificial vagina when neither transrectal massage nor electro-stimulation yielded a semen sample adequate for evaluation on multiple occasions. The author will make a deliberate effort at forcing each bull to extend his penis during electrostimulation. This serves two purposes: direct examination of the penis is possible and the tip of the penis can be placed directly at the mouth of the semen tube, thus avoiding chilling of the semen against a cold collection cone or contamination of the semen inside the prepuce. This can be accomplished by firmly pressing against the distal curvature of the sigmoid flexure of the penis. This structure is most commonly located well caudal of the neck of the scrotum and can be difficult to push against in obese bulls or those too tightly squeezed in a squeeze chute. 10. Semen evaluation: The SFT approach requires that three aspects of semen quality be evaluated, namely progressive motility of spermatozoa; spermatozoal morphology and the presence and type of somatic cells in the semen.

205

a. Progressive motility: The revised guidelines of the SFT no longer support the use of “mass” or “gross” or “wave” motility as an indication of the percentage of individual spermatozoa that are progressively motile. The percentage of progressively motile spermatozoa is to be determined by examining a thin wet mount, preferably using phase contrast microscopy. A thin wet mount can be prepared by placing a very small drop of raw semen under a coverslip or by dilution of the raw semen prior to preparing the wet mount. Semen can be diluted with fresh normal saline for this purpose. Operators must ensure that the saline has not become hyperosmotic while being stored in a syringe for periods of time or by allowing a small drop of saline to sit on a warm glass slide for even a few minutes. As the volumes of semen and diluent will be small, care must be taken to ensure that all glass ware is warmed to body temperature prior to coming into contact with semen. A suitably prepared wet mount allows the observer to recognize individual spermatozoa, all in the same focal plane. The sperm density in the sample is too high when individual cells obscure each other during examination. The volume under the coverslip, a function of sample drop size, is too high when individual cells appear in different focal planes. Drop size can be standardized by using an adjustable micropipette. Pipette tips must also be warmed prior to use. Bifocal phase contrast microscopes can be purchased for between $2 000 and $10 000. Upgrading an existing bright field microscope to a phase contrast microscope is technically very simple and often costs much less money. The SFT BSE certificates no longer require that an actual percentage be recorded for progressive motility. A simple “yes” or “no” for adequate motility has been introduced when the latest certificates were published earlier in 2019. However, as in the past, the suggested minimum % of progressively motile spermatozoa remains at 30%. b. Sperm morphology: The structure of individual spermatozoa can be evaluated under phase contrast or bright field microscopy at 100x magnification. Fixing semen smears for phase contrast microscopy requires special fixatives (usually glutaraldehyde), not commonly used for other applications in veterinary practice. Staining semen smears with a supravital stain is most common. This “morphology stain” comes as a mixture of eosin and nigrosin, dissolved in buffered saline. Neither stain is toxic to spermatozoa. Eosin is excluded by live cells only, whereas nigrosin is excluded by live and dead cells. Therefore, live cells remain white and dead cells become pink. Both are crisply outlined against the dark background provided by the nigrosine stain. Semen smears for the evaluation of sperm morphology can be prepared in many different ways. The author prefers to place a drop of the stain onto a warm glass slide for 10 seconds to allow the stain to come to the same temperature as the semen. A drop of semen is added to the stain and the two liquids are gently mixed using the edge of a second slide. Once mixed, the slide used for mixing the stain and semen is placed

206

on a third warm slide and then moved across the slide in a push-stop-push-stop motion to make a smear. As soon as the smear is made it is flame fixed, using a cigarette lighter. This rapid method of fixation is preferred over air drying the smear, because it rapidly dehydrates the smear, preventing the eosin to penetrate the now killed spermatozoa. Slower drying techniques often result in the partial eosin staining of spermatozoa. In the opinion of others any method of drying the semen smears after staining is acceptable as it is no longer customary to report the percentage of unstained spermatozoa on the BSE report or certificate. Using the stop-start-stop-start smear technique creates areas of greater and lesser darkness and sperm densities across the slide. This will facilitate evaluation when an area of optimum sperm density and staining can be found on virtually any smear, regardless of the sperm concentration in the raw semen or in the stain-semen mixture. This, in turn, is useful when sperm morphology is evaluated at a later time. Morphological defects have been assigned descriptive names in order to distinguish specific defects from one another. This detail has not been, and still is not, recorded on the SFT BSE sheets, but illustrations of, and appropriate designations for, the most commonly encountered defects in sperm structure are now provided with every new pad of triplicate certificates acquired from the SFT. As of 2019, the morphological traits are now grouped into four categories: normal, head defects, midpiece defects and tail defects. Until 2019 defects were grouped into primary (of testicular origin) and secondary (of epididymal origin). Other morphological classifications allow for the differentiation between major and minor defects, or between compensatory or noncompensatory defects. The latter classifications appear to have required too much knowledge of the impact of specific defects on the fertilizing ability of structurally defective spermatozoa on the part of the examiner, leading to variable interpretations and hence non-uniform conclusions. The latest changes to the reporting of morphological defects require that the examiner (certifier) interprets the significance of observed defects for each bull. The “comments” section of the BSE certificate can be used for this purpose. Yet another change to the SFT guidelines for breeding soundness of bulls introduced in 2019 is that spermatozoa with distal cytoplasmic droplets and spermatozoa with abaxially implanted flagella be classified as morphologically normal. This change was driven by the recognition that there was no evidence that these morphological forms impacted the fertilizing ability of spermatozoa. In the author’s opinion, however, neither form is “normal” as the overwhelming percentage of spermatozoa in the semen of the overwhelming majority of bulls are not affected by these aberrations. If one goal of the breeding soundness evaluation of bulls is to maintain excellent semen quality during the selection of future breeding stock, any lowering of standards will result in the gradual lowering of semen quality. We have witnessed this gradual decline in semen quality in horses and dogs in which breeding soundness evaluations have always set only one standard, namely the estimation of a given male’s ability to impregnate a

207

certain number of females or, even worse, an estimation of the number of females that could be impregnated by a single male during a certain period of time. The question was “is he good enough or not?” The question was not “is he normal or not?” Most readers of bull breeding soundness certificates (cattlemen) are not aware of the fundamental differences between “reproductively normal” and “adequately fertile”. It is against this background that the author will continue to classify spermatozoa with distal cytoplasmic droplets and abaxial midpieces as abnormal. When either defect is present in high numbers the comments section of the breeding soundness certificate can be used to inform the reader about the normal fertilizing ability of the affected spermatozoa. The SFT still advocates that bull semen must contain at least 70% morphologically normal spermatozoa (incl. those with distal cytoplasmic droplets and abaxially attached midpieces). c. Somatic cells in semen: Somatic cells detected in semen can be of preputial, epididymal, testicular or accessory sex gland origin. Their mere presence is readily recognized on wet mounts during the evaluation of sperm motility under phase contrast microscopy. Some types of cells are also easily identified under phase illumination, but other cells require trichrome staining (DiffQuick) for their identification. Smears for DiffQuick staining are made from raw semen, using the same stop-start-stop-start technique described earlier. Smears are air dried prior to fixation. The author prefers to leave semen smears in the fixative solution for much longer (at least 3 minutes) than other cytology smears. Squamous cells originate from the surface of the penis or the lamina interna of the prepuce. It is very common to also find at least some neutrophils in semen samples that contain preputial squamous cells. However, in the absence of squamous cells, the presence of neutrophils is usually an indication of inflammation (infection) in some part of the reproductive system. The presence of ciliated epithelial cells points to epididymal disease; spermatogenic cells (spermatogonia, spermatocytes and or spermatids) and Sertoli cells (large, often with very active cytoplasma and irregularly shaped nuclei) indicate testicular degeneration, while neutrophils alone and in large numbers are most commonly encountered in bulls with seminal vesiculitis. 11. Conclusion/Interpretation: A bull is considered a “satisfactory potential breeder” if his eye sight, musculo-skeletal structure, body condition, external genitalia, internal genitalia and semen are all found to be normal during the breeding soundness evaluation. Bulls with one or more abnormality may still be considered “satisfactory prospects” if the abnormality is considered of no or minimal consequence to the intended user. Conversely, it needs to be recognized that bulls with no detected abnormalities can still fail when used for breeding. This most commonly happens when bulls with normal structure are affected by functional deficits (short penis, penile deviations during erection, poor libido, intermittent joint disease that flares

208

up during breeding). It can also happen when a young bull presents with normal feet for his first breeding soundness examination and returns a year later with signs of screw claw. Bulls are classified as “unsatisfactory potential breeders” when the examiner is of the opinion that the bull will never recover from whatever deficits were detected during the breeding soundness examination. Unsatisfactory breeding prospects are not necessarily infertile! For example, a bull with small testes is considered ”unsatisfactory”, but may very well be able to impregnate 40 cows in each of the next 10 breeding seasons. If the cows all deliver calves that are to be sold to feedlots for future slaughter, a client may very well use such a bull. The same holds true for a bull with screw claw or one in which a persistent penile frenulum had been transected at an earlier age. If the examiner is of the opinion that an unsatisfactory bull may improve to become a satisfactory one the breeding soundness decision may be deferred. This happens most commonly when bulls under the age of 18 months fail to produce semen with 70% morphologically normal spermatozoa. Other bulls may recover from seminal vesiculitis. Yet others may recover from a lameness or an injury to the reproductive organs. 12. Remarks/Interpretation: This section of the breeding soundness certificate/report can and should be used to convey the examiner’s personal opinion on one or more of his/her findings to the reader. Examples may include “not suitable for seed stock production”, or referring to a specific finding with an asterisk one may enter here “*not likely of significance”. One could even state in this space that a bull that was classified as “unsatisfactory” for some reason “is likely to achieve acceptable pregnancy rates in a herd of 3, 7 or 15 cows”. The author uses this space frequently when the purpose of the breeding soundness examination was very specific. Examples of such circumstances include a legal requirement that a bull be tested for tritrichomoniasis (remark will be “trich test pending”), or additional tests required of a bull whose semen is to be frozen for commercial use. The space can also be used to list additional examinations that are indicated. An example may be for a bull whose penis never extended beyond the preputial orifice during the examination: ”observe during natural mating to confirm successful penile extension, intromission and thrust”. A bull that appears to have a short penis might require “general anesthesia to better measure the actual length of his penis”.

209

210

Food Animal

Dave Smith, DVM, PHD, DACVPM

Professor and Beef Program Leader Mississippi State University College of Veterinary Medicine Mississippi State, Mississippi

211

212

Systems approach to bovine respiratory disease David R Smith, DVM, PhD, DACVPM (Epidemiology) Mississippi State University, College of Veterinary Medicine, Mississippi State, MS david.smith@msstate.edu Introduction Bovine respiratory disease (BRD) is the leading cause of death in beef calves three weeks of age to weaning, costing cow-calf producers approximately $165 million annually 23. The disease is even more common and more costly after weaning and is the leading cause of morbidity and mortality in beef feeding and finishing systems 5,12. The disease syndrome is complex and surprisingly difficult to accurately diagnose. The incidence of BRD has not waned despite widespread use of improved vaccines and antimicrobials 12. The anatomy and physiology of the bovine lung may make cattle inherently susceptible to BRD 22. However, many other factors contribute to its occurrence. Causal thinking Part of the challenge in controlling BRD is the confusing array of factors that sometimes seem to explain the disease, but sometimes do not. This lack of consistent effect of putative risk factors confounds our understanding of actions that might prevent the BRD from occurring. The concepts of component and sufficient causes help explain this phenomenon. Risk factors are causal factors because they contribute to the causal pathway of disease. Risk factors may include factors related to the disease-causing agents (e.g. pathogens or toxins), the ability of the host to resist the effects of the agents, or management and other environmental factors that may affect host and agent interactions. Key determinants are those causal factors which are under management control. In disease causal theory, each factor that contributes to the development of disease is a component cause 15. Clinical signs of disease are expressed when various component causes add up to complete a sufficient cause. Each outbreak of respiratory disease is the result of the completion of a sufficient cause, which might have also included components of viral and bacterial pathogens, a certain state of immunity, or other component causes of respiratory disease in cattle that we fail to understand. Disease is expressed when a sufficient cause is completed. This is why some known component causes of BRD may be observed even though the disease is not expressed. It may appear to the livestock owner that the component cause that completed a sufficient cause was the sole reason for the disease. For example, a sudden change in weather may precede an outbreak of BRD because it completed the sufficient cause, but viral, bacterial, and immune status were unrecognized component causes. Removing one component cause (now the key determinant) means that the sufficient cause is not completed and thus disease is not observed. Systems thinking Thinking about the system of production may provide some additional insight into the factors that cause BRD. The science of system dynamics helps us understand how actions and decisions far removed from the immediate problem could be a cause of the problem. Disease 1 213

events that we observe, such as the occurrence of BRD, usually have relationships with risk factors which are commonly the subject of epidemiologic research and the primary subject of this paper. However, it is important to understand that underlying systems produce those relationships and, ultimately, the occurrence of disease (Figure 1) 11. A better understanding of how the system may lead to disease outcomes may further our understanding of why BRD occurs and what we can do to mitigate it. For example, a large regional drought might cause cow-calf producers to decide to wean calves early, seek feedlot pens to house cows, or to depopulate their herds –all of which may have effects on feedlot management and health. Small cow-calf producers may decide not to dehorn, castrate, vaccinate, or deworm calves on the farm because they lack facilities or fail to recognize an economic signal to do so. Decisions made months ago at a farm, possibly hundreds of miles away, may result in increased morbidity and mortality in the feedlot 2. Those decisions don’t always reflect sub-par husbandry. For example, pneumonia in calves prior to weaning is a systems problem paradoxically associated with highly managed herds 25,26.

Figure 1. The iceberg structure of system dynamics. The disease events we observe have relationships with other causal factors that are often studied by epidemiologists and other animal health researchers, but the systems that produce those relationships and the ultimate events require further understanding.

The epidemiology of BRD Traditionally, disease control programs have focused on agent-host interactions with some consideration of environmental factors. However, political, social, economic, and cultural factors also contribute to disease ecology as it affects the movement of people, animals, and animal products. The failure of disease control programs, whether at a local, regional, or global level, frequently results from failure to consider or understand the system comprising the disease’s ecology, including the decisions made by people responding to factors within the system (e.g. economic factors). Pneumonia in calves prior to weaning Pneumonia is a leading cause of sickness and death of calves in some cow-calf herds –especially after the first few weeks of life 21. This is perplexing because ranch calves typically live in conditions of little stress and relative isolation. Surveys of beef cattle producers 25 and veterinarians 26 from the northern plains region and southeastern US indicate that pre-weaning BRD is a problem for approximately one out of five cattle producers. Pre-weaning BRD may affect up to 10% of U.S. beef calves 7, resulting in death of 0.6% - 1.4% of all calves 3,17,20. Calves 2 214

affected with pre-weaning BRD may weigh 17 - 37 pounds less at weaning, compared to calves not affected 17,24. As with all infectious diseases, the occurrence of BRD is affected by factors of host immunity, presence of specific pathogens, and opportunity for transmission of pathogens between or within herds. Although the bacterial pathogens of pneumonia are commonly found in the upper respiratory tract of cattle, the inciting damage is often due to viral infections that may not be present in all cattle herds all the time. Commonly recognized viral BRD pathogens are bovine herpes virus 1, bovine viral diarrhea virus, and bovine respiratory syncytial virus, but many others, including bovine coronavirus 9,10, are likely to be involved. Pathogen exposure may be necessary but it is not causally sufficient because it is difficult to replicate the clinical presentation of BRD through experimental challenge with bacteria or viruses alone. 18 In confinement systems, the opportunity for pathogen transmission is high because of animal density. But, even in extensive pasture-based systems typical of cow-calf production, the opportunities for pathogen transmission may be high because cattle congregate closely around water sources and feedbunks, in shade, and when bothered by flies. Some management practices such as pasture moves and gathering for sorting also result in high animal density and greater opportunity for pathogen transmission. Passively acquired maternal immunity is important for protecting young calves against respiratory pathogens. However, maternal antibodies wane with time. Approximately every 16 to 20 days after ingestion, the serum concentration of maternal antibodies is halved, so that by 96 to 120 days of age, a calf retains less than 2 percent of the antibodies it absorbed from colostrum. The immune system is functional but unprimed at birth, and prior to 5 to 8 months of age and the immune response of calves is weak, slow, and easy to overcome 1. Therefore, even in the absence of additional stressors, calves 3 to 5 months of age may be particularly susceptible to pneumonia. This age-related susceptibility due to loss of maternal immunity may explain sudden outbreaks of pre-weaning BRD in herds with managed breeding seasons. Herd immunity is the protection afforded to susceptible individuals because most of the individuals in the population are immune. In herds with a narrow calving window, calves are similar in age and herd immunity is lost over a short span of time as the majority of calves approach 90 to 120 days of age. However, the optimum vaccination protocol to prevent BRD in calves of this age remains an important subject of investigation. Weaning, commingling groups, and exposure to severe weather can be powerful stressors that further reduce a calfâ&#x20AC;&#x2122;s ability to resist disease. Other factors affecting risk for pre-weaning BRD Health records representing over 9,900 calves from 28 cattle management groups within 7 beef cattle ranches were analyzed to test the effect of calf gender and age of the dam (Smith et al, unpublished). We concluded that the sex of calves affects their risk for BRD (males at greater risk than females). Also, of calves affected with BRD, those calves born to 2-year-old dams were more likely to become sick at an earlier age. This is consistent with the knowledge that the male sex of other species has been associated with greater risk for pneumonia 6,27. The age of the dam may be a correlate of colostrum absorption. Colostrum ingestion may be delayed 3 215

for calves born to a young dam because of dystocia or poor mothering skills. Also, the young damâ&#x20AC;&#x2122;s colostrum may not contain as many antibodies, in quantity and range of protection, as older dams 13,14,16. Pneumonia in calves after weaning The first several days from farm of origin to the stocker operation or feedlot can result in the accumulation of stress events that are detrimental to calf health, especially increasing the risk for BRD. Most BRD morbidity occurs in the first 21 days after arrival in the stocker or feedlot operation. By far, the most common illness of stocker calves is BRD 12. Other important receiving period diseases are lameness, musculoskeletal injury, diarrhea (e.g. rumen acidosis, Salmonellosis and coccidiosis), and bloat 5. Many small farm operations lack enough natural, human, or capital resources to provide an optimum health program while the calf is on the home farm. For example, the farm may lack facilities, manpower, or knowledge to dehorn, castrate, or vaccinate calves prior to weaning. Weaning often occurs the same day the cattle are marketed from the home farm, resulting in an important abrupt stress event. In addition, the common systems of marketing calves contribute additional stressors to the auction market calf. Calves may not have access to adequate feed or water or may not know how to drink from tanks or consume feed from bunks during transportation to and from the auction market. Calves are likely to be commingled with other calves, and after long distance transportation, may spend several days in an order-buyer facility as other calves are purchased to fill an order. During the phase of marketing, calves may lose rumen fill from not eating, may have shrink from dehydration, and may be exposed to a variety of enteric and respiratory pathogens. By the time calves have moved through these marketing channels and arrive at the destination feedlot or stocker facility, they may be exhausted, dehydrated, challenged by a variety of social and physical stressors, and incubating a respiratory or enteric infection. Unfortunately, the marketing system may not reward the small cow-calf farmer for adopting practices that improve immunity and decrease stress. Calves marketed directly from the (typically larger) cow-calf farm to the stocker or feedlot operation may experience some, but often not all, of the stressors of auction market calves; however, because direct marketing is often based on the farmerâ&#x20AC;&#x2122;s reputation, these calves are more likely to have been preconditioned by receiving deworming treatment, vaccination at a prior to weaning, and castration and dehorning at a young age. Calves that are marketed directly, especially those undergoing a pre-conditioning program, may have less morbidity and mortality in the postweaning phase and are, therefore, often considered calves at low risk for disease. Conversely, commingled, low body condition, freshly weaned calves, transported long distances, and marketed through an auction market are often considered high risk for disease. It is a paradox that some cattle feeders and stocker operators prefer light weight high risk calves because they can be purchased for less total dollars and, if they survive, often grow efficiently because of compensatory gains 8.

4 216

Attempts to mitigate the risk for BRD in feeding or finishing systems, such as by vaccinating calves at arrival, may not reduce BRD incidence 19 and may sometimes increase BRD incidence, increase mortality, and lower growth performance 4. Mass medication of calves with injectable antimicrobials at arrival has been the most consistently effective method to reduce BRD incidence 8. Conclusions The risk factors for bovine respiratory disease include a complex set of component causes that include bacterial and viral pathogens, level of host immunity, and environmental conditions that favor pathogen transmission and stress-induced susceptibility. During the post-weaning phase, these factors are superimposed on a system of marketing, transportation, and economic opportunity that further increase the risk for BRD. Acknowledgements A contribution of the Beef Cattle Population Health and Reproduction Program at Mississippi State University. Supported by the Mikell and Mary Cheek Hall Davis Endowment for Beef Cattle Health. References 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Cortese VS. Neonatal immunology. Vet Clin North Am Food Anim Pract 2009;25:221-227. Duff GC, Galyean ML. Board-invited review: recent advances in management of highly stressed, newly received feedlot cattle. J Anim Sci 2007;85:823-840. Dutil L, Fecteau G, Bouchard E, et al. A questionnaire on the health, management, and performance of cow-calf herds in Quebec. Can Vet J 1999;40:649-656. Griffin CM, Scott JA, Karisch BB, et al. A randomized controlled trial to test the effect of onarrival vaccination and deworming on stocker cattle health and growth performance. Bov Pract (Stillwater) 2018;52:26-33. Griffin D. Feedlot diseases. Vet Clin North Am Food Anim Pract 1998;14:199-231. Gutierrez F, Masia M, Mirete C, et al. The influence of age and gender on the population-based incidence of community-acquired pneumonia caused by different microbial pathogens. J Infect 2006;53:166-174. Hanzlicek GA, Renter DR, White BJ, et al. Management practices associated with the rate of respiratory tract disease among preweaned beef calves in cow-calf operations in the United States. J Am Vet Med Assoc 2013;242:1271-1278. Ives SE, Richeson JT. Use of Antimicrobial Metaphylaxis for the Control of Bovine Respiratory Disease in High-Risk Cattle. Vet Clin North Am Food Anim Pract 2015;31:341-350, v. Kapil S, Goyal SM. Bovine coronavirus-associated respiratory disease. Compendium on Continuing Education for the Practicing Veterinarian 1995;17:1179-1181. McNulty MS, Bryson DG, Allan GM, et al. Coronavirus infection of the bovine respiratory tract. Vet Microbiol 1984;9:425-434. Meadows DH, Wright D. Thinking in systems : a primer. White River Junction, Vt.: Chelsea Green Pub., 2008. Miles DG. Overview of the North American beef cattle industry and the incidence of bovine respiratory disease (BRD). Anim Health ResRev 2009;10:101-103. Odde KG. Survival of the neonatal calf. Vet ClinNorth Am Food Anim Pract 1988;4:501-508.

5 217

14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27.

Odde KG. Reducing neonatal calf losses through selection, nutrition and management. AgriPractice 1996;17:12-15. Rothman KJ. Causes. American Journal of Epidemiology 1976;104:587-592. Schumann FJ, Townsend HG, Naylor JM. Risk factors for mortality from diarrhea in beef calves in Alberta. CanJ Vet Res 1990;54:366-372. Snowder GD, Van Vleck LD, Cundiff LV, et al. Influence of breed, heterozygosity, and disease incidence on estimates of variance components of respiratory disease in preweaned beef calves. J Anim Sci 2005;83:1247-1261. Taylor JD, Fulton RW, Lehenbauer TW, et al. The epidemiology of bovine respiratory disease: What is the evidence for predisposing factors? Can Vet J 2010;51:1095-1102. Taylor JD, Fulton RW, Lehenbauer TW, et al. The epidemiology of bovine respiratory disease: what is the evidence for preventive measures? Can Vet J 2010;51:1351-1359. USDA. Beef 2007â&#x20AC;&#x201C;08, Part IV: Reference of Beef Cow-calf Management Practices in the United States, 2007â&#x20AC;&#x201C;08. . USDA:APHIS:VS, CEAH Fort Collins, CO 2010;#523.0210. USDA. Cattle Death Loss In: U.S. Dept. of Agriculture ASB, National Agricultural Statistics Service, ed, 2011. Veit HP, Farrell RL. The anatomy and physiology of the bovine respiratory system relating to pulmonary disease. Cornell Vet 1978;68:555-581. Wang M, Schneider LG, Hubbard KJ, et al. Cost of bovine respiratory disease in preweaned calves on US beef cow-calf operations (2011-2015). J Am Vet Med Assoc 2018;253:624-631. Wittum TE, Salman M.D., King M.E., Mortimer R.G., Odde, K.E., Morris D.L. The influence of neonatal health on weanign weight of Colorado, USA beef calves. Prev Vet Med 1994;19:15-25. Woolums AR, Berghaus RD, Smith DR, et al. Producer survey of herd-level risk factors for nursing beef calf respiratory disease. J Am Vet Med Assoc 2013;243:538-547. Woolums AR, Berghaus RD, Smith DR, et al. A survey of veterinarians in 6 US states regarding their experience with nursing beef calf respiratory disease. Bovine Pract 2014;48:9. Yamamoto Y, Saito H, Setogawa T, et al. Sex differences in host resistance to Mycobacterium marinum infection in mice. Infect Immun 1991;59:4089-4096.

6 218

What does antimicrobial stewardship in cattle practice look like? David R Smith, DVM, PhD, DACVPM (Epidemiology) Mississippi State University, College of Veterinary Medicine, Mississippi State, MS david.smith@msstate.edu INTRODUCTION “Antimicrobial stewardship refers to the actions veterinarians take individually and as a profession to preserve the effectiveness and availability of antimicrobial drugs through conscientious oversight and responsible medical decision-making while safeguarding animal, public, and environmental health.” (AVMA, 2018) Antimicrobial stewardship reflects the commitment of veterinarians and animal care-givers to take actions that preserve the effectiveness of antibiotic without sacrificing animal health and welfare; making evidence-based decisions about the use of antimicrobial drugs; and using antimicrobials judiciously, sparingly, and with ongoing evaluation of the outcomes of therapy. Antimicrobial stewardship must occur in reasonable context of the animal care-giver’s available resources, which can present a challenge to veterinarians in practice. The American Veterinary Medical Association has defined five principles of antimicrobial stewardship: 1. Commit to stewardship 2. Advocate for a system of care to prevent common diseases 3. Select and use antimicrobial drugs judiciously 4. Evaluate antimicrobial drug use practices 5. Educate and build expertise (https://www.avma.org/KB/Policies/Pages/Antimicrobial-Stewardship-Definition-and-CorePrinciples.aspx. Accessed June 11, 2018) Stewardship is demonstrated, not by simply reducing antimicrobial use, but by doing the things that reduce risk for infections in the first place and having a strong clinical rationale for using antimicrobial therapy. Antimicrobials are used therapeutically for purposes of prevention, control, or treatment. The AVMA recently defined antimicrobial prevention, control, or treatment in individuals or populations, as follows: Antimicrobial prevention of disease (synonym: prophylaxis): 1) Prevention is the administration of an antimicrobial to an individual animal to mitigate the risk for acquiring disease or infection that is anticipated based on history, clinical judgement, or epidemiological knowledge. 2) On a population basis, prevention is the administration of an antimicrobial to a group of animals, none of which have evidence of disease or infection, when transmission of existing undiagnosed infections, or the introduction of pathogens, is anticipated based on history, clinical judgement or epidemiological knowledge. Antimicrobial control of disease (synonym: metaphylaxis):

219

1) Control is the administration of an antimicrobial to an individual animal with a subclinical infection to reduce the risk of the infection becoming clinically apparent, spreading to other tissues or organs, or being transmitted to other individuals. 2) On a population basis, control is the use of antimicrobials to reduce the incidence of infectious disease in a group of animals that already has some individuals with evidence of infectious disease or evidence of infection. Antimicrobial treatment of disease: 1) Treatment is the administration of an antimicrobial as a remedy for an individual animal with evidence of infectious disease. 2) On a population basis, treatment is the administration of an antimicrobial to those animals within the group with evidence of infectious disease. (https://www.avma.org/KB/Policies/Pages/AVMA-Definitions-of-Antimicrobial-Use-forTreatment-Control-and-Prevention.aspx. Accessed November 26, 2018) Central to antibiotic stewardship is the veterinarian’s role in helping the animal care-giver maintain a system of husbandry that avoids common bacterial illnesses, thereby reducing reliance on antibiotic therapy to maintain animal health. Systems approach to antibiotic stewardship Livestock production systems are complex adaptive systems. Food production is a system (systems have numerous parts that affect each other); the system is a complex mix of physical, behavioral, biological and economic components with unpredictable outcomes (the parts interact with each other to produce variable outcomes); and the system is adaptive because it changes over time in response to those outcomes. Even within a given food animal commodity (e.g. beef cow-calf, dairy, broiler, catfish) the specific components and outcomes of a production system are variable. For example, a beef-cow calf farm in the southeast US may not look or behave like a ranch on the high plains. These differences in the way food animals are produced are due to differences in environmental resources, human resources, and capital – factors which themselves change over time. Within this complexity are biological systems of people, animals, pests, and pathogens –which are also interactive. In spite of the complexity, people make adaptive management decisions hoping to maximize utility (profit, pride, productivity) while minimizing losses due to disease. However, managing complex adaptive systems is not easy because outcomes are difficult to predict. The need to treat bacterial infections today may be due to decisions made much earlier. System dynamics can help cattle producers and veterinarians understand how actions and decisions far removed from the immediate problem could cause a problem 1. For example, drought could cause cow-calf producers to wean calves early, house cows in feedlots, or to depopulate their herds –all of which may have effects on feedlot management and health. Small herd cow-calf producers may decide not to dehorn, castrate, vaccinate, or deworm calves on the farm because they lack facilities or fail to recognize an economic signal to do so. Decisions made months ago, possibly hundreds of miles away, can increase the risk for sickness or death in the feedlot 2. Those decisions don’t always reflect sub-par husbandry. For example,

220

pneumonia (bovine respiratory disease or BRD) in calves prior to weaning is a systems problem paradoxically associated with highly managed herds 3,4. Many small farm operations lack sufficient natural, human, or capital resources to provide an optimum health program while the calf is on the home farm. For example, the farm may lack facilities, manpower, or sufficient knowledge to dehorn, castrate, or vaccinate calves prior to weaning. Weaning often occurs the same day the cattle are marketed from the home farm resulting in an important abrupt stress event. In addition, the common systems of marketing calves contribute additional stressors to the auction market calf. Calves may not have access to adequate feed or water, or may not know how to drink from tanks or consume feed from bunks during transportation to and from the auction market. Calves are likely to be commingled with other calves, and after long distance transportation, may spend a number of days in an orderbuyer facility as other calves are purchased to fill an order. During the phase of marketing, calves may lose rumen fill from not eating, may have shrink from dehydration, and be exposed to a variety of enteric and respiratory pathogens. By the time calves have moved through these marketing channels and arrive at the destination feedlot or stocker facility, they may be exhausted, dehydrated, challenged by a variety of social and physical stressors, and incubating a respiratory or enteric infection. Unfortunately, the marketing system may not reward the small cow-calf farmer for adopting practices that improve immunity and decrease stress. In contrast, calves marketed directly from the (typically larger) cow-calf farm to the stocker or feedlot operation may experience some, but often not all of the stressors of auction market calves. Because direct marketing is often based on the farmerâ&#x20AC;&#x2122;s reputation, these calves are more likely to have been preconditioned by receiving deworming treatment, vaccination at a prior to weaning, and castration and dehorning at a young age. Calves that are marketed directly, especially those undergoing a preconditioning program, may have less morbidity and mortality in the post-weaning phase and are, therefore, often considered calves at low risk for disease. Interestingly, commingled, low body condition, freshly weaned calves, transported long distances, and marketed through a sale barn are often considered high risk for disease. Paradoxically, some cattle feeders and stocker operators have a preference for light weight high risk calves because they can be purchased for less total dollars and, if they survive, often grow efficiently because of compensatory gains. When calves are likely to be incubating bovine respiratory diseases, the receiving program may include mass medication with an antibiotic delivered in the feed, water, or by injection. Mass medication on arrival for the purpose of treating incubating but unapparent infections is termed metaphylaxis. Metaphylactic use of antibiotics has been shown in many studies to reduce morbidity. In keeping with antibiotic stewardship principles, there are certainly times when mass medication strategies are cost effective and improve animal health and well-being; however, more work is needed to objectively determine those particular conditions, and to provide scientifically justifiable indications for prophylactic or metaphylactic use of antibiotics. Conclusions

221

We can be good stewards of antimicrobials when battling bovine respiratory disease, but it is not always easy and may require a change in paradigm. The principles of antibiotic stewardship require that veterinarians commit to actions that preserve antibiotic effectiveness. As antibiotic stewards, veterinarians should help cattle producers in all stages of production implement systems of husbandry that reduce the risk for pneumonia. When pneumonia does occur, or is likely to occur, then antibiotics should be used judiciously and records should be used to evaluate therapeutic success. Antibiotic stewardship is an evolving concept requiring veterinarians to actively update their expertise on the subject and share that knowledge with others. Acknowledgements A contribution of the Beef Cattle Population Health and Reproduction Program at Mississippi State University. Funded by the Mikell and Mary Cheek Hall Davis Endowment for Beef Cattle Health and Pfizer Animal Health. References 1. 2. 3. 4.

222

Meadows DH, Wright D. Thinking in systems : a primer. White River Junction, Vt.: Chelsea Green Pub., 2008. Duff GC, Galyean ML. Board-invited review: recent advances in management of highly stressed, newly received feedlot cattle. J Anim Sci 2007;85:823-840. Woolums AR, Berghaus RD, Smith DR, et al. Producer survey of herd-level risk factors for nursing beef calf respiratory disease. J Am Vet Med Assoc 2013;243:538-547. Woolums AR, Berghaus RD, Smith DR, et al. A survey of veterinarians in 6 US states regarding their experience with nursing beef calf respiratory disease. Bovine Pract 2014;48:9.

Iâ&#x20AC;&#x2122;m not positive thatâ&#x20AC;&#x2122;s a positive -the art and science of making a better diagnosis David R. Smith, DVM, PhD, DACVPM (Epidemiology) Mississippi State University, College of Veterinary Medicine, Mississippi State, MS Introduction Diagnosis is central to the function of the medical professions, and yet, making a diagnosis is as much art as science. Diagnostic tests are sometimes useful as population-based tools for identifying reservoirs of disease or infection within a herd, preventing the introduction of infected animals into a herd, and assessing the level of existing infection within a herd. In this article the terms infection and disease are used as if they were synonymous to avoid unnecessary confusion; although of course infection is not synonymous with disease and it is important to understand the distinction. Diagnostic tests are not perfect and, therefore, some test results can be expected to be in error. Diagnostic test evaluation predicts what errors might occur among diseased and nondiseased populations and diagnostic test interpretation predicts how the errors might be distributed among test positive or negative populations.1-3 â&#x20AC;&#x201C;is the test result likely to be a truepositive or a false-positive? -true-negative or false-negative? This information could be used to predict the effect diagnostic errors might have on a population-based health program. Unfortunately, failure to understand cognitive error, causal logic, and the concepts of diagnostic interpretation have led many clinicians down preventable paths of incorrect diagnoses and inappropriate treatment decisions. Poor diagnostic interpretation applied to population-based decision making can lead to devastating and costly errors. Blind application of a diagnostic formula is not a substitute for clinical judgment, but neither is clinical judgment sufficient in the absence of quantitative thinking. Quantitative diagnostic interpretation complements clinical judgment to enhance the decision-making process. The formulae and concepts presented in this chapter are easily applied with common computer spreadsheet functions (Figs. 1 and 2). Computer spreadsheet software programs are now sufficiently userfriendly so that quantitative analysis is within the grasp of anyone with interest. Diagnostic testing, in the hands of a clinician with an appreciation for physical examination and history taking, aware of their own cognitive biases, and understanding of the importance of the predictive value of the test, becomes a powerful tool for helping clients improve the health of their cattle. Diagnostic Test Evaluation Diagnostic test performance is evaluated by the parameters sensitivity and specificity.1;2 Sensitivity and specificity are estimated by testing individuals of known (or suspected) disease (or infection) status. Sensitivity (SENS) is a conditional probability describing the probability that a diseased individual (D+) will have a positive test result (T+). It is important to note that the probability is expressed only for the population of individuals with disease. SENS = P(T+| D+)

223

Specificity (SPEC) is the conditional probability that a non-diseased (D-) individual will test negative (T-). The probability only applies to the population of individuals without disease. SPEC = P(T- |D-) Diagnostic Test Interpretation Sensitivity and specificity values by themselves are not useful for test interpretation because practitioners do not know the true disease status of the animals they test. Practitioners are most interested in the probability that the test result represents the true infection status of the individual. This probability is called the post-test probability or predictive value.1;2 Positive predictive value (PPV) is the conditional probability that an individual with a positive test result is truly infected. Restated: given a positive test result, what is the probability this animal is truly infected? Negative predictive value (NPV) is the conditional probability that an individual with a negative test result is truly not infected. Restated: given a negative test result, what is the probability this animal is truly not infected? PPV= P(D+ |T+) NPV= P(D- |T-) Experienced practitioners know intuitively that clinical judgment is necessary to interpret diagnostic test results. The importance of clinical judgment to test interpretation can be shown in quantitative models. Post-test probability is calculated by using information about test sensitivity and specificity as well as information called pre-test probability. Pre-test probability is the probability of the individual truly being diseased (P D) before considering test results. One could think of PD as the proportion of animals actually having the specific disease from an imaginary population of animals all with the same clinical presentation and history. We estimate PD using what we know from review of the literature (e.g. from surveys reporting prevalence), history and physical examination, or previous experience. The formulas for PPV and NPV in terms of SENS, SPEC, and PD are:1

PPV =

SENSxPD (SENSxPD ) + (1 − SPEC)x(1 − PD )

NPV =

SPECx(1- PD ) SPECx(1 − PD ) + (1 − SENS)xPD

Apparent Prevalence Apparent prevalence (AP) is the percentage of animals determined to be diseased (infected) based on diagnostic test results.2 Apparent prevalence may differ from true prevalence because of test error. If the parameters of test performance are known then AP can be predicted over a range of values for true prevalence (PD):

224

AP = SENS x PD + (1-SPEC) x (1-PD) Diagnostic Efficiency Tests may error as false positive or false negative results. False negative (FN) results are a function of SENS (FN = 1-SENS), and false positive (FP) results are a function of SPEC (FP = 1SPEC). Diagnostic efficiency (EFFIC) describes the proportion of individuals correctly classified by the test results. Diagnostic efficiency depends on the parameters of test performance and PD.3 EFFIC = SENS x PD + SPEC x (1-PD) Aggregative testing strategies -sampling to detect disease in a population Sometimes it is important to determine if a disease is present or absent within an aggregate of individuals, for example a litter, pen, barn, flock or herd (the term â&#x20AC;&#x153;herdâ&#x20AC;? will be used to designate any such group of animals). The probability of detecting evidence of disease or infection in a diseased herd is termed herd-level sensitivity (HSENS). If the disease status of a herd is determined by testing individuals then HSENS is a function of SENS, SPEC, P D, the number of reactors used to classify the herd as infected, the size of the herd, and the number of animals tested within the herd.4;5 If there is an expected minimum value for PD within infected herds and test performance has been evaluated, then the number of animals to test can be determined to assure a given value for HSENS. This is the number of animals that must be tested to detect the presence of infection with a probability equal to HSENS.5 Herds could be classified based on different cut-point values for the numbers of reactors (R) used to classify the herd as diseased. HSENS can be estimated using the binomial probability distribution given the probability of a given number of reactors being present in a sample of size n from the herd. The probability of a reactor is the sum of the probability of a true positive reactor (SENS x PD) plus the probability of a false positive reactor ((1-SPEC) x (1-PD)); this is the apparent prevalence (AP), as previously defined. Except for the unusual circumstance when a test of individuals is perfectly specific (SPEC = 1) it is possible for false positive reactors (FP = 1-SPEC) to result in a false positive herd classification. Therefore, consideration must also be given to herd-level specificity (HSPEC), the probability that the a non-diseased herd would be correctly classified.5 Often the sample size (n) is large relative to the herd size (N) (n/N > 0.05) and usually herd sampling is conducted without replacement (i.e. once tested, the animal is removed from the pool for selection). In these circumstances the hypergeometric distribution function is more appropriate for calculating HSENS and HSPEC.4 Calculation of the hypergeometric function requires inputs for R, n, N, and the number of infected animals in the herd (S).

225

HSENS = 1- P(x< R| n, p = AP in a diseased herd) = 1- P(x< R| n, S = (N x AP), N)

(Binomial distribution) (Hypergeometric distribution)

HSPEC = P(x< R| sample size = n, p = (1-SPEC)) = P(x< R| n, S = (N x (1-SPEC), N)

(Binomial distribution) (Hypergeometric distribution)

Models for herd-level positive and negative predictive value (HPV+, HPV-), apparent prevalence (HAP), and diagnostic efficiency (HEFFIC) can be developed by substituting HSENS for SENS, HSPEC for SPEC, and the proportion of herds containing infected individuals (HP D) for PD. into the appropriate formulas.5 Simulation models for herd-level test performance have also been described.6 The choice of sample size has important implications for herd surveillance and survey research. The outcome of surveys to detect diseased herds may be biased if sample size estimates failed to consider the effect of imperfect test performance, herd size, and clustering of disease in sub-populations.5 Sample size estimates are often obtained from software that use formulas assuming perfect test performance; however, serious errors in sample size estimation can result if test performance is not considered. Further, for a given sample size the accuracy of the herd’s disease classification will differ in different sized herds and in sub-populations where disease is expected to cluster differently.5 Summary Population-based diagnostic decisions are usually of high economic consequence to veterinary clients. There is an expectation that veterinary diagnoses are accurate and reliable. “Eye-ball” or “gut-feeling” decisions are difficult to justify, as is blind faith trust in a diagnostic test result. However, it is possible to make appropriate diagnostic decision, or at least to understand how reliable the diagnostic results are likely to be, by applying sound clinical judgment to the principles of diagnostic interpretation.

= Figure 1. Use of a spreadsheet to calculate positive predictive value (PPV), negative predictive value (NPV), apparent prevalence (AP) and diagnostic efficiency (Effic, proportion classified correctly) from inputs of test sensitivity, test specificity, and the true probability of disease in the population (pDisease, estimated from clinical judgment). Using this test in this population, we expect that 78 percent of animals with a positive test result would truly be infected (i.e. 22% of positive test results are false positive), and 99% of animals with a negative test result would not be infected (i.e. 1 percent of negative test results are false-negative). In this case NPV approximates what we knew about the population before testing and is, therefore, noninformative. If this test were used to survey this population the apparent prevalence of infection would be 22% over-estimated (due to false positive classifications), and, overall, 97% of the individuals would be classified correctly.

226

0.8

Probability

0.6 0.4

0.6 0.4 0.2

0.2

0 10

100 110

HPV+ HSPEC hypgeom

Sensitivity of the test (individuals) Specificity of the test (individuals) True prevalence in a diseased herd

0.95 0.97 0.1

Herd size Proportion of herds affected

400 0.1

Probability

HSENS hypgeom

100 110

Sample size

HPV-

1 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0 10

100 110

Sample size HEFFIC

HAP

HPD

Figure 2. The probability to correctly classify infected herds (HSENS), non-infected herds (HSPEC) by testing various numbers of animals from herds of 400 animals using the same testing scenario as in Figure 1 and assuming a single positive test classifies the herd as testpositive. As the sample size increases HSENS increases, but HSPEC decreases towards zero (i.e. all truly negative herds falsely classified as infected. If ten percent of herds in the population are truly infected (HPD), then as sample size increase the predictive value of a negative herd classification (HPV- increases, but the predictive value of a positive herd classification (HPV+) decreases. Because of false-positive herd classifications the apparent proportion of affected herds (HAP) approaches 100%, and only the truly infected herds are classified correctly (HEFFIC). Because of false-positive test results this test, by itself, is not useful for differentiating infected herds from non-infected herds regardless of sample size. A spreadsheet file for these calculations is available from the author. References 1. Martin SW: The evaluation of tests. Can J Comp Med 1977; 41:19-25 2. Martin SW: Estimating Disease Prevalence and the Interpretation of Screening Test Results. Prev Vet Med 1984; 2:463-472 3. Trajstman AC: Diagnostic tests, sensitivity, specificity, efficiency and prevalence. Aust Vet J 1979; 55:501-501 4. Jordan D: Aggregate testing for the evaluation of Johne's disease herd status. 1996; Aust Vet J 73:16-19 5. Martin SW, Shoukri M, Thorburn MA: Evaluating the health status of herds based on tests applied to individuals. Prev Vet Med 1992; 14:33-43 6. Jordan D, McEwen SA: Herd-level test performance based on uncertain estimates of individual test performance, individual true prevalence, and herd true prevalence. Prev Vet Med 1998; 36:187-209

227

NOTES

________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ ________________________________________________________________________________ 228

Food Animal

John T. Groves, DVM

Livestock Veterinary Service Eldon, Missouri

229

230

The Challenges and Rewards of Working with Stocker/Backgrounders John T. Groves, DVM Livestock Veterinary Service, Eldon MO 65026 Abstract

Veterinary practitioners and consultants serving stocker/backgrounder clients are faced with many challenges. In an effort to better serve this dynamic segment of the beef industry, veterinarians must understand the unique disease dynamics and business plans associated with these operations. This paper describes some changes made in my central Missouri practice to better serve stocker/backgrounder clients and grow my veterinary business.

Introduction

Delivering veterinary services to the stocker/backgrounder segment of the beef industry has been challenging for many practices. As stocker/backgrounder operations have grown over the years, they no longer require some of the services offered by traditional veterinary practices. In fact, many stocker/backgrounder producers operate successfully without a relationship with a veterinary practitioner, much to the concern of the public and veterinary profession. For the purpose of this paper a stocker/backgrounder is defined as an operation that owns and manages cattle between weaning and placement in a feed yard. Developing relationships with these kinds of producers requires

231

innovative thinking, trust, and commitment from both parties to achieve successful outcomes. This paper describes some things I have done in my central Missouri practice to meet the needs of the growing stocker/backgrounder industry in Missouri. In the past many practitioners and consultants have tried to apply lessons learned in the feedlot segment to the stocker/backgrounder segment with limited success. Due to the extremely dynamic and highly variable populations involved in these operations, producers and veterinarians must work together to solve the problems inherent to this segment of the beef industry. Important to developing the skills to work with stocker/backgrounder operations are: •

Understanding business plans

•

Understanding health and financial measures

•

Managing health risk

•

Managing information risk

•

Managing price and equity risk

•

Managing your practice to provide value

Understanding Business Plans

Knowing and understanding business plans as they relate to the stocker/backgrounder business is critical. Unlike the other segments of the cattle industry, the business plan for a stocker/backgrounder can be very complex. Business plans can vary from simple grazing operations to complex businesses

232

which include cattle markets, order buying facilities, starting yards, grass traps and custom grazing operations. It is difficult to help these operations until you understand their business objectives and where profits are derived. As market conditions change, complex operations often adapt their business plan to exploit an opportunity or avoid a loss. Keeping up with the pace of change in these operations can be difficult. Operations which have a hard time defining their business plan are destined to struggle. I have found facilitating business plan development has helped not only the producer but also my ability to bring value.

Understanding Health and Financial Measures

How an operation measures health and financial performance depends heavily on its business plan. For some traditional backgrounders these measures usually reflect similar parameters to those used in the feedlot industry in which defined starting and ending points are used. However, operations with complicated business plans and high throughput need other parameters to measure both production and financial success and failure. Many of these measures may be counterintuitive to those who are stuck in the feedlot paradigm. Working with stocker/backgrounder producers to best define these measures will benefit all parties involved. Lending institutions especially appreciate participation in how to best measure the performance of these operations.

Managing Health Risk

233

Managing health performance in stocker/backgrounder operations is better defined as managing health risk. Predictability, flexibility, and consistency are especially important when designing health and treatment protocols. Production management strategies which mitigate the impact of important pathogens are critical to the long term viability of an operation. Pathogen management strategies include metaphylaxis, PI BVDV testing, and cattle flow management. Risk factors associated with the existing cattle population should be an important consideration when designing receiving protocols. Pathogens associated with the existing cattle population may be more important to health and production performance of the operation than the risk factors associated with the new cattle coming in at purchase.

Managing Information Risk

Information risk can be defined as insufficient high quality data to use for decision making and planning. Many growing stocker/backgrounder operations have outgrown their ability to collect the information they need to run their business effectively. Lending institutions evaluate operations for their information risk as part of the loan approval process and have high expectations. Opportunities exist for veterinarians to be part of managing information risk.

Managing Price and Equity Risk

234

As stocker/backgrounder operations grow, price and equity risk protection becomes imperative. Lenders will require a strategy to protect equity at some level and business opportunities exist for practitioners to become a resource for producers as they become comfortable with the process. Producers often look to their veterinarian as a resource when learning new skills. Helping clients with financial risk management complements the entire package of services offered by the veterinary practice.

Managing Your Practice to Bring Value

Managing a veterinary practice that serves stocker/backgrounder clients can be a challenge due to the sheer volume of products used by this segment of the beef industry. There is a very large financial commitment for the practice to inventory all the supplies used by these types of operations. Working closely and honestly with producers is critical to finding novel solutions to some of the cash flow problems that arise. The ability to provide non-traditional services and the opportunity to learn new skills are central to the veterinarians and practices serving these clients.

Conclusion

235

There are many challenges and rewards in serving stocker/backgrounder clients. Great potential exists for those veterinarians who choose to think innovatively and find effective solutions to problems that plague this increasingly significant segment of the beef industry.

236

Food Animal

Lourens J Havenga, BVSc

Chief Executive Officer - Multimin USA Inc. Fort Collins, Colorado

237

238

Trace minerals in cattle: Maternal Transfer, Fluctuations and Production Cycle changes. Lourens J. Havenga, BVSc Chief Executive Officer Multimin USA Inc. Fort Collins, CO 80528, lourens@multiminusa.com Abstract: Reproductive performance is one of the key economic drivers in both beef and dairy production. The roles of various trace minerals in cattle reproduction have been well documented. Identifying key risk periods where an imbalance of these trace minerals due to normal physiological events like maternal transfer or environmental exposure to antagonistic minerals, may enable practitioners to formulate supplemental strategies to minimize the risk and improve or maintain herd reproductive performance. Key Words: cattle, trace minerals, reproduction Adequate trace mineral levels are thought necessary to optimize cow reproduction, bull reproduction and also calf health and calf performance 12, 2. Native forages grazed by beef cattle are generally marginal or deficient in Cu, Mn, Se, and Zn concentrations15.The most widely used means of trace mineral supplementation for grazing cattle is the free choice, salt based, granular supplement13, however cattle do not balance their own mineral needs when consuming a freechoice mineral supplement 1,5. The most significant limitation to using free-choice mineral supplements is variation in individual animal intake 5, 9. The mineral status of cattle also change significantly over time and is not a constant, with the most significant changes occurring around the event of calving.8 Changing mineral status in cattle using different oral mineral compounds takes several weeks to months7. The availability of injectable trace mineral formulations have provided us with more options where plasma changes are measurable within hours and liver mineral value changes within one day20. An additional difference between oral and injected trace minerals is the exposure and impact of antagonist minerals in the diet. The absorption, availability and use of oral minerals are impacted by these antagonists e.g. iron, molybdenum, sulfur and calcium at different rates, reducing the animal`s trace mineral status and the injected trace minerals are not exposed to this effect.16 Most minerals serve two distinctly different purposes, as a structural component in certain tissues or as a co-factor in enzyme systems (both regulatory and as antioxidants) 17. Breeding females have two risk areas with regards to trace mineral imbalances. The thirty to ninety days prior to breeding will impact the follicle, ovulation, formation of the corpus luteum as well as early embryonic development 11,12,14 Another key period is pregnancy, especially the last 90 days of gestation as maternal transfer into the calf liver occurs during this time period11. This transfer and the event of calving will lead to significant drop in maternal mineral status8, 11.

239

Calves are born with higher trace mineral levels than the dam11 , however cowâ&#x20AC;&#x2122;s milk is a very poor source of trace mineral3 and significant decline in mineral status compared to birth levels are evident at sixty to ninety days of age, declining further up to weaning 4,10. The risk areas for calves are their trace mineral status at birth, at first vaccination and at or before weaning. Both disease and vaccination with modified live vaccine will cause a further decline in mineral status of cattle.6 Trace mineral status impact bull breeding soundness in several ways. In developing bulls scrotal size, semen quality and semen quantity are impacted.18, 21 The key risk periods in developing bulls are prior to weaning, right up to final breeding soundness examination, prior to sale or at breeding time. In mature breeding bulls trace minerals may be particularly critical for normal spermatogenesis, sperm morphology, and sperm motility and as such there are significant risk prior to the last sperm developing cycle before breeding soundness examination and breeding (on average 61 days prior to intended use).2,19 Once all the risk areas are clearly understood, practitioners will know when and how to utilize oral and injectable technologies to adequately manage each risk. Acknowledgement of conflict of interest: Dr. Lourens Havenga is the CEO of Multimin USA Inc. the developer and supplier of the injectable trace mineral product, MultiminÂŽ 90. References: 1Adams

FW, Dent WE, Howell HB, Mehlig JP. Growth performance and blood and liver copper values in Hereford calves offered certain mineral elements free choice. J. Anim. Sci. 1956; 15:1103 2Amann

RP. Reproductive capacity of dairy bulls. IV. Spermatogenesis and testicular germ cell degeneration. Am. J. Anat. 1962; 110:69-78.

3Anderson

3050-3055

RR. Comparison of trace elements in milk of four species. J. Dairy Sci. 1992; 75:

4Arthington

JD. Moriel P. Martins PGMA, Lamb GC, Havenga LJ. Effects of trace mineral injections on measures of performance and trace mineral status of pre- and postweaned beef calves. J. Anim. Sci. 2014; 92:2630-2640. 5Arthington

J.D. and Swenson C.K. Effects of trace mineral source and feeding method on the productivity of grazing Braford cows. Prof. Anim. Sci. 2004; 20:155 6Arthington

JD and Havenga LJ. Effect of injectable trace minerals on the humoral immune response to multivalent vaccine administration in beef calves. J. Anim. Sci. 2012; 90: 1966-1971

240

7Arthington

JD, Yost GP, McDowell LR, Martin FG, Wilkinson NS, Swenson CK. Effect of copper source and level on the rate and extent of copper repletion in Holstein heifers. J. Dairy Sci. 2002; 85:3297-3303. 8Barling

KS, Carstens GE, Daugherty SR, Herd DB and Randel RD. Effects of prenatal and prebreeding trace mineral/ vitamin E injections on calf health and reproductive performance of beef cows. Pages 39-43 in 2002/2003 Beef Cattle Research in Texas. Texas A&M Univ., College Station 9Boadi

DA, Ominski KH and Wittenberg KM. Utilization of fortified cubes to deliver trace minerals and monensin in forage-based diets. Can. J. Anim. Sci. 2006; 86: 291 10Choi

YK, Puschner B, Tegzes JH and Thurmond MC. Influence of age, sex and production class on liver zinc concentration in calves. J. Vet. Diagn. Invest. 2004; 16: 278-282 11Christensen

DA, Gooneratne SR. A survey of maternal copper status and fetal tissue copper concentrations in Saskatchewan Bovine. Can, J. Anim. Sci. 1989 69: 141- 150 12Fujii

J, Luchi Y, Okada F. Fundamental roles of reactive oxygen species and protective mechanisms in the female reproductive systems. Reproductive Biology and Endocrinology. 2005; 3:43 13Greene

LW. Designing mineral supplementation of forage programs for beef cattle. J. Anim. Sci. 2000; 78(E-Suppl.): E13-E22 14Guerin

P, Mouatassim S, Menezo Y. Oxidative stress and protection against reactive oxygen species in the pre-implantation embryo and its surroundings. Human Reproduction Update. 2001; Vol 7 no. 2, p175-189 15Harbers

LH, Smith EF, Umoh JE. The effects of burning on mineral contents of Flint Hill range forages. J. Range Manage. 1982; 35:231 16Hartman

SJ, Genther-Schroeder ON, Hansen SL. Comparison of trace mineral repletion strategies in beef cattle to overcome a high antagonist diet. AVC proceedings 2016 17Michiels

C, Raes M, Toussaint O, Remacle J. Importance of Se-glutathione peroxidase, catalase, and Cu/Zn- SOD for cell survival against oxidative stress. Free Radical Biology and Medicine 17, 1994; 235-248. 18Miller

JK and Miller WJ. Experimental zinc deficiency and recovery of calves. J. Nutr.1962; 76:467-474

241

Parillo F, Sylla L, Palombi C, Monaci M, Stradaioli G. Immunocytochemical localization of phospholipid hydroperoxide glutathione peroxidase in bullâ&#x20AC;&#x2122;s spermatogenic cells. Ital. J. Anim. Sci. 2014; 13:677-683.

20Pogge

DJ, Richter EL, Drewnoski ME, Hansen SL. Mineral concentrations of plasma and liver after injection with a trace mineral complex differ among Angus and Simmental cattle. J. Anim. Sci. 2012; 90:2692-2698 21

242

Underwood EJ, Somers M. Studies on zinc nutrition in sheep. 1 The relation of zinc to growth, testicular development, and spermatogenesis in young rams. Aust. J. Agric. Res. 1969; 20:889-897.

Food Animal

David Pugh, MS, DVM, DACT, ACVN, ACVM Southerntraxx Veterinary Services and Forge Waverly, Alabama

243

blank page

244

9/9/2019

2020 Mo VMA Summer Meeting Ruminant Nutrition DG Pugh

Herd Health

Nutrition Parasite Control (Internal & External)

Biosecurity Reproduction

(cows, heifers, bulls, calving management, etc)

Vaccination Genomic Stress Management

Feeding Livestock

What do you feed? What ever the Good Lord provides ! Alabama Livestock Producer

Beef Nutrition • Water- fresh/clean, free flowing, always available • Energy- forages, minimal concentrate, assess with BCS, highest requirements in early lactation, hardest to supply in late gestation/late winter

Feeding Beef Cattle • Feed related costs account for >60% of total expenditures for beef cattle herds • Four-Step Supplementation 1) Energy 2) Protein – maintain 7-8% CP for entire diet when not lactating

3) Vitamin – supplement / inject 4) Minerals – free choice salt w/ 8-12% Ca & P, and TM (S Wikse)

Broodcow Nutrition To maximize nutritional program: Shorten calving season (~63d) ….difficult to plan a feeding program for cows in different stages of production

• Protein- 7 –8% for maintenance, 10% late gestation, 12-14% in lactation

1 245

9/9/2019

Feeding and Management of Brood Cows

Feeding in General Heifers - breed more than needed - Breed 30 days before the mature cows - Palpate 60 days after breeding season -Cows > 10 years of age; the physical condition will diminish - Bulls - during intense breeding season; requirements may increase by 2-3 X - If forage is limiting, feed bulls separate 



– 30 days before calving – 70 days after calving  growth

of calf efficiency of cow  Lactation  Rebreeding  reproduction

Thin Cows • Thin cows have calves who are slower to nurse • Decreased CP and/or E feeding pre-calving reduces calves ability to generate heat (~10%)…dystocia further reduces calf heat production by ~ 10-20%

Feeding Beef Cows • In USA, >75% calves born in spring • 50d pre-calving…usually late winter…… - poor feeding results in decrease quality colostrum  lower calf survival/milk production/calf weaning wts & increase postpartum interval

critical time of nutrition

Winter Feeding Plan • • • • •

Sort into groups: 1) replacement heifers 2) older, thin cows/first calf heifers 3) cows BCS >5 Cull old, open, poor producing => 3-5 A pasture/cow

BCS • Body Condition Score • Estimation of body fat • Scale of 1 to 9 • Most cows score from 3 to 7

– BCS 3 = 7 to 9% fat. – BCS 5 = 15 to 18% fat. – BCS 7 = 25 to 27% fat.

2 246

9/9/2019

Feeding Cattle in Wyoming 1,200# lactating beef cow requires ~19 Mcals NE, or 33# good quality alfalfa hay (63% TDN) daily in early lactation 1,200# cow post weaning requires 10 Mcals NE, or 19# good quality alfalfa hay (63% TDN) daily

Feeding Cattle in Wyoming “2# whole corn fed to grazing cattle can reduce forage digestion enough to negate any benefits provided by the corn”. (Mount, U Wy Coop Ext, MP-111.06 Oct, 2005)

(Mount, U Wy Coop Ext, MP-111.06 Oct, 2005)

Winter Feeding Cows Supplements - If forage ~7% CP, grain supplement should be restricted to <0.5% BW/d - > 5# cereal grain/d => decrease forage intake by 6#/day for each # of grain Rule of Thumb - provide supplement @ 0.2-0.5 % BW… depending on BCS (2-5 #/cow/d)

Feeding Broodcows • When feeding weathered or poor quality forages / pasture… feed supplemental protein • When feeding good quality forages  protein is probably not needed, …. but supplemental energy may required

Feeding Broodcows Begin supplementation - with killing frost - prior to BCS loss - during periods of drought… duh

Protein supplement improves rumen digestion • Malnutrition in the cow is almost always accompanied by malnutrition of the rumen microbes. – Low protein forage

• Rumen maldigestion accelerates and magnifies the consequences of malnutrition • Protein supplementation markedly improves digestion and utilization of hay and grazing

3 247

9/9/2019

Protein Expensive ingredient

Feeds for supplementation

Examples are oilmeals (SBM, CSM)



Animal origin (fish meal, meat meal, tankage) (nonruminant products only) Byproducts (distillers grains,brewers grain, corn gluten, broiler litter) Protein substitutes, NPN (urea, biuret)

Protein supplementation and anthelmintic treatment in cattle resulted in higher weight gains than in cattle receiving an anthelmintic treatment only. Between those groups, no significant differences could be observed in fecal worm egg counts and hematocrit (Magaya et al., J. S. Afr. Vet. Assoc 71, 2000, pp. 31-37).

     

Oilseed meals Grain Breeder/range cubes Protein blocks Liquid feeds (protein or protein/energy) Syrup blocks or tubs Hays

Feeding protein at 130% of the required level to ewes will actually abolish the periparturient rise (PPR) in fecal egg count. Donaldson et al, JAnimal Science 1998; 67:523-33.

Ewes that were fed high quality protein early in pregnancy developed more body fat. Near lambing time, ewes supplemented with protein early in their pregnancy were able to prevent establishment of an experimental larval challenge better than the unsupplemented counterparts, even though their nutritional plane at time of challenge was the same. The “fatter” more resistant ewes had higher serum leptin levels, suggesting that leptin might be a link between nutritional status and immune function

Nematode infected ruminants have higher protein requirements, caused by anorexia, the predominant effect of helminth infections (sheep) (Coop and Holmes, 1996)

Cattle benefit from anthelmintic treatment and/or protein supplementation …. But the added value of protein supplementation was unclear from the study.

Valderrabano et al, Vet Parasitol, 141:122-131, 2006.

CP REQUIREMENTS--- Cows Immediately Post-Weaning - 6% 60 days Pre-Calving - 7.5 to 9% 60 days Post-Calving - 10 to 12% Heifer - 10.5% decrease

(Veronique, Veterinary Parasitology, 235: 15, Pages 113-122)

4 248

9/9/2019

CP - Forages Winter annuals - 20-30%

Natural Protein HIGH protein - ALL natural products generally contain 40% protein Hot mix Estimated range of salt intake of cattle fed salt-limited supplements

Stockpiled Fescue - 15-17% Warm season perennials - 11-15%

Body Wt (lbs.) 300 500 700 900 1100

Salt consumption # /day Low Avg. 0.3 0.5 0.5 0.6 0.6 0.7 0.7 0.9 0.8 1.1

High 0.6 0.7 0.9 1.1 1.3

Will consistently improve both intake (2 to 7 lbs) and digestibility (up to 15%) of forage

Protien Blocks, lick tubs and cubes are the most convenient ways to feed Care should be taken to prevent overeating Overeating can be partially controlled by feeding plenty of roughage and supplying plenty of fresh water

Urea or Non-Protein Nitrogen (NPN) Low rumen pH reduces absorption of ammonia to the blood, and reduces the incidence of ammonia toxicity

When urea is fed, Sulfur (S), Potassium (K), and Phosphorus (P) must be supplemented

Classes of Feeds cont.  NPN= non-protein nitrogen urea, ammoniated molasses or chloride, biruet, etc Urea = 45% Nitrogen X 6.25 = 281% protein equivalent

Urea or Non-Protein Nitrogen (NPN):  Urea is used to: - Increase diet organic matter digestion (urea treatment of straw)

- Increase microbial protein synthesis  Possible Problems: - Ammonia Toxicity - Reduced Feed Intake  Never Exceed when using Urea: - 1% of the diet dry matter - 1/3 of the total dietary protein

5 249

9/9/2019

Parasites in Cattle

Proper nutrition => Increase herd immunity => healthy cows => Better Productivity Use adult cows as “vacuum cleaners”

Diet Effects on Immunity Protein During disease or infection, proteins and amino acids are diverted from normal functions to support the synthesis of immunoglobulins and T-cell- and Bcell-mediated immunity, and they are catabolized for energy production (Scrimshaw and SanGiovanni 1997). Inadequate protein nutrition impairs cell-mediated immunity and immunoglobulin production

Diet Effects on Immunity

What Is Immunity? • The Ability To Resist Disease • Must Balance Protection and Challenge • Vaccination vs. Immunization

–NOT THE SAME THING!

Low intake (low nutrient intake) => decrease immune function Good diet supplies the substrates that are required for the development, maintenance, and function of the immune system (Klasing 2002). Nutrients needed for immune system support: energy, protein-amino acids, minerals, vitamins, & specific fats.

Diet Effects on Immunity

Energy serves as fuel for the synthesis and function of immune cells, & protein regulates and serves as structural component & for cells and antibodies. Minerals are required for proper function of the immune components (selenium, zinc, copper) Vitamins (A, E, B6, B12, C) are essential for immune function.

Mineral Nutrition • Deficient /Sub-optimal mineral intake rarely affects BCS….but will affect immune system

6 250

9/9/2019

Diagnosis of TM Deficiency

 Pasture (1-3 inches above the ground, all plants they eat) place in zip-loc bag

 Liver biopsy (Cu)…clip, scrub, rinse with distilled-deionized water (altered by gestation, disease, etc)  Whole blood (Se)…prefer green top tube  Serum (Zn)…TM / royal blue top tubes  Hair  Check 10% of herd

 Hay (core sample diagonally 10 % of bales)  Water (sulfate, etc)

Diet Effects on Immunity Minerals are required for proper function of the immune components (selenium, zinc, copper) Vitamins (A, E, B6, B12, C) are essential for immune function.

Trace minerals include: Cu, Zn, Se, Ar, Cr, F, I, Fe, Mn, Ni, Si, T, Va, ?

Released into environment by combustion of fossil fuels: As, Cd, Cr, Mn, Mg, Pb, Ni, etc Pesticide associated contamination: As, Pb, Hg,…. Fertilizer associated contamination: As, Cd, Cr, Ni, Zn,…..

Mineral Feeding  Trace mineral salt intake is governed by a drive for Na  Anything that alters TM salt palatability (Mg, DiCal, etc) or a diet that supplies adequate Na will result in inadequate TM salt intake

“Copper and zinc are probably the two trace minerals that western rangelands are typically deficient in.” (Steve Paisley, University of Wyoming Extension beef specialist)

Wyoming, cattle may have 2nd or ‘conditioned’ deficiencies (Natasha Wheeler Wy Livestock Roundup)

7 251

9/9/2019

Hay / Forage Analysis in USA • Alfalfa – deficient Zn in ~ 63% - excessive to sufficient in Ca - deficient to sufficient in P

Zn deficiency: parakeratosis, alopecia of head and legs, footrot, small testicles (goats & Holsteins), depressed libido Dx – Zn conc from liver biopsy / non-hemolysed serum (plasma) in non butyl rubber tubes, skin biopsy (eosinophils in lamas)

Diet Effects on Immunity Zinc Research with stressed calves has demonstrated that zinc supplementation can decrease bovine respiratory disease associated deaths by 52% (Carroll and Foresberg 2007)

Zinc absorption is: - enhanced by Vit C - inhibited by Ca, Cd, Fe, Sn, oxalates, phytates, organophosphates, Most consitently deficient mineral (>60% of forages - alfalfa) More Zn available from forage than cereal grains

Diet Effects on Immunity

Tx – Reduce legumes to < 1/3 of diet If < 1% dietary Ca …..offer zinc sulfate (1 – 4 g/d) or Chelated Zn (Zn methionine 1-4 g/d) Prevention – 50# TM salt, 50# DiCal, 10# ZinPro 100 (10,000 ppm Zn methionine), 50# molasis free choice…1 to 4 oz/d

Copper Copper’s immunological role has been reported to serve in antibody production, inflammation, and neutrophil phagocytosis (Erickson et al 2000; Schrimshaw and Sangiovanni 1997, Carroll and Forsberg 2007).

Copper supplementation has not been reported in summary literature to improve cattle performance or morbidity (Galyean et al. 1999, Carroll and Foresberg 2007; Duff and Galyean 2007).

8 252

9/9/2019

Copper Nutrition Copper absorption is: -enhanced by L-aa’s, Vit A, lactose, acid soils -inhibited by Mo/S, Cd, Zn, Fe, Se, Vit C, alkaline soils More is available from hay than grass Cu:Mo (3) 4:1 => 10 (13):1 Fe 250-1200 ppm (Spears J Nutri 2003, Prabowo JAS 1988)) S?

Mineral Nutrition • Cu Toxicity…only toxicity in literature (Junge JAVMA 1989, Mullaney Am Assoc Vet Lab Diag 1996, Weaver Can Vet J 1999, Carmalt Can Vet J 2001, Pugh J Camel Prac Res 1999) still…………. NWC appear more resistant to toxicity than sheep …in these cases Cu:Mo ratio >16:1

What to look for (2-4 oz) Salt Calcium Phosphorus Magnesium Copper Zinc Selenium

15-30% 6-12% 6-12% $$$ 0-4% (8-14%) .09-.18% .18-.36% .0026-.0052%

In anaerobic environment of rumen (C1) reduces Cu, and allows the formation of Mo-S complexes => decreased available Cu (<4:1 Cu:Mo, >2000 ppm S)

High dietary Fe => decreased available Cu ( >200 ppm Fe)

Exotic Cattle breed have greater requirements than British breeds (~50% higher)

Selenium

Diet Effects on Immunity

Supplemental selenium increase or enhance neutrophils & macrohphage phagocytosis (Duff and Galyean 2007; Erickson et al. 2000)

- antibody response / production of some specific antibodies (Carroll and Forsberg 2007).

Mineral Intake • Beef cow eats ~ 70 – 80# of salt/yr • Na is only mineral ingested in reliable fashion….so used as carrier • Na requirements 0.1% DM intake for nonlactating, and 0.2% DM intake for lactating cows • Will double salt consumption if go from blocks to granular

9 253

9/9/2019

Recipe Supply minerals by free choice feeding of a good quality mineral mixture with 10-12% Ca, 8-10% P, salt and trace minerals Commercial or ………….. 50# DiCal + 50# TM salt..throughly mixed

1:1 Trace mineral salt and dicalcium phosphate

Mineral Feeding Supply minerals by free choice feeding of a good quality mineral mixture with 10-12% Ca, 8-10% P, salt and trace minerals Commercial or ………….. 50# DiCal + 50# TM salt..throughly mixed)

Mineral for corn silage • Ground limestone - 50# • Dicalcium phosphate - 50# • TM salt -50# Offered free choice

Major Minerals cont’

Mineral Feeding Mineral for crop residues • Dicalcium phosphate - 50# • TM salt - 50# Offered free choice



Magnesium 

Low in lush spring grass—Grass Tetany is a common deficiency



Salt



Potassium



Sulfur



Sodium requirement, most feeds are low in sodium High in forages, low in grains. Needed when urea is added. Toxicity is concern

10 254

9/9/2019

Mineral Feeding • Granular molasis

– 10#

• Mg0

- 30#

• Dicalcium phophate – 30# • TM salt - 30# Provide free choice….adjust molasis to adjust intake (4 - 8 oz/d)

Mineral Feeding • Mineral for Grass Tetany Prevention

& CP are also needed

• Soybean meal/CSM or • Ground corn • Dicalcium phosphate • MgO • TM salt Offered free choice

where E

- 50#

- 50# - 50# - 50# - 50#

Mineral Feeding Feeding Inorganic (sulfates-chelated Cu, Co, Mn, Zn) vs Organic (chelated complexes of same) supplements final 95d gestation The supplements allowed the same levels of these TM’s, which were above the NRC Cows fed the Organic treatment weaned calves that were 53 lbs heavier than the Control and 28 lbs heavier than the Inorganic. (Marques et al, 2015)

Mineral Feeding Organic supplemented minerals resulted in improved calf health, less calves respiratory disease while on feed, and carcass wt 42 lbs heavier than control & 20 lbs heavier than Inorganic supplemented cows. (Marques et al, 2015)

 Chelates – allow the mineral to compete for binding and absorption at a non traditional site, as they are absorbed along with AA’s  Easily chelated minerals include: Cu, Co, Fe, Mn, Zn

Winter Feeding – Vitamin A

 Feeding 1/13 ‘green’ roughage  If feeding moderate to poor quality hay (brown) …supplement with 30,000 IU of Vitamin A daily in a feed or 200,000IU/lb of salt mixture  Vitamin A (im), October or November

11 255

9/9/2019

Post de-worming, turn out onto contaminated pasture Never keep replacement heifers that are dewormed and placed on clean pasture Never use permanent pastures for young stock Use long-acting dewormers for stockers going to feedyards ONLY !

“Important” Nematodes

Haemonchus placei & Cooperia sp

Calves Stocker (mostly), Warm Season parasite Cattle develop immunity by yearlings (usually) Mature cows will have low numbers and may serve as source of pasture contamination

Cooperia & Haemonchus spp resistant to ML’s are Dx in > 50% of cattle operations, when examined (reduced feed intake reduced productivity  economic losses) (Gasbarre, Vet Parasit, 2014)

H placei - Ivermectin resistance

Parasites in Cattle

Rotate pastures to maximize nutrition and pasture use, not to control parasites (but.. will help with parasites)

(Kaplan, NAVC, 2010)

Parasites in Cattle Do not under-dose animals & (teach) follow label directions for storage

Deworm with multiple classes of anthelmintics on arrival

Never deworm all animals pre turnout onto clean pastures (ML’s worst) => Refugia Killer

Drylot for 24‐48 hours then turn out onto contaminated pasture

Never deworm older cows pre summer in the south

Cull “poor doers”

Parasites in Cattle Pastures grazed by other livestock species

Cows ‘clean’ stocker pastures grazed by cows Non-permanent pastures (tilled & planted, hay pastures, crops) are clean (Navarre, personal communication, 2017)

12 256

9/9/2019

Parasites in Cattle

Smart grazing management:

Proper nutrition => Increase herd immunity => healthy cows => Better Productivity Use adult cows as “vacuum cleaners”

Avoid graze below about 5-6 cm (2-3 inches) pasture height. Over 80% of larvae are within 3 cm of the soil surface. Manage pasture quality: To ensure high quality regrowth for next time it is grazed 1- Goat to cattle system; 5-6 cm deep pasture left behind by the goats, it is acceptable to production from cattle. 2 - Goats + cattle Integrated system: cattle and goats prefer different species of forage. - Goats + cattle (do not share the same parasite species)

- Goats + sheep

(share the same parasite species)

- Cattle + Sheep

Perform McMaster’s technique for quantitative fecal egg counts. If sample is 0 on McMaster’s, perform a Wisconsin Double Centrifugal Sugar Flotation. Consider turning pooled fecal samples pre and post treatment for parasite species identification via coproculture (C Navarre , 2017)

Fecal Egg Count – In cattle, McMasters & Modified Wisconsin double centrifigation have good correlation.

(Divide cow number by 2.3 to compare more favorably with Double Centrigation Tech’s)

What can we do ?

Develop sustainable parasite control protocols which place less selective pressures on the parasites but maintain good productivity ex: Simultaneous

use of multiple classes of anthelmintics with different modes of action

Targeted/selective treatment of different classes of animals avoid blanket treatment (Gasbarre, Vet Parasit 204:3, 2014)

Any Questions?

13 257

258

9/9/2019

Herd Health Internal Nematode Parasites in Cattle DG Pugh

Nutrition Parasite Control (Internal & External)

Biosecurity Reproduction

(cows, heifers, bulls, calving management, etc)

Vaccination Genomic Stress Management

GI Nematodes can cause dramatic performance loss without overt signs of disease.

What do Cattle Producers Do? • “WE ARE GRASS FARMERS” (Gordon Hazard, DVM)

• We are Green • Converting Grass to Beef • Feeding People

Gastro-intestinal Parasites

• Appetite suppression • Protein loss • Host expenditures

– Tissue repair – Mounting an immune response

Most of production loss is due to decreased appetite

Parasites Generally • Have more impact on younger animals in the herd Calves > replacement heifers = second calf heifers > adult animals

• Most parasitism is SUBCLINICAL in nature – Clinical parasitism is rare

1 259

9/9/2019

BENEFITS OF DEWORMING - Improved Health -

Better Immune Status, feed efficiency

(Gasbarre and Stromberg, 1994)

• Increased Weaning Weights - >17-37# ….. Milk production & calf growth

(L Jones, WVC 2014)

• Increased Breeding Efficiency - Fertility, Onset of Puberty • Reduced Pasture Contamination

Increase resistance by the parasites to a dewormer - Deworm entire group & move to a ‘clean ‘pasture Graze stocker calves on a permanent pasture

Drug Resistance

Refugia – The proportion of the population

(Haemonchus - goats & sheep, Ostertagia & Cooperia – cattle)

that is not selected by drug treatment

It provides a pool or reservoir of drugsusceptible genes and dilutes the prevalence of resistant genes, and maintains biodiversity within a species (Martin, Int J Parasit 1981; Van Wyk, Onderstpoort J Vet Res 2001; Sissay, Vet Parasit 2006; Miller, Pugh, Kaplan, Sheep & Goat Med 2, 2012)

How to Recognize a Resistance Problem The warning signs: 

Lower than expected weight gain

Diarrhea  Rough hair coat  Delayed conception  Increased incidence of disease 

If you suspect a resistance problem => Fecal Egg Count Reduction Test (FECRT) 14 days after the last treatment.

Strongyle Parasites in Cattle

ML resistance in cattle documented 2003, and suspected in Al, Tn, Fl, La, SC, NC, ???... But inj IVM still >90%

reduction

Strategic Deworming…deworm early in the grazing season.

Anthelmintic resistance has continued to increase over the past ~15 years

Why do we now see anthelmintic resistance ?

Poor-ons poorly absorbed

Probably the use of very effective nematode control programs

C puncta, Nematadirus, Haemonchus the most significant internal nematode parasites

Programs which place selective pressure on the parasite genetics  Resistance

(improved the productivity)

And … Ostertagia less significant. ( Gasbarre , AVC, Denver 2012)

2 260

9/9/2019

“Now, we are forced to accept the reality

that chemical control of helminths is not, by itself, sustainable. Strategically and effectively applied chemical intervention, coupled with a raft of non-chemical measures designed to lessen ‘economic parasitism’ is the recommendation that most parasitologists appear to be advocating.” (Yazwinski et al, Proceed KVMA, 2018)

“Important” Nematodes

Haemonchus placei & Cooperia sp Calves Stocker (mostly) Warm Season parasite

Cattle develop immunity by yearlings (usually)

Mature cows will have low numbers and may serve as source of pasture contamination Cooperia & Haemonchus spp resistant to ML’s are Dx in > 50% of cattle operations, when examined (reduced feed intake, reduced productivity, economic losses) (Gasbarre, Vet Parasit, 2014; Kaplan, NAVC, 2010)

“Important” Nematodes • #1 Ostertagia ostertagi

• Can impact Young & Mature cow productivity • Cool season lover & do not survive well in hot environments

• Arrested development in animal – Hypobiosis - Summer in South – - Winter in the North

Some Bulls with Type ll Ostertagia will have scarred gut , poor condition and low FEC (r/o Johnes) Brahama and x’s have very poor immunity to Ostertagia

“Important” Nematodes Haemonchus placei Barber pole worm Likes it hot

Ivermectin resistance

(Kaplan, 2010)

Cooperia species

Prolific egg producers

Not notorious pathogen, but …stockers White wormers – good control

Ivermectin resistance

(Kaplan,, 2010; Yazwinski, 2014)

(Driven by pour-on’s) (Jones, 2014)

Parasite Problems in Cattle Stocker operations => buildup of anthelmintic resistance parasites Intensive rotational grazing + young animals + frequent deworming + Cooperia => Resistant Parasites

ML resistant Cooperia & Haemonchus spp can survive a single TX with a single ML and be transported in the calf from southeastern USA to Mid western states. A combo of ML & levamisole was very effective in decreasing the transport of ML surviving parasite to the upper Mid west (LL Smith, 2013)

3 261

9/9/2019

Topical generic Ivermectin efficacy (%’s) against: Cooperia oncophora - 93.0 C. punctata - 73.4

ML’s

Topical moxidectin efficacy (%’s) against:

 Improved clinical efficacy against GI resistant nematodes

Injectable moxidectin efficacy (%’s) against: Cooperia oncophora - 46.1 C. punctata - 93.6

SC – enhanced absorption, increased systemic availability/reduced drug

Cooperia oncophora - 99.3 C. punctata - 99.9

PO – reduced systemic availability high conc at site of GI parasite  enhanced parasite exposure to active drug at mucosa and GI lumen

conc in GI lumen  reduced exposure to GI located nematodes to active drug

This data suggest Tx of calves soon after weaning with topical moxidectin is effective (>90% efficacy) for all common nematodes in Boehringer Ingelheim Vetmedica, Inc. cattle; where, injectable MOX & Topical IVM have limited effectiveness against Cooperia spp.

 Limited efficacy (Lanusse et al , Vet Parasit, 204;18, 2014) Jenee S. Odani, DVM, DACVP

(Yazwinski et al, Vet Parasit, 195: 95-101, 2013)

Evaluation of long-acting eprinomectin compared to conventional anthelmintics in cow/calf production MOX + OXF ( PO & Orally) vs LAE in fall born, weaned heifer calves over 182 d ~~ ? OXF vs LAE in Spring calving cows were treated, weaning weights were lower (P=0.03) for LAE compared to OXF. (Backes, PHD dissertation UA, ProQuest Dissertations Publishing, 2016)

122 yearling pastured heifers with a history of anthelmintic resistance (California), moved to dry lot (Idaho) Fifty highest FEC were examined for Tx and FECRT

Ivermectin treatment (SC) resulted in no reduction in adult Cooperia spp. vs Moxidectin TX (SC) caused an 88% parasite reduction (Edmonds +, Vet Parasit 2010)

2017 Stocker cattle study: Cattle were treated w/ saline, OR doramectin (INJ) + albendazole (PO) OR eprinomectin extended-release injection then continuously grazed by treatment group for 118d This study cattle were treated with Injectable ivermectin, doramectin, and moxidectin Day 15 post TX FEC were: FEC FECR Drug 177 57% Ivermectin 335 41.2% Doramectin 28 91.2% Moxidectin

Parasites Problems in Cattle Cow-calf herds are less likely to experience resistance (although documented) Stocker heifers redirected back to cow-calf may intro resistant parasites Deworming all prior to turnout to summer pastures unused (refugia killer)

Coproculture larvae populations were mostly Haemonchus placei & Cooperia punctate

(Yazwinski ++ Bovine Practitioner, 2017)

4 262

9/9/2019

Parasite control - Maintain Refugia Avoid deworming all prior to turn out onto clean pastures (worse with ML’s) Avoid deworming adult cows going into summer

Treat Replacement heifers differently than stockers

Parasite control Avoid permanent pastures for stockers, yr after yr If use LA products ++> feedlot, till ground, use for hay, and keep replacement heifers off Stocker pastures (?)

Parasite control

- Cull poor doers

- Graze adult cows (or horses/goats) after calves… Thus using adult cows as ‘vacuum cleaners’ for calf parasites

- Avoid Generic pour-ons, dose accurately, handle drugs properly

- Avoid ‘resistant worms’ being introduced to the herd - Deworm with multiple classes of dewormer (or MOX)  drylot for 2 day  then move to contaminated pasture - Proper nutrition (enhance overall immunity)

Parasites in Cattle

Rotate pastures to maximize nutrition and pasture use, not to control parasites (but.. will help with parasites)

Drylot for 24‐48 hours then turn out onto contaminated pasture

Parasites in Cattle Do not under-dose animals

& (teach) follow label directions for storage Never deworm all animals pre turnout onto clean pastures (ML’s worst) => Refugia Killer

Never deworm older cows pre summer in the south

5 263

9/9/2019

Parasites in Cattle Pastures grazed by other livestock species Cows ‘clean’ stocker pastures Non-permanent pastures (tilled & planted, hay pastures, crops) are clean (Navarre, personal communication, 2017)

Macrocyclic lactones have been available for >30 years in the USA ML resistance has been reported and appears to be increasing in U.S.

Obstacles to change

Cattle producers are traditionally reluctant to abandon historical practices

Heritability for GIT resistance by cattle is

Veterinary Practitioners have not traditionally worked with parasite epidemiology

~0.3

Pharmaceutical companies stockholders have “strong economic incentives for maintaining the status quo” (McArthur & Reinemyer, Vet Parasit 204:34, 2014)

What can we do ?

Develop sustainable parasite control protocols which place less selective pressures on the parasites but maintain good productivity ex: simultaneous

In Southern USA Deworm -- 1st to 2nd calf Heifers (unless Zebu x) (Zebu & x’s have very poor immunity to Ostertagia)

-- Adult cows with <5 BCS

use of multiple classes of anthelmintics with different modes of action

-- Spring born calves in Mid Summer near or at Weaning

targeted/selective treatment of different classes of animals avoid blanket treatment

-- Bulls pre breeding

(Gasbarre, Vet Parasit 204:3, 2014)

-- Fall born calves near or at weaning (Some Bulls with Type ll Ostertagia will have scarred gut , poor condition, and low FEC - r/o Johnes)

6 264

9/9/2019

Fecal Egg Counts (FEC)

Beef Cow BCS

-- BCS 6  pregnancy rate should approach 100%

Fecal Egg Reduction Test (FERT) – 90+ %  good 85 %  OK <70 %  BAD

(if bulls, mineral, etc, etc are normal…???, Spitzer, 1995)

-- BCS 5  pregnancy rate should approach 94%

Fecal Egg Count (FEC) adult cow – 10 -

At calving FEC will rise (Immune suppression)

-- <BCS 5  deworm (?)

(Bagley)

20 (Navarre)

Usually Lush feed intake  increase FEC Dry feed intake  decrease FEC Stocker & Replacement Heifers have highest FEC from 6-18 mo of age then immunity

Fecal Egg Count

calf - 50  500

Young/new calves will shed few eggs until mid summer

To detect Anthelmintic Resistance in Cows Collect 20 fecal samples from rectum into plastic bag of similar aged animals at time of deworming. Remove excess air & refrigerate Perform a McMasters In 14 d collect sample from the 10 highest initial EPG cows Sample 1 EPG- Sample 2 EPG Sample 1 EPG

X100 = % reduction in EPG

-- Consider pooled samples for coproculture and sp ID (C Navarre , 2017)

• Short grass favors more aggressive parasite transmission. – Cows and especially calves

• Cattle concentration from feeding further increases parasite loads • Malnutrition diminishes parasite resistance – Calves may require additional deworming in early summer.

Fecal Egg Count – In cattle, McMasters & Modified Wisconsin double centrifugation have good correlation. (Divide cow number by 2.3 to compare more favorably with Double Centrifugation Tech’s)

Parasitism- is it connected to nutrition? • Poor nutrition (protein specifically) diminishes already acquired resistance to parasites. • PPRI periparturient relaxation of immunity – Diminshed parasite immunity right after birth • •

Nutritional sensitivity of periparturient resistance to nematode parasites in twobreeds of sheep with different nutrient demands. Br J Nutr. 2010 Nov;104(10):1477-86 . Proc Nutr Soc. 2001 Nov;60(4):515-25. Nutrient partitioning between reproductive and immune functions in animals. Houdijk JG(1), Jessop NS, Kyriazakis I.

• Short pasture markedly increases parasite transmission.

– Heavy fecal pat density increases parasite deposition and survival.

7 265

9/9/2019

Parasites in Cattle

Proper nutrition => Increase herd immunity => healthy cows => Better Productivity

Nematode infected ruminants have higher protein requirements, caused by anorexia, the predominant effect of helminth infections (sheep) (Coop and Holmes, 1996)

Use adult cows as “vacuum cleaners”

Cattle benefit from anthelmintic treatment and/or protein supplementation …. But the added value of protein supplementation was unclear from the study. (Veronique, Veterinary Parasitology, 235: 15, Pages 113-122)

Protein supplementation and anthelmintic treatment in cattle resulted in higher weight gains than in cattle receiving an anthelmintic treatment only.

Any Questions?

Between those groups, no significant differences could be observed in fecal worm egg counts and hematocrit (Magaya et al., J. S. Afr. Vet. Assoc 71, 2000, pp. 31-37).

8 266

Tips for Fly Control

External Parasites of Livestock Flies cost the Cattle industry > $80 million/ yr

DG Pugh DVM, MS, MAG Dipl ACT, ACVN, & ACVM

External Parasites of Livestock Blood‐suckers

Horn Flies – most economically important Difficult to control Face fly, Stable fly, House Fly - good sanitation Horse flies and deer flies Not much you can do…stay away from areas where they are… Lice, mosquitoes, ticks, grubs, mange and scab mites, black flies or buffalo gnats

External Parasites of Livestock Heribility of fly resistance is high ~.58 Increased hair follicles=> increase in the 2 oil glands & 1 sweat gland per hair follicle => increase in ‘stuff’ secreted by these glands Possibly more factors ( color ) ????

(Pugh DG, Ext ANR-2083, 2014, pp1-8)

Horn Fly (Haematobia irritans)

Why control horn flies? - If >200 flies on a calf - • > 10,000 flies/cow - Blood loss and stress – Weight reduction 15‐50 lbs of weaning weight Or…up to an extra 1.5 pounds per week

– Milk production reduction in dairy cow output up to 20%, 0.5 liters per day

267

Why control horn flies? • Transmit bovine mastitis (summer mastitis) (Oliver et al. 1998, Edwards et al. 2000)

Identifying Horn Fly

Rigid piecing mouthparts – Horn fly: rest on animal between feedings; most often on back, shoulders, sides; feed 10 – 20 times a day

– 53% flies collected from cattle are positive for S. aureus (Anderson et al. 2012, NC)

A little Horn fly biology

Horn Fly

• Less in feedlots, dairy farm or indoor operations

Must have an intact cowpat for larvae to complete development

• Entire cycle – approximately 2 weeks

• Generation – 10 or more per year

• Population peaks High density of animals trample and squash cowpats, accelerates drying and makes them unsuited for larval development

– In early summer then in fall (May through September in Bama)

• Number of eggs per female ≈500

• Preferred fresh dung – Grass manure of pastured cattle

Face Fly Musca autumnalis • Eggs are laid just below the surface of fresh cow manure.

• Larvae will either pupate in dry cow dung or in

the adjacent soil. Adult flies overwinter in farm buildings.

268

Face Fly

Spongy mouthparts, hairy legs, & sticky foot pads pick up pathogens, including Moraxella bovis, the bacteria associated with pinkeye, and Thelazia rhodesii , the eye

worm.

Longer season than the Horn Fly

Musca domestica …. “Housefly" • Sucking or ‘lapping’ ……."vomit drop feeder."

Stomoxys calcitrans - "Stable fly" Widely distributed throughout North America One of the most important sources of annoyance to livestock

Mass attack of flies => loss of blood, loss of flesh, lowered milk production & reduced butterfat content, reduced vitality, loss of pasturing time, & damage to the victim's tissues & hide Stress of fly bites, the animal may be more susceptible to disease.

“Balling” caused by stable fly feeding. Feed on the lower legs

Identifying Stable fly

Rigid piecing mouthparts

Stable fly: on animal only while feeding; Feed principally on the legs

Options for Control

Back Rubbers and Face Rubbers

• Back Rubbers and Face Rubbers • Pour‐on and Sprays • Feed Through • Dust bags • Ear tags

• They have to use it….often

Insecticide impregnated

• New chemicals • New formulation and delivering systems

269

• Choose effective insecticides and recharge every 2 to 3 weeks (or weekly) • Place in areas where cattle ‘move through’ Use High Quality Mineral oil or Fuel oil (not motor oil)

Pour‐on and Sprays • Delice, Atroban, Ectiban (permethrin) (Face Fly) • Cylence (cyfluthrin) – 1‐4 week control (Face Fly) • Saber – residual permethrin (Face Fly)

Strongyle Parasites in Cattle

ML resistance in cattle documented 2003, and suspected in Al, Tn, Fl, La, SC, NC, ???... But

injectable IVM still >90% reduction

Poor-ons poorly absorbed

• Macrocyclic lactones (doramectin, eprinomectin, ivermectin) (Horn Fly)

Feed‐Thru Through

Results will be extremely variable

--All animals must eat a nutritional or mineral supplement containing an IGR on a regular basis --Herds or horses need to be isolated - Start feeding these products just before the beginning of fly season and continue to feed until the first hard frost in the fall

Dust Bags

• Effective when used in ‘forced‐use’ situation (~80% - 90% fly reduction)

• Less effective if uncovered (wet), in high humidity conditions, or ‘non forced-use’ situations (~25% - 50% fly reduction) Options : Co‐Ral 1% D (coumaphos), Rabon 3% D, Methoxychlor 5% Dust (Horn fly) Ectiban - Permectrin 0.25% D (Face Fly)

270

Cattle

Feed‐Thru Through

IGR -Methoprene (Altosid) is the active in most block, tub and liquid products: ¼ ‐ ½ pound per month - Diflubenzuron (ClariFly) ( Vigilante Bolus)

OP –Tetrachlorvinphos (Rabon) is available as a premix – 70 mg per day

Horses IGR -Diflubenzuron (Equitrol II and Simplifly) -Cyromazine a triazine (Solitude) OP -Tetrachlorvinphos (Rabon, Equitrol)

Ear Tags (????) Do not use a pyrethroid more than once every three years (Best for Face Flies) Do not use an organophosphate more than 2 years in a row (Horn Flies) Remove the tags at the end of the season (or when they quit working & burn/bury) Do not tag cattle more than once in a year

Ear tags Pyrethroids – Face Flies ? Organophosphates – Horn Flies ??? Pyrethroids + Organophosphates Not Recommended !

Ear tags…… • Do no tagging when <200 fly per animal

• Use XP820 (abamectin) or Avenger (Chlorinated hydrocarbon) • permethrin ???? • Rotate classes of insecticides (Not Brand Names) every year to alleviate insecticide resistance • Wear gloves • Take tags out at the end of the season

Fly Traps

271

Other Classes of Ear tags • Chlorinated hydrocarbon – Avenger

(endosulfan ) (Horn Fly) • XP 820 – Abamectin (Horn Fly) • Fipronil is not allowed for use on cattle in US (phenylpyrazole)

Other Fly control Options

• Residual fly sprays • Biological control Parasitic wasp release programs (Replenish monthly April => September) Non‐native dung beetle to shrink manure pats Fire ant ? Contact sprays, fogs or space sprays Fly Baits • Manure sprays or feed through (IGR: methoprene, diflubenzuron)

Mechanical Methods

• A simple and economical option, dislodged flies will congregate on the translucent sides and top of the trap and die from desiccation – Flies trapped and die between slats and outer screened sides – Reduce fly number by 50‐70%

Non‐chemical prevention and control ‐ Drag harrow or Chain

Large tunnel‐like fly traps (Modified Bruce traps) – Place at pasture gates where animals must pass through regularly

‐ Con: Pasture less attractive to cattle (harm dung beetle)

‐ Pro: Cowpats unsuitable for fly development

Save the Dung Beetle

Family Tree for Endectocides

In the 1980’s, studies showed the use of avermectins (ivermectin,

Macrocyclic Lactones

eprinomectin, doramectin) adversely affected

dung beetle larvae.

Avermectins

Milbemycins Many Others

Mortality of larvae occurred in dung from several days to several weeks after treatment. These drugs are commonly used to control internal parasites in livestock After routine deworming of livestock with avermectins, the breeding capacity of further generations is reduced for many species of Dung Beetles.

Abamectin Bio-synthetic Semi-synthetic Ivermectin Doramectin (DECTOMAX) (IVOMEC) Eprinomectin (EPRINEX)

Semi-synthetic Milbemycin Oxime (INTERCEPTOR)

• Horse flies and deer flies Not much you can do…stay away from areas where they are… Tabanus

Semi-synthetic Moxidectin (CYDECTIN)

64x Less Toxic

MOX minimal tox to dung beetles -

(Errouiss, Vet Rec, 2001; Ridsdill-Smith, Vet Parasit, 1993; Lumaret et al, J App Ecology, 1993; Fincher, Environ Ent, 1992, Floate et al, Annn Rev Entomol, 2005; Kadiri et al Ann Soc Entomol Fr, 1999; Lumaret et al, Vet Res, 2002)

External Parasites of Livestock Blood‐suckers

Nemadectin

Lumart, Current Pharm & Bio Tech 13:10041060, 2012

Fly control Options - Reduce

Fly Breeding Areas

- Residual fly sprays – harborage areas

- Biological control Parasitic wasp release programs Non‐native dung beetle to shrink manure pats

- Contact sprays, fogs or space sprays

Chrysops

- Fly Baits - Feed throughs (IGR) (Pugh, ANR-2083, 2014; Pugh, Eq Vet Sci, 2013)

Keep the Faith

272

Equine

273

274

Equine

Fairfield Bain, MBA, DVM, ACVIM, ACVP, ACVEC Equine Veterinary Professional Services - Merck Animal Health Placitas, New Mexico

275

276

A Review of the Equine Colic Examination – Is there anything new? Fairfield T. Bain, DVM, MBA, Diplomate ACVIM, ACVP, ACVECC Associate Director, Equine Life Cycle Management Placitas, New Mexico Preamble The colic examination is part of the “bread and butter” of equine practice. We often take it for granted, however, the basic skills of the physical examination – particularly focusing on the animal with clinical signs of colic – remains an art with certain amounts of skilled observation and intuition being important. These skills require practice like any other and build on experience. Veterinary educational institutions are challenged in providing these experiences, and the temptation is often to leap past the basic examination to other diagnostics to obtain the most expedient answer. The challenge here is that following this rapid program can occasionally result in a missed diagnosis. We tend to undervalue the most basic components – the signalment, history, observation, and complete physical examination – which can occasionally point to some source of pain outside the gastrointestinal tract or even outside the abdominal cavity. The goal of this presentation is to review the components of the physical examination of the colic patient, and then describe the commonly available diagnostic tools and where they fit in to the scheme. The goal is to provide the most expedient route to finding an answer for a diagnosis – and helping the owner answer questions as to the best medical or surgical management of the problem. Introduction Besides being an astute observer of the horse, its behavior, appearance, stance, and its environment, the physical examination remains a key piece of information gathering for the colic patient. We all start with the basic vital signs – temperature, heart rate, and respiratory rate. While accumulating that initial information, we can be hands on with the horse (if safe to do with an animal showing acute abdominal pain). Never forget that “colic” is simply pain – most often attributable to problems of the gastrointestinal tract within the abdomen – but can occur with a variety of medical issues external to the abdomen. Observation, auscultation, and percussion are important components of the exam. The rectal exam is also part of the colic evaluation where important information can be obtained. It is also a risk – of injury to the horse and to the veterinarian – that needs to be considered. The next piece of information commonly available to the practitioner is whether there is presence of gastric reflux on passage of a nasogastric tube. The culmination of this basic information gathering should allow the practitioner to place the patient into a certain category suspect of a anatomic and pathophysiological process, which will help in decision-making. The Colic Quadrant is a graphic representation of the author’s thought processes when approaching a colic patient. It is represented below.

277

Introduction to Abdominal Ultrasound for Colic Evaluation Besides the physical examination, ultrasound is often the author’s next step in the evaluation of the critical, recurrent, or complicated colic patient. Rectal examination remains a useful and important diagnostic tool but is occasionally limited to structures in the caudal abdomen that are within reach of the examiner. The abdominal cavity reaches cranially to the diaphragm just caudal to the heart. A systematic approach to the ultrasonographic evaluation of the abdomen allows for rapid assessment of location, characterization, and content of multiple intra-abdominal structures. Understanding Ultrasound Equipment A variety of options are available in the offerings of ultrasound equipment. Newer, more portable devices are coming on the market each year – both digital and in laptop configurations. Some understanding of the physics of ultrasound is necessary – mainly in understanding the principles of frequency. The higher frequency wavelengths provide more detailed images, but less (more shallow) tissue penetration. An example being a 12- mHz probe is usually used for tendon imaging… providing excellent image quality with fine detail, but unable to visualize anatomic structures more than a few centimeters deep to the skin. Alternatively, a 1.9-mHz probe provides adequate depth of penetration to image the entire equine heart but does not produce the fine detail image of the high frequency probe. The type of probe used should be appropriate to the body region being evaluated. The smaller, microconvex probes are good for accessing small body parts, especially in tight confined areas such as the inguinal region. The curvilinear 3.5 mHz probe is probably the best all-around probe for general abdominal imaging of the colic patient. Various other probes may be used for additional evaluation (higher frequency, higher

278

detail probes for more detail of the serosal surfaces, or lower frequency probes to penetrate large volume effusions or to evaluate the pregnant uterus). Patient Preparation Preparation of the area to be imaged is also an issue. Some coupling material is required for the sound waves to penetrate the hair and skin. For most situations, isopropyl alcohol alone is used to wet down the hair coat without clipping. This may degrade the surface material of the probe over time. On some occasions, clipping the hair and application of a contact gel will be required to achieve the best detail in the image. The Ultrasound Exam The practical part of the ultrasound examination is that it can be quickly performed immediately following the physical examination. In some situations, it can be performed prior to the rectal examination. For the abdomen, a systematic approach is helpful as with the physical examination. The author prefers a system starting cranially on one side â&#x20AC;&#x201C; just caudal to the elbow, progressing caudally, imaging all appropriate structures on that side, and then repeating the process on the contralateral side. This way, a complete examination of the body cavity is performed in an effort to determine the nature of the disease process. On the left side, one would start near the elbow â&#x20AC;&#x201C; scanning dorsal-to-ventral in each intercostal space to include the ventral lung margin and diaphragm. Most cranially - observing the liver, moving caudally to observe the stomach and its contents (mainly looking for excessive fluid volume as would occur with intestinal obstruction), and the spleen. The spleen-stomach relationship is important to identify on the left side (Fig. 1). Evaluation of the stomach content and size can be determined. The typical adult gastric profile is visible over 3-4 intercostal spaces. Colonic displacements or epiploic foramen entrapments can obscure the normal stomach-spleen image. Small intestinal segments are usually observed in the caudal-ventral abdomen just medial to the ventral margin of the spleen. Normal small intestine rarely contains luminal fluid and will often be seen as variably motile structures between the medial surface of the spleen and the colon.

279

Figure 1. Spleen-stomach relationship on the left side.

In the recently postpartum mare, imaging just beneath the flank fold and caudally into the inguinal region can be helpful in evaluating the broad ligament for the presence of hematomas. In the dorsal-caudal abdomen, the left kidney and nephrosplenic space should be visible (Fig. 2). Moving to the right side, beginning again at the elbow, the colon wall will be seen just caudal to the diaphragm. In some patients, some segments of small intestine can be present. Moving caudally, beneath the diaphragm the liver can be identified, and eventually, the duodenum will be present between the ventral-medial surface of the liver and the right dorsal colon (Fig. 3). Its course can be traced caudally to its turn medially just beneath the right kidney. This is important to be able to identify for evaluation of distension from small intestinal obstructive diseases or thickening as would occur with primary diseases of the duodenum such as the gastroduodenual ulcer syndrome. In older horses (teens and upward), the right lobe of the liver will often have atrophied and may not be visible beneath the right lung margin. Ventrally and caudally, the colonic and cecal surfaces can be seen. In the mid-ventral abdomen, some segments of small intestine may be visible. When evaluating for colonic displacements, identification of the vasculature of the medial mesocolon can be useful. The presence of the vasculature of the large colon against the body wall implies either a displacement or at least a partial torsion of the colon.

280

Figure 2. Spleen, left kidney, and nephrosplenic space on caudodorsal left abdomen.

Figure 3. Normal duodenum, between ventralmedial aspect of liver and right dorsal colon.

Gastric Disorders Gastric distension usually implies a more distal obstructive process as opposed to primary gastric obstruction (Fig. 4). Most often ultrasound cannot differentiate gastric distension from intestinal obstruction from that caused by ileus. Profound distension of the stomach with free-floating omentum may imply impending gastric rupture. The earlier the gastric distension is detected during the examination process, the sooner relief of pain can be provided by passage of a nasogastric tube. In fact, ultrasound can be useful in evaluating the success of gastric decompression. If the patientâ&#x20AC;&#x2122;s heart rate remains high, or it remains painful, and a distended stomach is still observed during ultrasound examination, then the decompression may not have been successful and should be repeated.

Figure 4. Fluid distension in the stomach.

281

Gastric impaction is difficult to diagnose on ultrasound alone, but can be inferred by observing the presence of an expanded gastric profile over a larger than normal area on the left side (5-7+ intercostal spaces). Additional evaluation, including gastroscopy, may be necessary to be confident of the diagnosis. Serial evaluation using ultrasound can be performed to evaluate response to management. Small Intestinal Disorders Often, the challenge is to identify the presence of small intestinal distention before it is palpable per rectum, or to differentiate between a strangulating obstruction of the small intestine and nonstrangulating disorders such as ileus or enteritis. The presence of fluid or gas filled small intestine should be considered abnormal. Strangulating obstructions (volvulus or entrapment by strangulating lipomas) can result in profoundly distended, non-motile segments of small intestine with tendency toward sedimentation of luminal contents to the ventral aspect of the abdomen (Fig. 5). In the Gulf Coast and southern US, the incidence of ileal impactions is much higher, and this lesion can appear very similar to strangulating obstruction of the small intestine (Fig. 6). Clinical experience and evaluation of the patientâ&#x20AC;&#x2122;s history and clinical course must be taken into account when observing fluid-distended, poorly motile small intestine in geographic regions where this entity is common. Additional clinical diagnostic measures (such as abdominocentesis) may be needed to differentiate ileal impaction from strangulating lesions of the small intestine. Enteritis is generally viewed as fluid distension of the lumen, with variable motility and variable thickening of the intestinal walls (Fig. 7). Ileus often appears similar to (and can occur concurrently with) enteritis with variably motility and variable thickening of the intestinal wall, and with molding of the intestinal segments against each other. Strangulating obstructions of the small intestine tend to have more profound luminal distension with minimal motility and tendency toward sedimentation of particulate material to the ventral aspect. There is a time course involved with changing appearance over time following strangulation. Early in the course,

Figure 5. Non-motile, fluid-distended small intestine consistent with strangulating obstruction.

Figure 6. Small intestinal fluid distension with variable motility with ileal impaction.

the intestinal wall thickness may be thin with some persisting motility present, and with progression of strangulation and vascular congestion, the wall thickness increases with devitalized small intestinal having a markedly thickened wall and a less distinct serosal surface.

282

Clinical information such as concurrent fever and leukopenia and neutropenia will be supportive of the diagnosis of enteritis. Some specific small intestinal lesions include epiploic foramen entrapment â&#x20AC;&#x201C; suggested by multiple segments of poorly motile small intestine in the left cranial abdomen, and ileocecal intussusception â&#x20AC;&#x201C; sometimes the small intestinal segment can be observed within the cecal lumen if surrounded by fluid. Scrotal and inguinal herniation of small intestine is generally self-evident, and the contents of the hernia can be rapidly confirmed using ultrasound (Fig. 8).

Figure 7. Fluid-distended small intestine with indistinct serosal surfaces and variable motility consistent with enteritis.

Figure 8. Intestine present with the vaginal tunic consistent with scrotal hernia.

Large Intestinal Disorders Ultrasound can be used to evaluate the position and contents of the large intestine. Cecal Disorders As just mentioned, ileocecal intussusceptions can be occasionally identified on ultrasound. Cecocolic and cecocecal intussusceptions can also be identified, generally with the thicker multiple edematous layers of the intussuscepted portion being visible within the liquid contents of the colon (Figs. 9 and 10). Cecal impaction is generally not easily identifiable by ultrasound alone.

283

Figure 9. Longitudinal view of trilayer appearance of edematous cecal wall within lumen of right ventral colon consistent with cecocolic intussception.

Figure 10. Transverse view of trilayer appearance of edematous cecal wall consistent with cecocecal intussusception.

Large Colon Disorders Ultrasound has become a tool to aid in identification of colonic displacements with the nephrosplenic entrapment being most commonly and easily identified. Generally, the presence of colon along the dorsal aspect of the left peritoneal cavity with some evidence of medial displacement of the lateral splenic capsule is confirmation of this lesion (Fig. 11). Right dorsal displacements and colon torsions can result in observation of the medial colonic vasculature against the body wall (Fig. 12). Rectal examination is still useful in further characterization of colon position within the abdomen, and to further evaluate colonic contents. Colon impaction still requires rectal palpation for detection and confirmation, as it is difficult to differentiate the character of solid colonic contents on ultrasound alone. Large colon volvulus often presents with characteristic clinical signs of acute onset of profound abdominal pain and abundant gas distended colon palpable on rectal examination. In some situations where abdominal ultrasound is performed on these patients, the operator may observe edema of the wall of the large colon (Fig. 13). Other Abdominal Disorders Ultrasound can be useful in identifying various disorders within the abdominal cavity that do not have a primary intestinal lesion. Postpartum disorders like uterine artery rupture with hemoperitoneum or peritonitis secondary to a uterine tear are common scenarios where ultrasound provides critical diagnostic information. It is also helpful in characterizing peritonitis secondary to gastrointestinal rupture. An uncommon disorder that can be identified using ultrasound is a diaphragmatic hernia. In some cases, the muscular portion of the diaphragm will be absent with intestinal or other abdominal structures being observed directly adjacent to the heart or lungs.

284

Figure 11. Nephrosplenic entrapment with large colon present in the nephrosplenic space, obscuring observation of the left kidney and displacing the spleen medially.

Figure 12. Vessels of medial mesocolon of the large colon positioned laterally against right body wall with right dorsal displacement.

Figure 13. Thickening of the wall of the large colon with edema secondary to large colon volvulus.

Non-GI, non-abdominal causes Lastly, be aware that there are some disorders that cause clinical signs of colic that exist outside the abdominal cavity. Examples might include the Friesian with aortic rupture that may present as “colic” signs, horses with ventricular arrhythmias are often described as having signs of “colic” pain (possibly from abnormal blood flow?), and horses with pleural disease and rib fractures can present with signs that can be confused with abdominal pain. In these cases, imaging of more specific locations might be needed to determine a diagnosis.

285

Additional diagnostics for colic While the physical examination, rectal examination, nasogastric intubation, and in certain situations, abdominal ultrasound will point to a specific diagnosis, additional “patient side” diagnostic tools can occasionally provide helpful information. Probably the most common tools currently available to the practitioner that may fit this “real time” information gathering process are serum amyloid A (SAA) and lactate. Serum amyloid A is an acute phase protein (like fibrinogen) that responds more rapidly to inflammatory triggers – within about 6 hours compared to 24+ for fibrinogen – and is suggested to be more actively induced by an infectious process. Given this background, it may be helpful in differentiating early cases of sepsis from a variety of causes, and enteritis, or intestinal compromise resulting in peritonitis. Some authors have even suggested that SAA might rise prior to onset of the febrile response. In general, it is absent in the normal horse, however, minor amounts – up to 10-50 mg/L may be present. Concentrations higher than 20-50 mg/L are suggestive of a significant inflammatory process. In fact, levels of 1,000-2,000 are commonly present in animals with significant suppurative inflammation. Additionally, the SAA may be more “real time” in monitoring the response of an inflammatory insult to treatment – often declining more rapidly than fibrinogen or the white blood cell count. Lactate is also occasionally useful in colic management. Normal lactate concentrations are considered < 2mmol/L. It has been used as a prognostic tool – extremely high concentrations (> 20 mmol/L) might be indicative of significant effects of poor perfusion – systemically and perhaps related to intestinal ischemia, however, there is often much overlap between categories of survivors and non-survivors. It is possibly more useful when evaluating response to intravenous fluid resuscitation – the trend towards normal being encouraging and failure of lactate concentration to decline with therapy being a negative prognostic indicator. Summary The art of medicine – the tools of physical examination, rectal exam, and nasogastric intubation – remains the most important skills in evaluating the horse with colic signs. The “extras” – abdominal ultrasound, and other “real time” diagnostic aids such as serum amyloid A and lactate may help answer additional questions to help the owner make decisions for treatment.

286

Equine

Earl Michael Gaughan, DVM

Equine Veterinary Professional Services - Merck Animal Health Sedalia, Colorado

287

288

Wounds near synovial structures EM Gaughan, DVM Diplomate ACVS Merck Animal Health

Wounds involving the synovial compartments of joints, tendon sheaths, and bursae can be debilitating and career if not life threatening injuries. Unlike juvenile forms of joint sepsis the most common route for inoculation of adult synovial structures is via direct penetration during wounding. Inoculation of these structures can be obvious from an open wound or more subtle from puncture wounds or extension from distant injury. It is vital to treatment success that wounds associated with synovial structures are considered contaminated until proven otherwise. Horses with wounds of synovial structures can have obvious trauma with tissue disruption and/or loss or they may require examination due to very subtle wounds as with puncture trauma. Lameness is usually present but can vary in severity. Acute wounds that open a joint may not have lameness that would be typical of synovial sepsis but more consistent with the pain of only the wound itself. Many horses with open and draining septic joints do not demonstrate severe lameness until the outflow is occluded with granulation tissue. When this occurs or the wound is such that a closed synovial environment remains, the horse can demonstrate lameness of grades 4-5/5. Physical examination of horses with this type of wound should include determination of the type of wound and then concentrate on determination of synovial compartment involvement. Lacerations, de-gloving injury, and puncture wounds are the most common means of involving equine joints and synovial sheaths and bursae. Extension from wounds distant from these structures can occur and the possibility should be investigated. Other supporting tissue and normal interior tissue (ie; tendon) should be evaluated to determine the total extent of the traumatic wound. Lameness can again be variable dependant on the timing of evaluation in relation to wounding, the tissues involved, and the ultimate presence of contaminants. The horse should be examined for systemic repercussions from the wound and any resultant complications. The diagnosis that a wound does indeed involve a synovial structure can be obvious on physical examination or may require some extensive investigation. When performing an examination on the suspected tissue it is recommended to handle the tissue in an aseptic manner to avoid iatrogenic inoculation of these special tissues. A rule of thumb would be to handle the tissue as if it remains sterile when examining it and assume it is infected when treating that structure. It may be essential to clean the wounded region before further diagnostic procedures can be safely performed. Lavage with sterile aqueous solutions is recommended unless heavy contamination is obvious, when tap water is acceptable. When the wounded tissue is appropriately cleaned, a sterile probe can assist diagnosis by investigating the depths of a particular wound. It is preferable to probe gently so as not to puncture into an otherwise normal structure. A sterile hypodermic needle can be placed into the structure under question to aspirate synovial fluid for evaluation and to administer a

289

sterile balanced polyionic solution. It is best to place the needle as distant from the wound as possible to avoid inadvertent contamination. Sterile solution is injected with volume and pressure sufficient to distend the synovial compartment. The wound should be observed during this procedure. If the fluid is seen to flow from the depths of the wounded tissue then the synovial structure should be considered contaminated and potentially infected even if synovial fluid samples demonstrate normal cellular and protein contents. Definitive diagnosis continues to rest on culture and sensitivity identification of microorganisms from the synovial environment. Cytology and gram stain results can provide a preliminary working diagnosis. After physical examination and manipulations, imaging studies may be necessary either for diagnosis or for establishment of a baseline imaging study. Plain film radiography is the most common imaging modality used. Gas patterns with in the synovial compartment in question can be consistent with involvement with a wound. Obvious disturbance of related osseous structures can confirm joint involvement. If the examination is performed after sufficient time, loss of cartilage and lysis of subchondral bone may be evident as repercussions of synovial compartment sepsis. If a needle can be placed in the joint, a positive contrast intra-synovial study can demonstrate communication with a wound. After proper cleansing preparation, a catheter (large IV or small animal urinary) can be placed into the depths of the wound and positive contrast medium injected. The resulting fistulogram may also demonstrate communication between the wound and the synovial structure in question. When a wound is confirmed or under strong suspicion to involve a synovial structure, treatment should be initiated at the earliest possible opportunity. When faced with an open wound into a synovial compartment, two options are immediately possible. Primary closure of the capsule of these structures requires that the internal environment be as clean as possible and ideally sterile. This decision is usually made based on the amount of obvious contamination of the tissue and the duration since wounding when treatment can be initiated. If the synovial compartment has been sharply opened with minimal trauma and contamination and the horse is available for immediate post-injury treatment, primary suture closure can be successful. The ability to appropriately close wounds of this type is infrequent and may be most dependant on husbandry practices. Wounds with obvious contamination and longer duration may be best treated as open wounds or have drainage systems placed within the synovial compartment. The goals of treatment are to remove the contaminant, prevent it from establishing infection, preserve the synovial environment, and return the tissue to the functional status of pre-wounding. These goals are best achieved by thorough lavage to physically remove debris and microorganisms, systemic antibiotic administration, and anti-inflammatory therapy. The reduction in the inflammatory insult to the synovial structure can be accomplished by administration of systemic non-steroidal antiinflammatory drugs (NSAID) and local administration of dimethylsulfoxide (DMSO) and sodium hyaluronate (HA). The use of HA has been clinically beneficial in the face of sepsis, however, there may be some early evidence that it may bind compliment in a similar manner as polysulfated glycosaminoglycans. Therefore caution is suggested. Treatment of puncture wounds and wounds that contaminate a synovial structure

290

from indirect extension require similar treatment as open wounds. Lavage can be best accomplished with arthroscopic guidance and administration. Greater volumes of lavage solution can be delivered and debris can be visualized and removed from the intra-synovial space. This may also be the best way to lavage structures involved with large open wounds. A schedule of lavage is difficult to prescribe as each wound can be very different in nature and response to treatment. Every other day lavage has been suggested. This can be amended to more or less frequent administration dependant on the horse's clinical improvement and results of serial synovial fluid analyses. Steadily decreasing lameness and return to a normal synovial fluid profile is solid evidence of improvement. Indwelling positive suction drains have been reported as successful in horses with septic arthritis and tenosynovitis. Long term antibiotic therapy is often necessary (up to 8 weeks) to totally rid the synovial environment of microorganisms. Regional perfusion of antibiotics is an accepted modality for increasing local antimicrobial treatment in a specific site. With a tourniquet placed above the septic site, antibiotics can be administered intravenously, into joint spaces and in to the medullary cavity of long bones. Dosing schedules have been somewhat arbitrary but most practitioners repeat doses every 24 to 48 hours. Dosage quantities have also been somewhat variable (full systemic body does to 1/3 this dose at each administration). The benefit of regional perfusion is gaining higher local presence of antibiotics at the septic synovial site and therefore, more likely effect of the chosen drug. Horses that survive the treatment of synovial structure wounds can benefit from additional ancillary therapy. Passive motion and staged active use of the wounded limb(s) can encourage return to a normal synovial compartment. Adhesions can be modified with exercise and reduced in severity or lengthened so as to not influence range of motion in tendon sheaths and joint capsules. Recent evidence supports the use of HA in tendon sheaths to reduce or prevent adhesions after insult to these tissues. The same may be true for joints. The administration of PSGAG may assist the synovial compartment return to normal but care must be taken that this agent is not placed into the synovial space when microorganisms are still present. The compliment binding of the PSGAG can allow complications or reestablishment of infection. The prognosis for horses with wounds into synovial structures is always guarded to poor for return to athletic soundness. This prognostic picture can change dramatically with appropriate treatment. This is especially true when aggressive treatment can be initiated in as early and timely a manner as possible.

291

292

Equine

Bo Brock, DVM, DAVBP Brock Veterinary Clinic Lamesa, Texas

293

294

THE HORSE IN MOTION The moving horse uses a series of events involving muscles, bones, tendons, nerves, and joints to propel itself across the ground. Motion involves strides which consist of phases involving the use of various muscles which deliver the limb to a point in which it can grab the earth and pull the animal across it. Movement occurs through a series of cycles in which each leg takes a turn delivering a force which will propel the horse in the desired direction at a desired rate. We will begin evaluating this process with the foot of the horse just leaving the ground. The horse must swing the leg forward in order to get in position for the next stride, the next period of weight bearing. A large number of muscles cooperate to accomplish this protraction phase of the stride but only the major muscle will be discussed here. Figure 1 shows the attachments of the straplike brachiocepalicus and fan like serratus muscles. As the serratus thoracis muscle is pulling the scapula down and back, the brachiocephalicus is pulling the humerus forward.

Figure 1 These combined actions cause the leg to swing forward around the center of rotation of the leg which is an area around the midpoint of the humerus. The pectoral muscle is attached to the humerus at about this rotational midpoint and serves to further protract the limb with its contraction. As the leg swings forward it flexes at the carpus. This is a labor saving mechanism engineered into the system which greatly decreases the length of the

295

lever arm and thus the amount of energy and force required to move the leg forward. This effectively reduces the moment of inertia of the leg and allows the center of rotation to be higher up.

Figure 2 Now the leg is almost fully protracted (figure 2). The muscles of the forearm, particularly the extensor carpi radialis, assist the simple swinging movement of the leg by extending the carpus in preparation for putting the foot on the ground (impact). Once the foot is on the ground the stance phase of the stride begins. This involves the reciprocal muscle of the swing phase that were relaxed to allow protraction. The reciprocal muscle of the brachiocephalicus is the Latissimus Dorsi. This muscle will contract as the brachiocephalicus relaxes, causing the humerus to begin moving caudally and thus start pulling the body of the horse forward. The reciprocal muscle of the serratus thracis is the serratus cervicis. As the thoracis relaxes, the cervicis contracts, thus pulling the scapula up and forward resulting in more force being applied to forward movement of the horse. The leg is already swinging down and back when the foot hits the ground. This is extremely important. If the leg is swinging back at the same speed as the horseâ&#x20AC;&#x2122;s body is moving forward, the horse is running at or near a constant speed and the only load applied to the leg by the horseâ&#x20AC;&#x2122;s body weight is straight down. If he wants to run slower, he slows down the speed of the backward swing of the leg, while the opposite holds true for acceleration. The body weight of the horse is now applied to the foreleg, and the leg must sustain or support that weight as well as try to move it forward. For mechanical

296

purposes, the weight of the horse is considered to be concentrated at a single point, the center of gravity. This is a point at which the horse could be suspended from and balance. It is clear that the pull exerted by the weight of the horse, acting at the center of gravity, will tend to pull the leg down and back, a tendency that must be resisted. As seen in figure 2, the pull of the center of gravity acting through the serratus thoracis will move the scapula down and back, flexing or closing the angle of the shoulder joint. This movement is resisted by the biceps brachii as well as contraction of the serratus cervicis. The elbow will also tend to flex, in the opposite direction but for the same reason and this is resisted by the tricepts muscle (figure 3). Body weight forces the fetlock and coffin joints to flex which is resisted by the suspensory ligament and flexor tendons. The check ligaments are in place to allow resistance of the tendency of the various joints of the lower limb to succumb to the effects of the weight of the body without having to use muscles of propulsion. In fact, the small muscles of the forearm are used mostly not to cause motion, but prevent it.

Figure 3

The primary function of the forelegs are to support weight, absorb shock, and lift the animal from the ground for the flight phase of the stride, while the rear legs provide the main propulsion. The secondary function of the forelegs is to assist in moving the horse forward. The serratus cervicis and the triceps are the major muscle groups which pulling the leg to the rear and consequently moving the body forward. Toward the end of the stride, just before the hoof clears the ground, the large deep flexor muscle provides a strong pull on the hoof, lifting the horse up and forward.

297

We will start with the hind limb just as the forelimb with the foot just leaving the ground. The hip, stifle, and hock joint all flex to decrease the moment of interia, enabling the horse to move the leg forward with the least possible muscular effort.

Figure 4. The iliopsoas, only muscle shown in top picture, causes protraction The hip is flexed by the action of the iliopsoas muscle (figure 4). The stifle is flexed by a portion of the biceps femoris muscle. The hock is automatically flexed by a system of muscles that run on the from and back of the tibia. The peroneus tertius and superficial flexor (figure 4) are almost entirely tendinous structures that connect the stifle to the hock causing these two joints to work together synchronously when the foot is off the ground. There is no way you can pick up a horses foot without the fetlock, hock, and stifle all flexing synchronously. The leg protracts and then begins to swing back in retraction in preparation for impact. The massive gluteus muscle (figure 5) contracts moving the proximal femur forward, thus pushing the body forward. The hamstring muscle also

298

contracts assisting the glueus in propelling the animals forward. The quadriceps contract extending the stifle which in turn causes hock flexion.

Figure 5. The center of rotation of the hind limb is the approximate center of the tibia. As the rear leg drives back, pushing the horse forward, the hip joint angle opens; the stifle joint flexes slightly, while the hock first dorsiflexes and then extends. Unlike when the foot is off the ground, while propelling the horse, the hock extends while the stifle flexes.

299

PHASES OF THE STRIDE There are five phases to the stride of the horse as defined in Adam’s Lameness. Each phase requires different body structures with different stressors. The phases should be understood and the areas of stress should be analyzed as the horse moves and during examination.

Landing – the hoof touches the ground and the limb begins to receive the impact of the body’s weight. Loading – the body moves forward, and the horse’s center of gravity passes over the hoof. Usually, this is when the fetlock descends (extends) to it’s lowest point, sometimes resulting in an almost horizontal pastern. Stance – The fetlock rises to a configuration comparable to the horse’s stance at rest. The transition between the loading phase and the stance phase is VERY stressful to the internal structures of the hoof and lower limb. The horses center of gravity moves ahead of the hoof. The flexor apparatus lifts the weight of the horse and rider and the fetlock begins to move upward. The pastern straightens and the limb begins pushing up off the ground. Breakover – This is the phase when the hoof leaves the ground. It starts when the heels lift and the hoof begins to pivot at the toe. The knee or hock relaxes and begins to flex. Breakover is measured from the time the heels leave the ground to the time the toe leaves the ground. The deep digital flexor tendon (assisted by the suspensory ligament) is still stretched just prior to the beginning of breakover, to counteract the downward pressure of weight of the horse’s body. Swing – The limb moves through the air and straightens out in preparation for landing.

300

Landing

Stance

301

Breakover heel lift

Breakover toe Pivot

CONFORMATION

Diagrammatic depiction of assessing balance during conformation evaluation. Three circles (from left to right: forehand, midbody, hind quarters) are visualized and should overlap by one third. Excessive overlapping of circles (short coupled) or barley overlapping of circles (long, weak in back) are common conformational abnormalities. Body length (x) should be equal to or slightly longer than withers height (Y), and withers height and rump height (Z) should be the same.

302

Balance

Horses with good balance are likely to be good athletes and have less lameness problems. Horses with a short thick neck (quarter horse build) are often straight in the shoulders and have a center of gravity farther forward causing more weight to be distributed on the front end and often times more lower limb problems. A horse with a short back has closer spinous processes and may be predisposed to impingement of these spinous protrusions, whereas a horse with a long back may have difficulty engaging the hind limbs properly. A horse that is taller behind than in front will carry more weight on the front half of the body and is predisposed to front end lameness

303

Assessment of lengths, angles and heights

Shoulder length â&#x20AC;&#x201C; Top of withers to point of shoulder. May be related directly to stride length, and horses with longer shoulders usually have longer strides. Shoulder angle â&#x20AC;&#x201C; often related to shoulder length. Long shoulder often gives a more sloping shoulder whereas a short shoulder often gives a straighter angle and thusly a more choppy gait and shorter stride. Shoulder angle in faster horses has been found to be close to 45 degrees and equal to pastern angle in well balanced conformation. A long radius coupled with a short, strong cannon bone is desirable for speed of stride and maximum stride length. Rump length is also important in determining stride length, and a longer length of the rump is desirable. Many horses with long rumps have flatter rump angles (flat croup). Horses with short, steep rumps often have choppy gaits and many hindlimb lamenesses. This is due to the steepness of the angle shifting the center of gravity caudally which puts more weight on the hindlimbs.

304

LIMBS FORELIMB CONFROMATION Base wide

Base narrow

Wing in (paddle)

305

Wing out

Horses with a base wide conformation in the front end usually have a narrow chest. This base wide build overloads the medial aspect of the lower limb, predisposing to lameness. Horses with base wide, toed in, tend to wing out or paddle during protraction which predisposes to interference with the ipsilateral hind limb during a trot. Horses that are base wide, toed out, are often uncorrected carpal valgal deformitites and result in excessive loading on the medial aspect of the foot and misshapen feet. This also concentrates the weight on the medial aspect of the carpus and metacarpus. Base narrow horses overload the outside of the lower limb and foot. Bow-legged or out at the knee conformation predisposes the animal to abnormal forces on the lateral area of the entire distal limb and may result in osteoarthritis of the carpus, fetlock or lateral suspensory branch desmitis and sesmoiditis. Offset or â&#x20AC;&#x153;benchâ&#x20AC;? knees â&#x20AC;&#x201C; lateral positioning of the metacarpal region relative to the central axis of the radius. This conformation is often associated with carpal or metacarpal lameness. Toed in horses often wing out (paddle) and are subject to problems with the lateral splint bone, lateral fetlock joint problems, lateral suspensory problems, ringbone, and degeneration of the carpal joint. These symptoms often become clinical at the prime of the horses life and the horses are often very athletic. Toed out horses often wing in and wear the inside aspect of the foot. Often seen with base narrow stance and have problems with the medial splint bone.

306

HINDLIMB CONFORMATION

A = Sickle hock B = Straight hock C = Camped under D = Camped out Straight behind – post- legged. These horses have larger stifle and hock angles but smaller fetlock joint angles. Often develop upward fixation of the patella, suspensory desmitis, and fetlock osteoarthritis. Horses with normal hock angles may develop straight hocks secondary to severe suspensory desmitis. Sickle hock – one of the most common rear end conformation abnormalities. Leads to soft tissue problems of the tarsus and plantar area of the limb. Smaller than normal hock angle. Called a “curby” conformation due to the fact that curb often is a sequella to the effects of the conformation. Load is concentrated on the distal, plantar aspect of the hock resulting in soft tissue stress and joint pain.

307

EVALUATION OF MOVEMENT Considering all that we have gone over up to this point, it is now possible to gather information about potential problem areas on a moving horse. The best gait to evaluate a horse for lameness is a slow trot. This is a diagonal two beat gait which affords the opposite front and rear limbs contact with the ground at the same time. The exam is best done on a hard surface and the animal should be evaluated coming toward and going away from the observer as well as from the side. The horse should be seen going in a straight line as well as in a circle and should be observed going up and down a slight incline. The horse handler should allow the horse to “have it’s head” and not constrain the natural motion of the horse any more than is needed. When observing a lame horse in motion, one should have a set system by which the exam is done and a understanding of “normal” for the type of horse being observed. It is often helpful to begin with a broad classification and work into a more specific diagnosis. GENERAL PRINICPLES:

308

•

Type of lameness 1) Pain – lameness caused by painful stimulation interfering with normal function of a particular area 2) Mechanical – area in question has become limited in normal ability to move or perform intended function 3) Neurological – problem originating from the central or peripheral nervous system which effects the ability of the horse to move normally.

•

Grade of lameness (AAEP guidelines) Grade 1 – Difficult to observe; not consistently apparent regardless of circumstance. Grade 2 – Lameness difficult to observe at a walk or at a trot in a straight line. Consistently apparent under some circumstances (weight carrying, circling, inclines, ect) Grade 3 – Lameness consistently apparent at a trot under all circumstances. Grade 4 – Lameness obvious; marked nodding, hitching, and or shortened stride Grade 5 – Minimal to no weight bearing in motion or at rest

•

Action of head and hips Head goes down on sound front leg or down on unsound hindlimb. Pelvic hike on unsound limb or gluteal rise on sound limb

309

•

Placement of foot When considering the boney column, horse will place to foot on the ground “toward” the lesion. In other words, if the horse has pain in some section of the pillar of hard tissue that comprises the weight bearing structures of the leg, it will move that foot toward the area of pain in order to distribute the pressure down the column on the opposite side. Examples of this include axial placement of the hind foot with medial joint pain in the hock. Other examples include moving the feet forward with laminitis in order to keep more weight on the back of the boney column.

•

Limb flight In normal horses, the length of stride of the paired forelimbs and hindlimbs, measured from hoof imprint to hoof imprint, is nearly identical. From a clinical perspective, the length of the stride of the affected limb cranial to the stance position of the contralateral limb is called the cranial phase (A) of the stride, and the length of stride caudal to the stance position of the contralateral limb is called the caudal phase (P) of the stride.

â&#x20AC;˘

310

Limb flight continued In many lame horses, the cranial phase of the affected limb is shortened. The caudal phase is lengthened to maintain a near equal overall stride length side to side. If the stride length did not remain the same, the horse would veer toward the shortened side due to a shorter amount of distance covered at a constant speed with the unaffected side. Loss of propulsion or an unwillingness to push off with the lame leg may be an explanation for a decreased cranial phase. Another explanation may be stresses applied in the soft or boney tissue which increase pain when the limb bears weight at the end or cranial part of the stride.

Equine

Peter Morresey, MVM, DACT, DACVIM Rood and Riddle Equine Hospital Lexington, Kentucky

311

312

Peripartum mare and foal: what to look for, what to do Peter R. Morresey BVSc MVM Rood and Riddle Equine Hospital Lexington, KY 40580

Introduction For the foal, a successful transition to extrauterine life may be complicated by events both before and during parturition. Once exposed to the external environment, the neonate must rapidly develop altered cardiovascular, respiratory and gastrointestinal function; stand; suckle; achieve coordinated limb movements, and develop defenses against a myriad of infectious challenges. Although born immune deficient through a lack of pre-suckle antibodies, the foal can successfully mount a response to many infectious challenges once sufficient colostrum has been ingested and immunoglobulins absorbed. When problems occur, common presenting signs include depression, weakness, lack of suckle reflex, fever, hypothermia, sepsis, and neurological dysfunction. The mare is optimally managed by maintaining a 12 month foaling interval. This requires that mares are first rebred on their foal heat (average interval to conception in these mares is 25 days). During this period the mare must recover physically from parturition, involute her uterus, re-establish her estrous cycle, lactate sufficiently to support the foal, and consume feed sufficiently to achieve all these aims. The foal 1. Examination of the foal At birth, a foal is approximately 10% of its mature body weight, reaching 30% by 3 months of age. The most rapid period of growth occurs close to parturition meaning any nutritional or physiological checks at this time may have significant effects. As in utero residence increases, continuing skeletal growth exceeds placental function, leading to a relative placental insufficiency and premature delivery. Congenital abnormalities are generally uncommon but can be serious, and include microophthalmia, cleft palate, dental malalignment (wry nose, prognathism, brachynathism, â&#x20AC;&#x2DC;parrot mouthâ&#x20AC;&#x2122;), scoliosis, and hydrocephalus. More common conditions include herniation and orthopedic abnormalities (limb deviations, tendinous laxity and contracture, supernumerary digits). Cardiorespiratory Physiological murmur (patent ductus arteriosus) present at birth can persist for up to 4 days. Persistence of fetal circulation past this time suggests an anatomic cardiac anomaly (septal defect, valvular incompetence, stenosis) or pulmonary disease rendering pulmonary pressures elevated. Thoracic excursion is an indication of respiratory effort. Tachypnea during disease is most consistently related to diffuse pulmonary changes however pain, excitement, or fever can increase rate. Nostril flaring may also indicate increased effort. Nasal discharge should never be present, a mucoid discharge may indicate a respiratory tract infection, and a milk discharge can be associated with congenital abnormalities (cleft palate, pharynx) or an inability to swallow milk correctly. Rib fractures are most common in primiparous mares or following dystocia. Ribs 3 through 8 on the left side are most commonly affected. They have been demonstrated to be most readily detected by ultrasonography. If suspected, the chest should be palpated to assess for the presence of rib fractures (crepitus and subcutaneous fluid swelling if the site is unstable). Pain and altered thoracic excursion may be seen. A flail segment (unstable due to discontinuity in more than one portion of the rib) may move in a paradoxical fashion.

313

Orthopedic Ossification of the cuboidal bones occurs within the last two to three months of gestation. Immaturity and dysmaturity of the foal can affect this process as can short gestation, placental abnormalities, and maternal illness. Conformation examination should involve observing the foal standing and at the walk. A small degree of carpal valgus causing uneven weight loading of the carpus is common at birth. The observer should position themselves perpendicular to the limb, not the foal, as rotation can give the appearance of limb deviation. A toe out conformation of the front limbs is common in neonates due to incomplete thoracic expansion which occurs with increased age and muscularity. Where acute lameness in noted, sepsis of physes or synovial surfaces should be considered the primary rule out before trauma is considered. Leukocytosis is an inconsistent finding, although inflammatory markers (fibrinogen, serum amyloid A) are commonly elevated. Umbilical region Umbilical herniation appears as a smooth pendulous swelling at the site of the umbilicus. This may be soft and easily reducible, or firm and irreducible if incarceration of content (omentum, intestine) or abscessation has occurred. With urachal patency, urine leakage causes wetting of the hair in the umbilical stump area, regional scalding and dermatitis which further promotes infection. Heat, swelling and pain upon palpation are found with infection of the umbilical stump. General malaise, fever, depression, polysynovitis, septic arthritis and septic physitis may follow bacteremia sourced from the umbilical infection. Inguinal region Inguinal and scrotal herniations are usually easily reducible and resolve with time. Colic is rare unless gut becomes incarcerated, this being suspected where the hernia content becomes firm, painful and unable to be reduced. 2. Times of importance to the neonatal foal Sternal Recumbency: the foal should right itself and be able to remain sternal within minutes of birth. Standing: within 60 minutes (range of 15-165 minutes). Compromised neonates tend to remain recumbent longer, further exposing themselves to pathogens. Suckle reflex: usually develops within 20 minutes of birth, although may be much sooner. Suckling: the foal should suckle the mare within 2 hours (range 35 minutes to 7 hours). Urination: first urination occurs at 6 hours for colts, 10 hours for fillies. Urine production: approximately 6 mL/kg/hr. Decreases may result from decreased fluid intake, increased losses or compromises in renal function. Obstruction or disruption due to rupture and uroperitoneum are possible in the compromised neonate, or one which sustained trauma during parturition. Defecation: foals display abdominal straining within the first few hours after of birth, and pass meconium completely within 24 hours. Colostrum stimulates GI motility. Any interference with GI motility will prolong passage of meconium increasing the likelihood of impaction. 3. Differential diagnosis of the depressed neonate Intrauterine growth retardation (IUGR) Compromised placental function affecting either the maternal or fetal side results in accumulation of cellular damage and derangements of endocrine, metabolic, and cardiovascular processes. Nutrients and oxygen supplied to, and wastes removed from, both the fetus and the placenta are diminished. Outcome of IUGR is dependent on the severity and duration of

314

changes, as well as the concurrent fetal developmental events. Many cases require intensive nursing care over the initial neonatal period, this including nutritional and fluid support, orthopedic management of any congenital issues, and pre-emptive measures to manage neurological dysfunction. This level of continuous care is very difficult to provide in a field setting. Hypoxic ischemic encephalopathy (HIE)/Perinatal asphyxia syndrome (PAS) Initially, behavior changes such as loss of affinity for mare, depression, and wandering may be all that is apparent. Loss of suckle reflex may develop. Later, seizure activity beginning as focal muscle tremors progressing to generalized seizures may occur. Concurrent vital organ dysfunction may be detected on routine examination. Where compatible clinical signs are present, due to the multi-system compromise that may be present, referral for continuous care should be recommended. Sepsis

Initial clinical signs are vague and non-specific, mimicking hypoxic insult or neonatal isoerythrolysis. Severe complications can occur: septic arthritis, multiple organ dysfunction, and death. Infections rapidly become overwhelming with clinical deterioration occurring over several hours. When sepsis is suspected, immediate institution of broad spectrum antibacterial coverage is essential. Due to likely compromised circulatory performance, oral and intramuscular antibacterials are unlikely to be sufficiently absorbed to provide adequate coverage. Intravenous catheter placement is necessary. Neonatal isoerythrolysis (NI) Clinical signs of NI may be subclinical or clinical, and depend upon the degree of hemolysis. Foals appear healthy at birth and the onset of clinical signs occurs from several hours to as late as seven days after ingestion of colostrum. Foals become progressively lethargic, weak, and depressed. Mucous membranes may become pale and later icteric. Breathing may become shallow, rapid, and labored. A rapid heart rate also may develop. In many cases transfusion of compatible blood will be required to bridge the period of hemolytic crisis. These foals are also at high risk for sepsis and should be managed as such. Uroperitoneum Progressive abdominal distension, mild to moderate colic, generalized depression and diminished suckling activity are commonly present. Abdominal distension may not be present until the volume of urine retained is considerable, or the rate of accumulation exceeds fluid absorption across the peritoneum. Affected foals will strain to urinate. The most clinically important result is a disturbance of serum electrolyte values, chiefly potassium. Elevated potassium levels result in arrhythmias, bradycardia, and can progress to cardiac arrest in severe cases. This is a medical emergency with a surgical correction. Fluid support (potassium free) will be necessary, however exacerbation of abdominal distension may occur compromising breathing efforts. Placement of a urinary catheter may allow some ducting of urine externally. Referral is recommended as soon as the diagnosis is made. Meconium impaction or retention Affected foals will display kyphosis (dorsoflexion) while straining to defecate. Meconium impaction results from accumulation of meconium at the pelvic inlet, and can result in urinary tract rupture from increased intra-abdominal pressure during abdominal straining, and direct pressure of retained meconium at the pelvic inlet on the colon and bladder wall. Meconium retention is an accumulation of meconium high in the colon sufficient to cause obstruction. Significant pain and abdominal distension may be associated with this condition. Continuous

315

analgesia may be necessary. Severe cases may progress to peritonitis from devitalization of the gut wall. The great majority of affected foals with resolve with a retention enema (acetylcysteine) however many will require nutritional and fluid support until gastrointestinal distension has resolved. 4. Triage of the compromised neonate Title: Care of the neonate: the first 48 hours Author: Peter R. Morresey BVSc MVM MACVSc DACT DACVIM (LA) CVA Address: Rood and Riddle Equine Hospital PO Box 12070 Lexington, KY 40580 Phone: 859-233-0371 Fax: 859-255-5367 pmorresey@roodandriddle.com

316

Care of the neonate: the first 48 hours Peter R. Morresey BVSc MVM MACVSc DACT DACVIM (LA) CVA Rood and Riddle Equine Hospital PO Box 12070 Lexington, KY 40580 Introduction For the foal, a successful transition to extrauterine life may be complicated by events both before and during parturition. Once exposed to the external environment, the neonate must rapidly develop altered cardiovascular, respiratory and gastrointestinal function; stand; suckle; achieve coordinated limb movements, and develop defenses against a myriad of infectious challenges. Although born immune deficient through a lack of pre-suckle antibodies, the foal can successfully mount a response to many infectious challenges once sufficient colostrum has been ingested and immunoglobulins absorbed. When problems occur, common presenting signs include depression, weakness, lack of suckle reflex, fever, hypothermia, sepsis, and neurological dysfunction. The neonate 1. Prediction of the High Risk Neonate Maternal Conditions: • Systemic problems: fever, concurrent debilitating disease process, gastrointestinal compromise with potential for endotoxemia, and surgical manipulation. • Reproductive problems: history of previous neonatal compromise, placental pathology, poor perineal conformation, and prepartum loss of colostrum. Parturient Events: • Abnormal gestation length • Abnormalities of the birth canal, prolonged labor, dystocia, premature placental separation, and premature rupture of the umbilical cord. • Meconium in the amniotic fluid or amnion (may be the only indication of aspiration intially). Neonatal Conditions: • In utero growth retardation (low birth weight, decreased muscle mass), meconium staining, or placental disease. • Immaturity as indicated by short soft hair coat, flaccid ears and lips, and tendinous laxity. • Angular limb deformation and incomplete ossification of the cuboidal bones of the carpus and tarsus potentially impedes initially ambulation and ultimately future athleticism. • Trauma during delivery may have effects that are not apparent until a few days of age. Abnormal behavior and the inability to stand (30-60 minutes) and suckle (up to 2 hours) lead to a lack of colostrum intake, preventing adequate transfer of passive immunity. 2. Examination of the foal At birth, a foal is approximately 10% of its mature body weight, reaching 30% by 3 months of age. The most rapid period of growth occurs close to parturition meaning any nutritional or physiological checks at this time may have significant effects. As in utero residence increases, continuing skeletal growth exceeds placental function, leading to a relative placental insufficiency and premature delivery. Congenital abnormalities are generally uncommon but can be serious, these include microophthalmia, cleft palate, dental malalignment (wry nose, prognathism, brachynathism, ‘parrot mouth’), scoliosis, and hydrocephalus. More common conditions include herniation and

317

orthopedic abnormalities (limb deviations, tendinous laxity and contracture, supernumerary digits). Cardiorespiratory Physiological murmur (patent ductus arteriosus) present at birth can persist for up to 4 days. Persistence of fetal circulation past this time suggests an anatomic cardiac anomaly (septal defect, valvular incompetence, stenosis) or pulmonary disease rendering pulmonary pressures elevated. Thoracic excursion is an indication of ventilatory effort. Tachypnea during disease is most consistently related to diffuse pulmonary changes however pain, excitement, or fever can increase rate. Nostril flaring may also indicate increased effort. Nasal discharge should never be present: a mucoid discharge may indicate a respiratory tract infection, and a milk discharge can be associated with congenital abnormalities (cleft palate, pharynx) or an inability to swallow milk correctly. Rib fractures are most common in primiparous mares or following dystocia. Ribs 3 through 8 on the left side are most commonly affected. They have been demonstrated to be most readily detected by ultrasonography. If suspected, the chest should be palpated to assess for the presence of rib fractures (crepitus and subcutaneous fluid swelling if the site is unstable). Pain and altered thoracic excursion may be seen. A flail segment (unstable due to discontinuity in more than one portion of the rib) may move in a paradoxical fashion. Orthopedic Ossification of the cuboidal bones occurs within the last two to three months of gestation. Immaturity and dysmaturity of the foal can affect this process as can short gestation, placental abnormalities, and maternal illness. Conformation examination should involve observing the foal standing and at the walk. A small degree of carpal valgus causing uneven weight loading of the carpus is common at birth. The observer should position themselves perpendicular to the limb, not the foal, as rotation can give the appearance of limb deviation. A toe out conformation of the front limbs is common in neonates due to incomplete thoracic expansion which occurs with increased age and muscularity. Where acute lameness in noted, sepsis of physes or synovial surfaces should be considered the primary rule out before trauma is considered. Leukocytosis is an inconsistent finding, although inflammatory markers (fibrinogen, serum amyloid A) are commonly elevated. Umbilical region Umbilical herniation appears as a smooth pendulous swelling at the site of the umbilicus. This may be soft and easily reducible, or firm and irreducible if incarceration of content (omentum, intestine) or abscessation has occurred. With urachal patency, urine leakage causes wetting of the hair in the umbilical stump area, regional scalding and dermatitis which further promotes infection. Heat, swelling and pain upon palpation are found with infection of the umbilical stump. General malaise, fever, depression, polysynovitis, septic arthritis and septic physitis may follow bacteremia sourced from the umbilical infection. Inguinal region Inguinal and scrotal herniations are usually easily reducible and resolve with time. Colic is rare unless gut becomes incarcerated, this being suspected where the hernia content becomes firm, painful and unable to be reduced. 3. Times of importance to the neonatal foal1

318

Sternal Recumbency: the foal should right itself and be able to remain sternal within minutes of birth. Standing: within 60 minutes (range of 15-165 minutes). Compromised neonates tend to remain recumbent longer, further exposing themselves to pathogens. Suckle reflex: usually develops within 20 minutes of birth, although may be much sooner. Suckling: the foal should suckle the mare within 2 hours (range 35 minutes to 7 hours). Urination: first urination occurs at 6 hours for colts, 10 hours for fillies. Urine production: approximately 6 mL/kg/hr. Decreases may result from decreased fluid intake, increased losses or compromises in renal function. Bladder rupture and uroperitoneum are possible in the compromised neonate, or one which sustained trauma during parturition. Defecation: foals display abdominal straining within the first few hours after of birth, and pass meconium completely within 24 hours. Colostrum stimulates GI motility. Any interference with GI motility will prolong passage of meconium increasing the likelihood of impaction. 4. Differential diagnosis of the depressed neonate Intrauterine growth retardation (IUGR) Compromised placental function affecting either the maternal or fetal side results in accumulation of cellular damage and derangements of endocrine, metabolic, and cardiovascular processes. Nutrients and oxygen supplied to, and wastes removed from, both the fetus and the placenta are diminished. Outcome of IUGR is dependent on the severity and duration of changes, as well as the concurrent fetal developmental events. Many cases require intensive nursing care over the initial neonatal period, this including nutritional and fluid support, orthopedic management of any congenital issues, and pre-emptive measures to manage neurological dysfunction. This level of continuous care is very difficult to provide in a field setting. Hypoxic ischemic encephalopathy (HIE)/Perinatal asphyxia syndrome (PAS) Initially, behavior changes such as loss of affinity for mare, depression, and wandering may be all that is apparent. Loss of suckle reflex may develop. Later, seizure activity beginning as focal muscle tremors progressing to generalized seizures may occur. Concurrent vital organ dysfunction may be detected on routine examination. Where compatible clinical signs are present, due to the multi-system compromise that may be present, referral for continuous care should be recommended. Sepsis

319

Uroperitoneum Progressive abdominal distension, mild to moderate colic, generalized depression and diminished suckling activity are commonly present. Abdominal distension may not be present until the volume of urine retained is considerable, or the rate of accumulation exceeds fluid absorption across the peritoneum. Affected foals will strain to urinate. The most clinically important result is a disturbance of serum electrolyte values, chiefly potassium. Elevated potassium levels result in arrhythmias, bradycardia, and can progress to cardiac arrest in severe cases. This is a medical emergency with a surgical correction. Fluid support (potassium free) will be necessary, however exacerbation of abdominal distension may occur compromising breathing efforts. Placement of a urinary catheter may allow some ducting of urine externally. Referral is recommended as soon as the diagnosis is made. Meconium impaction or retention Affected foals will display kyphosis (dorsoflexion) while straining to defecate. Meconium impaction results from accumulation of meconium at the pelvic inlet, and can result in urinary tract rupture from increased intra-abdominal pressure during abdominal straining, and direct pressure of retained meconium at the pelvic inlet on the colon and bladder wall. Meconium retention is an accumulation of meconium high in the colon sufficient to cause obstruction. Significant pain and abdominal distension may be associated with this condition. Continuous analgesia may be necessary. Severe cases may progress to peritonitis from devitalization of the gut wall. The great majority of affected foals with resolve with a retention enema (acetylcysteine) however many will require nutritional and fluid support until gastrointestinal distension has resolved. 5. Triage of the equine neonate When infection is suspected it should be aggressively managed. Any signs of neurological dysfunction should similarly prompt intensive supportive care on farm, and initiate a conversation regarding potential for referral. In the uncomplicated but compromised neonate, fluid therapy and meeting of nutritional needs are the most common obstacles to overcome. Type of fluid Choice of fluid will be made following assessment of the biochemical profile and clinical appearance of the patient. The initial replacement fluid is usually an isotonic crystalloid fluid such as LRS or an equivalent solution with a bicarbonate precursor. In situations of excessive K (uroperitoneum, HYPP) 0.9% NaCl, a K-deficient fluid, is used. Hypertonic saline is beneficial for transient intravascular fluid (IVF) expansion where interstitial fluids store is still adequate. Isotonic crystalloids should be used prior to or concurrently with colloids or hypertonic crystalloids. Volume Three separate fluid volumes must be considered: existing fluid deficit, maintenance requirements, and abnormal on-going fluid losses. Volume requirements in liters are calculated by addition of the calculated existing deficit (%dehydration x bodyweight in kg), maintenance requirements (up to 10% bodyweight/day in neonates) and on-going losses (estimated). Rate of administration This is determined by the severity of the presenting condition, body mass of the foal, volume calculated to be required, estimated on-going losses, and time available for administration. Up to 100 mL/kg may be administered in situations of severe hypovolemia until correction occurs. A practical method of administering this volume is by giving 1L LRS

320

(corresponds to 20mL/kg for a 50kg foal) as a bolus every 15 minutes and assessing response. A maximum of 4 boluses is administered and should correction of hypovolemia not be achieved this is as strong indication to consider referral care. Higher rates of administration should be avoided in patients with decreased plasma proteins or cardiac insufficiency. Rapid IVF expansion may cause diuresis before transference to the extravascular fluid, therefore maintenance rates should be established once volume deficits are corrected. Supplementation with mareâ&#x20AC;&#x2122;s milk During the first 24 hours of enteral support a suggested initial rate of milk delivery is 2ml/kg body weight per hour. This provides 2.4L of milk to a 50kg foal, being near 5% of bodyweight. Extreme caution should be exercised to avoid aspiration in the compromised neonate, therefore placement of an indwelling feeding tube transiently is recommended. Additional calories can be provided intravenously (dextrose solution, parenteral nutrition). This feeding rate can be gradually increased to achieve 10% to 15% of body weight as milk intake daily. The mare 1. Examination of the mare Systemic signs Fever, when present, is indicative of an inflammatory process. In the postpartum mare, uterine or intestinal mural devitalization may allow leakage of inflammatory mediators or translocation of bacteria into the peritoneal cavity initiating a systemic response. Where sepsis is overwhelming, decreased rectal temperature may be present. While a useful indicator, heart rate may be variably elevated due to individual tolerance to pain, and heart rate alone cannot be relied upon to predict outcome. When elevated, hypovolemia must be considered especially if signs of circulatory compromise are present. Of note, a heart rate within the expected range may be present in the face of significant gastrointestinal compromise. Pulse quality can be assessed at the distal extremities or the facial artery. Poor pulse pressure is suggestive of hypovolemia, shock, or cardiac insufficiency. A bounding pulse may indicate the early phase of endotoxemia. Elevation of respiratory rate and effort may indicate pain, acid-base disturbances, impediment to the diaphragmatic movement from visceral distension or pleural space disease (pleuritis) which may cause pain in its own right. Physical exam Pale mucous membranes are associated with hypovolemia or hemorrhagic shock, bright red membranes indicate the early stages of endotoxemia, while a toxic line (dark blue/purple gingival margin) suggests intestinal devitalization and bacterial translocation. Mucous membrane color has been considered a reliable prognostic indicator in some colic studies. Increased intestinal sounds are seen with irritant conditions with favorable outcomes e.g. colitis. Hypoperistalsis may be caused by sudden feed changes, carbohydrate overload, or infectious agents. When intestinal sounds are decreased, scant fecal production and acute pain are associated with conditions with a less favorable prognosis. Visual body condition scoring is augmented by palpation of fat deposits, chiefly over the ribs, tail head and vertebral spines which avoids the effects of abdominal distension and elongated haircoat. Dental work is often delayed due to pregnancy, whether for concerns regarding sedation or potential bacteremia in the presence of gingivitis or decay. The nutritional stress the lactating mare faces to meet the needs of the rapidly growing foal necessitates timely and effective dental care, therefore examination of the oral cavity and particularly the teeth is important. The ability to consume an adequate ration and digest the contents depends upon integrity of the

321

dental arcade. Malalignment and pain compromise mastication, potentially reducing digestibility of the ration and increasing the chances of esophageal obstruction. Lameness limits mobility regardless of the source (hoof, joint) and may precipitate stress with any associated pain. Ability to forage is reduced. Elevation of stress hormones exacerbates insulin resistance and depresses hormones involved in promoting cyclical activity. Reproductive system Integrity of the perineum is vital for health of the reproductive tract. Early placement of a Caslick suture post foaling is shown to improve reproductive performance, with mares sutured at 48 hour post foaling having increased pregnancy rates over those sutured at foal heat, making it imperative that any further delay is avoided. Where perineal laceration has occurred, or recto-vaginal fistula formation is confirmed, antibacterial coverage in the postpartum period coupled with dietary management to promote fecal passage will be necessary. Referral for surgical correction is delayed until granulation tissue has formed sufficiently to allow repair. If rectal of vaginal tearing extend to the peritoneal cavity this is a surgical emergency requiring immediate referral. Limited to the post foaling mare, careful evaluation of the vagina by manual palpation may reveal defects in the vaginal mucosa or full-thickness lacerations. The integrity of the uterine lumen may also be assessed with deeper palpation. 2. Differential diagnosis of the compromised periparturient mare Abdominal pain - gastrointestinal Colic in the prepartum mare presents a serious diagnostic challenge to the practitioner through limitations imposed upon examination by the presence of the gravid uterus. Accurate differentiation between gastrointestinal conditions and reproductive conditions is essential but difficult in many cases. Trauma to the gut may result in ischemic necrosis of the affected areas. Compromise to the gastrointestinal tract results in the onset of endotoxemia with profound circulatory dysfunction and proinflammatory stimuli occurring. Peripartum gastrointestinal conditions include large colon volvulus or displacement, cecal rupture, small intestinal volvulus, enterocolitis and direct trauma to the intestine. The most common site of postpartum rupture is the tip of the cecum. Small colon may suffer bruising from compression during foaling, or avascular necrosis from disruption of the mesenteric attachments. The small colon has a relatively short mesocolon which can tear with passage of the fetus. Lesser trauma may result in impaction and colic with variable signs of systemic disease. Increased peritoneal fluid with inflammatory changes in conjunction with signs of endotoxemia may be the first indication of small colon devitalization. With ultrasonography small intestinal strangulation can be suspected when distension, mural thickening and loss of motility are noted. The large colon is at increased risk of torsion in postpartum mares, being the most common diagnosis for referral emergency presentations of postpartum mares in one review. Impaction may result from diminished water intake, depressed motility due to systemic disease and inappetence, and pain resulting from perineal trauma slowing fecal passage. Altered feed intake and quality, and the addition of medications (e.g. anitbacterials) may induce enteritis or enterocolitis. Pain results from intestinal inflammation, and diminished motility promoting increased gas distension. Assessment of the majority of the intestinal tract by ultrasonography is difficult. Response to nasogastric intubation, clinical impression and evaluation of blood work aids diagnosis. Abdominal pain - genitourinary Reproductive problems in the peripartum period with apparent colic as a presenting clinical sign include hemorrhage of the blood vessels supplying the reproductive tract, uterine torsion, uterine rupture, uterine laceration, and uterine bruising.

322

Rupture of and subsequent hemorrhage from the uterine artery is the most common cause of death in mares post partum. Hemoperitoneum itself is a significant cause of abdominal discomfort in the horse. Although usually considered a problem of the postpartum period, reports exist of cases in the prepartum period. Peripartum hemorrhage has been reported to occur at any age, however older mares are considered to be at greater risk due to age-related degeneration of arterial vessels. Hemorrhage can occur into the peritoneal cavity, within the broad ligament of the uterus, within the uterine wall (mural hemorrhage), or into the uterine lumen. Combinations of these may occur. Hemorrhage into the peritoneal cavity leads to profound hypovolemia, pain and sometimes peracute death. If confined to the broad ligament or uterine wall, pain can be significant but prognosis for life better. Broad ligament hematomas may be incidental findings during routine reproductive examinations, or may be come acutely apparent a variable time after foaling following rupture causing abdominal hemorrhage and pain. Luminal hemorrhage is usually of less significance due to the relatively small amount of blood lost and lack of significant uterine distension. The hematoma initially appears uniformly hyperechoic before developing a heterogenous appearance with separation of the blood into anechoic fluid and hyperechoic organizing tissue. Tearing of the broad ligament in the acute to subacute phase will allow leakage of blood into the peritoneal cavity and systemic signs. There is no reported predilection for side of rupture. Torsion is most prevalent within the final three months of gestation, but is not usually associated with parturition. Mild to moderate abdominal pain is often seen. Devitalization of the uterine wall can lead to rupture and systemic illness. Diagnosis is made by rectal palpation, with the broad ligament coursing over the dorsum of the uterus indicative of the direction of torsion i.e. the ligament can be traced dorsally from its origin, across the dorsum of the uterine body, ending ventrally in the direction of torsion. An inverted uterine horn tip may occur following uncoordinated uterine contractions or uterine fatigue post foaling. Alternately, overzealous traction in cases of placental retention may iatrogenically invert the uterine horn. The characteristic target sign appearance may be difficult to obtain with transabdominal ultrasonography but is usually readily obtained transrectally. Chronic low grade pain is often seen with spontaneous cases, progressing in later stages to display fever and depression as uterine wall becomes devitalized. Iatrogenic cases may often develop severe pain at the time of placental traction. Laceration, mural hematoma and necrosis may result from vigorous expulsive efforts by the mare or misdirected obstetrical manipulations. The time course of clinical signs is dependent on the extent of the laceration and its location (dorsal versus ventral) allowing spillage of uterine content and aspiration of air. Pain results from ensuing peritonitis, with profound endotoxemia developing over 24 hours in most patients. Sudden onset of colic signs following uterine lavage with concurrent appearance of a large volume of relatively anechoic peritoneal fluid is highly suggestive of uterine perforation. Necrotic vaginitis may result from fetal oversize and prolonged obstetrical manipulations. Abrasion of the vaginal mucosa may lead to cellulitis, with deeper trauma causing hematoma formation which may progress to abscessation. Outright vaginal, rectal and perineal laceration may occur. Discomfort results from local inflammation and impediment of appropriate fecal passage. Nutrition Mares that foal in decreased body condition, or those that lose body reserves in early lactation, have reduced reproductive performance requiring more time to initiate cyclicity and more cycles to conceive. Feed requirements increase markedly over maintenance once lactation begins, with mares dry matter intake regularly achieves 2-3% of body weight , with energy and protein needs also challenging to meet. Where forage quality is average,

323

concentrate intakes should be in the range of 0.5-1% of body weight. Where lower quality forage is given or intake restricted, larger amounts of concentrates are needed. Therefore higher quality forages should be provided for lactating mares when possible. High concentrate intakes should be divided into two or three servings per day. Lactating mares in moderate body condition tended to skip a breeding season, and body condition score 5 proved to be marginally acceptable in lactating mares. 3. Triage of the compromised perinatal mare The peripartum mare can experience the full range of colic diagnoses, however the recently gravid uterus provides unique challenges to examination and decision making. Compromise to the uterine wall tends to progress steadily to peritonitis and discomfort once perforation has occurred, this being immediate with laceration or delayed with mural bruising and necrosis. Fever, depression, inattention to the foal and a lack of milk production are compatible findings. Gastrointestinal lesions result in more rapid deterioration and varying degrees of abdominal pain where translocation of bacteria or spillage of content has occurred. These lesions can outwardly appear similar to uterine pathology in the early stages. Rapid onset of profound abdominal pain in the postpartum mare should always be considered a large colon accident until proven otherwise. Where placental remnants remain or are suspected, protect the systemic health of the mare by appropriate use of antimicrobials and anti-inflammatories. In the case of prolonged retention, anti-endotoxic medications and localized treatment to forestall laminitic changes in the hooves are indicated. Uterine lavage should be repeated to physically remove infectious agents and the products of inflammation, and to stimulate uterine contractility. When needed, uterotonics to stimulate contractility to facilitate expulsion of placenta remnants, fluid and to decrease overall uterine luminal space are indicated. Summary The majority of neonatal foals and post parturient mares transition without difficulty. Health of the mare during gestation may impact the foal therefore, where potential for compromise is suspected, a proactive approach to the neonate should be taken. Observation of both foal and mare in the immediate postpartum period is essential to detect sometimes subtle signs of potentially catastrophic impending conditions. References/Suggested Reading

Abutarbush SM. Use of ultrasonography to diagnose large colon volvulus in horses. J Am Vet Med Assoc 2006;228:409-413. Arnold CE, Payne M, Thompson JA et al. Periparturient hemorrhage in mares: 73 cases (1998-2005). J Am Vet Med Assoc 2008;232:1345-1351. Carr EA. Field triage of the neonatal foal. Vet Clin Nth Amer: Eq Pract 2014;30:283-300. Dembek KA, Hurcombe SD, Frazer ML et al. Development of a likelihood of survival scoring system for hospitalized equine neonates using generalized boosted regression modeling. PloS one. 2014;9:e109212. Dolente BA, Sullivan EK, Boston R et al. Mares admitted to a referral hospital for postpartum emergencies: 163 cases (1992-2002). J Vet Emerg and Crit Care 2005;15:193-200. Fielding CL. Practical Fluid Therapy and Treatment Modalities for Field Conditions for Horses and Foals with Gastrointestinal Problems. Vet Clin Nth Amer: Eq Pract 2018;34:155-68. Frazer GS. Post partum complications in the mare. Part 2: Fetal membrane retention and conditions of the gastrointestinal tract, bladder and vagina. Equine Vet Ed 2003;15:91-100. Jean D, Picandet V, Maciera S et al. Detection of rib trauma in newborn foals in an equine critical care unit: a comparison of ultrasonography, radiography and physical examination. Equine Vet J 2007;39:158-163. Klohnen A, Vachon AM, Fischer AT. Use of diagnostic ultrasonography in horses with signs of acute abdominal pain. J Am Vet Med Assoc 1996;209:1597-1601. Marsh PS, Palmer JE. Bacterial isolates from blood and their susceptibility patterns in critically ill foals: 543 cases (1991â&#x20AC;&#x201C;1998). J Am Vet Med Assoc 2001;218:1608-10.

324

Perkins NR, Robertson JT, Colon LA. Uterine torsion and uterine tear in a mare. J Am Vet Med Assoc 1992;201:9294. Platt H. Caecal rupture in parturient mares. J Comp Path 1983;93:343-346. Williams NM and Bryant UK. Periparturient Arterial Rupture in Mares: A Postmortem Study. J Eq Vet Sci 2012;32:281-284.

325

326

Diarrhea and respiratory conditions in the growing foal. Peter R. Morresey BVSc MVM Rood and Riddle Equine Hospital Lexington, KY 40580

Introduction The journey from newborn foal to adulthood is not without its challenges. In addition to the numerous opportunities for injury that are an accepted risk with the horse, infectious diseases pose a repeated and sometimes significant threat. Many infectious agents are resident in the environment and exposure cannot be avoided. Diarrhea In many cases an etiological agent is not found, however during a clinical examination of an affected foal the following differential diagnoses should be considered and presumptively managed if signs are suggestive. In the absence of a definitive diagnosis, appropriate fluid therapy and general supportive care are indicated. A. Common diarrheal conditions 1. Infectious agents: bacterial Salmonella In highly concentrated populations of horses, Salmonella infection is of particular concern. Stressors such as dietary changes, surgery, transport, heat exposure and concurrent illness increase the likelihood of infection. Clinical signs of Salmonellosis are variable, ranging from mild enteritis to sepsis and shock. Intestinal fluid loss occurs due to active fluid loss through hypersecretion, and passive fluid loss by malabsorption due to profound inflammation. Diagnosis of Salmonella is confirmed by positive fecal or blood cultures. Treatment for Salmonella infection is aimed at maintaining hydration and electrolyte balance. As neonates and younger foals are at high risk for bacteremia systemic antimicrobials are necessary to counter the potential for infection of physeal and synovial structures. Intestinal Clostridiosis These bacteria are found in the intestinal tracts of domestic animals and are widely distributed throughout the environment, including the soil. Endospore production enables survival under adverse environmental condition. Potent exotoxins are responsible for a variety of intestinal diseases in domestic animals. Clinical disease results from Clostridium perfringens biotypes A and C and Clostridium difficile. Diarrhea induced by Clostridium sp. is more common during the early neonatal period. Disease induced by Cl. perfringens biotype C is associated with abdominal distention, colic, shock, hemorrhagic diarrhea and high mortality. The syndrome is commonly seen within the first 48 hours of life, usually in vigorous foals with high milk intake. Enteric disease associated with C. perfringens biotype A has been seen in newborn foals, with transient and variable clinical presentation. This biotype is however also present in the feces of healthy young foals. Clostridium difficile is found in the feces of healthy horses and foals, implying healthy foals may function as a potential reservoir. Toxins act synergistically to cause intestinal disruption. Diagnosis is confirmed by identifying toxin within the feces or intestinal luminal content, and recovery of the organism and biotyping by polymerase chain reaction( PCR) for toxin gene identification. Treatment is often unrewarding in established cases. Antimicrobial agents (penicillin and metronidazole), NSAID, plasma, correction of fluid and electrolyte derangements, and C. perfringens biotype C antitoxin are indicated. Prevalence varies with geographic location but C.

327

difficile appears to be a rare isolate in older suckling foals. Treatment is as above for C. perfringens without specific antitoxin. Samples should be collected and shipped in an appropriate container. The isolation of C. difficile is usually considered significant in foals of all ages but it is not uncommon to identify foals that are culture positive but toxin-negative. Recovery of C. perfringens from diarrheic foals without toxin presence is also of questionable significance because the organism, particularly C. perfringens biotype A, is commonly found in the feces of healthy foals. Enterococcus durans Enterococcus durans has been isolated from diarrhea cases in many species. It is commonly isolated from the feces of young foals with diarrhea in association with other potential diarrhea pathogens. Diarrhea is likely to be age dependent in its severity. Lawsonia intracellularis Equine proliferative enteropathy (EPE) is a fecal-oral transmissible enteric disease caused by Lawsonia intracellularis. Although the condition is considered to have a sporadic case distribution, apparent outbreaks are reported. Equine proliferative enteropathy affects weanling foals chiefly between the ages of three and six months although yearling cases occur. Presenting signs include depression, fever, weight loss, colic, diarrhea, and ventral edema. Clinical pathology findings include leukocytosis, anemia, mild to severe hypoalbuminemia and variably hyperfibrinogenemia. Hyponatremia, hypokalemia, hypocalcaemia, and metabolic acidosis are present. Abdominal ultrasonography reveals loops of thickened small intestinal wall, and in severe cases the entire small intestine is affected with apparent large colon involvement in some cases. Antemortem diagnosis of EPE depends on a combination of characteristic clinical findings, serological testing for L. intracellularis antibodies, and detection by PCR in feces. Gross pathologic lesions in EPE are characteristic with mucosal hypertrophy of the ileum and terminal jejunum, sometimes involving the entire small intestine. Treatment entails correction of fluid and electrolyte deficits. A combination of crystalloid and colloid therapy will be required. Anti-inflammatory, antidiarrheal, antiulcer therapy and pain management will be necessary. A number of antimicrobials have proven effective in this condition including macrolides, chloramphenicol, oxytetracycline and doxycycline. 2. Infectious agents: viral Rotavirus The virus invades the intestinal epithelium affecting the brush border of the villi which are responsible for small intestinal degradation of disaccharides to enable absorption. Loss of the brush border decreases lactase resulting in lactose maldigestion. Lactose remaining in the intestine is highly osmotically active drawing fluid intraluminally. Clinical signs of disease occur most often in young foals, usually 3 months of age or less. Diarrhea, abdominal distension, colic, depression and anorexia occur. Rotavirus is reported as the most common cause of diarrhea in foals in a Kentucky study. Infected foals may shed rotavirus for up to 10 days. The virus is environmentally persistent for 9 months. Diagnosis requires detection of the virus in feces by PCR, ELISA, latex agglutination or electron microscopy. As there is no specific treatment for rotavirus infection, therapies are empirical and symptomatic, consisting of fluid therapy and supportive care. Vaccination of pregnant mares may be of use in control on infected farms. Coronavirus Coronavirus has been isolated from the feces of diarrheic foals however the significance and true incidence or infection is not known.

328

3. Infectious agents: Protozoal Cryptosporidia Infection appears `widespread therefore the role of cryptosporidium in foal diarrhea remains controversial. In one study the number of foals with diarrhea was not significantly different between positive and negative foals. Detection of oocysts in fecal samples requires acid-fast staining, immunofluorescence assays, or flow cytometry. Treatment is generally supportive and centers on fluid and electrolyte replacement. Prevention includes environmental disinfection and isolation of infected foals. Giardia

Prevalence is considered to be as high as 35% but data associating shedding with disease are lacking. Suckling foals with diarrhea and high Giardia counts have been reported to respond to metronidazole administration. 4. Infectious agents: helminth parasites Foals and weanlings are susceptible to a wide range of gastrointestinal parasites as, unlike adults, they have not developed any degree of resistance to infestation. The most likely to cause disease is the ascarid Parascaris equorum. Following the tissue migratory phase (lung, liver) the parasite comes to reside in the small intestine where enteritis, diarrhea and impaction can result. Cyathostomes, strongyles, pinworms and tapeworms may also be problematic. 5. Non-infectious: management, nutritional, iatrogenic Lactose intolerance Lactose intolerance is a secondary problem most commonly associated with rotavirus infection, but it can be caused by any condition affecting the small intestine. Continued ingestion of lactose in severely diarrheic foals is therefore detrimental, exacerbating fluid and electrolyte losses by osmotic draw. Dietary alterations Commensal flora can be easily disrupted, compromising its role in suppressing pathogen overgrowth. Dietary alteration has been identified in one study as an important risk factor for Salmonella sp. in hospitalized horses. Changes in the intestinal microflora and alterations in villus structure increasing the potential for diarrhea can occur with prolonged fasting, emphasizing the importance of a consistent feeding program. Disturbances of colonic flora â&#x20AC;&#x201C; antimicrobial associated diarrhea Any broad-spectrum antibiotic has the potential to disrupt local protective flora and to allow intestinal overgrowth of potential pathogens. Loss of colonization resistance through alterations in the gastrointestinal microflora, altered colonic fermentation, and increased toxin production by overgrowing pathogenic organisms are major causative factors. A recent equine study confirmed the association or antimicrobial usage with diarrhea but did not implicate any particular class of antimicrobials. B. Diagnostic procedures Physical examination Fever or hypothermia may be present. Depression, dehydration and abdominal pain are commonplace. Foal heart rate elevations are variable due to individual tolerance to pain and varying response to hypovolemia. Poor pulse pressure is suggestive of hypovolemic or distributive shock. A bounding pulse may indicate the early hyperdynamic phase of

329

endotoxemia. Respiratory rate and depth may increase in compensation for developing metabolic acidosis secondary to hypovolemia. Abdominal distension sometimes occurs due to severe fluid accumulation in the colon. With more serious infectious causes such as Salmonella in foals less than 2 months of age extra-intestinal disease is common and includes uveitis, infective synovitis, osteomyelitis, pneumonia, and meningitis. Ultrasonography Rapid assessment can be made of gastrointestinal wall thickness, small and large intestinal diameter, content and motility, stomach size, quantity and nature of peritoneal fluid, and position of the viscera and intestinal tract. The presence of a mesenteric lymphadenopathy or abscess suggesting extrapulmonary R. equi infection could be detected which may be then confirmed, in some cases, by tracheal aspiration. Clinical pathology With more serious infectious causes of diarrhea, a complete blood count may find neutropenia with a toxic left shift in the initial stages, progressing to a rebound neutrophilia as the disease becomes of longer duration. Anemia may be present in chronic cases. Fibrinogen will be variably elevated depending on severity of colonic inflammation and the presence of secondary inflammatory foci (pneumonia, synovitis). Hypoproteinemia (chiefly albumin although globulin will decrease in chronic or severe cases) will result from depressed feed intake and gastrointestinal losses. Electrolyte derangements also occur, with hyponatremia being the most clinically significant. Sodium is lost with the electrolyte rich fluids of the gastrointestinal content. Also, as Na is bound to albumin levels are further depressed. Serum levels may be further depressed by overconsumption of fresh water causing a dilutional effect. Other findings include hypochloremia, decreased bicarbonate, and elevated lactate. Azotemia may occur with hypovolemia and dehydration. Non-specific elevations of hepatic enzymes secondary to hypoxia (from hypovolemia) and inflammatory changes may occur. In neonatal cases, an assessment of colostral immunoglobulin transfer and blood culture are important to perform. Pathogen testing Diarrhea associated with the most serious infectious neonatal differentials (Salmonella, rotavirus, Clostridia) is most often clinically indistinguishable making establishment of a specific etiology vitally important where targeted treatment is possible. Fecal culture (serial, up to five in the presence of suspected Salmonella) and PCR is advisable in all cases. While PCR is more rapid, it is unable to differentiate between viable and inactivated pathogens, and does not provide the sensitivity information successful culture does. In the case of clostridial diarrhea, toxin production is thought more important as nontoxigenic strains of both C. difficile and C. perfringens are found in normal feces, and the organism is difficult to grow in culture. Toxins A and B for C. difficile are detectable by PCR or ELISA. Rotavirus may be diagnosed by latex agglutination or ELISA testing. Electron microscopy can be used as a non-specific screen for viral particles however the clinical significance of all recovered cannot be certain. Cryptosporidia may be seen with acid fast stain although considerable expertise is required for detection. Fecal samples for parasite egg presence is advisable in older foals. C. Individual case management Diarrhea treatment may be extensive depending on severity and chronicity, requiring fluid and electrolyte replacement, correction of acid-base disturbances, control of hypoproteinemia, diminishment of inflammation, countering of endotoxin effects if present, analgesia if required, topical mucosal treatments aimed at protection and repair, and the judicious use of antimicrobials when indicated by signalment or clinical suspicion of a specific causative infectious agent.

330

Fluid therapy Calculation of required resuscitative and maintenance volumes is essential as the underestimation of fluid volumes required in the diarrheic foal is commonplace. Three fluid volumes must be considered: maintenance, deficit and ongoing losses. • Maintenance: can be assumed to be 10% of foal bodyweight. • Deficit: mild (5%), moderate (8%), severe (10%) of bodyweight. • Ongoing losses: estimate volume of diarrhea or reflux. Bolus crystalloid fluids can be given in the initial stages of resuscitation (20ml/kg incremental loads over 15 - 30 minutes). Colloids are also useful to administer in a bolus fashion during initial treatment of hypovolemia, with incremental doses of 3 – 10 ml/kg. Following each dose, reassessment of volume status to determine further need for fluids is required. Once stable, the foal can be transitioned to a maintenance rate of fluids (5 – 10% of bodyweight over 24h). Concurrent or sequential administration of both crystalloids and colloids is advantageous. Crystalloids distribute to the extracellular fluid space, with approximately 75% distributing to the interstitial fluid space, allowing interstitial rehydration. Colloids however are restricted to the intravascular space making them useful in hypovolemic shock as they allow rapid intravascular fluid expansion. The increase in colloid oncotic pressure by the administration of colloids causes increased retention of crystalloid fluids within the intravascular fluid compartment. Plasma supplies albumin for oncotic pressure and drug carriage, along with antithrombin and immunoglobulins. Hetastarch is less expensive, has only oncotic properties, and cannot be measured by a refractometer. The author prefers to give both products in tandem. Antidiarrheals/absorbents A number of absorbent materials are in common usage. Bentonite clay and dioctahedral smectite act as absorbents. Bismuth subsalicylate has both toxin absorbent and local antiinflammatory effects. Activated charcoal is very effective for adsorbing bacterial enterotoxins and endotoxins. Kaolin and pectin are often used in combination to absorb toxins however clinical studies have not demonstrated unequivocal benefits from administration. Gastric ulcer prophylaxis Some cases of ulceration are clinically silent until serious sequelae have occurred. Compatible clinical signs include any or all of decreased suckling, poor body condition, diarrhea, bruxism, ptyalism and intermittent colic of varying severity. The use of H2 receptor blockers (cimetidine, ranitidine) or proton pump inhibitors (omeprazole) is recommended in diarrheic foals. Mucosal protectants (sucralfate) are also of use. The use of these medications in foals should be considered on an individual basis as ulcer prophylaxis in a hospital setting has been associated with higher rates of diarrhea. Analgesics and anti-inflammatories Non-steroidal anti-inflammatory drug (NSAID) usage is widely practiced in diarrhea cases for the control of fever, mucosal inflammation, and analgesia. Care in their usage must be practiced as in compromised patients exacerbation of renal pathology is possible. Therefore correction of fluid and protein deficits must be prior to or concurrent with NSAID administration. Antimicrobials As a large number of diarrhea and colitis cases do not have a specific infectious agent recovered the indiscriminant use of antimicrobials is to be discouraged, however protection of the severely neutropenic or neonatal foal from secondary infections (pneumonia, catheter site

331

sepsis) by the use of parenteral antimicrobials is rational. Neonates and younger foals are at considerably higher risk from bacteremia during colitis, with infection of synovial and physeal tissues having potentially devastating consequences. In one study, half of foals less than 30 days of age admitted to a referral hospital for diarrhea were bacteremic. Electrolyte supplementation Hypokalemia can be managed by addition of KCl to intravenous replacement fluids (2040 mEq/L) and can be administrated safely if the rate of administration does not exceed 0.5 mEq/kg/h (do not bolus). KCl can also be administered orally for several days. Sodium bicarbonate may be used in severe metabolic acidosis not corrected with volume expansion. Half the calculated dose is given slowly intravenously over 20 minutes, and the rest of the dose in crystalloid fluids over 4 hours. Oral supplementation is also possible. Nutritional requirements Loss of body condition and protein-energy requirements during convalescence must be met. Intravenous glucose containing solutions are incomplete and appropriate for only shortterm (24 hour) usage. Solutions containing 5% dextrose are easily made and readily available. Caloric content of a 5% dextrose solution is 0.17 kcal/mL, so to provide approximately 40 kcal/kg/d an infusion of 10 mL/kg/h must be used. For an average foal (50kg bodyweight) a daily volume of 10 mL/kg/h x 50 kg x 24 hours = 12 L must be given. This volume will likely not be well tolerated by the foal. Therefore the established maintenance rate of fluids (4-5 mL/kg/h) will only provide less than half the required caloric intake. Parenteral nutrition enables nutritional support without worsening diarrhea however considerable attention must be paid to sterile technique and monitoring these foals (blood glucose) rendering this difficult to perform in farm situations. Probiotic usage Although in widespread usage, some studies have shown no benefit in the use of probiotic preparations with regards to disturbances of fecal flora (Salmonella sp. shedding), duration of hospitalization or prevalence of clinical signs. Anecdotally probiotics may be useful as both treatment for the affected foal and as a preventative for other newborn foals on the property. The use of Saccharomyces boulardii has been reviewed favorably. Respiratory system disorders Respiratory disorders are the second most common reason for poor performance in the athletic adult horse. During the growing phase, respiratory conditions can stunt growth or lead to long-term loss of pulmonary capacity. A. Common respiratory conditions Pulmonary infection Bacterial pneumonia is the most common cause of respiratory disease in foals. Bacterial pneumonia can be secondary to sepsis or prolonged recumbency in the devitalized neonate. The most common bacterial organisms associated with pulmonary disease in neonatal foals are the same as those responsible for systemic sepsis, chiefly Escherichia coli, Streptococcus spp, Klebsiella pneumoniae, Pasturella spp, and Actinobacillus spp. Less commonly, Salmonella spp, Pseudomonas spp and Staphylococcus spp are involved. In a study of bacteremic foals, 19% (79/423) were concurrently diagnosed with pneumonia. Pneumonia derived from sepsis tends to have a generalized distribution throughout the lung. Additionally, the development of deleterious responses to sepsis (acute lung injury, respiratory distress syndrome) can exacerbate severity of the bacterial disease. Aspiration of feed material or saliva can also contribute to the development of pneumonia, whether during suckling by

332

compromised individuals (sepsis, perinatal asphyxia) or iatrogenically during assisted feeding. Distribution in these cases tends to be cranioventral. As the foal progresses to the juvenile stage, bacterial pneumonia remains a problem, whether an extension of viral challenge, or secondary to the stresses of weaning, comingling, concurrent devitalizing conditions, and overwhelming challenge. Viral pneumonia in the neonate through the juvenile stage is chiefly the result of infection with Equine herpesvirus 1 or 4 (EHV), and sometimes Equine arteritis virus (EAV). Clinical signs in neonatal foals can closely mimic sepsis, with icterus, neutropenia and petechiation present. Affected foals suffer from decreased pulmonary compliance and pulmonary edema. Pleural space disease This may involve an extension of infectious pulmonary disease, or loss of negative pleural pressure due to the presence of fluid or gas. Pleural fluid can be septic and inflammatory as a result of pulmonary disease, hemorrhagic due to thoracic wall trauma (fractured ribs in the neonate) or a coagulopathy, a transudate resulting from hypoproteinemia, or an extension of peritoneal fluid (peritonitis, uroperitoneum) accessing the pleural space via discontinuity in the diaphragm. Gas (air) can accumulate from pulmonary lacerations (fractured ribs, iatrogenic) or rupture of the lung parenchyma (formation of bullae, iatrogenic due to overinflation during resuscitation efforts). Acute respiratory distress syndrome Of significance clinically, subsequent to infection and inflammation which may become profound, acute respiratory distress syndrome (ARDS) may develop. Considered multifactorial in origin, marked to severe dyspnea, tachypnea and respiratory effort result from ARDS, with hypoxic damage of multiple organs possible. B. Physical examination Rectal temperature The presence of an infectious agent is expected to raise rectal temperature in the early stages of infection. However, rectal temperature is often an unreliable indicator of disease. In the neonate, as the infection becomes chronic and the foal fatigues, normo- to hypothermia may ensue. Tachypnea may raise rectal temperature due to increased exertion, especially in older foals. Auscultation Lung sounds tend to be louder in foals than in adults as the body wall is much thinner. There is poor correlation between auscultation and the presence of lung pathology. Normal bronchovesicular sounds may still be heard in foals with lung consolidation as sounds may radiate from airflow in unaffected adjacent areas. Airway changes (crackles due to airway collapse, wheezes due to airway narrowing) and mucus rattles are indicative of pathology. Respiratory effort Parenchymal disease of the lungs can greatly increase the respiratory effort required due to loss of compliance. Paradoxical thoracic wall motions can be seen in the neonate: inward motion during inspiration, and outward motion during expiration. In older foals, increases in respiratory rate and greatly diminished thoracic excursion, sometimes with abdominal motion, is seen with respiratory distress. Loss of negative pleural pressure from fluid or air similarly increases the work of breathing as transference of forces generated by the thoracic wall and diaphragm to the lung becomes less efficient. Nostril flaring and extension of the neck are attempts to minimize upper airway resistance. Open mouth breathing is a sign of severe respiratory distress and indicates a life threatening emergency situation.

333

A decreased respiratory effort should not always be interpreted as a positive sign in all cases of respiratory disease, as in the neonate fatigue may have ensued. Older foals have a more rigid thoracic wall and do not expend as much energy during the active portions of ventilation. C. Diagnostic techniques Physical exam findings are augmented by the use of advanced imaging techniques, microbiological testing and clinicopathological findings. Ultrasonography Ultrasonography allows rapid assessment of the pleural space and superficial lung parenchyma, with deeper structures visible where consolidation or abscessation is present. The probe is generally placed perpendicular to the thoracic wall however areas shielded by the ribs can be assessed by sweeping the ultrasound beam horizontally. Assessment of the cranial thorax (cranial to the third ICS) presents some difficulty as the triceps musculature covers this area, however the probe can be placed under the right triceps musculature with the probe angled towards the left shoulder to image the cranial mediastinum. Radiography Radiography allows deeper structures to be visualized. Aspiration pneumonia is located in the cranioventral lung fields, whereas that resulting from bacteremia is more diffuse. Inflammatory changes are indicated by increased radiodensity centered on the airways initially, coalescing to a generalized opacity in interstitial pneumonia and ARDS. Discrete areas of consolidation and deep abscessation may be noted. Tracheal aspiration Aspiration of fluid and mucopus from the lower respiratory tract allows cytological evaluation, bacterial culture and antimicrobial sensitivity analysis. This can be obtained by percutaneous or endoscopic means. Endoscopy has the advantage of avoiding tracheal penetration and direct visualization of the upper airway, but requires a greater investment in equipment and personnel. D. Treatment The central tenets of treatment of respiratory disease in the foal include: ▪ Reversal of hypoxemia and hypoxia ▪ Reduction of respiratory effort via bronchodilation, improved pulmonary compliance and resolution of pleural space disease (if present) ▪ Improved ventilation ▪ Enhanced mucociliary clearance ▪ Control of infection ▪ Control of inflammation (and pain if present) ▪ Supportive care 1. Increased inspired oxygen tension Intranasal oxygen is the established treatment for hypoxemia. Hypercapnia, however, is a more difficult clinical syndrome to manage as this indicates problems with diffusion or depressed ventilation. Oxygen can be readily administered in field situations. 2. Medications Anti-inflammatories Control of inflammation improves pulmonary function, diminishes fever, and reduces pain (pleural, pulmonary, thoracic wall). Inflammatory syndromes of importance to the neonate

334

include bacterial infection and aspiration of irritant compounds. Older foals may experience significant inflammation from both viral and bacterial conditions. Where the potential for sepsis exists, antimicrobial treatment should be used concurrently. Antimicrobials The mainstays of infectious respiratory disease treatment are oral and parenteral antimicrobials. However, the low bioavailability of many drugs administered by these routes limits their concentration in the lung parenchyma and distal airways. Bronchodilators Sympathomimetic agents (ď ˘2 adrenergic agonists) stimulate receptors on smooth muscle cells of the airway walls, promoting relaxation of muscle and bronchodilation. Stimulation of mucociliary motility also results. Parasympatholytic agents also stimulate bronchodilation, however tachycardia and ileus can result from prolonged usage. Mucolytics Mucolytic drugs decrease the viscosity of mucus enabling more efficient transport up the tracheobronchial tree for clearance. 3. Aerosol therapies The ability to localize treatments directly to the tracheobronchial tree is the chief advantage of aerosol therapy. Higher local concentrations of antimicrobials can be achieved due to bypassing of gastrointestinal barriers limiting bioavailability and avoidance of metabolic inactivation. Inhaled bronchodilators have been shown to be more efficacious than systemic administration of the same compound in their ability to counter bronchoconstriction. An increase in mucociliary clearance has also been reported with the use of ď ˘2 adrenergic agonists, by enhancing ciliary activity and facilitating productive coughing by airway dilation. Sterile water, sterile saline and N-acetylcysteine are all shown to decrease the viscosity of mucus and are therefore useful adjuncts to inhalant therapies. 4. Supportive care Provision of nutrition and fluids should be made if the foal is unable to provide for itself. In situations where aspiration is occurring, if parenteral feeding is not possible, placement of an indwelling nasogastric tube allows bypassing of a dysfunctional pharynx while treatment is attempted. Older foals may benefit from increased concentrate ration during periods of catabolism. 5. Resolve pleural space disease (if present) Aspiration of air and fluid under ultrasonographic guidance (to reduce volume of the pleural space) increases pulmonary compliance by improving transference of the thoracic excursion to the lung surface enabling expansion. Summary Respiratory tract infection is commonplace in the growing foal. Disease may be mild and self-limiting or may rapidly progress to severe life-threatening respiratory distress where inflammation is significant. Diarrhea can be similarly self-limiting or life-threatening depending on the causative agent, the immune status of the foal, and the therapeutic response to infection by the owner and veterinarian. Many infectious agents are widespread in the equine population, and cause problems when resistance to infection is overcome or sufficient numbers of infectious organisms accumulate in the environment.

335

Rhodococcus equi 1. Epidemiology A number of management factors have been found to be associated with infection: large farm size, high numbers of mares and foals, high stocking densities and transient horses. This is the result of variations in environment (temperature, soil parameters, and presence of high dust levels), management of the horses with respect to handling and other stressors, and variations in the virulence of individual isolates. Airborne R. equi concentration in stables increases when warmer, drier and windier weather conditions arise, and this correlates with an increased disease occurrence. The particular susceptibility of the foal is not fully understood but can be explained in part by a combination of heavy challenge through the respiratory route coinciding with declining maternally derived antibody in the absence of fully competent foal cellular immune mechanisms. Healthy foals on endemic farms have been shown to exhale virulent R. equi suggesting that these foals may harbor the organism in the absence of clinical problems. This is a significant factor regarding the occurrence and persistence of disease on individual farms. Susceptible foals that encounter high concentrations of airborne virulent R. equi are at great risk for disease. 2. Pathogenesis of infection Infection follows ingestion but predominantly inhalation of the virulent organism, with a dust aerosol considered to be the major route of pulmonary infection. Pneumonia is typically chronic, however the incubation period is not well defined and ranges from 6 to 18 days in experimentally infected foals. An incubation period of 49 days, based on age of onset of clinical signs and age at death, was calculated in another study that assumed a point source of infection. Virulence factors enable R. equi to survive and replicate in phagocytic cells. Clearance of R. equi relies on both humoral and cellular components of the immune system. Cytokine secretion, chiefly interferon gamma (IFN-ď §) is important. A competent cellular immune system and local pulmonary response is required to prevent pneumonia and death. 3. Disease manifestation Pulmonary disease Pneumonia resulting from R. equi infection is a common condition of foals and weanlings, with clinical signs of disease most often appearing prior to 4 months of age. Chronic suppurative bronchopneumonia with abscessation and lymphadenitis occurs, with initially a slow spread of disease and a considerable compensatory ability of the foal to manage a progressive loss of lung function making early diagnosis difficult. A mild fever and increase in resting respiratory rate may only become apparent when foals are stressed by handling. As disease becomes more profound anorexia, lethargy, respiratory distress and high fever become apparent. In most cases mucopurulent nasal discharge is an inconsistent finding. Extrapulmonary disease Extrapulmonary disease in foals has also been widely reported. In one study 74% of affected foals had at least one extrapulmonary manifestation of R. equi. Up to half of affected foals had intestinal lesions (mesenteric lymphadenitis, severe erosive mucosal inflammation) although signs of enteric disease were not present. Uveitis is also reported. In another retrospective study, one-third of affected foals displayed immune-mediated polysynovitis, most often affecting the tibiotarsal and femorotibial joints. Sporadic cases of diarrhea may result from extrapulmonary disease, inflammation secondary to infection of the mesenteric lymph nodes or the presence of a mesenteric or peritoneal abscess is responsible. 4. Diagnosis

336

As yet there is no readily available single diagnostic technique of high specificity and sensitivity for R. equi pneumonia. Instead, diagnosis is based on clinical presentation, hematological abnormalities, compatible imaging findings and microbiological confirmation of infection. 5. Clinical presentation Clinical presentation includes high fever, depression, increased respiratory rate and effort, and mucopurulent nasal discharge. Extrapulmonary disease includes abdominal abscessation, uveitis and polysynovitis. Persistent ill-thrift and poor weight gain may be all that is apparent in some chronic, insidious cases. While infection most often results in respiratory signs, intestinal involvement may cause chronic diarrhea, and lameness may result from septic arthritis or osteomyelitis. 6. Clinical pathology Leukocytosis with hyperfibrinogenemia is a common finding, however, changes in hematology may be small to absent in some foals. 7. Imaging Radiography has been largely superseded by the use of ultrasonography in the diagnosis of R. equi pulmonary involvement, although it is invaluable in the investigation of extrapulmonary disease which may include osteomyelitis of long bones or vertebrae. Ultrasonography allows a presumptive diagnosis of R. equi pneumonia to be made from visualization of variably sized abscesses within the lung. It is useful as both a diagnostic aid and a screening tool on farms with endemic disease at high prevalence. Ultrasonographic screening of foals on endemic farms is empirically recommended to begin between 3â&#x20AC;&#x201C;6 weeks of age. Despite its increased usage, ultrasonography is limited to detecting peripheral lung lesions, and it cannot discriminate other causes of bacterial pneumonia that may cause comparable lesions. Controversy exists regarding at what size of abscessation treatment becomes necessary. Although deleterious effects were not noted initially, a rapid increase in resistance to antimicrobial treatment has been noted with a proactive policy of treatment based on ultrasonographic screening. Prophylactic treatment similarly increases usage of antimicrobials, with no proven reduction in disease prevalence. The decision to treat is based on clinician experience, with anecdotal evidence that subclinically affected foals with a solitary abscess, or a small number less than 10cm in aggregated diameter, can resolve spontaneously without antimicrobial treatment. 8. Microbiological evaluation Confirmation of R. equi infection is advisable as the specificity of antimicrobial agents used in treatment may not provide effective control of other bacterial causes. Culture of tracheal aspirates is considered to be the definitive diagnostic technique for R. equi pneumonia. When accessible, PCR provides a rapid diagnostic test. Cytological findings compatible with R. equi infection included intracellular Gram positive or acid fast coccobacilli. Infection of extrapulmonary sites must be diagnosed by culture or PCR evaluation of samples from those sites. However, this is not possible with some extrapulmonary manifestations of disease (polysynovitis, uveitis, enteric). 9. Treatment Antimicrobials Azithromycin and clarithromycin have the advantage of good efficacy, less frequent administration and reduced occurrence of deleterious side effects. Although generally well-

337

tolerated, hyperthermia and enterocolitis can still be observed. Rifampin co-administration with clarithromycin has been shown to reduce clarithromycin concentrations, although efficacy has not been affected. The development of antimicrobial resistance continues, however, as crossresistance occurs within the macrolides. Doxycycline has demonstrated good efficacy against R. equi with oral administration, having the added benefit of a relatively broad spectrum. Adjunctive treatments Along with appropriate supportive care and a favorable stall environment (minimize particulate irritants, avoid ammonia build-up, minimize humidity, air conditioning), the use of bronchodilators, anti-inflammatory doses of corticosteroids, inhalant delivery of medications and intranasal oxygen have been of benefit in more severe cases. 10. Prognosis The prognosis for recovered cases is favorable. Residual pulmonary pathology is not present in recovered horses that were diagnosed as infected while foals. Subsequent racing performance is indistinguishable from that of the general horse population. The diagnosis of a mixed infection, with other bacteria and fungi isolated alongside R. equi by tracheobronchial aspiration, does not negatively impact survival. 11. Preventative measures Aspects of herd management that affect disease occurrence Aerosol exposure to the pathogen and the resulting prevalence and severity disease is affected by stocking density. A direct relationship between grouping of mares and foals with the concentration of airborne R. equi has been demonstrated. Increased foal density promotes foalto-foal respiratory spread. Management strategies should attempt to limit the time foals congregate in crowded areas and decrease the size of groups. Environmental management to minimize disease Minimizing dust in holding pens and transit areas, maintaining good pasture cover, and reducing time in stables area were all associated with a decreased incidence of R. equi pneumonia in one study. Alternative bedding materials and airborne decontaminants have been suggested as useful to decrease the concentration of airborne virulent R. equi in stables. Plasma prophylaxis While reduction in both prevalence and severity of R. equi pneumonia has been shown with the use of hyperimmune plasma in some studies, results are inconsistent as several studies demonstrated only safety with no protective effects. Considerable debate over to the appropriate timing of plasma administration to susceptible foals and the correct amount to achieve a protective effect exists, this being likely responsible for the variation in response to plasma administration reported. Great variation in IgG content has been demonstrated between batches of plasma, and even bags from the same batch, contributing to the great variation in response. Antimicrobial prophylaxis Prophylactic treatment with azithromycin in young foals cannot be relied upon to prevent R. equi pneumonia. Study results are conflicting: one study performed on endemic farms in Texas significantly reduced prevalence of R. equi pneumonia in foals that received prophylactic therapy compared to untreated controls, however, a similar study in Germany found no significant difference in the frequency of R. equi pneumonia between controls and foals treated prophylactically with azithromycin for the first 4 weeks of life. This increased usage of therapeutic antimicrobials theoretically accelerates the onset of bacterial resistance. Summary: R. equi It is unlikely that exposure to R. equi can be avoided by neonatal foals during their period of susceptibility to infection due to the ubiquitous nature of the organism. Foals vary

338

widely in their susceptibility, the result of genetic factors and infectious dose. Management factors to minimize exposure should center upon reduction of airborne irritants and avoidance of overcrowding. Screening for disease is effectively achieved by ultrasonography however judicious use of antimicrobials is needed to avoid treatment of foals that would spontaneously resolve lower levels of abscessation. References/suggested reading

Ainsworth DM, Eicker SW, Yeagar AE, et al. Associations between physical examination, laboratory, and radiographic findings and outcome and subsequent racing performance of foals with Rhodococcus equi infection: 115 cases (1984-1992). J Am Vet Med Assoc 1998;213(4):510-5. Baldwin DR, Honeybourne D and Wise R. Pulmonary disposition of antimicrobial agents: methodological considerations. Antimicrob Agents Chemother 1992;36(6):1171-5. Barr BS, Waldridge BM, Morresey PR, et al. Antimicrobial-associated diarrhoea in three equine referral practices. Equine Vet J 2012;45(2):154-8. Baverud V, Gustafsson A, Franklin A, et al. Clostridium difficile: prevalence in horses and environment, and antimicrobial susceptibility. Equine Vet J 2003;35(5):465-71. Bihr TP. Protein-losing enteropathy caused by Lawsonia intracellularis in a weanling foal. Canadian Vet J 2003;44(1):65-6. Chaffin MK, Cohen ND, Martens RJ, et al. Foal-related risk factors associated with development of Rhodococcus equi pneumonia on farms with endemic infection. J Am Vet Med Assoc 2003;223(12):1791-9. Cook VL and Bain FT. Volume (crystalloid) replacement in the ICU patient. Clinical Techniques in Equine Practice 2003;2(2):122-9. Cooper DM and Gebhart CJ. Comparative aspects of proliferative enteritis. J Am Vet Med Assoc 1998;212(9):144651. Davis E, Rush BR, Cox J, et al. Neonatal enterocolitis associated with coronavirus infection in a foal: a case report. J Vet Diagn Invest 2000;12(2):153-6. Desrochers AM, Dolente BA, Roy MF, et al. Efficacy of Saccharomyces boulardii for treatment of horses with acute enterocolitis. J Am Vet Med Assoc 2005;227(6):954-9. Hird DW, Casebolt DB, Carter JD, et al. Risk factors for salmonellosis in hospitalized horses. J Am Vet Med Assoc 1986;188(2):173-7. Hollis AR, Wilkins PA, Palmer JE, et al. Bacteremia in equine neonatal diarrhea: a retrospective study (1990-2007). J Vet Intern Med 2008;22(5):1203-9. Magdesian KG. Colloid replacement in the ICU. Clinical Techniques in Equine Practice 2003;2(2):130-7. Mallicote M, House AM and Sanchez LC. A review of foal diarrhoea from birth to weaning. Equine Vet Educ 2012;24(4):206-14. Pusterla N and Gebhart C. Equine proliferative enteropathy caused by Lawsonia intracellularis. Equine Vet Educ 2009;21(8):415-9. Reuss SM, Chaffin MK and Cohen ND. Extrapulmonary disorders associated with Rhodococcus equi infection in foals: 150 cases (1987-2007). J Am Vet Med Assoc 2009;235(7):855-63. Sanchez LC, GiguĂ¨re S and Lester GD. Factors associated with survival of neonatal foals with bacteremia and racing performance of surviving Thoroughbreds: 423 cases (1982-2007). J Am Vet Med Assoc 2008;233(9):1446-52. Seahorn JL and Seahorn TL. Fluid therapy in horses with gastrointestinal disease. Vet Clin Nth Amer: Eq Pract 2003;19(3):665-79. Tillotson K and Traub-Dargatz JL. Gastrointestinal protectants and cathartics. Vet Clin Nth Amer: Eq Pract 2003;19(3):599-615. Traub-Dargatz JL, Salman MD and Jones RL. Epidemiologic study of salmonellae shedding in the feces of horses and potential risk factors for development of the infection in hospitalized horses. J Am Vet Med Assoc 1990;196(10):1617-22. Tzipori S, Hayes J, Sims L, et al. Streptococcus durans: an unexpected enteropathogen of foals. J Infect Dis 1984;150(4):589-93. Walker RL, Madigan JE, Hird DW, et al. An outbreak of equine neonatal salmonellosis. J Vet Diagn Invest 1991;3(3):223-7. Weese JS, Parsons DA and Staempfli HR. Association of Clostridium difficile with enterocolitis and lactose intolerance in a foal. J Am Vet Med Assoc 1999;214(2):229-32, 205. Womble A, Giguere S and Lee EA. Pharmacokinetics of oral doxycycline and concentrations in body fluids and bronchoalveolar cells of foals. J Vet Pharmacol Ther 2007;30(3):187-93. Wong GA, Pierce TH, Goldstein E, et al. Penetration of antimicrobial agents into bronchial secretions. Am J Med 1975;59(2):219-23.

339

340

Basic Science Review

341

342

Basic Science Review

Christopher Baines, PhD and Brian Flesner, DVM, MS, DACVIM

Department of Biomedical Sciences and Department of Veterinary Medicine and Surgery College of Veterinary Medicine, University of Missouri Columbia, Missouri

343

344

Dr. Jekyll and Mr. Hyde: cancer vs. cardiac cell killing by anthracyclines Christopher P Baines, PhD1, Brian K Flesner, DVM, MS, DAVCIM (Oncology)2 1

Department of Biomedical Sciences, 2Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri, Columbia, MO 65211, USA. Anthracyclines, such as doxorubicin, are some of the most commonly used chemotherapeutic agents in both animals and humans. They are effective cancer cellkilling drugs and are indicated for the treatment of both solid and hematologic cancers. Doxorubicin is intrinsically important in the treatment of lymphomatous neoplasms; it is the best single agent drug against lymphoma and is the anchor of the CHOP protocol. However, the clinical use of anthracyclines in dogs and people is greatly hampered by the predilection of the compounds to induce dilated cardiomyopathy and life-ending arrhythmias. This can result in early termination of a doxorubicin-based protocol and/or having to switch to other potentially less efficacious chemotherapeutics, especially in dog breeds pre-disposed to cardiomyopathy (i.e. Doberman Pinscher, Boxer). Despite significant research into the development of adjunct therapies to prevent the cardiotoxic effects of anthracyclines, the only co-drug clinically approved for use in animal and human patients is the iron-chelator dexrazoxane (Zinecard). Unfortunately, dexrazoxane is very expensive, has a narrow therapeutic window, can lead to myelosuppression, and may even reduce the anti-cancer potency of anthracyclines. Thus, there is a great need to better understand the cellular mechanisms by which anthracyclines induce cancer cell vs. myocardial cell death. Such new mechanistic insight is especially important, as it will allow us to avoid areas of molecular overlap and exploit differential pathways thereby reducing the cardiotoxic effects of anthracyclines while maintaining their cancer killing efficiency in the clinical setting.

345

346

Basic Science Review

Lane Clark, DVM, PhD and Philip Johnson, DVM, DACVIM University of Missouri - College of Veterinary Medicine Columbia, Missouri

347

348

Gastrointestinal complications of phenylbutazone treatment in horses: pathophysiological and clinical considerations. Philip J. Johnson, Lane Clarke University of Missouri College of Veterinary Medicine

Introductory comments: Phenylbutazone (butazolidine or ‘bute’) is probably the most commonly used non-steroidal antiinflammatory drug (NSAID) in horses. Phenylbutazone is no longer approved for human medical use in the United States and United Kingdom because it can cause severe adverse effects. Phenylbutazone was implicated in the 2013 meat adulteration scandal. Therefore, the use of phenylbutazone should be restricted to those horses not intended for human food because metabolites of phenylbutazone can cause aplastic anemia in people. In 1968, the winner of the Kentucky Derby, Dancer's Image, was disqualified because traces of phenylbutazone were identified in the horse’s post-race urinalysis. In horses, phenylbutazone is routinely used for its analgesic, anti-inflammatory, and antipyretic properties during the management of infections and musculoskeletal disorders such as sprains, overuse injuries, tendinitis, osteoarthritis, and laminitis. Although the plasma elimination half-life for phenylbutazone is only 4–8 hours, its elimination half-life in inflammatory exudate is ~24 hours, so once daily dosing can be useful. Phenylbutazone is regarded as reasonably non-toxic when used at appropriate doses (2.2-4.4 mg/kg/day) and may be administered orally (via paste, powder, or in feed) or intravenously. It is often used on a twice daily administration basis for the management of more severe conditions (such as painful laminitis). Phenylbutazone is a non-selective inhibitor of cyclooxygenase (COX), therefore exerting its antiinflammatory action through inhibition of prostaglandin production. The alimentary tract and kidneys represent the principal sites of phenylbutazone toxicity in horses. The potential of phenylbutazone to provoke ulceration in the alimentary tract (‘ulcerogenicity’) is greater than that that associated with other commonly-used NSAIDs such as flunixin meglumine and ketoprofen. The COX-1 sparing (selective) inhibitor firocoxib appears to be less ulcerogenic. Phenylbutazone toxicity is more likely when higher doses of the drug are used and when the drug is administered over longer periods of time. Some individuals appear to be inherently more susceptible or sensitive to phenylbutazone toxicity, with toxic sides effects developing even with conservative doses over the course of only a few days. Toxic side effects arise regardless of the route of administration of phenylbutazone (oral and intravenous). NSAID toxicosis is more likely when more than one NSAID is being administered to the same patient at the same time (the combined use of phenylbutazone and flunixin meglumine is sometimes referred to as ‘NSAID stacking’). Other factors that predispose to phenylbutazone toxicosis include dehydration, sepsis (systemic inflammation), preexisting or comorbid hepatopathy, and pre-existing renal disease. Although ulcerative gastritis and right dorsal colitis are the most commonly-encountered gastrointestinal complications of phenylbutazone treatment, it should be emphasized that other ulcerative and motility-altering actions of phenylbutazone may affect other parts of the alimentary tract. Clinical consequences of phenylbutazone toxicosis: Before embarking on a phenylbutazone treatment protocol, it is recommended that the owner/handler/trainer of the horse should be carefully appraised of the clinical signs associated with toxicity. Scrutiny for early signs of toxicity leads to prompter initiation of appropriate actions, such as discontinuation of phenylbutazone treatment. In those cases for which a protracted period of phenylbutazone treatment is planned/anticipated, some pre-treatment baseline data may be obtained (examples might include measurement of the plasma albumin and creatinine concentrations). Clinical signs of phenylbutazone toxicity may arise within days or weeks following commencement of therapy. It is important to carefully ascertain if and when (and how much) phenylbutazone (and/or other NSAIDs) had been administered to a patient if signs consistent with toxicity are identified. Phenylbutazone-induced ulceration in the oral cavity (ulcerative glossitis/stomatitis) and lining of the esophagus (esophagitis) can result in difficulties (slowing) with prehension and mastication, ptyalism, and signs of discomfort during swallowing (neck stretching and groaning). Signs of ulcerative gastritis include loss of interest in food (inappetence, anorexia), altered interest in different food components, colic (recumbency following a meal), bruxism, ptyalism, and behavioral signs such as resentment of flank handling, ‘girthiness’, and exercise intolerance. It should be noted that most cases of ulcerative gastritis in adult horses do not result from NSAID use; NSAID use can lead to ulceration in both the squamous and glandular aspects of the gastric epithelial lining (glandular lesions are more common than squamous ulceration). A complete discussion regarding the specific clinical manifestations

349

of the equine gastric ulcer syndrome (EGUS) represents a weighty topic unto itself and is beyond the scope of this abstract. Phenylbutazone toxicity may also lead to inflammation and ulceration of the large intestinal lining. The development of ulcerative colitis may complicate NSAID treatments. Although phenylbutazone may cause generalized ulcerative colitis, the more common large intestinal clinical syndrome is the syndrome of right dorsal colitis (sometimes referred to as ‘’colon ulcers”). Unlike generalized colitis in which diarrhea, endotoxemia, dehydration, hypoproteinemia and systemic inflammation are prominent, right dorsal colitis does not so commonly lead to diarrhea or marked systemic inflammation. However, diarrhea or soft stools are reported for some cases of right dorsal colitis, along with signs of activated systemic inflammation (fever, tachycardia, endotoxemia, etc). More commonly, phenylbutazone-induced right dorsal colitis leads to anorexia/inappetance, lethargy, loss of bodily condition, colic (predisposing to ascending colon impaction), hypoproteinemia (especially hypoalbuminemia), and subcutaneous edema. Hypoproteinemia results from leakage of plasma proteins (especially albumin) into the lumen of the colon; this protein-losing colonopathy may be present in the absence of overt ulceration. Chronic cases of right dorsal colitis tend to be characterized by weight loss, hypoalbuminemia (with subcutaneous edema), soft stools, and recurrent bouts of colic. It should also be emphasized that phenylbutazone may predispose to common forms of colic (colon impaction and gas) by virtue of an effect on bowel motility (in the absence of ulceration and protein loss). Phenylbutazone toxicity can also lead to renal papillary necrosis, especially in the face of dehydration. Hemorrhage and ulceration in the bladder have also been recognized as complications of phenylbutazone treatment. Pathophysiological considerations: The parietal cells of gastric pits express the gastric H+/K+ exchanging ATPase (ATP4A) known as the gastric proton pump. The source of protons for the pump involves the catalyzed and spontaneous hydration of membrane permeable CO2 which generates of H2CO3 that serves as the source of H+ ions. The pump exports H+ in exchange for K+ which, in turn, is recycled back into the pit lumen via a K+ channels KCNE2/KCNQ1. Bicarbonate generated during the dissociation of H2CO3 is removed from the parietal cell into the interstitial fluid via Cl-/HCO3exchangers AE2/SLC26A7, thus alkalizing the plasma, which is responsible for the postprandial ‘alkaline tide’. Chloride entering the parietal cell by the exchange process provides for the concomitant secretion of Cl- via an apical Cl- channel thus forming luminal hydrochloric acid. Regulation of the parietal cell H+/K+ ATPase involves the actions of 1) the parasympathetic nervous system, which mediates both unconditioned reflexes of appetite and responses to food filling, via directly stimulating the parietal cell, inducing release of gastrin from antral G cells and histamine from subepithelial enterochromaffin cells (ECLs); 2) circulating gastrin which also stimulates the parietal cell directly and causes release of histamine from ECL cells. Gastrin release from G cells is stimulated both by neural action (muscarinic, gastrin releasing peptide neurotransmission) and by luminal amino acids and food buffering (increase in gastric pH due to food buffering the acid); and 3) paracrine ECL release of histamine which greatly amplifies stimulation of the parietal cell H+/K+ ATPase (~80%). Defense against gastric acidity involves the gastroduodenal mucosal barrier which is regulated by prostaglandins generated by the cyclooxygenase (COX) enzymes I and II which catalyze arachidonic acid released from acid-damaged mucosal cells. Different complements of prostanoids are generated by the two COX enzymes. Products of the constitutive COX I enzyme complex (HETES, lipoxins, prostaglandins) have potent antiinflammatory action that regulates the components of the gastroduodenal mucosal barrier by stimulating mucus release and secretion of HCO3- from the gastroduodenal epithelium. This so-called alkaline mucus barrier provides titration of H+s entering the surface mucus from luminal gastric acid, thereby increasing the pH next to the epithelium to near neutrality. A second facet of the COX I products causes increased blood flow to the upper gastrointestinal tract which supports a high metabolic rate of the epithelium and provides rapid removal of H+s crossing tight junctions between the epithelial cells which are neutralized by the blood buffer system. The third facet of the COX I products is the stimulation of restitution of the epithelium. The first stage of repair and protection against luminal content is the ability of the epithelium to dedifferentiate to a squamous morphology and cover the exposed submucosal tissue. This response expands the surface area of the epithelial cells adjacent to the site of epithelial loss by ~5-fold to cover the insult. Treatment of horses with phenylbutazone or any of the nonselective COX inhibitors (both COX I and II) compromises the integrity of the gastroduodenal barrier leading to ulcer formation. In contrast to regulating the barrier, the inducible COX II products (prostaglandins, prostanoids) are involved in pain sensation and the regulation of inflammation. Hence the development of COX II selective inhibitors which selectively spare the gastroduodenal barrier regulation by COX I products and provide analgesia. Renal disease resulting from non-selective NSAIDS (phenylbutazone) use in the horse can be manifested by a severe condition known as renal papillary necrosis. Prostaglandins generated from the COX enzyme

350

complexes do not significantly affect the overall renal blood flow or glomerular filtration rate in healthy animals. However, the use of non-selective NSAIDS and possibly COX II inhibitors (COX II is constitutively expressed in the kidney) can have an important localized action at the renal papilla, particularly during volume contraction. The vasculature of the papilla, which supports the collecting ducts, is much reduced in size compared to the medullary circulation and therefore the papilla is considered a mildly hypoxic tissue. Non-selective NSAID inhibitors can concentrate to approximately 10-fold in the renal papilla as compared to the plasma concentration and can prevent the vasodilatory action of renal prostaglandins (particularly PGE2, PGI2). These prostanoids counteract the vasoconstriction of volume/salt depletion by moderating the vasoconstrictor effects of angiotensin II, norepinephrine and vasopressin in the papillary vasculature. Thus, non-selective NSAID use in combination with dehydration or volume loss can lead to interstitial ischemia, swelling that further compromises the papillary circulation and necrosis that, at its worse, can be sloughed into the renal pelvis and block the opening to the ureter. Diagnosis of phenylbutazone toxicity: Phenylbutazone toxicity should be suspected when the aforementioned clinical signs are recognized in the context of phenylbutazone treatment. As noted above, toxicity is more likely when higher doses of the drug are administered for longer periods. However, some individual horses appear to be at higher risk and may develop toxicity within days of initiating a conservative dosing protocol. In most instances, abnormalities identified on hematology and plasma biochemistry include hypoproteinemia and hypoalbuminemia. Other abnormalities may be identified through routine blood and urine testing if co-morbid renal disease is present (isosthenuria, azotemia, etc) or if systemic inflammation, endotoxemia, and dehydration are present (leukocyte abnormalities, electrolyte disturbances, etc). Other diagnostic procedures that are helpful to substantiate phenylbutazone toxicosis include a careful oral cavity examination (via sedation using a speculum), gastroesophageal endoscopy (esophagitis, EGUS), and ultrasonographic imaging of the large intestine, especially the right dorsal colon (to demonstrate edema and thickening in the colon lining). Confident corroborative diagnosis of right dorsal colitis is challenging. The condition may be affirmed if ultrasonographic evidence of right dorsal colon thickening or edema is found (in appropriate cases and especially if hypoalbuminemia is present) but it should be noted that it is not possible to visualize the entirety of the wall of the equine right dorsal colon with ultrasonography. The urinary tract should also be further examined using ultrasonography of the kidneys, urinalysis, and â&#x20AC;&#x201C; if ulcerative cystitis is suspected â&#x20AC;&#x201C; bladder endoscopy. The most commonly reported laboratory abnormality associated with NSAID-induced renal papillary necrosis is isosthenuria. Other abnormalities may include azotemia and hematuria (grossly evident or occult). Ultrasonographic imaging of the kidneys may also reveal abnormalities that result from renal papillary necrosis. Uncommonly, severe colitis (with deep ulceration) may be complicated by the development of peritonitis. However, in most cases of right dorsal colitis, analysis of peritoneal fluid does not reveal any abnormalities. Severe generalized ulcerative colitis can be fatal. The use of phenylbutazone also increases the risk of cecal impaction, commonly encountered in hospitalized horses being managed for orthopedic conditions. Treatment of phenylbutazone toxicity: When phenylbutazone toxicity has been identified, further treatment with phenylbutazone (or other NSAID) should be curtailed. Both gastric lavage and the administration of mineral oil are recommended for instances of acute toxicosis (accidental or inadvertent overdose) in order to decrease drug absorption. Inhibition of gastric hydrochloric acid secretion with omeprazole should help to facilitate resolution of EGUS following discontinuation of phenylbutazone treatment. The therapeutic impact of omeprazole may be promoted by coadministration of sucralfate and/or misoprostol (synthetic prostaglandin analogue) in some cases. Effectiveness of orally-administered omeprazole monotherapy should be evaluated via follow-up endoscopy after 3-4 weeks; if endoscopic evidence of EGUS is still evident, treatment using a long-acting IM form of omeprazole may also be considered. Treatment of right dorsal colitis requires dietary adjustment using a ration characterized by a low fiber load. Horses affected with right dorsal colitis should usually not be fed roughage (hay/alfalfa) and may not tolerate pasture (roughage) grazing. Diet should be constructed using a complete pelleted ration (such as Purina Horse Chowâ&#x201E;˘) provided as small volume feedings and made available on a frequent basis throughout the day. If necessary, dietary energy content may be increased by adding corn oil to the daily ration. Other treatments that have been advocated as helpful for the management of right dorsal colitis include misoprostol, psyllium mucilloid, sucralfate, n-3 (omega-3) polyunsaturated fatty acid supplements, dietary supplements that contain combination of zinc and butyric acid, and metronidazole.

351

Treatment for right dorsal colitis may also necessitate management of colon impaction (adjusted feeding, stool softeners, analgesia, etc). It should be emphasized that treatment for right dorsal colitis is not predictably or uniformly effective; this condition often leads to long-term debilitation with fibrosis and cicatrization of the colonic lumen, thus further predisposing to obstruction and impaction. In those chronic cases with secondary luminal narrowing, surgical treatment may be attempted in order to facilitate by-pass of the narrowed right dorsal colon. In some instances, phenylbutazone treatment leads to a more extensive and generalized ulcerative colitis in which the clinical presentation is characterized by diarrhea, protein loss, dehydration, endotoxemia (systemic inflammation), colic, and fever. In those cases, treatment approaches usually include intravenous fluid therapy (crystalloid and colloid fluids), analgesia (emphasis on minimizing the use of NSAIDs), parenteral antibiosis (in some cases, if sepsis is suspected), and laminitis mitigation (address the feet, icing). Severe hypoproteinemia calls for plasma transfusion in many of these cases. Recommended approaches to minimize risks associated with phenylbutazone treatment: ¥ Avoid the use of phenylbutazone in horses and ponies with known risk factors for toxicosis. ¥ Avoid the use of phenylbutazone at higher doses or for long periods of time if the clinical circumstances allow for a more conservative approach. ¥ Avoid using phenylbutazone at the same time as other NSAIDs and/or corticosteroids. ¥ Client education – teach the owner/handler about the clinical signs of phenylbutazone toxicosis and emphasize that veterinary attention should be sought as early as possible if those signs arise (so as to optimize clinical outcomes). ¥ Consider using COX-1 sparing NSAIDs (such as firocoxib, meloxicam) for the long-term management of orthopedic conditions. ¥ Evaluate blood work for a patient in which phenylbutazone use is being planned (is there pre-existing evidence for hypoalbuminemia, renal disease, or hepatopathy?). ¥ Recommend that, where practical, the owner should monitor water consumption for horses being treated with phenylbutazone. ¥ Consider concurrent treatment with omeprazole (and/or sucralfate, misoprostol) when phenylbutazone treatment is being started. ¥ Monitor feces (frequency, quantity, and consistency) during phenylbutazone treatment. ¥ Monitor plasma (albumin) and urine (USG) during phenylbutazone treatment. References: Available upon request

352

Basic Science Review

Nicole Nichols, PhD and Matthew Hull, DVM University of Missouri - College of Veterinary Medicine Columbia, Missouri

353

354

Mineralocorticoids and a Clinical Review of Hydroadrenocorticism

Mineralocorticoids

Nicole Nichols, PhD - Department of Biomedical Sciences, Mizzou Matthew Hull, DVM - Resident in Small Animal Internal Medicine, Mizzou

Nicole Nichols, PhD – Department of Biomedical Sciences, Mizzou

MINERALOCORTICOIDS - OBJECTIVES

MINERALOCORTICOIDS - OUTLINE

Should be able to describe where the adrenal glands are located, and what regions and layers they consist of (e.g. cortex vs. medulla).

Gland structure and layers

Should be able to describe what controls aldosterone production and secretion. -role of renin -role of plasma Na+ -role of plasma K+

Functions of aldosterone

Aldosterone production and control of secretion

Aldosteronism and Addison’s Disease

Should be able to describe the functions of aldosterone. -actions on renal Na+, K+, and H+ -actions on intestinal Na+ and K+ Should be able to identify the causes, signs, symptoms, and treatment of Aldosteronism and Addison’s Disease.

The adrenal glands are located on top of the kidneys. Within each adrenal gland there is an outer cortex and an inner medulla.

355

Adrenal Cortex is divided into several layers

MINERALOCORTICOIDS - OUTLINE Gland structure and layers Aldosterone production and control of secretion Functions of aldosterone Aldosteronism and Addison’s Disease

Zona Glomerulosa produces mineralocorticoids • Steroid Hormones • Primarily aldosterone

Zona Glomerulosa produces mineralocorticoids • Steroid Hormones • Primarily aldosterone –Secretion regulated by kidney (reninangiotensin)

Control of Mineralocorticoid secretion • Angiotensin – formed from action of renin on angiotensinogen – Renin released in response to:

• Decreased blood pressure • Decreased [Na+] in distal tubular fluid • Sympathetic stimulation • Decreased blood volume

• Decreased plasma Na+ • Increased plasma K+

356

MINERALOCORTICOIDS - OUTLINE Gland structure and layers Aldosterone production and control of secretion

Functions of Aldosterone • Controls Na+ and K+ content in body directly and water indirectly.

Functions of aldosterone Aldosteronism and Addison’s Disease

– Increases renal absorption of Na+ – Increases renal H+ secretion – Increases renal K+ secretion – Increases ECF volume and blood pressure

Cellular Actions of Aldosterone

Renal Sodium Transport

Renal Na+ Reabsorption

Distal Tubule, Collecting Duct

Na+

Basolateral Membrane

Luminal Membrane

Na+

Cellular Actions of Aldosterone Renal Na+ Reabsorption

• Binding to Mineralocorticoid receptor (MR) • Stimulates transcription • Protein synthesis

Mechanism of Aldosterone Action Renal K+ Secretion

Distal Tubule, Collecting Duct

K+

• Increase basolateral Na+K+ATPase activity • Activate luminal Na+ (ENaC) channels

K+ 0 mV

357

-70 mV

-50 mV

Aldosterone and H+ Secretion

Mechanism of Aldosterone Action Renal K+ Secretion

• Distal tubule and collecting duct – Direct – Increased K+ Secretion

• Na+K+ ATPase • Increased luminal permeability to K+ • Increased negative luminal potential – (due to Na+ reabsorption)

• Hypokalemia => ion shifts • Increased H+ secretion

– Tubular transepithelial potential difference

• Can result in metabolic alkalosis

Control of Volume

Functions of Aldosterone • GI – Na+ absorption – K+ secretion

• Other – Sweat, salivary glands – K+ uptake – muscle, liver, adipose, nervous tissue

Intestinal Na+ Transport Intestinal Na+ Transport

• Colon – increases Na+ absorption • Stimulates Na+K+ ATPase • Increases luminal permeability to Na+ – Increases opening of ENaCs – Insertion of ENaCs into luminal membrane – Synthesis of ENaCs

358

Intestinal K+ Transport

Intestinal K+ Transport • Passive K+ secretion – Increases negative potential of lumen • Due primarily to Na+ absorption

• Active K+ secretion – Stimulates Na+K+ ATPase – Increases K+ channel activity (BK channels)

MINERALOCORTICOIDS - OUTLINE

Aldosteronism

Gland structure and layers Aldosterone production and control of secretion Functions of aldosterone Aldosteronism and Addison’s Disease

• Causes – Tumor of adrenal cortex (renin/angiotensin levels would be low) – Activation of renin/angiotensin system – due to: • • • •

Aldosteronism • Signs and Symptoms – – – – – –

Hypernatremia Hypokalemia Alkalosis Edema Increased ECF volume Hypertension

• Treatment

– Tumor removal – Administration of aldosterone antagonists (spironolactone)

359

Congestive heart failure Afferent arteriolar constriction Cirrhosis Conditions associated with massive edema

Addison’s Disease • Caused by:

– Autoimmune destruction of adrenal cortex

• Signs and Symptoms – – – – – – –

Hypoglycemia Hyperpigmentation Hyponatremia Hyperkalemia Decreased ECF volume Hypotension Acidosis

Addisonâ&#x20AC;&#x2122;s Disease â&#x20AC;˘ Treatment: â&#x20AC;&#x201C; Cortisol and Aldosterone

â&#x20AC;˘ Secondary Adrenal Insufficiency â&#x20AC;&#x201C; Caused by deficiency of ACTH â&#x20AC;&#x201C; Signs and Symptoms â&#x20AC;˘ Generally same as Addisonâ&#x20AC;&#x2122;s EXCEPT â&#x20AC;&#x201C; Aldosterone levels are normal and ACTH is low â&#x20AC;&#x201C; No hyperpigmentation

Â&#x192;Â&#x2013;Â&#x2013;Â&#x160;Â&#x2021;Â&#x2122; Â&#x2014;Â&#x17D;Â&#x17D;ÇĄ Â&#x2021;Â&#x2022;Â&#x2039;Â&#x2020;Â&#x2021;Â?Â&#x2013;ÇĄ Â?Â&#x192;Â&#x17D;Â&#x17D; Â?Â&#x2039;Â?Â&#x192;Â&#x17D; Â?Â&#x2013;Â&#x2021;Â&#x201D;Â?Â&#x192;Â&#x17D; Â&#x2021;Â&#x2020;Â&#x2039;Â&#x2026;Â&#x2039;Â?Â&#x2021;

PHYSICAL EXAM

SIGNALMENT AND HISTORY â&#x20AC;˘ 3 YO FS mixed breed dog â&#x20AC;˘ Presented for 2 day history of vomiting and lethargy â&#x20AC;˘ Received a large ham bone as a treat from the owners

â&#x20AC;˘ Following day began vomiting pieces of bone and

acting lethargic â&#x20AC;˘ Vomited twice day of presentation and became inappetant â&#x20AC;˘ Historically healthy dog otherwise

TRIAGE DIAGNOSTICS â&#x20AC;˘ PCV/TP: 65% / 9 g/dl â&#x20AC;˘ BG: 20 mg/dl â&#x20AC;˘ Lactate: 2.9 mmol/l â&#x20AC;˘ Blood pressure: could not obtain â&#x20AC;˘ Chem8: hyponatremia (132 mmol/L; 140-155

mmol/L), hyperkalemia (7.4 mmol; 3.5-5.0 mmol/L), azotemia (BUN/creatinine 61/3.9 mg/dL; 5-35/0.5-1.5 mg/dLČ&#x152;

360

â&#x20AC;˘ Dull, lethargic, became laterally recumbent

during initial physical exam â&#x20AC;˘ T â&#x20AC;&#x201C; 97.7 Pulse â&#x20AC;&#x201C; 160 with thready femoral pulses RR â&#x20AC;&#x201C; 24 â&#x20AC;˘ MM hyperemic, CRT >3 seconds â&#x20AC;˘ Remainder of physical exam unremarkable

Â&#x201D;Â&#x2018;Â&#x201E;Â&#x17D;Â&#x2021;Â? Â&#x17D;Â&#x2039;Â&#x2022;Â&#x2013;

â&#x20AC;˘ Â&#x2018;Â?Â&#x2039;Â&#x2013;Â&#x2039;Â?Â&#x2030;

Â&#x2039;Â&#x2C6;Â&#x2C6;Â&#x2021;Â&#x201D;Â&#x2021;Â?Â&#x2013;Â&#x2039;Â&#x192;Â&#x17D;Â&#x2022;ÇŤ

â&#x20AC;˘ Septic peritonitis

â&#x20AC;˘ Â&#x2021;Â&#x2013;Â&#x160;Â&#x192;Â&#x201D;Â&#x2030;Â&#x203A;Č&#x20AC;Â&#x2018;Â&#x201E;Â&#x2013;Â&#x2014;Â?Â&#x2020;Â&#x2021;Â&#x2020;

â&#x20AC;˘ Intestinal foreign

â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2021;Â&#x201D;Â?Â&#x192;Â&#x17D;Â&#x2021;Â?Â&#x2039;Â&#x192;

â&#x20AC;˘ Pancreatitis

Â?Â&#x2021;Â?Â&#x2013;Â&#x192;Â&#x2013;Â&#x2039;Â&#x2018;Â?

â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2018;Â&#x2DC;Â&#x2018;Â&#x17D;Â&#x2021;Â?Â&#x2039;Â&#x2026; Â&#x2022;Â&#x160;Â&#x2018;Â&#x2026;Â? â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2018;Â&#x2030;Â&#x17D;Â&#x203A;Â&#x2026;Â&#x2021;Â?Â&#x2039;Â&#x192;

â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2018;Â?Â&#x192;Â&#x2013;Â&#x201D;Â&#x2021;Â?Â&#x2039;Â&#x192; â&#x20AC;˘ Â&#x153;Â&#x2018;Â&#x2013;Â&#x2021;Â?Â&#x2039;Â&#x192;

body (potentially perforated)

â&#x20AC;˘ Acute kidney injury â&#x20AC;˘ Hypoadrenocorticism

â&#x20AC;˘ CBC Č&#x201A; Mild eosinophilia, otherwise WNL â&#x20AC;˘ PT/PTT - WNL

â&#x20AC;˘ UA Č&#x201A; USG â&#x20AC;&#x201C; 1.013 Č&#x201A; 15 WBC per HPF, 4+ bacteria

â&#x20AC;˘ Chemistry Panel Č&#x201A; Hyponatremia (130 mmol/L;

â&#x20AC;˘ Thoracic radiographs â&#x20AC;&#x201C; WNL

â&#x20AC;˘ Abdominal Radiographs â&#x20AC;&#x201C; marked hip

dysplasia, otherwise WNL

140-155 mmol/L) Č&#x201A; Hyperkalemia (8.5 mmol/L; 3.5-5.0 mmol/L) Č&#x201A; Hyperphosphatemia (12.2 mmol/L) Č&#x201A; Azotemia ( BUN/creatinine 53/3.3 mg/dL) Č&#x201A; Hypoalbuminemia (1.9 mg/dL; 2.8-4.0 mg/dL) Č&#x201A; Hypocholesterolemia (72 mg/dL; 132-350 mg/dL)

DIFFERENTIALS? â&#x20AC;˘ Vomiting Č&#x201A; GI vs. Non-GI? â&#x20AC;˘ Hypoglycemia Č&#x201A; Depletion of glycogen stores, liver failure, paraneoplastic (insulinoma), hypoadrenocorticism, artifact

â&#x20AC;˘ Azotemia Č&#x201A; Pre-renal, renal, or post-renal?

â&#x20AC;˘ Hypoalbumemia Č&#x201A; PLN, PLE, hepatic failure, third spacing, acute inflammatory response (acute phase protein)

â&#x20AC;˘ Â&#x2018;Â?Â&#x2039;Â&#x2013;Â&#x2039;Â?Â&#x2030;

â&#x20AC;˘ Â&#x2021;Â&#x2013;Â&#x160;Â&#x192;Â&#x201D;Â&#x2030;Â&#x203A;Č&#x20AC;Â&#x2018;Â&#x201E;Â&#x2013;Â&#x2014;Â?Â&#x2020;Â&#x2021;Â&#x2020;

Â?Â&#x2021;Â?Â&#x2013;Â&#x192;Â&#x2013;Â&#x2039;Â&#x2018;Â? â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2018;Â&#x2030;Â&#x17D;Â&#x203A;Â&#x2026;Â&#x2021;Â?Â&#x2039;Â&#x192; â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2018;Â&#x2013;Â&#x2021;Â?Â&#x2022;Â&#x2039;Â&#x2018;Â? â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2018;Â?Â&#x192;Â&#x2013;Â&#x201D;Â&#x2021;Â?Â&#x2039;Â&#x192; â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2021;Â&#x201D;Â?Â&#x192;Â&#x17D;Â&#x2021;Â?Â&#x2039;Â&#x192;

â&#x20AC;˘ Â&#x153;Â&#x2018;Â&#x2013;Â&#x2021;Â?Â&#x2039;Â&#x192;

â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2021;Â&#x201D;Â&#x2019;Â&#x160;Â&#x2018;Â&#x2022;Â&#x2019;Â&#x160;Â&#x192;Â&#x2013;Â&#x2021;Â?Â&#x2039;Â&#x192; â&#x20AC;˘ Â&#x2018;Â&#x2022;Â&#x2039;Â?Â&#x2018;Â&#x2019;Â&#x160;Â&#x2039;Â&#x17D;Â&#x2039;Â&#x192;

â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2018;Â&#x192;Â&#x17D;Â&#x201E;Â&#x2014;Â?Â&#x2039;Â?Â&#x2021;Â?Â&#x2039;Â&#x192;

â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2018;Â&#x2026;Â&#x160;Â&#x2018;Â&#x17D;Â&#x2021;Â&#x2022;Â&#x2013;Â&#x2021;Â&#x201D;Â&#x2018;Â&#x17D;Â&#x2021;Â?Â&#x2039;Â&#x192; â&#x20AC;˘

ÇŤ

â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2018;Â&#x192;Â&#x2020;Â&#x201D;Â&#x2021;Â?Â&#x2018;Â&#x2026;Â&#x2018;Â&#x201D;Â&#x2013;Â&#x2039;Â&#x2026;Â&#x2039;Â&#x2022;Â?

â&#x20AC;˘ Â&#x2021;Â?Â&#x192;Â&#x17D; Â&#x2C6;Â&#x192;Â&#x2039;Â&#x17D;Â&#x2014;Â&#x201D;Â&#x2021; Č&#x2039;Â&#x192;Â&#x2026;Â&#x2014;Â&#x2013;Â&#x2021; Â&#x2018;Â&#x201D; Â&#x2026;Â&#x160;Â&#x201D;Â&#x2018;Â?Â&#x2039;Â&#x2026;Č&#x152;

â&#x20AC;˘ Â&#x192;Â&#x201D;Â&#x192;Â&#x2022;Â&#x2039;Â&#x2013;Â&#x2039;Â&#x2026; Â&#x2039;Â?Â&#x2C6;Â&#x2021;Â&#x2026;Â&#x2013;Â&#x2039;Â&#x2018;Â? Č&#x2039;Â&#x2019;Â&#x2022;Â&#x2021;Â&#x2014;Â&#x2020;Â&#x2018;ÇŚ Â&#x2020;Â&#x2020;Â&#x2039;Â&#x2022;Â&#x2018;Â?Â&#x2039;Â&#x192;Â?

Â&#x2122;Â&#x160;Â&#x2039;Â&#x2019;Â&#x2122;Â&#x2018;Â&#x201D;Â? Â&#x2039;Â?Â&#x2C6;Â&#x2021;Â&#x2026;Â&#x2013;Â&#x2039;Â&#x2018;Â?Č&#x152; â&#x20AC;˘ Â&#x201D;Â&#x2039;Â?Â&#x192;Â&#x201D;Â&#x203A; Â&#x2018;Â&#x201E;Â&#x2022;Â&#x2013;Â&#x201D;Â&#x2014;Â&#x2026;Â&#x2013;Â&#x2039;Â&#x2018;Â?Č&#x20AC;Â&#x2014;Â&#x201D;Â&#x2018;Â&#x192;Â&#x201E;Â&#x2020;Â&#x2018;Â?Â&#x2021;Â? â&#x20AC;˘ Â&#x160;Â&#x201D;Â&#x2018;Â?Â&#x2039;Â&#x2026; Â&#x2021;Â&#x2C6;Â&#x2C6;Â&#x2014;Â&#x2022;Â&#x2039;Â&#x2018;Â? â&#x20AC;˘ Â&#x2018;Â?Â&#x2030;Â&#x2021;Â&#x2022;Â&#x2013;Â&#x2039;Â&#x2DC;Â&#x2021; Â&#x160;Â&#x2021;Â&#x192;Â&#x201D;Â&#x2013; Â&#x2C6;Â&#x192;Â&#x2039;Â&#x17D;Â&#x2014;Â&#x201D;Â&#x2021; â&#x20AC;˘ Â&#x2039;Â&#x192;Â&#x201E;Â&#x2021;Â&#x2013;Â&#x2021;Â&#x2022; Â&#x2021;Â&#x17D;Â&#x17D;Â&#x2039;Â&#x2013;Â&#x2014;Â&#x2022; â&#x20AC;˘

Â&#x2020;Â&#x2039;Â&#x2022;Â&#x2021;Â&#x192;Â&#x2022;Â&#x2021;

Â&#x2018;Â&#x2019; Â&#x2018;Â?Â&#x2019;Â&#x192;Â?Â&#x2039;Â&#x2018;Â? Â?Â&#x2039;Â? Â&#x2021;Â&#x2020;Ç¤ Í´Í˛ÍłÍś Â&#x2021;Â&#x2026;Ç˘Í´ÍťČ&#x2039;ÍśČ&#x152;ÇŁÍşÍşÇŚÍťÍˇÇĄ Textbook of Veterinary Internal MedicineÇĄ ÍşÂ&#x2013;Â&#x160; Â&#x2021;Â&#x2020;Ç¤ÇĄ Â&#x2019;Â&#x2019;Ç¤ ÍłÍşÍ´ÍˇČ&#x201A;ÍłÍşÍľÍľÇ¤

ÇŤ

HYPOADRENOCORTICISM

â&#x20AC;˘ Â&#x203A;Â&#x2019;Â&#x2018;Â&#x192;Â&#x2020;Â&#x201D;Â&#x2021;Â?Â&#x2018;Â&#x2026;Â&#x2018;Â&#x201D;Â&#x2013;Â&#x2039;Â&#x2026;Â&#x2039;Â&#x2022;Â?

â&#x20AC;˘ Â&#x2022;Â&#x2013;Â&#x2039;Â? Â&#x2022;Â&#x2014;Â&#x201E;Â?Â&#x2039;Â&#x2013;Â&#x2013;Â&#x2021;Â&#x2020; Č&#x201A; Â&#x192;Â&#x2022;Â&#x2021;Â&#x17D;Â&#x2039;Â?Â&#x2021; Â&#x2026;Â&#x2018;Â&#x201D;Â&#x2013;Â&#x2039;Â&#x2022;Â&#x2018;Â&#x17D; ÇŚ Î´Íł Â?Â?Â&#x2018;Â&#x17D;Č&#x20AC; Č&#x201A; Íł Â&#x160;Â&#x2018;Â&#x2014;Â&#x201D; Â&#x2019;Â&#x2018;Â&#x2022;Â&#x2013; ÇŚ Î´Íł Â?Â?Â&#x2018;Â&#x17D;Č&#x20AC;

Primary

Secondary H

Typical

Atypical

ACTH A

GLUCOCORTICOID GLUCOCORTICOID MINERALOCORTICOID

361

A A GLUCOCORTICOID

• Ȃ

• Ǧ ͵ • 85-90% of cortex must be destroyed before clinical signs manifest

Ȃ • • • • •

Ȃ Ǥ • ͷǦͳͲΨ Ȃ ǲ ǳ • • α

Ǥ ʹͲͳͶ ǢʹͻȋͶȌǣͺͺǦͻͷ

• ȋͳͲǦʹͲΨȌ Ȃ

• • Ȃ Mineralocorticoid production intact

Textbook of Veterinary Internal Medicineǡ ͺ Ǥǡ Ǥ ͳͺʹͷȂͳͺ͵͵Ǥ

• Ȃ Ȃ •

• • • Ǥ

362

• Ȁ Æ

Ȃ ǡ ǡ

• •

Textbook of Veterinary Internal Medicineǡ ͺ Ǥǡ Ǥ ͳͺʹͷȂͳͺ͵͵Ǥ

Ǥ ʹͲͲ͹ ǢͳͲͶȋ͵ȌǣͳͻͷǦʹͲͳ

Ȃ ǡ

ǡ ǡ Ȃ ͳͲ •

• Ȃ ǡ ǡ ǡ ǡ • Ȃ Ͷ Ǥ ʹͲͳͶ ǢʹͻȋͶȌǣͺͺǦͻͷ

• • Æ • • ΪȀ Æ

•

โ ข โ ข โ ข โ ข โ ข โ ข โ ข

ย ย ย ย ย ย

ย ย ย ย ย ย ย ย ย ย ย ศ ย ย ย ย ย ย ย ย วฃ อบอบฮจ ย ย อปอทฮจ ย ย ย ย ย ย ย ศ ย ย ย ย วฃ อบอทฮจ ย ย อปอทฮจ ย ย ย ย ย ย ย ศ ย ย ย ย ย ย ย ย ย ย ย ย ย วฃ อธอบฮจ ย ย อนอทฮจ ย ย ย ย ย ย ย วฃ อทอณฮจ ย ย อนอทฮจ ย ย ย ย ย ย ย ย ย วฃ อถอฒฮจ ย ย อทอฒฮจ ย ย ย ย ย ย ย ศ ย ย ย ย ย ย ย ย ย ย ย ย วฃ อตอทฮจ วฒEvery time we travel or have friends overโ ฆ.โ

โ ข โ ข โ ข โ ข โ ข

ศ ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ศ ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย โ Resolves with symptomatic care then relapses p when they y go g homeโ

โ ข โ ข โ ข โ ข โ ข โ ข โ ข โ ข โ ข โ ข

ย ย ย ศ ย ย ย ย ย ย ย ย วฃ อบอนฮจ ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย วฃ อบอดฮจ ย ย ย ย ย ย ย วฃ อธอปฮจ ย ย ย ย ย ย ย ย ย ย วฃ อถอดฮจ ย ย ย ย ศ ย ย ย ย ย ย ย ย วฃ อดอปฮจ ย ย ย ย ย ย ย ย ย ย วฃ อณอทฮจ ย ย อตอถฮจ ย ย ย ย ย ย ย ย ย ย วฃ อดอทฮจ ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย วฃ อดอดฮจ ย ย ย ย ย ศ ย ย ย ย ย ย ย ย ย ย ย ย วฃ อณอนฮจ ย ย ย ย ย ย ย ย ย ย ย ย วฃ อนฮจ

Dog with collapseโ ฆshockโ ฆan d bradycardiaโ ฆ.

วฏ วจ ศ ย ย ย ย ย ศ

โ ข ศ ย ย ย ย ย ย ย ย ย ย ย ย ศ Lack of stress leukogram in an ill animal (92%) ศ ย ย ย ย ย ย ย ย ย ย ย ศ อดอฒฮจศ ศ Lymphocytosis (10%)

โ ข ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ศ ย ย ย ย ย ย ย ย ย วก ย ย ย ย ย ย ย ย ย ย ย ย วก ย ย ย วฆย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย

ศ อดอนฮจศ

โ ข ย ย ย ย ย ย ย ย ย ย ย ย ย โ ข

ย ย ย ย ย ย ย ย ย ย ศ

ย ย ย ย ย ย ย ย โ ข ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย

ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย วค อดอฒอณอถ ย ย วขอดอปศ อถศ วฃอบอบวฆอปอท Textbook of Veterinary Internal Medicineวก อบย ย ย ย วควก ย ย วค อณอบอดอทศ อณอบอตอตวค

ย ย ย ย ย ย ย ย ย ย ย ย ย ย ฮฑ ย ย ย ย ย ย โ ข ย ย ย ย ย ย ย ย วซ

363

โ ข ย ย ย ย ย ย ย ย ย ย ย โ ข Gold standard for diagnosis โ ข ย ย ย ย ย ย ย ย ย ย อท ย ย ศ ย ย โ ข ย ย ย ย ย ย อดอทอฒ ย ย ศ ย ย ย โ ข อณ ย ย ศ ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย โ ข ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย วจ

โ ข Steroid interference in testing โ ข Dexamethasone generally will not interfere โ ข ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย โ ข ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย ย

• Correct hypovolemia Ȃ

• • Ȃ ǫ

•

• Rapid acting glucocorticoids

Ȃ First priority behind fluids! Ȃ ͲǤͳ Ȁ

• Ǧ

• Ǧ Ȃ GI protectants Ȃ ǡ ǡ ΪȀǦ Ȃ

Ȃ ȋͲǤͳǦͲǤʹ Ȁ Ȍ Ȃ ȋͲǤͷǦͳ Ȁ Ȍ

Ǥ ʹͲͳͶ ǢʹͻȋͶȌǣͺͺǦͻͷ Textbook of Veterinary Internal Medicineǡ ͺ Ǥǡ Ǥ ͳͺʹͷȂͳͺ͵͵Ǥ

• Ȁ Ȃ ͲǤʹǦͲǤʹͷ Ȁ daily Ȃ Stress (hospitalization, surgery, trauma, environment change) increases cortisol demand

• Ȃ Ȃ Ȃ ͲǤͲͳǦͲǤͲʹ Ȁ Ȁ • ȋͷͲΨ Ȍ

• ʹǦͳͲ Æ

Ȃ Ȃ ʹǤʹ Ȁ • ͳǦʹ Ǧ ǡ ͵Ǧ͸

Ȃ Monotherapy for “atypical”

and secondary hypoadrenocorticism

Ǥ ʹͲͳͶ ǢʹͻȋͶȌǣͺͺǦͻͷ Textbook of Veterinary Internal Medicineǡ ͺ Ǥǡ Ǥ ͳͺʹͷȂͳͺ͵͵Ǥ

Ǥ ʹͲͳͶ ǢʹͻȋͶȌǣͺͺǦͻͷǡ Textbook of Veterinary Internal Medicineǡ ͺ Ǥǡ Ǥ ͳͺʹͷȂͳͺ͵͵Ǥ

DOCP COST $$$ ̈́ͶͶ ʹͷ Ǣ ̈́͸Ͷͷ Ȁ ̈́ͳʹͲ ʹͷ Ǣ ̈́ ̈́ ̈́ͳǡ͹ͷͲ Ȁ

̈́ͳ͹͸ ʹͷ Ǣ ̈́ʹǡ͸ͲͲ Ȁ

364

•

͵͸ǦͻͲ

•

̈́ͶͲͲ ʹͷ Ǣ ̈́ͷǡͻͲͲ Ȁ

• ͳǦͳǤͷ Ȁ

• ͳͲΨ

at same dose interval

• Young animals more likely to

need more frequently or at higher dose

•

• ǡ

• Ȃ Ȃ Ȃ

Ǥ ʹͲͳͶ ǢʹͻȋͶȌǣͺͺǦͻͷ

365

blank page

366

Basic Science Review

Leah Cohn, PhD, DVM

Professor - Director of Graduate Studies Associate Department Chair, Veterinary Medicine and Surgery University of Missouri - College of Veterinary Medicine Columbia, Missouri

367

368

Cytauxzoonosis + Other Feline VBD Leah A. Cohn, DVM, PhD, DACVIM (SAIM) Professor, University of Missouri Cytauxzoon felis is a protozoal organism transmitted by ticks that causes potentially fatal illness in domestic cats. C. felis infects only domestic and wild cats, with no age or sex predisposition. Outdoor cats with tick exposure in endemic areas are at risk. Specific risk factors include urban-edge habitats and close proximity to wooded or unmanaged areas. It is common for multiple cats from the same household or neighborhood to become infected. C. felis infection has been reported in the south central and southeastern United States, but its range appears to be expanding north and east, corresponding to changes in distribution of the tick Amblyomma americanum. Most cases occur between March and September, with a peak incidence between March and June and a second wave of infections occurring in August and September. The natural host is thought to be the eastern bobcat (Lynx rufus rufus), which develops a mild or subclinical infection compared to the rapidly progressive and usually fatal disease seen in domestic cats. The organism is transmitted by A. americanum (suspected predominant vector) or Dermacentor variabilis ticks during feeding.Sporozoites released from the tick salivary glands infect macrophages. Asexual reproduction occurs within the host macrophage during the schizogenous phase, causing infected cells to grow to enormous size (â&#x2030;Ľ250 microns in diameter). These schizont-laden macrophages then occlude arterioles, venules, and capillaries, causing organ failure and clinical illness.When the schizonts rupture, merozoites are released to infect erythrocytes. Merozoites are minimally pathogenic but may cause initial hemolysis.Healthy, recovered cats can harbor erythrocyte piroplasms for years; they can transmit the pathogen to ticks during feeding. Domestic cats usually develop the disease, acute cytauxzoonosis (classic severe illness), about 2 weeks after the bit of an infected tick. Recovered cats (and a few that are acutely infected) harbor the pathogen without illness. These chronic carrier cats may be discovered to have incidental erythroparasitemia. Importantly, recovered domestic cats can act as reservoirs of infection.

369

Clinical signs of illness are acute and nonspecific and include acute onset of anorexia, lethargy, dyspnea, icterus, and pallor. Cats may be reported to seem as if in pain and often the third eyelid is elevated. Affected cats are usually febrile (103°F-107°F [39.4°C-41.7°C]), but hypothermia is seen in moribund cats. Icterus and/or pallor are common, as is elevation of the nictitans. Abdominal palpation reveals splenomegaly and hepatomegaly. Tachypnea, tachycardia, altered mentation, vocalization, seizures, and coma can be seen in the later stages of disease. Most cases exhibit a rapid course, with death occurring within 1 week of onset of signs if left untreated. Diagnosis is usually through blood smear examination when a clinical suspicion exists. Although most often diagnosed by microscopic identification of piroplasms in red blood cells (RBCs) on blood smear, illness can occur before appearance of piroplasms, and piroplasms may be seen in low number in chronic carriers. On the other hand, identification of schizontladen macrophage on the feathered edge of a blood smear or by cytology of fine-needle aspirates is pathognomonic for disease. Pleomorphic (round, oval, anaplasmoid, bipolar [binucleated], or rod-shaped) organisms in RBC are often seen in high numbers; the round and oval piroplasm forms are most common (0.8-2.2 microns in diameter; typical erythrocyte diameter ≈8 microns). Infected macrophages may occasionally be seen on the feathered edge and may be mistaken for platelet clumps at low power. If cytauxzoonosis is suspected but not immediately detected by examination of a blood smear, tissue aspirates of lymph node, liver, and spleen are indicated to identify infected macrophages. These cells range in size from 15-250 microns in diameter, typically have a large distinct nucleolus, and their cytoplasm is filled with numerous small (1-2 micron) basophilic particles (i.e., developing merozoites). CBC findings include pancytopenia (normocytic, normochromic, nonregenerative anemia, leukopenia, and thrombocytopenia), but monocytopenias or bicytopenias may occur. Serum biochemistry profile often demonstrates elevated liver enzymes (frequently lower than expected for the degree of hyperbilirubinemia), hyperbilirubinemia (mild to moderate), and hyperglycemia. Azotemia is rare. Urinalysis reveals bilirubinuria. Coagulation testing may be consistent with disseminated intravascular coagulation (DIC)

370

Imaging studies do not contribute directly to the diagnosis. Abdominal imaging: splenomegaly and hepatomegaly common. Thoracic radiographs: ± pleural effusion, pulmonary infiltrates Polymerase chain reaction (PCR) testing can confirm infection before appearance of schizonts or piroplasms but will also be positive in chronic carriers. This send-out test means result often come “too late” to change the course of treatment, even if only delayed by a few days. Necropsy with histopathology can confirm the diagnosis and is usually how cytauxzoonosis is first recognized in regions that were previously considered nonendemic. New treatments with antiprotozoal therapy have proved effective along with supportive care in this disease, which was previously considered universally fatal. Because the disease progression is very rapid, specific treatment should be instituted immediately in suspected cases. Minimal stress and handling is recommended; early placement of nasogastric tube may facilitate administration of medication and nutrition with less stress. Crystalloid fluids are provided to correct dehydration, restore intravascular volume, and maintain perfusion. In anemic animals, oxygen delivery to tissues must be restored with a transfusion of whole blood (20 mL/kg IV administered over 4 hours) or packed RBCs (20 mL/kg IV administered over 4 hours)). Some clinicians treat/prevent DIC with heparin 100-300 IU/kg SQ q 8h or 18 IU/kg/h IV constant-rate infusion (CRI). Animals with respiratory compromise may require supplemental oxygen or thoracocentesis if pleural effusion is identified. Analgesia is recommended. The author prefers Buprenorphine 0.01-0.02 mg/kg SQ, IM, or IV q 6-12h prn over meloxicam. While the later can reduce fever, this is not always a good thing in my experience. Placement of a feeding tube eases administration of drugs and provision of nutritional support. Antiprotozoal therapy should be started immediately. The preferred option is Atovaquone 15 mg/kg PO q 8h administered with a fatty meal for 10 days combined with azithromycin 10 mg/kg PO q 24h for 10 days; this treatment is associated with survival rates of approximately 65%. The treatment is facilitated by placement of a feeding tube. Atovaquone is very viscous and therefore difficult to accurately dose. Fill the dosing syringe a few minutes before administration to allow the drug to settle in order to be sure that the entire dose is present (the thick drug can coat the sides of the syringe causing inadvertent underdosage). There are a few alternative antimalarials. One such drug is Imidocarb dipropionate (Imizol) 3-5 mg/kg IM then repeated in 7-14 days. Pretreat with atropine 0.04 mg/kg SQ to minimize

371

cholinergic side effects. Survival with imidocarb treatment ≈25% although some claim higher success rates. Another option is Diminazene aceturate (Ganaseg) 2 mg/kg IM repeated in 7 days. A small case series showed this to be a promising treatment, but it is not approved by the U.S. Food and Drug Administration (FDA) or available in the United States. Recently, the combination antmilarial Coartem was about 45% efficacious in a prospective study of naturally infected cats. The advantage of coartem is ease of administration for this pill with a course of treatment completed in three days. Doxycycline 5 mg/kg PO q 12-24h × 14 days may be considered as treatment for co-infection with other tick-borne pathogens. Without aggressive treatment, 95% of cats will die within a few days. Even with early diagnosis and atovaquone/azithromycin treatment, many cats will die within a day or two. Survivors may have a difficult course with severe clinical disease that lasts for 5-7 days before finally improving. The likelihood of survival varies regionally. In some areas, incidental discovery of erythroparasitemia is common (indicating that the cat survived acute infection), and in other areas, survival is rare even with aggressive treatment. All clinical, hematologic, and biochemical abnormalities resolve in 4-6 weeks. Chronic infection does not appear to be associated with decreased life span. Recurrent severe infections appear extremely rare in surviving animals, suggesting some degree of protective immunity, but re-infection is possible. Hypothermia, icterus, severe anemia, and seizures warrant a poor prognosis, and euthanasia should be discussed as a possibility for the most severely affected cats. In endemic areas, an effective acaricides and tick repellent should be used to prevent exposure to ticks. Both the Seresto collar (Bayer) and Revolution Plus (Zoetis) have been demonstrated to help prevent infection. The author has personally treated many cats that recived other types of ectoparasites control. Because infections have occurred despite acaricides treatment, keeping cats indoors in endemic areas is strongly recommended. Other Vector-Borne Infections in Cats Blood-sucking arthropods are common causes of disease in pets both directly (eg, itching, anemia) and indirectly (eg, pathogen transmission). Mosquitoes, flies, fleas, and ticks are each capable of transmitting a variety of microbes including parasitic worms, protozoa, viruses, and bacteria. Cats are susceptible to a number of vector-borne diseases (VBD). These include heartworm infection, hemotropic mycoplasmosis, leishmaniasis, anaplasmosis, ehrlichiosis, babesiosis, rickettsiosis, hepatozoonosis, bartonellosis, cytauxzoonosis, Q fever, tularemia, plague, trypanosomiasis, and borreliosis.

372

Of course, not all vector transmitted microbes are potential pathogens, and not all potential pathogens cause disease. Many microbes are well-adapted to a reservoir host and only rarely cause disease in the reservoir species (eg, Bartonella henselae rarely causes obvious/overt disease in cats). Disease may be more likely when the potential pathogen infects a nonreservoir host (eg, Cytauxzoon felis causes death in the vast majority of infected domestic cats but often only a mild, short lived illness in the reservoir host, the bobcat). The mechanism of pathogen transmission varies depending on the pathogenic organism and vector. Ticks feed for extended periods of time in a single site. During the long period of feeding, they not only “suck” blood from the host, but they also “spit” into the host. The salivary fluid inoculated during tick feeding includes anticoagulants, analgesics and antipruritics, immunomodulatory molecules, and pathogens. Many pathogens must be “activated” to move from the tick’s mid-gut to the salivary gland prior to inoculation. Although this movement may take some time, it is unwise to assume that there is always a risk-free period to mechanically remove ticks prior to pathogen transmission. Fleas can regurgitate during feeding, but flea feces (frass) is the more important cause of pathogen transmission. Pruritic animals scratch the dermis thereby helping to inoculate the frass on the skin surface. Hemotropic mycoplasma Hemoplasmas (haemotropic Mycoplasma spp) are gram negative, epicellular bacteria lacking a cell wall. While there are several species that infect cats, the most pathogenic is M. haemofelis (formerly known as Hemobartonella felis). Found world-wide, fleas are thought to be the predominant arthropod vector although ticks, flies, or other such arthropods might also transmit infection (mosquitoes do not seem to be an important vector). Blood transfusion, fighting behavior, and perinatal transmission are alternative routes of transmission. In addition to these risk factors, retroviral infections FeLV and FIV predispose cats to infection, or at least to illness from infection. M. haemofelis generally causes an acute hemolytic anemia that can be life-threatening or mild. Cats that survive this acute stage often become subclinical carriers with mild anemia, or may have a waxing and waning course of chronic, recurrent anemia. Clinical signs are all related to hemolytic anemia and can include lethargy, weakness, anorexia, fever, pallor, icterus, splenomegaly, lympadenomegaly, and physiologic heart murmur. Typically anemia is regenerative (variable severity) and is Coomb’s positive. Chemistry abnormalities often include hyperglobulinemia, hyperbilirubinemia, and increased liver enzymes. The most common point-of-care diagnostic test is a simple blood smear, but both false negative and false positives occur. The organism is epicellular not intracellular, and cell attachment is mediated by calcium. Blood collected in EDTA allows the organisms to “fall off” the cells when calcium is

373

chelated thus causing a false negative. It is best to make fresh smears from blood not treated with anticoagulants. Even then, the parasite load is variable and absence of visible parasites does not rule out infection. Stain precipitate, Howell-Jolly bodies, siderotic inclusions, basophilic stippling, or other parasites can be confused for M. haemofelis organisms microscopically. PCR is very sensitive, and all blood donors should be screened by PCR before use rather than relying solely on blood smear review. The species M. hemominutum is actually more prevalent than M. haemofelis, but it is less pathogenic. This, and several other hemotropic mycoplasma, are only likely to cause illness in cats with compromised immune systems. Regardless of the specific pathogen, treatment is doxycycline (or minocycline) as a first line at 5-10 mg/kg BID for 28 days. Fluoroquinolones are an alternative. Generally, it is assumed that treatment improves illness but does not eliminate infection entirely. Infection has apparently been cleared by using first a course of tetracycline followed by a further 2 weeks treatment with fluoroquinolone. Supportive care including blood transfusion plus/minus a short course of prednisolone to suppress immune mediated destructions of RBC may also be required. Prognosis for clinical recovery is fair to good with such treatment, but such recovered cats should not be used as blood donors. And of course, prognosis also depends on co-morbid conditions; a cat that developed Mycoplasma related hemolysis because it was immunosuppressed/ill is less likely to have a good outcome than would be an otherwise healthy cat. Bartonellosis Bartonella are gram negative intracellular bacteria. There are >38 different species in this genera, and they infect many, many species of animals. Those that are best recognized in cats are B. henselae, B. koehlerae, B. clarridgeiae, B. bovis, B. quintana, B. vinsonii sub. Berkoff. Cats are the established reservoir host for B. henselae and B. koehlerae, and likely for several other species as well. As for other VBD, the reservoir host is often well adapted to the pathogen. Cats with exposure to fleas, thought to be the likely primary means of transmission for Bartonella, are very commonly infected (up to 98% in several prevalence studies from warmer climates such as Brazil, and 0% in Norway, with ~30% on average for temperate climes). However, overt clinical disease is rare in the species. Experimental infection of cats with B. henselae can cause transient mild fever, lethargy, lympadenomegaly, and rarely CNS signs, reproductive failure, or anemia. Naturally infected cats have a higher leukocyte count and globulin than uninfected cats. Occasionally, myocarditis, endocarditis, or pyogranulomatous inflammation follow infection. And yet, most infected cats remain well. The greatest import for B. henselae is as a zoonotic pathogen rather than as a cause of feline disease.

374

Humans with bartonellosis can develop a variety of illnesses ranging from subclinical to self-limiting to fatal in outcome. The most common illness in immunocompetent people is â&#x20AC;&#x153;Cat Scratch Diseaseâ&#x20AC;? (CSD). CSD results in variable mild fever and regional painful lympadenomegaly that usually resolves over many months. Antimicrobial therapy does not speed recover, and organism is usually not viable leading to the proposal that an immunologic reaction to the pathogen causes disease. Bacillary angiomatosis is a more severe and often fatal form of illness related to B. henselae infection of immunocompromised people. A large variety of other manifestations of human infection has been documented including cancer and neurologic disease. Children are more likely to develop CSD than are adults, perhaps because they are more likely to play with cats in a way that leads to scratches. Kittens are more likely to be bacteremic than adult cats, and more likely to scratch and bite as well, meaning that kittens pose a greater risk of zoonosis than adult cats. Infection can be transmitted by dogs as well as cats, and human infection does not have to be preceded by a known scratch or bite. It is believed it is not the cat that causes infection directly, but rather the cat acts as a reservoir for fleas and pathogen, and that a scratch/bit inoculates flea frass mechanically. Options for diagnostic testing include serology, specialized blood culture with cell lysis or tissue culture, and a variety of PCR tests, including PCR testing after enrichment on a specialized media. All of these methods have major pitfalls, but enrichment PCR is likely the most sensitive and specific option (culture is considered the most specific method, but sensitivity is poor). Overt illness in cats due to bartonellosis is uncommon, but if no other explanation exists for clinical signs such as fever, testing may be worthwhile despite the pitfalls. In such a cat, treatment would be warranted if there is a positive PCR or a positive culture. Diagnostic testing is necessary for potential blood donor cats, with negative PCR as a minimal standard for donor use and negative serology, PCR, and culture as the optimal standard suggested in the ACVIM Consensus Statement on screening blood donors (JVIM 30:15-35, 2016). No known treatment clears the pathogen. For the rare cat with clinical illness believed to be due to bartonellosis, a combination of a fluoroquinolone and doxycycline for 28 days is often suggested. Due to rapid resistance, use of azithromycin is not recommended. Such cats should still not be used as blood donors. Healthy cats that are rejected as blood donors because of a positive test result do not require antimicrobial treatment simply because of the positive test result. Sometimes, pet owners come to veterinarians with a request to test a healthy cat because of a diagnosis of CSD in a person in the home, or because there is an immunosuppressed

375

person. Although there is some disagreement among experts, this is generally NOT warranted. A cat that tests negative may still have harbored the pathogen, and a cat that tests positive will often self-resolve high level bacteremia as the kitten/cat ages. As mentioned, there are a multitude of pitfalls of testing that can lead to false positive and negative tests, and the cat itself is not usually the reason for infection as much as are the cat’s fleas. Furthermore, there is no treatment known to eliminate the pathogen. Instead of testing, the owner should be educated regarding preventive measures for future exposure. This includes religious use of ectoparasites control products to eliminate fleas (and ideally keeping the cat indoors), avoiding rough play, trimming the cat’s nails or using SoftPaws nail covers, and washing any scratches or bites well with soap and water. For immunocompromised persons, it may be wise to adopt cats rather than kittens as they are less likely to 1) scratch/bite, and 2) have a high level bacteremia. Also, choosing cats from sources such as a breeder or a friend where flea exposure is less likely than from an animal shelter cat may be wise. I should point out that this opinion is not held uniformly, and a few experts would recommend testing and even antimicrobial administration for healthy, positive cats that live with immunocompromised persons or very young children. Often, veterinarians know far more about the zoonotic risk of disease than do physicians, and it may be helpful to ask that the owner’s physician get in touch either with you, with a veterinarian with expertise in infectious disease, or with a physician specialist in infectious disease. Q fever Caused by Coxiella burnetii, Q fever is more of an issue for livestock (especially small ruminants) and humans than for cats, although cats are certainly susceptible to infection. The bacterium is found at high concentrations in the birth products of infected ruminants as well as in the urine, feces, and milk. It is also found in the dust from pastures contaminated with these fluids. It is a VBD because it can be transmitted by tick bite, especially the brown dog tick Rhipicephalus sanguineus. Non-vector transmission seems to be more common, however, as a source of human exposure to this zoonotic pathogen. Farm cats are likely exposed via shed placenta or aborted fetuses, but infection of cats from non-rural areas are also reported. Most infected cats remain healthy. Lethargy, fever, an anorexia can occur. In intact queens, abortion and still births are common. Pregnancy loss and parturition are important routes of zoonotic transmission to humans because of the exposure to the products of conception from a pet cat that experiences abortion (always wear gloves and protective clothing when handling cats or dogs experiencing abortion…don’t forget brucellosis is also zoonotic), or when trying to resuscitate weak kittens at parturition. Culture of the bacteria is possible but not advised unless biosafety level 3 facilities are available. Diagnosis in cats is usually based on a fourfold increase

376

in IgG on paired serum samples, but there can be cross reaction with Bartonella genera organisms. Treatment for cats is not well described. Tetracyclines, fluoroquinolones, and chloramphenicol are the treatments of choice for Q fever in humans and are likely effective for cats. Prevention of Vector Borne Disease Very few vector borne infections have available vaccines for disease prevention. For most VBD, the best prevention is prevention of ectoparasites. Even in the case of heartworms this may be true, with increased emphasis on prevention of mosquito bite in addition to simply killing the immature parasite once transmitted. Flea and tick prevention should be used on all cats year round. Not all products have equal efficacy on all arthropod vectors, and even those effective for ticks do not possess equal efficacy against all species of ticks. For example, the Lone Star Tick (Amblyomma americanum) is especially difficult to kill. A variety of considerations should apply when recommending these products to pet owners, including: Safety for use on cats (many dog products are very toxic to cats) Spectrum of efficacy Repellency Speed of Kill Owner Compliance ▪ Ease of application ▪ Frequency of application ▪ Aesthetic considerations ▪ Cost • Efficacy throughout treatment interval • • • • •

At present, there is no oral product available for use in cats. Collars and topical products are readily available but must be applied correctly and at the correct time. Please see https://capcvet.org/parasite-product-applications for product details.

377

Vectors and Diseases They Transmit Lone Star ticks

Brown dog ticks

American Dog ticks

Black legged ticks

Soft bodied ticks

Granulocytic ehrlichiosis

Canine monocytic ehrlichiosis

Rocky Mountain spotted fever

Lyme disease

Tick borne relapsing fever

Q fever

Cyclic thrombocytopenia

Bartonellosis

Granulocytic anaplasmosis

Tularemia

Rocky Mountain spotted fever

Tularemia

Cytauxzoonosis

Babesiosis

Panola Mountain ehrlichiosis

Hepatozoonosis (H. canis)

Human monocytic ehrlichiosis

Tularemia

Fleas Biting insects

Hemotropic Mycoplasma

Gulf coast ticks

Chagas disease

Bartonellosis

Hepatozoonosis (H. americanum)

Leishmaniosis

Plague

Suggested Readings Alvarez-Fernandez a, et al. Bartonella infections in cats and dogs including zoonotic aspects. Parasit Vectors. December 2018;11(1):624. Bergmann M, et al. Risk factors of different hemoplasma species infections in cats. BMC Vet Res. February 13(1):52. 2017. Brianti E, et al. Efficacy of a slow-release imidacloprid (10%)/flumethrin (4.5%) collar for the prevention of canine leishmaniosis. Parasit Vectors. 14;7:327. 2014. Brunt J, et al. American Association of Feline Practitioners 2006 Panel report on diagnosis, treatment, and prevention of Bartonella spp. infections Journal of Feline Medicine and Surgery 8: 213-226, 2006. Clarke CF, et al. Emergence of autochthonous cutaneous leishmaniasis in northeaster Texas and Southeastern Oklahoma. The American Journal of Tropical Medicien and Hygine. 88:157-161. 2013. Drummond MR, et al. Improvement of Bartonella henselae DNA Detection in Cat Blood Samples by Combining Molecular and Culture Methods. J Clin Microbiol. 56(5).2018. Grazia G. Effectiveness of a 10% imidacloprid/4.5% flumethrin polymer matrix collar in reducing the risk of Bartonella spp. infection in privately owned cats. Parasit Vectors. 2019 February; 12(1):69. LA Cohn, et al.: Efficacy of atovaquone and azithromycin or imidocarb dipropionate in cats with acute cytauxzoonosis. J Vet Intern Med. 25:55-60 2011 21143646 ME Schreeg, et al.: Pharmacogenomics of Cytauxzoon felis cytochrome b: implications for atovaquone and azithromycin therapy in domestic cats with cytauxzoonosis. J Clin Microbiol. 51:3066-3069 2013 23784135

Minard HM, et al. Pathology in practice. Journal of the American Veterinary Medical Association. 251:57-59, 2017. MK Sherrill, et al.: Cytauxzoonosis: diagnosis and treatment of an emerging disease. J Feline Medi Surg. 17:940-948 2015

Pennisi, Maria Grazia, and Maria Flaminia Persichetti. Feline leishmaniosis: Is the cat a small dog?. Veterinary parasitology 251: 131-137. 2018. Shaprio AJ, et al. Q Fever (Coxiella burnetii) Knowledge and Attitudes of Australian Cat Breeders and Their Husbandry Practices. Zoonoses Public Health. 64(4):252-261. 2017. Sykes, Jane E. Feline hemotropic mycoplasmas. Journal of veterinary emergency and critical care 20): 62-69. 2010. Tasker, S. Haemotropic mycoplasmas: what's their real significance in cats? Journal of feline medicine and surgery 12: 369-381.2010. Trainor, K. E., et al. Eight cases of feline cutaneous leishmaniasis in Texas. Veterinary pathology 47: 1076-1081. 2010. Weingart C, et al. Infection with haemoplasma species in 22 cats with anaemia. J Feline Med Surg. 18(2):12936. 2016.

378

Basic Science Review

Alison LaCarruba, DVM, ABVP (Equine)

Associate Teaching Professor University of Missouri - College of Veterinary Medicine Columbia, Missouri

379

380

Equine Endocrine Dysfunction Pituitary Pars Intermedia Dysfunction Pituitary Adenoma Intermediate lobe Disease of older horses, typically >15 years, slowly progressive Hyperplasia, Hypertrophy Loss of dopaminergic inhibition Oxidative damage Hyperplasia/hypertrophy of melantropes – PI MSH/Beta endorphin related peptides – induce a 6 X increase in steroidogenic properties of ACTH Clinical Signs Hypertrichosis (Hirsuitism), 55-80% of cases Long, thick, curly, failure to shed, shed and grow winter coat early Patchy alopecia, represents progressed disease Polyuria/Polydypsia - Up to 76% of horses Unclear pathogenesis, hyperglycemia Cortisol, ADH, Increased GFR due to increased glucocorticoids? Combination of factors Weight loss – Early clinical sign +/- obese or normal Pendulous abdomen, Muscle loss/weakness Swayback Unclear role of POMC hormones on energy metabolism and muscle wasting Lethargy, Decreased responsiveness, Increased B-END Hyperhidrosis, Dermatitis, Infertility, Neurological Impairment (Uncommon) Diagnosis No perfect test, Preliminary lab data is helpful - CBC, Chem, UA Typically normal +/- Anemia, neutrophilia, lymphopenia, hyperglycemia, glucosuria Baseline ACTH Recheck multiple times, seasonality, not a perfect test, moderate to advanced signs TRH Stimulation: ACTH – More sensitive Horses with equivocal signs, best to diagnose earlier onset disease Dexamethasone suppression test Not frequently used, not helpful for early onset

381

Insulin Resistance Supportive Endogenous ACTH False positives Stress, travel, etc Seasonality Fall values are increased in all horses Different reference range False negatives Other clinical signs noted but normal ACTH No perfect test! Insulin Resistance - Supportive POMC peptides - Unable to measure Dexamethasone Suppression Test- Supportive Baseline Cortisol not helpful Baseline ACTH EDTA plasma purple-top. Mix blood and keep cold. Separate plasma from cells within 4 hours after collection. After centrifugation transfer plasma sample to a vial (plastic) suitable for frozen storage and shipping. Refrigerate if shipping same day, freeze if shipping the following day or later. The sample should be received cold. Baseline ACTH- Medication should be given as normal if monitoring treatment effect. (Pergolide). Excitement, exercise, and/or severe illness can elevate ACTH concentration. ACTH is very unstable in whole blood and serum samples. Do NOT send whole blood. TRH Stimulation -TRH is presently available as a compounded product through Wedgewood Pharmacy. The Wedgewood Pharmacy product is called “Protirelin”. Collect a Pre (or baseline) blood specimen into a purple-top (EDTA) tube. Inject 1 mg TRH intravenously (IV) for horses >250 kg; inject 0.5 mg TRH IV for horses and ponies <250 kg. Collect an additional EDTA blood specimen at exactly 10 minutes Feed grass hay only 12 hours prior to testing Do not perform within 24 hours after oral sugar testSide effects – transient coughing, Flehmen response, yawning, testing in fall not recommended

382

Treatment Pergolide - Dopaminergic agonist, 2 mcg/kg once daily, adjust to affect Not to exceed 4 mcg/kg daily Pergolide Side effects -most common - decreased appetite, weight loss, lethargy, behavioral changes, aggression, nervousness, increased activity As a dopamine receptor agonist, and synthetic ergot derivative, it may interfere with lactation.

Equine Metabolic Syndrome A collection of risk factors predisposing to endocrinopathic laminitis Insulin dysregulation is a consistent and important part of the syndrome Generalized/regional adiposity, weight loss resistance, weight gain Altered adipokine concentrations EMS defined as insulin dysregulation along with one or more risk factors. A combination of resting hyperinsulinemia, postprandial hyperinsulinemia, or insulin resistance (IR) - A central feature of EMS ID can occur in some horses with PPID, or other

systemic illness Causes - genetic and environmental Breed predispositions Ponies, Andalusians, Gaited horses, Morgans, Miniature horses “Easy Keepers” Require fewer calories, Enhanced appetite - Evolutionary adaptation Glucocorticoids, Adipokines, stress, chronic inflammation, high glycemic diet Genetics and Environment collide, not all fat is created equal . . . Adipocytes secrete adipokines – similar to cortisol Activation cortisone to cortisol via 11β-hydroxysteroid dehydrogenase type 1 enzyme Insulin resistance, vasospasticity, laminitis Clinical Signs OBESITY – Generalized or Regional adipocity -“Cresty” neck, supraorbital fat LAMINITIS - Insulin dysregulation Infertility

383

How to diagnose Insulin dysregulation Two dynamic tests Oral Sugar Test (OST) Preferred-more complete Digestion and absorption of sugars Incretin hormone response Secretion of insulin Insulin Tolerance Test (ITT) Sole focus is tissue insulin sensitivity Oral Sugar Test Advantages Readily available (corn syrup), ease of administration, assessment of insulin responsiveness to ingested sugars. Disadvantages Horses must be fasted 3-12 hours Low “within horse” repeatability Variability of results Differences in gastric/intestinal transit times, digestion/absorption of sugars, incretin responses and insulin secretion Helpful when monitoring over time, major shifts in insulin concentrations (>30uU/ml) are significant, test performance improved by administering 0.45 ml corn syrup/kg instead of 0.15 mg/kg. Fast 3-12 hours. Administer corn syrup orally and collect blood at 60 and 90 minutes. Measure insulin and glucose >45 uU/ml positive Insulin Tolerance Test Advantages Does not require pre-test fasting Blood glucose measured with glucometer so preliminary results ready on site. Disadvantages Cost of insulin, risk of clinical hypoglycemia Have IV dextrose ready to administer Fed – pasture or hay only. DO NOT FAST Collect blood – time O Administer 0.10 IU/kg regular insulin Collect blood 30 min, measure glucose, feed meal immediately after sample <50% decrease in blood glucose concentration from baseline consistent with IR Resting Insulin A single sample collected in the fed horse - hay or pasture, NOT grain (4 hours)

384

Detect resting hyperinsulinemia Can be used to asses the insulinemic effect and laminitis risk of the forage component of the diet <20uU/ml –non-diagnostic – Dynamic testing 20-50uU/ml – ID suspect –Dynamic testing >50 uU/ml – insulin dysregulation – manage Two Step Approach to the

Diagnosis of ID Testing has not shown to cause laminitis, but if owner is concerned . . . Measure resting insulin to screen for hyperinsulinemia at rest If resting insulin normal, move on to dynamic testing Blood glucose – important. Diabetes mellitus is uncommon but could occur Additional Testing Adiponectin – Not available in USA -Concentrations <3.2 ug/ml are consistent with metabolic abnormalities in adipose tissue and increased risk of laminitis Leptin – (Available) Higher leptin associated with increase adiposity and metabolic derangement. More associated with obesity than ID Triglycerides – Hypertriglyceridemia associated with ID and obesity. Predictive of laminitis risk in ponies. Dietary Management - Obese EMS Horse Restrict or eliminate grazing, Hay with low NSC - Feed 1.5% BW Weight tape/scale every 30 days - Lower to 1.2% BW Dry lot, avoid stress, soak hay in cold water for 60 min - Decrease water soluble CHO Slow feeder nets, feed multiple small meals, ration balancer High dose levothyroxine Weight loss resistant horses Obesity with acute lamintis 48 mg/500kg horse Gradual weaning with weight loss over 3-6 months Metformin Persistent hyperinsulinemia 30mg/kg 30 min prior to feeding up to 3 times daily Recheck insulin

385

Diseases of the Equine Thyroid Hypothyroidism – true adult hypothyroidism is RARE Thyroid hormone deficiency Deficient thyroid activity Disruption of HPT axis Primary Iodine disturbances Neoplasia Thyroiditis (Hashimoto) Thyroid agenesis Secondary Pituitary or hypothalamic dysfunction (PPID, other diseases) Tertiary Defect in TH use NOT IN HORSES Not life threatening Clinical symptoms Obesity, alopecia, infertility, exercise intolerance, possibly anhydrosis, concurrent disease, Iodine deficiency Diagnosis -Single T3/T4 unreliable, TSH stimulation, TRH Stimulation PPID Combination of Clinical signs Consistent low T3/T4 No response to TRH Rule out other diseases Hypothyroidism Treatment Iodine – areas of low soil iodine (Great Lakes Region) Levothyroxine Hyperthyroidism UNCOMMON Physiologic states – Pregnancy, late term fetus, newborn Neoplasia – adenocarcinoma, adenomatous thyroid tumor Clinical symptoms – Tachycardia, tachypnea, polyphagia, behavior changes, heat intolerance, aged >20 yrs Parathyroid Dysfunction Primary hyperparathyroidism - Rare Parathyroid adenoma or hyperplasia – no neg feedback Blood levels - Increased PTH and Ca, Low phosphorous

386

Loss of cortical bone, osteodystrophia fibrosa Lameness, enlarged facial bones, poor body condition, osseous proliferation maxilla and mandible, loose cheek teeth. Secondary Hyperparathyroidism Excessive PTH secretion in response to chronic hypocalcemia Hyperphosphatemia or BOTH - Big head disease Nutritional - Most common form, Multiple animals 3:1 phosphorous:Ca or higher, Diets low in Ca High in phosphorous OR high in oxalates binds dietary Ca Clinical Signs Enlarged facial bones, respiratory noise, lameness Dx: PTH, urinary excretion of Ca, urinary excretion of phosphorous Tx: Ca supplementation Pseudohyperparathyroidism Paraneoplastic disease Documented in humans and animals Tumors secrete PTH-like substances Hypercalcemia Lymphosarcoma, squamous cell carcinoma, mesothelioma, few others. Hypoparathyroidism â&#x20AC;&#x201C; RARE, Hypocalcemia, Hyperphosphatemia Decreased PTH Primary disease - Synthesis/secretion PTH Secondary disease - Not described in horses More commonly Hypocalcemia 2Â° to. . Cantharidin toxicosis Lactation tetany Extreme exercise Acute renal failure Endotoxemia Adrenal Dysfunction Hyperadrenocorticism Excessive cortisol production PPID is major cause

387

Adrenal tumors – rare Adrenocortical adenoma Adrenal insufficiency Adrenal exhaustion “Turn out syndrome” Lack of aldosterone mineralcorticoid Lack of ACTH response Intense training Extensive exogenous corticosteroid use Critical care/sepsis Foals Diabetes Mellitus RARE Type II - IR/hypoinsulinemia Differenttials EMS, PPID Type I - Insulin dependent, Very unusual Diabetes Insipidus Neurogenic ADH deficiency Nephrogenic

Inability to react to ADH Familial, drug induced Produce large amounts of dilute urine, followed by polydipsia

388

Soft Skills

389

390

Soft Skills

Brian Patrick, DVM

Senior Technical Services Veterinarian Bayer Animal Health Columbia, Illinois

391

392

11/26/2019

Building Trust with Clients

Today’s Objectives  Identify specific communication tools to increase confidence in client interactions  Commit to using 2 tools in practice

Our Plan…  Essential communication tools • • • • •

Power of Nonverbal Questioning skills: History taking / building trust Active Listening Empathy Ask‐Tell‐Ask

 Translation to practice

393

11/26/2019

Why does communication matter?

Reason 1 Reason 2

Five reasons communication is key in veterinary practice Reason 3 Reason 4 Reason 5

Reason 1

 History taking

Diagnostic Accuracy

 Up to 85% of data necessary to accurately obtain a diagnosis comes from the history  History alone has significantly higher correlation to accurate diagnosis than any other diagnostic modality alone (PE, basic tests, imaging)  Missed diagnoses are most often (56%) the result of breakdowns related to history taking (Paley et al 2011, Schattner 2012, Kaplan et al., 1995, Marvel et al., 1999; Peterson et al., 1992; Rabinowitz et al., 2004, Stewart et al., 1986; Jagosh et al 2011; Singh et al 2013)

394

11/26/2019

Barriers How long does it take a doctor to interrupt a patient?

Diagnostic Accuracy  18 seconds (Beckman & Frankel 1984)  23 seconds (Marvel et al 1999)  12 seconds (Rhoads et al 2001)

Only 1 of 52 interrupted patients returned to or completed their concerns

Patients have an average of 3 concerns per office visit

Reason 2

Improved Adherence

Adherence in vet med

 Range between 23‐65%  Problems cited: • information Communication • Trust not established • Lack of follow‐up • Client opinion not considered (AAHA 2009; AAHA 2003; Adams, V 2002)

Quality of Patient Care Reason 3 • Ineffective team communication is the root cause of 66% of reported medical errors • Patient care suffers

Communication

JCAHO Root Causes & Percentages for Sentinel Events ‐ All Categories (Jan 1995−Dec 2005); TeamSTEPPS, Agency for Healthcare Research and Quality and Dept of Defense, 2008

395

11/26/2019

Formal Complaints Liability Reason 4 Up to 82% of formal complaints and malpractice cases are because     

Clients felt misinformed Informed consent not obtained Client reported feeling disrespected Felt like opinion did not matter Procedure not explained

Communication

Satisfaction Client/Team Reason 5

Client’s perception = Your reality

Communication

Domains of Communication Content

396

• “What” we say

Nonverbal

• “How” we say it

Perception

• Our internal thoughts and feelings

11/26/2019

Building Client Trust What’s your welcoming ritual? • 78% patients want their doctors to shake hands • 93% want to be greeted by name • 96% want Dr. to intro by name (Makoul, 2007)

Building Trust: Essential Tools Nonverbal awareness Open-ended Questions /Funneling

AskTell-Ask

Active Listening/ Empathy

Why non-verbal awareness?

 Up to 80% of communication is nonverbal  Awareness takes no extra time

 With mixed messages,

nonverbal message is more accurate of feelings and will predict behavior

397

11/26/2019

What is nonverbal communication? Definition All of our behavior signals exclusive of verbal content

Categories  Kinesics  Proxemics  Paralanguage  Autonomic changes

Categories: Kinesics  Facial expressions  Body tension  Gestures  Touch  Posture

Categories: Proxemics  Spatial relationships

398

 Barriers

 Interpersonal distance

 Exam table

 Vertical height distance

 Medical record

 Angle of facing

 The pet

11/26/2019

Categories: Paralanguage  Voice tone  Rate  Rhythm  Volume  Emphasis

Categories: Autonomic changes  Flushing  Blanching  Tearing  Sweating  Changes in breathing  Changes in pupil size  Involuntary swallowing

Client nonverbal messages… What assumptions do we make?

399

11/26/2019

Nonverbal messages… Colleagues

Client nonverbal messages… What assumptions do we make

Exercise! Non-verbal communication OBSERVE CAREFULLY Content

Nonverbal

400

• “What” is said • “How” it is said

11/26/2019

Movie Time

Observe and take notes… 1. Clip #1 and #2, words exchanged are identical 

Notice nonverbal behavior



What is the impact on the client?

2. In clip #3 and #4, the client sends a mixed message. 

How does the veterinarian address the mixed message?



What is the impact on the client? 1

Building Trust: Essential Tools Nonverbal awareness

Open-ended Questions /Funneling

Ask-TellAsk

Active Listening/ Empathy

401

11/26/2019

Asking Questions

History-taking…getting the story

Video Case Study Let’s observe initial history taking TASK: Take notes

What I liked

What I’d do differently

Data to share with veterinarian

Client history-taking: What’s your style?

     

402

“Tell me what happened..” “Go on…” “How are you holding up?” “What are your thoughts?” “What were you hoping…” “How’s the family doing with this?”

11/26/2019

Open-Ended Questions

 Encourage clients to tell their story

Without interrupting!

Photograph used with permission from University of Wisconsin School of Veterinary Medicine

Skill drill: Open-ended Questions How would you open up these closed questions?

“Is he eating?” “Are you walking him?” “Did you give her the medication?” “Is there blood in the vomit?” “Have you made a decision yet?”

Open-Ended Questions How are we doing as a profession? Research findings: Data gathering from clients •During 300 visits: •13 closed‐ended questions •2 open‐ended questions •No open‐ended questions in 25% of appointments (Shaw, Adams, Bonnett, Roter, 2004)

403

11/26/2019

Funnel it…

Closed-ended Clarify.. Refine.. Fill gaps

Exercise Let’s again observe our veterinary technician

What I liked

What I’d do differently

Additional data to share with veterinarian

Building Trust: Essential Tools Nonverbal awareness Open-ended Questions /Funneling

AskTell-Ask

Active Listening/ Empathy

404

11/26/2019

Essential tool: Active Listening Definition Stating back (in your own words) the content or feelings behind the message

Active Listening “So, you’re saying….you’re frustrated..” “It sounds like…this worked out better than we originally thought..” “You’re wondering if.…this surgery is…” “I hear you saying….you’re not sure you’re ready to consider euthanasia…”

Building Trust: Essential Tools Nonverbal awareness Open-ended Questions /Funneling

AskTell-Ask

Active Listening/ Empathy

405

11/26/2019

Empathy  Being seen  Being heard  Being accepted

“Brutus is an important part of the family”

“I can see you are worried”

Empathy is the

single most important skill in building client relationships and leading to positive outcomes Yet…

Empathy

statements expressed in

only 7% of veterinary appointments (Shaw, Adams, Bonnett, Roter, 2004)

Word choice… Convey Empathy  “Sounds rough…”  “I worry about those things too…”  “I can see you how hard this decision is for you…”  “This was not what you were expecting…”  “You gave him a great life…”

406

11/26/2019

Building Trust: Essential Tools Nonverbal awareness Open-ended Questions /Funneling

Ask-Tell-Ask

Active Listening/ Empathy

EDUCATION TOOL

ASK-TELL-ASK

ASK

Ask what the client already knows

TELL

Customize your message to the level of client understanding

ASK

Ask client to repeat key elements (Kemp, Floyd, McCord‐Duncan, & Lang, 2008)

WHY USE ASK-TELL-ASK?  Half of people leave the doctor’s office confused • • • •

Diagnosis Recommendations Home care instructions Follow‐up IOM, Health Literacy (2004); Harvard School of Public Health: Health Literacy

407

11/26/2019

Ask

ASK – Tell – Ask what the client already knows

“You mentioned your previous dog had hip surgery. What is your understanding of this surgery?”

“What do you know about diabetes?”

Ask -

TELL

- Ask

“So, you’ve had some difficult experiences with surgery in the past…”

Ask -

TELL

- Ask

Use concrete instructions “Dissolve the medication and squirt it into her mouth with this syringe.”

“Mix a teaspoon of the powder (demonstrate with a teaspoon) into Buddy’s food in the morning.”

408

11/26/2019

Ask – Tell – ASK “Close the loop”

ASK

TELL

“I’ve given you lots of information that’s hard for anyone to remember. I know you’ll be talking to … about this. Can we go over what you’ll be telling him to be sure we’re all on the same page?”

EXERCISE: Ask – Tell – ASK  Select a topic you’re comfortable talking about  Select 3 key instructive points on this topic  In pairs, practice ASK-TELL-ASK (Begin by ASKING their knowledge of this topic)  TELL them the 3 points. Be clear & brief.  ASK them to review the 3 points  Switch roles

Essential Tools for Practice     

409

Non‐verbal communication Open‐ended questions Active listening Express empathy Ask‐Tell‐Ask

11/26/2019

Benefits of Effective Communication

Next stepsâ&#x20AC;Ś What 1 or 2 tools will you try in your practice?

410

11/26/2019

Making a CLEAR recommendation

Module Objectives  Identify specific recommendations that practice teams make routinely  Incorporate “why” in addition to “what” into recommendations  Develop language for our most common recommendations  Demonstrate a method to better assess client understanding

Now with your partner… • Make at least one recommendation • Trade roles • Ask your partner if you explained “why” they should follow this recommendation

411

11/26/2019

Simon Sinek ‐ Why

Let’s try it again… • Think about “why” you are making the recommendation • Think of “why” in words you would use with the client • Try it out with your partner • Ask your partner if it is clear “why” they should follow your recommendation

412

11/26/2019

Client Education Why do clients visit your practice? What do they pay you for? • Information • Peace of mind

Client Education What do clients care about? • Long life • Comfortable • Sometimes $$

We must have perspective…

413

11/26/2019

On the Same Page What do you clients care about? What do they understand?

On the Same Page • Are we talking about what matters most to our clients? • Or are we talking about what we think matters most?

Veterinarians value exams….

Q34. Please indicate the extent to which you agree or disagree with each of the following statements using the scale provided. Base: All respondents (n=401)

Bayer Veterinary Care Usage Study

414

11/26/2019

How much are clients hearing/understanding?

Bayer Veterinary Care Usage Study

Client Education

This is what I know

This is what I can communicate to others

This is how much other people understand from my communication

Making recommendations Is your recommendation explicit and specific to that pet? “We recommend year round prevention. See the ladies up front…”

“If you decide to do this, the estimate is good for a year. Call the front desk to set it up.”

“We should get his teeth cleaned soon.”

(Schwartzberg 2007)

415

11/26/2019

Making recommendations Is your recommendation explicit and specific to that pet? “We should start heartworm prevention today. We recommend….”

“We need to see Max back to recheck his ears in two weeks. Let’s get that set up right now.”

“We need to get those teeth cleaned in the next three months.”

(Schwartzberg 2007)

How much are clients hearing/understanding?

Bayer Veterinary Care Usage Study

Making recommendations  Avoid jargon  Speak at their level  Limit to 3 key points  PAUSE

(Schwartzberg 2007)

416

11/26/2019

Making recommendations  Use visuals  Keep it slow  Chunk and check

(Schwartzberg 2007)

Things that make recommendations challenging…  Characteristics of the recommendation • level of complexity • length or duration • client lifestyle/client‐animal bond • cost, accessibility

Assess confidence in the recommendation “How confident are you that you’ll be able to give this medication to Toby three times a day?”

417

11/26/2019

Assess confidence in the recommendation Ask the client to quantify confidence

“On a scale from 0 to 10 - with 0 being not confident at all to 10 being very confident - How confident are you that you will be able to give this medication 3 times a day to Toby?”

Recommendation Create an action plan  Write - understandable language  Personalize practice handouts  Follow-up  Reminders  Heartworm test  Chronic medication refills  Annual exams

Recommendation follow-up What worked well

What I would do differently

What clear recommendations were made?

418

11/26/2019

Clear Recommendations • Clients must know “why” • Deliver information clear and simple language – Chunk and check

• Utilize core skills • Assess their understanding – Scale of 1 to 10

Recommendation Checklist Remember: It always starts with the “WHY”!

 Was my recommendation clear/specific?  Did I assess understanding/confidence?  Did we agree to a simple plan?  Is the follow-up plan in place?

What are your “take away” points from today? What questions do you have?

419

420

11/26/2019

Empathy: What’s the big deal?

Our Plan…  Benefits of conveying empathy in practice  Your practice experiences, and how we can improve on them?  Skill practice using video clips  Practice words of empathy to try with clients…

What is Empathy?

421

11/26/2019

Empathy  Being seen  Being heard  Being accepted

“Brutus is an important part of the family”

“I can see you are worried”

Why all members of the team should use empathy?     

Makes a connection Builds trust Validates feelings Decreases anxiety Increases adherence

Clients feel understood

What gets in our way?  Our worries: • Taking too much time • Will open a “can of worms”  Not comfortable for me  Our belief “it’s not my job”

422

11/26/2019

3 steps for communicating empathy 1) Focus ….look and listen (suspend your judgment) 2) What do you imagine your client is experiencing? 3) Start there -communicate your understanding

“Mrs. Jones, it sounds like you’re really worried about..”

Empathy is the

single most important skill in building client relationships and leading to positive outcomes Yet…

Empathy

statements expressed in

only 7% of veterinary appointments (Shaw, Adams, Bonnett, Roter, 2004)

What has your experience been so far trying empathy out with your clients?

423

11/26/2019

“This was not what you were expecting…”

Tips and word choice…

“Sounds rough...”

“I worry about those things too…”

“Lots of people feel that way…it’s totally understandable”

Part 1: Focus – look and listen What do you imagine this client is experiencing?

If you wanted to talk to this client about dental, heartworm, medication use, grooming at home, etc. how ready are they to listen? 0 Not ready

10 Very ready

Part 2: Now that you’ve imagined what the client might be feeling, what will you say?

Write down the exact words

You may want to start with “It sounds like you are feeling ….”

424

11/26/2019

Empathy…takes many forms… Restate Reflect

• “Sounds like you’re concerned that Sadie…”

Normalize

• “Anyone would feel scared…”

Selfdisclosure

• “I stopped feeling bad about using a crate when I realized she liked it for a safe-haven.”

Partnership

• “I think WE can figure this out together…”

Responding to Client Empathic Opportunities Emotions ‐ Feeling – Concerns “I’m worried Jasper has cancer like my other dog did.” YOU: “I could see how you’d be worried since you’ve been through it before.”

Progress – Positive talk “I bring him for long walks now that the weather’s nice.” YOU: “That’s terrific and sounds enjoyable for you both.”

Challenge – Difficulties “I can’t give her pills. She spits them out or I end up fighting with her.”

YOU: “I hear you. That’s frustrating, for sure.”

Things to avoid DON’T  Interrupt  Interrogate  Change the subject  Discount the clients’ feelings  Get “hooked” into an angry emotional exchange

425

(Salem, R. 2003)

11/26/2019

Caveats  Empathy does NOT mean “I understand” or “I know how you feel” – You don’t!! Try saying: “I imagine that feels…”

 You don’t have to agree with the emotion  You don’t always get it right! Remember: Empathy SAVES time and prevents problems

Seize the Opportunity Insert Empathy here

Mrs. Johnson, I can see that….

Next steps… Look for opportunities for empathy and practice! Notice what effects it has on the client (and you!).

426

11/26/2019

Elephant in the Room Money talk in the Veterinarian‐Client Relationship

Module Objectives By the end of the module learners will:  Identify emotional or behavioral responses to financial issues  Describe 3 factors which may influence discussion of financial issues with clients  Identify 2 skills to effectively communicate about financial issues with clients  Choose 2 communication skills to practice discussing financial issues with your clients

Module overview  Rationale  Premises  Demonstration video and exercise  Skills training: A review  Demonstration video and final exercise

427

11/26/2019

Rationale:

Why a module on money?

 Veterinarians nor clients do an effective job  Impacts your relationship with clients  Client’s lack of financial resources is a common source of non-adherence  Financial impact on the practice  Written treatment plans are infrequently used in practice  It won’t go away by ignoring it (Alexander, Casalino, & Meltzer, 2003; Hardee, Platt & Kasper, 2005; Coe, Adams & Bonnett, 2009; Bonvicini & Perlin, 2010)

“The Elephant”  Tremendous strides in veterinary medicine  Care for elderly animals more costly  Strong human-animal bond yet few people budget for unexpected vet care (Smith, 1994; Brown & Silverman, 1999; Lue et al, 2008)

“The Elephant”  “Sticker shock” of veterinary care  Vet care has been artificially low for years (Smith, 1994; Brown & Silverman, 1999)

428

11/26/2019

Premise 1

Discussing money CAN be difficult “Money is our secret both in private and in public.”  Messages about money are passed down through generations  Money may arouse high emotions  Explicit money discussions are uncommon in veterinary visits (Coe, Adams & Bonnet, 2009; Orman 1997)

Veterinarian Experience

Issues at stake are important, yet outcomes are uncertain

Identity implicated

Challenge of discussing money

Money paired with perception of caring

429

Emotions aroused

11/26/2019

Client Experience Issues at stake are important, yet outcomes are uncertain

Identity implicated

Challenge of discussing money

Money paired with perception of caring

Emotions aroused

Veterinary discussions of money • Only 29% of appointments include discussion of cost • Written treatment plan provided in 14% of appointments

(Coe, J Am Vet Med Assoc, 2009)

Premise 2: Pet owners want to know benefit for their pet

• Care of animal precedence over $$ aspects • Expect veterinarians to initiate conversation regarding cost • Money discussion related to outcome for pet including well-being and health (Coe, J Am Vet Med Assoc, 2007)

430

11/26/2019

Simon Sinek ‐ Why

Now with your partner… • Make at least one recommendation • Trade roles • Ask your partner if you explained “why” they should follow this recommendation

431

11/26/2019

Client Education Why do clients visit your practice? What do they pay you for? • Information • Peace of mind

Client Education What do clients care about? • Long life • Comfortable • Sometimes $$

Premise 3: Money linked to identity Veterinarian

Client

Touches on both feeling and identity issues for clients and vets.

Touches on feelings and values

432

11/26/2019

Premise 4: Meaning we give to money arouses strong emotions  Meaning is different for each person  Differences in experience account for differences in perception

Money decisions: Human animal bond

This is an animal I am less attached to. I am not willing to spend resources on him.

This is an animal I am very attached to. I am willing to spend inordinate resources on her.

CLIENT – “I’M THE LOSER”

433

11/26/2019

Premise 5: Assumptions hinder money discussions We make assumptions based on our own:

Assumptions about being judged I don’t dare bring up my financial concerns. She’ll think I don’t care about Miles’.

I shouldn’t raise the issue of cost unless he brings it up. He’s going to think all I care about is the money if I bring up the cost of these services.

Assumptions about others He can certainly afford to pay for his dog’s care.

434

She’s so young. Her services should cost me less.

11/26/2019

Assumption: Attachment & commitment Those kids are really attached to that dog. I’m sure they will want to go ahead with the surgery.

The last thing I’m going to do is pay for surgery on a dog that is destroying our house! He’s going to think I’m a terrible mother.

The responsibility is not yours alone

 Clear practice policies are helpful  Responsibility can be designated or shared

HOWEVER: The designated team member(s) who discuss $$ with clients need to be trained and supported

Exercise  Work in teams of 4 with 2 assigned to be “veterinarian” and 2 assigned to be “client”  Review video case vet- client interaction  From your assigned role as the vet or client, list any assumptions made about the “other”  List reasons for your assumptions  Discuss potential implications for vet-client communication Workbook pg. 21

435

11/26/2019

Skill Training: A Review

 Acknowledge the Issue  Discover Meaning  Opportunities to Show Compassion  Boundaries - Adjust  Extend the System

Acknowledge Be aware of your own cues and clues Understand your own financial triggers.

Be aware if/which money issues will be a personal “hook” for you.

Acknowledge Be aware of your own cues and clues Understand your clients’ feelings are not necessarily directed at you, but more at the general situation Lagoni, Butler & Hetts, 1994

436

11/26/2019

Acknowledge Be aware of your client’s cues and clues “You’ve mentioned financial concerns before. The treatment we’ve discussed is certainly costly to undertake. Should we talk some more about that before we make any decisions?”

Acknowledge Be aware of your client’s cues and clues “You’re being so quiet over there. Is there something we should talk about?”

What is Empathy?

437

11/26/2019

Empathy is the

single most important skill in building client relationships and leading to positive outcomes Yet…

Empathy

statements expressed in

only 7% of veterinary appointments (Shaw, Adams, Bonnett, Roter, 2004)

Empathy conveys  I see you  I hear you  I understand you  I accept you Particularly when responding to emotions

What has your experience been so far trying empathy out with your clients?

438

11/26/2019

Acknowledge: Accept the challenge  Acknowledging issues does not mean that you have to fix it  Acknowledging issues does not need to take extra time  Have words ready

Acknowledge: Accept the challenge “That’s so “You’re right. Medical care is expensive.” costly. We’re so used to

insurance we tend to forget that sometimes.” “I can see where you are

“I can’t afford this!” coming from. It can be hard to fit unexpected expenses into our budgets. Especially when we’re forced to balance our finances against our animals’ health.”

Skill Training: A Review

 Acknowledge the Issue  Discover Meaning  Opportunities to Show Compassion  Boundaries - Adjust  Extend the System

439

11/26/2019

Discover Meaning for the Client  If you don’t know, ask “ Would you like to discuss what this treatment means financially?” “Are these costs what you expected?”  Check client understanding of how their money and effort may benefit their pet  Include a written treatment plan (Coe, Adams & Bonnett, 2007, 2009; Klingborg & Klingborg, 2007)

Discover Meaning: Your Own Sympathetic “I understand how painful it is not to be able to pay for something you want so badly.”

Irritated “Pets are a luxury. Why would you take on an animal without accepting the cost of the care it involves?”

Photograph from Argus Institute, CSU

Discover Meaning

Find common ground  Recognize value of both perspectives

 Express desire to

problem-solve together

440

11/26/2019

Skill Training: A Review

 Acknowledge the Issue  Discover Meaning  Opportunities to Show Compassion  Boundaries - Adjust  Extend the System

Opportunities for Compassion Listen for opportunities for client compassion

Verbalize or demonstrate empathic responses

What are some opportunities to show compassion to clients when discussing finances?

441

11/26/2019

Opportunities for Compassion  Timing and context “Mr. Fisher, it’s clear you care about Toby and unsure whether you are ready to commit to the cost of this eye surgery.”

 Feelings, thoughts “It can be uncomfortable when balancing the care you want with the amount of money you have to spend. These decisions are hard for everyone.”

Exercise: Words of ADOBE • Work in pairs and review portion of “Teddy” scenario • Develop your response together.

Workbook pg 28

Practice…Practice • Reflect on each of the client statements in your workbook. • Using your tools, how might you respond? • Write the exact words you would say.

“I can’t afford this!!!!” Workbook pg 29-30

442

11/26/2019

Adjust boundaries Content

Roles

Time

Practice Policies

Adjust boundaries: Time  Allow for time to talk about monetary issues • Educate client about short and long-term costs • Provide treatment options and associated costs • Emphasize potential benefits and value for their pet.

Invest time now

“Pay now or pay later”

Adjust boundaries: Clarify expectations

“It’s important you let me know what you’re thinking…”

443

11/26/2019

Adjust Boundaries

Open boundaries around content  Listen for financial issues raised by the client.

Acknowledge and include them in your discussion.

 Use the client’s words whenever possible:

“I hear you when you say you’re feeling financially very ‘tight’ right now and want to spend your money wisely.”

Adjust Boundaries

Close boundaries around content  Repetitive concerns about costs: Redirect content “I know you’d like it if this treatment were less expensive. It might be helpful to talk about some less expensive options for Molly’s care.”

 Client that won’t be redirected: Clarify boundaries “I’m happy to talk about options to reduce expenses for Jasper’s care. Our fees have been set with a lot of thought and we feel they are reasonable.”

Adjust Boundaries

Develop clear practice policies  Establish clear billing and payment policies

 Agree to be consistent  Clarify who discusses client monetary issues

 Ensure practice team is

trained for fee discussions

444

11/26/2019

Exercise: ADOBE practice  Review video interaction.  Pick up from where the video leaves off. How should the conversation proceed?  In teams of three, practice the ADOBE skills. Assign who will be the “vet”, “client”, and “observer.”  Discuss what “worked” in each interaction  Discuss ways to improve the interaction. Workbook pg. 39

Skill Training: A Review

 Acknowledge the Issue  Discover Meaning  Opportunities to Show Compassion  Boundaries - Adjust  Extend the System

Extend the system

Is additional help needed?  Referral to less expensive services  Pet insurance  Payment plan/Care Credit  Have printed resource information on hand

445

11/26/2019

Extend the system

What are possible resources?  Family members or friends  Other veterinary medicine professionals  Community and other support services

Summary: The Response

 Acknowledge the Issue  Discover Meaning  Opportunities to Show Compassion

 Boundaries - Adjust  Extend the System

Next steps… What 2-3 tools/skills will you try out in practice?

446

Soft Skills

Rebecca A. Johnson, PhD, RN, FAAN, FNAP Professor Emerita - University of Missouri Columbia, MO

447

448

The Client-Animal-Veterinarian Bond: Imperative for Health Rebecca A. Johnson, PhD, RN, FAAN, FNAP Professor Emerita University of Missouri Columbia, MO Rapid changes in society and heavy reliance on ever emerging technologies make special challenges for helping professions such as veterinary medicine. In this presentation, the importance of human-animal and human-human bond that drives veterinary medical practice will be discussed. In particular, the presentation will address challenges associated with maintaining professional distance yet engaging effectively while treating animals that may be the lifeblood, or livelihood of clients. Some of these challenges include need for empathy, use of open communication strategies, importance of follow-through, ways to build client loyalty to the practice, and ways to recognize and address compassion fatigue. The importance of clear verbal and non-verbal communication will be discussed, as will ways to project to clients, ways in which practices embrace the human-animal and human-human bond.

449

450

Expanding Small Animal Practice: TigerPlace, A Pet Encouraging Retirement Residence Rebecca A. Johnson, PhD, RN, FAAN, FNAP Professor Emerita University of Missouri Columbia, MO While the human animal bond has always been a foundation for small animal veterinary medicine, given the rapidly expanding population of adults over age 65, the bond is perhaps more central than ever to the success of small animal practices serving older clients. Pets remain as important to older adults as they are to younger counterparts, perhaps more important. One focus of the field of successful aging hinges on the concept of aging-in-place. This concept has taken many forms but essentially means that older adults need not move from their homes as they need more assistance and eventually care. This presentation will use the TigerPlace aging-in-place retirement residence as a case study to demonstrate ways in which small animal veterinary practices can expand their remit from the clinic to the community to assist this growing population of pet owners/clients.

451

452

Soft Skills

Zoe Agnew-Svoboda

PAWS Place Program Coordinator - Rose Brooks Center Kansas City, Missouri

453

454

455

POWER AND CONTROL WHEEL

456

❖ Has anyone ever threatened harm or harmed your pet? ❖ Has anyone ever threatened harm or harmed you? ❖ Do you feel unsafe at home? If you answered “yes” to any of these questions Talk to a staff member about Rose Brooks Center Partnering with Rose Brooks Center to create a safer community.

457

458

Practice Management

459

460

Practice Management

David Galloway, DVM, DACVS-SA

U.S. Army Veterinary Corps Officer - Retired Program Manager - Veterinary Corpsâ&#x20AC;&#x2122; FYGVE Program Falls Church, Virginia

461

462

Select SLIDE MASTER to Insert Briefing Title Here

US Army Veterinary Corps US Army Veterinary Corps Update First Year Graduate Veterinary Education (FYGVE) David S. Galloway david.s.galloway.civ@mail.mil 703-681-7757 571-278-2737

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 1

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

•

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 2

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Why we serve.

FYGVE PM: David Galloway • •

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

UG (USMA, KSU); CVM (KSU, 95); MS/Sx Res (OkSU, 2003) Army Lifer: 1982-90 (USMA, AD), 1991-95 (KSARNG), 19962012 (VC), 2012-UTC (VC FYGVE) Assignments: VETCOM / SOF / MTOE / Army Staff – USA: Benning, Bragg, FSHTX, Leavenworth, McPherson, National Capital, Riley, Rucker, Stewart, West Point – Overseas: Korea, Japan, Germany – Deployments: Reforger ‘88 (Certain Challenge), South America, Iraq Jobs: – Infantry x 10 yrs – Veterinary Branch OIC – Special Opeations Vet – Command x 11 yrs • Rifle Company, MDVM, DVC, MDVS – Coffee Boy… OTSG/DODVSA – FYGVE Program Manager (2012-UTC) Hobbies: Fishing, FYGVE

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 3

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 4

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Agenda

• Veterinary Corps Update – – – –

A lot of stuff to do. A lot of places. Veterinary Corps Soldiers Veterinary Corps Missions Veterinary Corps Accessions

Veterinary Corps Update

• FYGVE Internship Program – – – –

FYGVE = First Year Graduate Veterinary Education. Why: New CVM Grads need [and want] Mentorship. How: A different kind of internship! End-State: Competent, Confident Veterinarian-Leaders.

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

463

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 5

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 6

2-Nov-19

MVMA Convention 20 JAN 2020

Veterinary Corps Update Select SLIDE MASTER to Insert Briefing Title Here

Select SLIDE MASTER to Insert Briefing Title Here

A Time for Change

• Veterinary Corps Mission • Veterinary Corps Soldiers • Veterinary Corps Accessions

“All great changes are preceded by chaos.” - Deepak Chopra

“Change is hard at first, messy in the middle and gorgeous at the end.” - Robin Sharma

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 7

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 8

2-Nov-19

MVMA Convention 20 JAN 2020

Veterinary Corps Mission

US Strategic Guidance Documents: Nested Drivers of Change 2017 National Security Strategy : Protect, Promote Prosperity, Preserve Peace through Strength, Advance Influence

2018 National Defense Strategy: Build More Lethal Force, Strengthen Alliances, Reform the DOD Hon Esper

Build Readiness, Reform, Strengthen and Partnerships

Hon McCarthy GEN McConville

LTG Dingle

Army VC Update / FYGVE Internship Program

Select SLIDE MASTER to Insert Briefing Title Here

A Path of Change

2018 Army Strategy: Modernize, Alliances

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

2018 Army Medicine Campaign Plan: Readiness & Health, Healthcare Delivery, Force Development, Take Care of Ourselves, and Families DOD & Army Medicine Reform

• The US Army Veterinary Corps' mission is

to protect the Warfighter and support the National Military Strategy. This is accomplished by providing veterinary public health capabilities through: – Veterinary medical and surgical care. – Food safety and defense. – Biomedical research and development.

BG Eric Torring (26th Veterinary Corps Chief) FYGVE End State: “... agile and adaptive VCOs who are prepared to effectively operate and achieve success in an environment of a constant state of flux while navigating to and through an unknown and unknowable future.” Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 9

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 10

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Global Health Engagement

It’s more than MWDs, Family Pets, and Food Safety

• DOD Global Health Engagement activities (GHE) are

conducted to assist in achieving Theater Campaign Plan objectives. Army Vets impact global security in ways that no others can...

• Animal health impacts the economy, human health, and human security.

• Strategically employed and properly targeted veterinary GHE activities can improve animal and human health, and strengthen livelihoods while meeting DoD and USG goals.

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

464

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 11

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 12

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Veterinary Corps Officers (VCOs) • • • •

Veterinary Corps Officers (VCOs)

64A – Field Veterinary Service Officers (Initial entry VCOs) – Entry Level Veterinarian – Doctorate in Veterinary Medicine, maintain practice licensure, NVAP 64B – Veterinary Preventive Medicine Officer – Masters (MPH) or PhD (e.g. Public Health, Epidemiology, Food Science, etc.) – Board certification in the American College of Veterinary Preventive Medicine 64C – Laboratory Animal Medicine Officer – Postdoctoral training in laboratory animal medicine – Board certification in the American College of Laboratory Animal Medicine 64D – Veterinary Pathologist – Postdoctoral training in veterinary pathology – Board certification in the American College of Veterinary Pathologists

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 13

2-Nov-19

MVMA Convention 20 JAN 2020

•

64E – Veterinary Comparative Medicine Officer – PhD degree in microbiology, immunology, physiology, pharmacology, toxicology, etc. – R&D and Science Management 64F – Veterinary Clinical Medicine Officer – Postdoctoral training in a veterinary clinical discipline recognized by the AVMA – Board certification in clinical specialty (e.g. Veterinary Emergency and Critical Care, Surgery, Internal Medicine, Radiology, Ophthalmology, etc.) 64Z - Senior VCO – Senior VCOs in AOCs 64B-F selected for key leader positions 640A – Food Safety Officer (VC warrant officer) – Food Protection (Food Safety and Defense) Subject Matter Experts

•

• •

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

Select SLIDE MASTER to Insert Briefing Title Here

• VCOs

– 64A Field Veterinary Service Officers – 64B Veterinary Preventive Medicine Officer – 64C Laboratory Animal Medicine Officer – 64D Veterinary Pathologist – 64E Veterinary Comparative Medicine Officer • FSOs – 640A Food Safety Officers [VC Warrant Officers] • VC Enlisted Soldiers – 68T Veterinary Technicians – 68R Veterinary Food Inspectors Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 15

MVMA Convention 20 JAN 2020

VS Demographics

Veterinary Corps Soldiers

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

2-Nov-19

Slide 14

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Veterinary Corps AC/RC 600

532

400

265

200 0

Active Component VCOs by AOC

69 VCO VCO (Veterinarian)

1000 500 0

64A 64B 229

WO WO (Food Safety Officer)

64C 64D 64E 64F

Enlisted Strength AC/RC 1500

116

1004 595

438 68R 68R (Food Inspector)

RC 180

68T 68T (Vet Tech)

AC VCO Age • • • •

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

AC VCO Gender

< 30 16% 30 to 39 45% 40 to 49 30% ≥50 9%

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

• •

Slide 16

Female 60% (322) Male 40% (210)

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

VC Alma Matters

VCO Life Cycle

SOURCE: Human Resources Command, Mar 19 Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

465

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 17

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 18

2-Nov-19

MVMA Convention 20 JAN 2020

Accession & Compensation Select SLIDE MASTER to Insert Briefing Title Here

Select SLIDE MASTER to Insert Briefing Title Here

VC Special Pays and Incentives • Health Professions Loan Repayment Programs (for

• Accession Programs: – – – –

qualifying Educational Loans):

Direct Commission Educational Delay Health Professions Scholarship Program (HPSP) Early Commissioning Program (ECP)

– Active Duty: $40,000 / year (up to $120,000 for 3 years) – Reserves: $20,000 per year, $60,000 (lifetime maximum)

• $15,000 new accession bonus • Incentive Pays: $5,000 per Year • Board Certification Pay: $6,000 per Year • Retention Bonuses

• Compensation; – – – –

< 2 Years: 2 Years: 3 Years: 4 Years:

$56,960.68 $61,700.47 $64,937.07 $69,040.82

– 2 Year - $2,500 – 3 Year - $3,750 – 4 Year - $5,000

• Average Annual Military Compensation which combines Basic Pay, Special Pay, BAS, BAH (Based On Locale): - includes Tax Advantage from Untaxed Allowances.

• Available: Family Tricare medical, dental, and vision insurance • Available: Life Insurance (SGLI): 400k service member/100k spouse

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 19

2-Nov-19

MVMA Convention 20 JAN 2020

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 21

– PhD In Physiology, Pharmacology, Toxicology, Microbiology, Pathology, Public Health – Masters In Internal Medicine, Surgery, Radiology, Food Animal/Preventive Medicine, Emergency Medicine, Public Health, Food Technology, Human Animal Bond 2-Nov-19

MVMA Convention 20 JAN 2020

• Health Professions Loan Repayment Programs – Up to $40,000 / year (max. $120,000 for 3 yrs)

466

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 22

2-Nov-19

MVMA Convention 20 JAN 2020

Points of Contact

– Full tuition paid – Monthly stipend: $2100/ month x 10.5 mon/yr – Reimbursement for books, required instruments, health insurance, & associated expenses – 2nd Lieutenant AD pay: $2900/ month x 1.5 mon/yr • Active Duty (AD) at Mil Vet Clinics... San Antonio (MWD Center), San Diego (Marine Mammal Program), Belvoir (DC), etc. – Vet Corps offering primarily 3 year scholarships  Application period 1st semester of CVM Yr 1.

Slide 23

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Select SLIDE MASTER to Insert Briefing Title Here

• Health Professions Scholarship Program:

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

2-Nov-19

MVMA Convention 20 JAN 2020

• Long Term Health Education Training

Select SLIDE MASTER to Insert Briefing Title Here

Army VC Update / FYGVE Internship Program

Slide 20

– Laboratory Animal Medicine – Veterinary Pathology – Animal Medicine • Internal Medicine • Emergency / Critical Care • Surgery • Animal Behavior • Radiology

Vet School Scholarships

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

• Residency Programs

• Medical Coverage • Dental Coverage • Low Cost Life Insurance • Paid Continuing Education • Post-DVM Educational Opportunities • Leadership and Practice Management Opportunities • Thrift Savings Plan (~ 401k) • 30 Days Annual Leave Plus 10 Federal Holidays • Paid Moving Expenses - Household/Personal Army VC Update / FYGVE Internship Program

Army VC Update / FYGVE Internship Program

Select SLIDE MASTER to Insert Briefing Title Here Educational Opportunities

Benefits

Select SLIDE MASTER to Insert Briefing Title Here

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

2-Nov-19

MVMA Convention 20 JAN 2020

• Active Duty: Assistant Veterinary Corps

Chief, Corps Specific Branch Proponent Officer (CSBPO) – COL Dwayne Bechtol: dwayne.c.bechtol.mil@mail.mil – Phone: 210-221-6564

• Reserves: Assistant Veterinary Corps Chief, Mobilization & Reserve Affairs – COL Jacob Johnson: jacob.a.johnson4.mil@mail.mil

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 24

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Questions & Discussion

FYGVE Internship Program

facebook.com/ArmyVetCorps facebook.com/ArmyVetCorpsChief

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 25

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 26

2-Nov-19

MVMA Convention 20 JAN 2020

Why FYGVE?

FYGVE Internship Program Select SLIDE MASTER to Insert Briefing Title Here

Select SLIDE MASTER to Insert Briefing Title Here

• Today’s CVM graduates:

– The least desired job placement = “business owner.” – JAVMA 2019: 87.6% entering internships

• FYGVE = First Year Graduate Veterinary Education. • Why: New CVM Grads need [and want] Mentorship. • How: A different kind of internship! • End-State: Competent, Confident Veterinarian-Leaders. Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 27

2-Nov-19

MVMA Convention 20 JAN 2020

Why FYGVE?

Select SLIDE MASTER to Insert Briefing Title Here

63.3% to prepare for residency or qualify for a desired position 24.6% wanted to practice better-quality veterinary medicine 10.3% believed they needed more hands-on training ... high rate of satisfaction among veterinarians who completed internship programs: exposure to a wide variety of training and clinical experiences; appropriate levels of supervision.

– And many arrive with a measure of insecurity about professional competence due to always standing 4th in line from the patient during their senior CVM year. • Patient  Specialist  Resident  Intern  Vet Student

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 28

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

FYGVE Sites

• Historically, @ 72% of new VCOs received initial isolated

•

assignments. – VCO captains are required to be veterinarians, “business owners,”… and so much more. ...without direct supervision and mentorship. Overwhelmed VC Captains. – 2006: VC Junior Officer Council raised “Overwhelmed CPT Syndrome” to the Corps Chief. – 2007-2008: Internship proposal developed & socialized. – 2009: US Army Medical Command ordered development of a Veterinary Corps Internship Program. – 2010: FYGVE launched 1 site. – 2011-2013: Established 6 additional sites.

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

467

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 29

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 30

2-Nov-19

MVMA Convention 20 JAN 2020

Why FYGVE?

Select SLIDE MASTER to Insert Briefing Title Here

• New accessions want [and need] a year of supervised training.

FYGVE 2020

• Solution: A different kind of internship…

Rotating , Multidisciplinary... based on competencies required to be a successful VCO.

• FYGVE Program • FYGVE Mission • FYGVE intent

• Key Competencies:

– Animal Medicine – Veterinary Public Health – Veterinary Leadership and Mission Oversight

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 31

2-Nov-19

MVMA Convention 20 JAN 2020

FYGVE Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 33

Slide 32

2-Nov-19

MVMA Convention 20 JAN 2020

MISSION: The Veterinary Corps’ FYGVE Program provides entry level Veterinary Corps Officers with an initial year of post-graduate training to prepare them for success as Army Medical Department leaders responsible for performing comprehensive military veterinary support in support of installations and DOD Global Operations.

* MEDCOM OPERATION ORDER 09-38 (VETERINARY CORPS FIRST YEAR GRADUATE MEDICAL EDUCATION (FYGME) PROGRAM) [10 April 2009] ordered development of a Veterinary Corps Internship Program. Phased execution the FYGVE Program was outlined in implementation FRAGOs 1-4.

2-Nov-19

MVMA Convention 20 JAN 2020

FYGVE Program Intent

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 34

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

The intent of the one year FYGVE internship is to acclimate FYGVE interns to Army and AMEDD culture while increasing their veterinary technical skill-set and leadership confidence and competencies so that they will succeed in the execution of the Army’s military veterinary mission, including animal health care, food protection, and veterinary public health, for the Department of Defense (DOD).

End State (FYGVE Vision): FYGVE graduates are capable General Practitioner Level VCOs, confident in their ability to apply and continually improve acquired animal medicine, veterinary public health, and Veterinarian-Leader competencies in the execution of assigned mission sets. They are agile and adaptive VCOs who are prepared to effectively operate and achieve success in an environment of a constant state of flux while navigating to and through an unknown and unknowable future. To achieve this end state, FYGVE graduates must be technically competent Veterinarian-Leaders of Character who: * Pursue Excellence. * Pursue life-long Veterinarian-Leader professional competency and resiliency development. * Contribute to the Veterinary Corps / Public Health Team. * Enhance personal and organizational impact by Strengthening Partnerships. * Enhance a Culture of Competence, Dignity, and Respect within their units.

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

468

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Select SLIDE MASTER to Insert Briefing Title Here

The US Army Veterinary Corps’ First Year Graduate Veterinary Education (FYGVE) Program is a one year rotating internship designed to reinforce critical food protection, public health, animal health, business management, and leadership knowledge, skills, and attributes that are introduced in veterinary school curricula and at the AMEDD Basic Officer Leadership Course, but not developed adequately to ensure initial and continuing success of new Veterinary Corps Officers.

Army VC Update / FYGVE Internship Program

FYGVE Mission

Select SLIDE MASTER to Insert Briefing Title Here

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 35

FYGVE Program Vision

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 36

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

FYGVE Sites Roll-Up FYGVE

FYGVE 2020 • • • • •

FYGVE Administration Completion Requirements 2020 FYGVE Year Critical Exposures FYGVE Program Elements

• HPSP Accessions are required to attend FYGVE. • Direct Accession VCOs can volunteer. • FYGVE Capacity = 42 interns. Average class size = 31 interns. Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 37

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

Select SLIDE MASTER to Insert Briefing Title Here

OPORD 09-38) under the direction and guidance of the Veterinary Corps Chief. • COL Steve T. Greiner – FYGVE Oversight Committee = “Council of Colonels”: – Deputy Veterinary Corps Chief • COL Margery M. Hanfelt – Director, DCSPH-VS • COL Steve T. Greiner – Director, APHC VSPHS • COL John C. Beach – Veterinary Corps CSBPO • COL Dwayne C. Bechtol Program Manager – Dr. David Galloway @ Corps Chief’s Office (DHHQ, DCSPH)

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 39

2-Nov-19

MVMA Convention 20 JAN 2020

2020 Cadre

• The FYGVE Program is executed PHC (OTSG / MEDCSM

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Slide 38

Select SLIDE MASTER to Insert Briefing Title Here

FYGVE Administration

•

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

• Belvoir • •

• Campbell – VPH: MAJ Amos K. Peterson – VPH: MAJ Morgan C. Mander – AM: MAJ Tiffany L. Kimbrell (Sx) – AM: LTC Scott C. Chamberlin (ECC) Benning • Carson – VPH: MAJ Taylor K. Opel – VPH: MAJ Lauren M. Seal – AM: MAJ Katie S. Barry (Sx) – AM: LTC Andrew J. Kay (SMR) Bragg • Hood – VPH: MAJ Dustin J. Staab – VPH: MAJ Elizabeth A. Williams – AM: LTC Eileen K. Jenkins (IM) – AM: MAJ Scott J. Anderson (Sx) • JBLM – VPH: MAJ Elizabeth A. James – AM: MAJ Suzanne C. Skerrett (Sx)

Cadre : Intern Ratio @ 1:2

2-Nov-19

MVMA Convention 20 JAN 2020

2020 Interns

Select SLIDE MASTER to Insert Briefing Title Here

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 40

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

AY20 Requirements 1/2 • Unrestricted US State Veterinary License. • APHC Auditor Certification. • APHC Clinical Credentialing. • NVAP Category 2 Accreditation. • Veterinary Corps Chief (VCC) Readiness Targets. • Army Fitness and Body Composition Standards. • DEA National Provider Identifier. • Mandatory Training.

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

469

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 41

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 42

2-Nov-19

MVMA Convention 20 JAN 2020

Critical Exposures

Select SLIDE MASTER to Insert Briefing Title Here

AY20 Requirements 2/2

• 48 Reportable Events... 377 Required Exposures

• Complete Critical Exposures. • CE Level Formal Presentation. • 3ea CE Level Site Professional Presentations. • Army Writing Style Proficiency. • 64A Individual Critical Tasks Proficiency. • Officer Values / Technical skills / Leadership.

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 43

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Statement(s) • NCOERSFs / NCOERs • OERSF / OER • Good News Storyboard • Information Papers • Publication

• 3ea CE Level On-Site Professional Presentations (AM, VPH, LDR). – Internal Audience – Intern Led Training

Slide 45

Slide 44

2-Nov-19

MVMA Convention 20 JAN 2020

• Memorandums

• EXSUM • Counseling

– External Audience

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Army Writing Style Reqs

• CE Level Formal Presentation

Army VC Update / FYGVE Internship Program

Select SLIDE MASTER to Insert Briefing Title Here

Formal Presentations

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

– MWD Medical Readiness Status – Clinical Policy – VPH Policy – MWD Disposition • Awards

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 46

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

FYGVE Year 2020

FYGVE AY20: FYGVE Year

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

470

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 47

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 48

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

FYGVE Weeks

Program Elements

• Rotational Weeks • Non-Rotational Weeks • Critical Exposures [Reportable Events] • FYGVE Intern Leader • FYGVE Site Intern Leader duties – Site Weekly Report

• Site Thursday Training • FYGVE 3rd Thursday Collective Training • Multi-day Collective Training Short Courses • Leadership Book Reading • Special Training Events Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 49

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

– 3 Mayhem Rotation Weeks

• Interns given a VS mission set… Plan, Execute, AAR.

– Elective Week [optional]

• Intern selected activity, e.g. Dog Center, Specialty Clinic, Lab Animals.

– 1 Attending Clinic

– 1 Off-Site Visit

• Goal: Week of peer mentorship in Branch Operations / Leadership.

Slide 51

2-Nov-19

MVMA Convention 20 JAN 2020

• Non-Rotational Weeks

– 13 Non-Rotational Weeks • Coming / 3ea Initial Weeks / 3ea Short Courses / Going – Initial Weeks – Orientation – Clinical Privileging • Initial 2 weeks to get interns privledged as providers in the VTF. – VPH Inspection 101 • Week of VPH didactic and group inspections to prepare intern for VPH missions. Conduct Commissary, shopette, food court, warehouse, animal facility inspections as a group.

471

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 52

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

FYGVE Weeks

Slide 53

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Critical Exposures

Select SLIDE MASTER to Insert Briefing Title Here

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

– Mayhem Weeks (3 ea): Cadre provide intern leader with a week mission set. Interns plan and execute the week. Frequent leadership changes. Frequent mission changes. – Intern Scheduled Rotations Weeks: Interns who are on a successful critical exposure glide path at the rotational midpoint are be allowed to schedule their own rotation weeks, as long as they remain on a successful glide path. Interns desiring self-scheduled Rotations Weeks have to coordinate with cadre and other interns for scheduling that benefits all. It’s a reward, and also an exercise in planning, coordination, and forward thinking: schedules are set at least 3 weeks out.

• Goal: See what a “normal” clinic looks like. • Often mission back-fill. ... Independence. Confidence.

Army VC Update / FYGVE Internship Program

2-Nov-19

MVMA Convention 20 JAN 2020

– 2 Week Rotations: Animal Medicine, Veterinary Public Health, Mission Oversight.

• 2020 rotation weeks are 50% AM, 25% VPH, & 25% LDR.

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Slide 50

• Rotational Weeks

– 37 Rotational Weeks

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

FYGVE Weeks

• Rotational Weeks

Army VC Update / FYGVE Internship Program

Select SLIDE MASTER to Insert Briefing Title Here

FYGVE Weeks

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

2-Nov-19

MVMA Convention 20 JAN 2020

• 48 Reportable Events... 377 Required Exposures

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 54

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Critical Exposure Explanations

FYGVE Intern Leader

• Critical exposures

• Primary means of FYGVE Captains getting leadership experience. – Peer Leadership – Planning and conduct of Site Operations – Site Administration • Weekly Report. • Owning it: When in charge, be in charge!

– Exposure definitions include program policy review and leader interactions [Knowing & Doing] – All exposures are requirements / not goals.

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 55

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

Select SLIDE MASTER to Insert Briefing Title Here

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 56

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Didactics: Site Thursday Training

FYGVE Site Intern Leader duties

• FYGVE Site Thursday Training Scheduling • ** Adult Leader Model, discussion... not briefing (no PPT except to

• Site Weekly Report – W: AAR – W+1:

guide discussion). REQUIRES participant PREP!

• Planned Activities (W+1): Bullets about planned key activities. • Thursday Training (W+1) – Time / Activity / Trainer / Topic • Site dial-in information. • Indication of Off-site Training: includes location and POC information.

– W+2 thru W+6: akin to W+1... Progressive detail – Mid-Term/ Long Term Training Plan • Calendar Items

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

• Field Trips / Other Training Slide 57

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

Select SLIDE MASTER to Insert Briefing Title Here

• Cadre Animal Medicine Topic

– Leadership vignette / discussion

– Monthly one-hour session. Typically AM Case Challenge.

• Cadre Veterinary Public Health Topic

• TED Videos! • HBR Must Reads

– Monthly one-hour session. Typically VPH Case Challenge.

• Intern Led Training (ILT)

– Weekly one-hour session – Present a professional presentation – Intent: peer instruction and discussion of topics specifically of interest to VCOs in the execution of their duties. Officer Professional Development (OPD) – PHA/PHC Directed Leader’s Time Training – Bi-weekly one-hour session – Didactic training on a VCO Competency related topic – Invited guest SME -OR- Intern presents.

Army VC Update / FYGVE Internship Program

472

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

2-Nov-19

MVMA Convention 20 JAN 2020

Site Thursday Training

• Leadership Lesson [Lessons in Leadership]

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Slide 58

Select SLIDE MASTER to Insert Briefing Title Here

Site Thursday Training

• •

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 59

2-Nov-19

MVMA Convention 20 JAN 2020

• VPH Current Event

• •

– Bi-weekly half-hour session. – Interns present a 20-30 minute talk on a current PH/VPH event. AM Current Event – Bi-weekly half-hour session. – Interns present a 20-30 minute talk on a current AM event. AM Case Rounds – Weekly half-hour session. AM interns share key lessons.

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 60

2-Nov-19

MVMA Convention 20 JAN 2020

3rd Thurs Collective Tng

Select SLIDE MASTER to Insert Briefing Title Here

Site Thursday Training

• VPH Rounds

– Weekly half-hour session. VPH interns share key lessons.

• PHA CUB (60 Min)

– PHA directed.

• PHA/PHC OPD (60 Min)

– PHA/PHC directed.

• Book Club •

•

– 5th week, one-hour session. – Discuss site directed professional book readings. FYGVE Weekly Training Meeting / AAR – Every Week – “Company” Training Meeting. – ARR & 6 week training schedule. Field Trips / Special Training Events

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 61

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

Select SLIDE MASTER to Insert Briefing Title Here

• Senior Leader Mentorship Talks

• JPC Practical Pathology Series (TC/DCS) • 3 Sessions x 2 hrs RACE CE – Introduction to Diagnostic Cytology – Improving Diagnostic Yield: Sampling Techniques and Submission – Cytology Challenge

•

• Cadre Talks

– 1 / Site – Intern suggestion… share Cadre SME knowledge. David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 63

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

HOOD BELVOIR JBLM

473

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 64

2-Nov-19

MVMA Convention 20 JAN 2020

• Animal Medicine Track

6-10 JAN 2020 3-7 FEB 2020 24-28 FEB 2020

– DODMWDVS Animal Behavior Short Course • 3 day course • Topics

– Dx and Tx of behavioral disorders in animals – Canine PTSD – MWD Bite Muzzle Assessment

• All courses are Alle Zusammen. • All courses during the Holiday Lull. • Course site & dates subject to change.

Army VC Update / FYGVE Internship Program

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Multi-day Courses

• Incl. Tactical Canine Casualty Care Workshop.

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

– Successful VCO leaders give brief mentorship talks that offer career reflections, challenges & success stories, leadership tips, leadership philosophy, etc; followed by a Q&A period with the interns. – Not an AOC recruiting talk. – 4 ea Near Miss Rounds – Discussion of Near Miss cases to improve clinical outcomes.

Select SLIDE MASTER to Insert Briefing Title Here

Multi-day Specialty Skill Courses • FYGVE BSC Week • FYGVE VPH Week • FYGVE MRCC Week

2-Nov-19

MVMA Convention 20 JAN 2020

3rd Thursday Training

• Cadre Huddle / Intern Leader Update

Army VC Update / FYGVE Internship Program

Slide 62

Select SLIDE MASTER to Insert Briefing Title Here

3rd Thursday Training

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

• 22 hrs RACE CE

Slide 65

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 66

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Multi-day Courses

• VPH Track

• Leadership Track

– Veterinary Public Health Week

–Medical Risk Communication Course

• 3 day course • Topics: – – – – –

• 2 day course • Topics:

Comprehensive Audit System Tri-Service Food Code HACCP Military Sanitary Inspections VC Demand Topics: » » » » »

–Learn about aspects of risk communication –Develop ability to communicate risk to the public – Risk-Benefit Communication – Controversial Issues (addressing concerns) – Crisis Communication

Key Leader Talks Human Animal Bond Emergency Preparedness Rabies Prevention Program Veterinary Support for Disease Outbreaks

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

• Practical Exercises tailored to VCO issues • 12 hrs RACE CE

TCCC Workshop – 3rd Day

Slide 67

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

– Often site backfill. – Requirement: 1 week.

• Other leadership reading by site.

• Off-Site Visit

4 Disciplines of Execution [Carson] The 4 tendencies (Gretchen Rubin) Leadership and Self-Deception (Arbinger) Lean In (Sheryl Sandberg) A Higher Standard (Ann Dunwoody) On Call in Hell (Richard Jadick) Others….

– Defined expectations. – Planned, Coordinated, Targeted Peer Mentorship @ a site with a solid Branch Chief. – Requirement: 1 week – “Best week” of their internship.

Slide 69

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 70

2-Nov-19

MVMA Convention 20 JAN 2020

FYGVE SitesEvents Special Training

Select SLIDE MASTER to Insert Briefing Title Here

• Events providing training not available at the

• Allowance for 1 week of intern selected

FYGVE Electives Sites Off-Site

FYGVE site: – Off-Site Training, e.g. ECC Procedures Lab – Local professional short courses. • Seafood HACCP or PMO Course – REQUIRED Exposure: Prep for next job. • e.g. MTOE Experience w/ local Med Unit. • e.g. Possibly visiting follow-on site.

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

474

2-Nov-19

MVMA Convention 20 JAN 2020

– Intent: Exposure to a non-VETCEN environment.

• Keller - The One Thing • Sinek - Start with Why • Marquet - Turn the Ship Around

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 68

• Attending Clinic

– Discussed during Collective Trng wks.

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

FYGVE Sites Other Sites

• 3 books for all sites.

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

Select SLIDE MASTER to Insert Briefing Title Here

Leadership Reading

– – – – – – –

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 71

Special Training. – Training at Dental Specialty Clinic – Week in DC at Vet R&D sites.

• Intern coordinated: [It’s your elective.]

– Special Training…. Usually Cadre LOE. – Electives…. Always intern LOE.

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 72

2-Nov-19

MVMA Convention 20 JAN 2020

Select SLIDE MASTER to Insert Briefing Title Here

Questions & Discussion

Crushing FYGVE!

• OWN IT!

– FYGVE isn’t a Corps, Cadre, or PM Program... – It’s a personal INTERN led Program: OWN IT! • Read the Book! Refer back to it. • Make a Personal Development Plan. • Execute Aggressively. • Crush It!

facebook.com/ArmyVetCorps facebook.com/ArmyVetCorpsChief

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

475

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 73

2-Nov-19

MVMA Convention 20 JAN 2020

Name/Office Symbol/(703) XXX-XXX (DSN XXX) / email address

Army VC Update / FYGVE Internship Program

David S. Galloway, DVM, MS, MMAS, Dipl ACVS-SA

Slide 74

2-Nov-19

MVMA Convention 20 JAN 2020

476

Practice Management

Elizabeth Johnson, DVM

Assistant Director of Outreach and Engagement International Council for Veterinary Assessment Atlanta, Georgia

477

478

479

480

6.5 hours

300 + 60 = 360 items

481

% !

$"" (( ( $!

( $# '( # ( $# +( ) * %

( " ( "

) ! ! $ % % 6675=03(9,2> 5- 9/, 60.2,9 2099,78 04 9/, -(775<04. 75538 5- ( 8<04, -(73 /(;, 6(2, >,225< +0(77/,( $/, 3(4(.,7 5- 9/, -(73 7,65798 9/(9 9/08 +0(77/,( 5**:78 8657(+0*(22> 04 2099,78 89(7904. (8 ,(72> (8 +(>8 5- (., (4+ 6,780898 :4902 9/, 60.2,98 (7, <,(4,+ (9 ()5:9 95 +(>8 5- (., 579(209> 7,8:2904. -753 9/08 +0(77/,( 08 30403(2 ):9 +,/>+7(9054 (4+ ( 6557 .75<9/ 7(9, 2,(+ 95 25<,7 <,(404. <,0./98 $7,(93,49 <09/ .,49(30*04 /(8 ),,4 04,--,*90;, 04 9/, 6(89 85 9/, 3(4(.,7 +5,8 459 97,(9 9/, 60.2,98 -57 9/, +0(77/,( &/0*/ 5- 9/, -5225<04. 08 9/, 3589 201,2> *(:8(2 (.,49 %( $# (

) ! ! $ % % 57*04, ,49,75;07:8

$7(4830880)2, .(8975,49,70908 ;07:8

#'* & ( " ( " ! '' ( $#' # " 57*04, # (8975049,8904(2 $ 49,767,9 *522,*9,+ 04-573(9054 (4+ ,89()208/ ( <57104. 57 -04(2 +0(.45808 57 *54*2:8054 "' " 5**0+05808

$ %

#!$

) # $ % " ## ## ( $'

(

+ #!$ $ % %&

* '%*&

" ! &) ) # ) # ' $ "' ' ' & )"% (! ) # ) # ! $%(!( & " "&'"'

) )!()! ( & '

482

Practice Management

Rob Bertman, CFA, CFP

Senior Consultant, Student Loan Planner St. Louis, Missouri

483

484

Veterinarians typically have a tough road paying back their student debt. Often they owe 2-4x their income. Despite this, veterinarians do have an optimal way to pay back their loans while still saving for the future. In this presentation, weâ&#x20AC;&#x2122;ll cover the common issues veterinarians face when paying back their student loans. We will explain the various ways to pay back loans including refinancing and the different income driven repayment options available. Weâ&#x20AC;&#x2122;ll deep dive and explain optimal ways to pay back student debt by examining case studies with fairly common veterinarian debt and income characteristics. The findings and presentation are based upon calculations and real-life scenarios weâ&#x20AC;&#x2122;ve seen in our more than 3,000 individual consults covering more than $750,000,000 of student debt.

485

486

Practice Management

Jean Schmidt, DVM

Assistant Missouri State Veterinarian Jefferson City, Missouri

Tom Lenz, DVM, MS, DACT

Private Practice - Equine Practitioner Louisburg, Kansas

487

488

The Veterinarianâ&#x20AC;&#x2122;s Role in Suspected Equine Neglect, Abuse and Mistreatment Tom Lenz, DVM, MS, DACT Veterinarians often face difficult situations in their practice including treating or observing animals that may have been neglected, mistreated and/or abused. When these situations occur, veterinarians have the ethical and professional responsibility to respond compassionately, effectively and in some cases legally. The American Veterinary Medical Association considers it the responsibility of the veterinarian to report suspected cases of animal abuse, when an educational approach is inappropriate or unsuccessful, to the appropriate authorities, whether or not reporting is mandated by state law. (www.avma.org/KB/Policies/Pages/Animal-Abuse-and-Animal-Neglect.aspx) However most states do have regulations requiring veterinarians to report cases of animal abuse so it is important to be familiar with animal abuse laws that apply in your city, county or state. With the recent increase in the publicâ&#x20AC;&#x2122;s interest in animal welfare issues, the nonfulfillment of these responsibilities may place the individual veterinarian at risk of adverse criticism or legal action. (Robertson, 2010). The American Veterinary Medical Association has published guidelines for veterinarians in suspected cases of animal cruelty, abuse and neglect. They include guidance on what constitutes animal neglect or abuse, protocols and procedures when investigating cases, client questionnaires, a decision tree, a listing of state laws and many other tools to aid veterinarians in dealing with suspected cases. (Practical Guidance for the Effective Response of Veterinarians to Suspect Animal Cruelty, Abuse and Neglect, AVMA) Currently, equine cruelty, neglect or abuse is more prevalent in our society because of the recent economic recession which prevents some owners from properly caring for their animals, the desire for a competitive edge in the performance horse, people holding on to horses for fear that if they sold them they might end up being processed for human consumption and the human psychological condition of hoarding. For most veterinarians, abuse will likely be first observed or suspected in their everyday practice while treating patients. Although serious abuse cases such as beating, starving, or intentionally harming an animal may occur, neglectful situations present themselves more routinely. Many of these are due to a lack of knowledge on the part of the animal caregiver or accidents and provide the veterinarian the opportunity to educate the client on the proper care of the animal. However, some cases may be due to the intentional actions of the client and should be reported to the appropriate authority. Once a suspected case of animal abuse or neglect is observed the practitioner is often faced with a confounding series of ethical, economic and practice management issues in attempting to arrive at an effective response that balances the interests of the animal, the client and their practice.

1 489

When reporting potential or suspected animal abuse it is not the duty of the veterinarian to determine guilt or innocence. Their responsibility is to report suspected cases and let the authorities investigate them. Unfortunately, many veterinarians are not unaware of the appropriate authorities to whom they should report because such authorities vary from state to state and even from locality to locality within a given state. Therefore, complicating the ease with which veterinarians are able to report known or suspected animal abuse. In most areas of the country, the appropriate animal welfare authority may include the local animal shelter, the sheriff or law enforcement officials, or the local HSUS or ASPCA organization. (Glasere 2016) The veterinarian’s role in cases of suspected neglect or abuse may be one or all of the following: • • •

Attending Clinician Forensic Medical Examiner Expert Witness

Regardless of the role they are expected to collect and preserve information which usually includes identifying and examining each animal, evaluating water and feed sources, and photographing housing as well as pastures and potential hazards. Evidence is defined as anything that can demonstrate or disprove a fact in contention. In equine abuse investigations, that can include everything from the photos of a horse’s injuries or body condition to moldy hay. (Eller 2016) Typical signs of equine abuse, neglect and starvation include: • • • • • • •

Weight and Body Conditions scoring (BCS) is less than optimal Recumbence and difficulty ambulating Dull and depressed demeanor Chronic open wounds and dermatitis without evidence of healing Overgrown hooves, lameness, laminitis, hoof disease Unkempt coat, dandruff, not shedding Dental disease – fractured or chipped teeth

To assist law enforcement with an investigation of potential animal abuse, the veterinarian must understand the basics of evidence identification, collection and preservation. (Gardner 2011) If called upon to be a forensic medical examiner or expert witness there are four areas that should be focused upon. • • • •

Document the condition of the facility upon arrival Document each animal and its environment Identify nonanimal issues Document the condition of the scene upon exit

2 490

Photographs are a fundamental component of documentation and should include all six sides of an animal with close-ups of lesions, abscesses, wounds, etc. It’s a good idea to identify the animal with signage and place a ruler next to the findings for measurement purposes. If there are a large number of animals, a good rule of thumb is to have a veterinary team for every 50 equids in order to complete examinations within a few days depending on the extent of the medical conditions present. Ideally, the team should include a veterinarian, handler, technician and scribe/photographer. Documentation of the scene upon arrival should include photos or videos of the area secured by law enforcement and may be done by law enforcement or the veterinary team. A thorough examination of each animal is conducted by the veterinarian and in cases where animals are near death or severely injured triage should be utilized to rapidly sort animals for examination and treatment based on their medical condition. During triage animals should be separated into categories and provided easily seen identification denoting their condition. For example, critical animals are often designated ‘red’ with noncritical animals in need of treatment designated ‘yellow’; animals ready for transport designated ‘green’ and animals exhibiting signs of infectious disease designated as ‘blue’. (Eller 2016) Critical animals require immediate treatment with documentation including a description of their medical condition and photographs taken before and after treatment is provided. Critical medical conditions include but are not limited to open fractures, seizures, hemorrhaging, colic, etc. Animals exhibiting signs of infectious disease should be placed in an isolation area set up in a barn or shelter off site if possible. It is imperative to document not only the individual animal’s physical condition but also their living conditions given they may hold information that will either contradict or corroborate the animal’s physical condition. This is especially true in cases of neglect. In addition, the veterinarian should note and document other details such as quids on the ground or toxic plants eaten along the fence line or in a dry lot. Once all live animals have been examined and their condition documented dead animals or skeletal remains on the property should be examined, photographed and catalogued. In addition, any nonanimal evidence pertinent to the case should be identified and photographed. Those might include medications, supplements, surgical supplies, horse shoes, training tools and caustic substances. The veterinarian’s role in an animal abuse case doesn’t end after the scene has been documented, evidence collected, and animals treated. The veterinarian is then usually required to provide a written opinion based on their findings. The facts regarding the history, medical examination findings, scene findings, diagnostics and forensic examinations are provided by the veterinarian in a final report that is often referred to as the ‘forensic veterinary statement’. The responsibility to prove or disprove a suspected case of neglect or abuse does not lie on the veterinarian. The veterinarian’s forensic statement is only part of the case and is provided to help the judge and jury understand the evidence. Therefore, it should be written for a lay audience and impartial. 3 491

Unfortunately, there is not a standard format for the veterinary forensic statement. However, it is more than just the physical examination. The following components are recommended for the forensic statement and should be completed for each animal if possible: (Eller 2016) 1. Introduction a. Investigating agency, lead officer, case number and animal identification b. Reason for the examination c. Date, time, and location of the examination d. Signalment and other identifying information as well as photographs of the animal(s) 2. Scene findings a. Personal observations or information provided b. Photographs where indicated 3. History a. A medical history for the animal(s) may or may not be available 4. Medical findings a. Physical examination and findings b. Pain assessment as applicable c. Diagnostic tests and results as well as an explanation of results d. Treatment provided and response 5. Necropsy results when indicated a. Gross description of findings b. Presentation of the body c. Postmortem changes d. Ancillary procedures and lab reports e. Photographs and lab results f. Cause and manner of death g. Interpretation and explanation of findings 6. Conclusions Involvement in many equine abuse or neglect cases often result in a veterinarian’s testimony before a court. That is because in order to be successful, prosecutors must show: • • •

The nature, severity and duration of an animal’s injury or abuse The cause of the injury or death In some cases, the degree to which the animal suffered or experienced pain as a result of its injuries.

All of which fall under the expertise of a veterinarian. 4 492

Testifying as an expert witness is often an unfamiliar and uncomfortable scenario for many so an understanding of what is to be expected of them is critical. Once a veterinarian is contacted by animal control officers, law enforcement officers or a humane shelter to aid in the seizure of an animal(s) or to examine and treat an animal(s) that is believed to have been mistreated or abused the veterinarian becomes a witness in the case. Therefore, it is imperative that the veterinarian’s written records, videos, photographs, necropsy findings and laboratory tests findings be well documented. Court appearances for an expert witness vary among states and municipalities. However, in most cases the animal control or law enforcement officer provides testimony as to what warranted the investigation or seizure of the animal(s), not the veterinarian. The veterinarian may then be called as an expert witness once criminal charges have been assigned and a trial date has been set. Prior to the court date, it is recommended to schedule an appointment with the prosecutor to review your qualifications and the medical condition of the equids that were seized or treated, the environment in which they were found, quality of feed, care, etc. When appearing in court, dress in business rather than work-related clothing as it implies you are a professional. Be prepared to provide the court proof of your current veterinary license, business license and identification. They are usually provided to the prosecution prior to the court appearance. Rule 702 of the Federal Rules of Evidence defines an expert witness as ‘a person that can provide knowledge on a subject that is not limited merely to the scientific and technical but extends to all specialized knowledge in that field’, thereby allowing for opinions within the parameters of the witness’s expertise. (Cornell Law School – 2011) To qualify you as an expert witness, the prosecutor will ask a series of questions about your education and professional employment as a veterinarian. Always be generous with your veterinary qualifications, professional accolades and publications as they all substantiate your title as an expert witness. Have dates of veterinary merits and provide articles you have authored. Once qualified, it’s important to remember that you know more about the subject than anyone else in the room. Be prepared for the defense attorneys to attempt to undermine your expertise. Use your time in the witness stand to educate both the prosecution and the defense. It is often difficult for the jury or court to understand how to assess a horse’s weight or Body Condition Score (BCS) in the field so bring a weight measuring tape along with a BCS Score chart for a visual effect. Photographs are always better than a description which may be inadequate for some jurors. Use lay terms rather than medical terms when describing body parts or medical conditions. Listen carefully to the question asked and answer concisely only that question. For instance, if the attorney asks if you know the coat color of the horse that was seized, the answer is either yes or no and not sorrel, dun, bay, etc. The prosecutor will guide your responses if more information is required. However, you do have the right to explain your answers beyond yes and no if that answer is incomplete. If you do not know an 5 493

answer to a question than state that you do not know the answer. ‘I do not know’ is an accurate and legitimate response. (Mason 2019) Veterinarians may become involved in a potential case of animal abuse or neglect by reporting a suspected or known case of animal abuse to the appropriate authority, by being asked by law enforcement to assist with the investigation of a case or by being called as an expert witness in a civil or criminal case. Therefore, it is important to be familiar with animal cruelty laws in a given jurisdiction as well as understand what enforcement authority has jurisdiction and should be contacted to report a suspected case of abuse or neglect. In addition, veterinarians assisting law enforcement must have a thorough understanding of their role and how to identify, collect and preserve forensic evidence.

Cornell Law School. Rule 792. Article seven. Testimony by expert witnesses. www.law.cornell.edu 2011: #792 Eller E, Touroo R. The Equine Veterinarian’s Role in Potential Cases of Animal Abuse. AAEP Proceedings 2016, Vol. 62, 199-207 Gardner RM, Practical Crime Scene Processing and Investigation. Boca Raton, FL: CRC Press 2011 Glasere ME, McCobb E. How can veterinarians report animal abuse if they don’t know who to report it to? J Am Vet Med Assoc 2016,248(9):992-993 Mason, CA, How to be An Effective Expert Witness In An Equine Abuse/Neglect Case, Publication pending Practical Guidance for the Effective Response by Veterinarians to Suspected Animal Cruelty, Abuse and Neglect. (www.avma.org) Robertson, IA. (2010) Legally protecting and compelling veterinarians in issues of animal abuse and domestic violence. New Zealand Veterinary Journal 58(3), 114-120

6 494

Special Interest

495

496

Special Interest

Michael R. Boeger

Administrator, Missouri Bureau of Narcotics and Dangerous Drugs Jefferson City, Missouri

497

498

Missouri Bureau of Narcotics & Dangerous Drugs

Michael R. Boeger, Administrator

REGISTRATION ISSUES Applications are available on our website at https://health.mo.gov/safety/bndd As a courtesy, reminder emails are sent out 60 days in advance of the expiration date. Registrations are issued at a Missouri practice location only, where patient care occurs and controlled substance activities take place. A separate mailing address may be provided on the application. Applications can be completed online.

Purchasing Controlled Substances You must have both a BNDD and DEA registration. You may delegate the ordering of controlled substances in Schedule III—V to another employee, however the registrant is responsible. Schedule II purchases and transfers require a DEA Form 222 Official Order Form, which may only be signed and executed by the DEA registrant. Another person may be authorized to execute the DEA form for the practitioner if there has been a Power of Attorney Form executed.

499

The Bureau’s Authority • Chapter 195, RSMo and the Controlled Substances Act • Record keeping • Security • No authority regarding clinical issues or proper treatment • No powers of arrest or monetary penalties

Registration Issues (Cont.) 9 If you change practice locations from what is printed on your registration, you must notify the Bureau within 30 days or your registration terminates. 9 Controlled substance activities require a BNDD registration. Associate DVMs who are employees may administer under their employer’s DEA number. 9 All veterinarians must have their own DEA number in order to prescribe controlled drugs. 9 Separate registrations are required for separate locations where controlled substances are stored.

Controlled Substance Storage • Do not leave drugs left un-attended in patient care areas. • Controlled substances must be stored in a securely locked, substantially built cabinet.

Initial Inventory • The first time you receive controlled substances, you must perform an initial inventory. • A specific “stand-alone” document on file. • Registrant name & DEA number • Date taken • Opening of Business or Close of Business or Time of Day inventory was taken • Drug name, drug strength, dosage form and quantity on hand. • Number of containers & doses in each container; • A Schedule II inventory shall be separate than A Schedule III—V inventory.

Annual Inventory Controlled substances must be inventoried at least once a year. This is a specific “stand-alone” document on file. A daily ongoing perpetual log is not sufficient. Registrant name and DEA number Date taken Opening of Business, Closing of Business, or Time of Day Drug name, drug strength, dosage form and quantity on hand. Number of containers and doses in each container. Schedule II inventories shall be separate from Schedule III—V inventories.

Receipt Records For Schedules III—V

Receipt Records for Schedule II

• You must maintain a record of all controlled substances received. • Supplier’s name, address and DEA number • Receiver’s name, address and DEA number • Drug name, drug strength, dosage form and quantity received DATE RECEIVED If you save invoices as your records of receipt, the date you received the drugs is not on the invoice so you must date each of these invoices.

• The DEA Form 222 Official Order Form is the record. • Once the drugs received have been “checked in”, the third copy of the Order Form must be initialed and dated to show what date the drugs were received.

Transferring Possession

Definitions

• Prescriptions are for patients only. A prescription may not be issued to obtain drugs for office stock. • Office stock must be purchased or transferred from another registrant. • Records of transfers received or transferred out may be stored with other receipt records. • Transfer records must include the same information as receipt records; names, addresses and DEA numbers of both registrants, date, drug name, drug strength, dosage form and quantity.

500

• Prescription: A written order to be filled at a pharmacy. It may be a written prescription or telephoned to the pharmacy. • Administer: To apply the drug to the patient yourself or observe the patient taking the drug. • Dispense: To give a supply of drugs to a patient for future use and allow them to leave your office with drugs in their possession.

Documenting Patient Charts All controlled substance activities regarding patients, must be documented in the patients’ charts. Prescriptions written or phoned in must be documented in the chart. Drugs administered in the office must be charted. Drugs dispensed must be charted. The information required on a prescription must be charted: date, drug name, drug strength, dosage form, quantity, instructions for use and refills authorized.

Dispensing Containers & Labels • Dispensing must be in containers approved by the U.S. Food & Drug Administration; • Child resistant containers must be used; • All dispensing laws regarding proper labeling must be followed; • Name and address of the dispensing practitioner; • Name of the patient • Drug name, drug strength, dosage form, quantity and directions for use; • Warning sticker/label advising it is illegal to transfer controlled substances to another individual.

Disposing of Unwanted Drugs Drugs and partial doses contaminated by patient contact may be destroyed on site. The drugs must be destroyed beyond reclamation. On the log, document all of the administration information, the amount wasted and the reason for the waste. The wastage must be witnessed by a second person and the second person must sign/initial the log. Unwanted drugs that are expired and not contaminated, must be transferred back to the manufacturer, distributor or a reverse distributor. Only destroy on site with permission from the DEA and DEA Form 41.

501

Administration & Dispensing Log Separate • Controlled substances that are dispensed from your office stock, must be recorded on a separate log, that is separate from the patients’ charts. • A separate log for drugs administered in the office is highly advisable so that you can review drug usage without examining hundreds of patient charts. • Date, patient name & owner/ address, drug name, dosage form, drug strength, quantity and initials of person administering or dispensing. (Veterinarians—species recorded)

Dispensing for a Herd • • • • •

Obtain the species of animal; (Hogs to be cut) Number of animals in the herd (150) Average weight and/or size (X pounds) Determine the average dose per animal (one vial) Multiply the number of doses times the number of animals in the herd. • Dispense the number of vials required • DOCUMENT YOUR WORK AND CALCULATIONS • Do not dispense a supply for “general future use”

General Record Keeping Issues • All controlled substance records must be maintained at the registered site. • All controlled substance records must be maintained for two years. • All controlled substance records are open for inspection & copying by the Bureau and law enforcement officers.

Documents Available on Website www.health.mo.gov/BNDD

Keeping a Closed Loop

Manufacturer

Reverse Distributor Destruction

Distributor

Practitioner

End User

PREVENT DRUG DIVERSION

200 3,200 3,400

Drugs administered and dispensed 1,600 Drugs sent to reverse distributor 100 Drugs contaminated/destroyed on site 10 Dosage Units no longer in your possession 1,710

Drugs that should be in your safe

5mg tablets 5mg tablets 5mg tablets

5mg 5mg 5mg 5mg

tablets tablets tablets tablets

• • • • •

502

• The practitioner may delegate duties and tasks, but compliance with all controlled substance laws is the responsibility of the registrant.

• Registrants should have policies and procedures in place to train and instruct staff on what is required. • The registrant should perform regular reviews to insure that policies, procedures and laws are being complied with.

3,400 – 1,710 = 1,690 tablets

Most Common Violations • • • • •

Application for Registration Change of Address Form Print your certificate Controlled Substances Transfer Form Dispensing Log Form List of Reverse Distributors Waiver Forms for Employees with Drug Crimes Practitioner’s Guide to Prescribing, Administering & Dispensing Controlled Substances in Missouri • Theft of Controlled Substances Report Form (State form only) • Preventing Prescription Fraud

Registrant Responsibility

Auditing Your Drugs Drugs on hand on annual inventory Drugs received since that date Total dosage units your responsible for

• • • • • • • •

Practitioner moved and did not notify the Bureau; Failure to maintain an annual inventory; Failure to document controlled substance prescriptions in patient chart; Invoices used for tracking receipt of drugs and date not documented; Schedule II annual inventory on same document as Schedule III—V annual inventory; Annual inventory is not marked as “Opening of Business”, “Closing of Business;” Unwanted drugs illegally destroyed and not reversed; Drugs wasted not witnessed and documented with a witness; Dispensing in unapproved containers; Dispensing in containers without proper labeling

Protecting Your Practice (Handout Provided)

• It is the professionally licensed practitioner that has the most knowledge. It is the registrant that has all the responsibility.

• Protect your controlled substance activities against diversion, but also have controls, policies and procedures in place to monitor your employees. • Violations are caused by the activities of the personnel in the practice. • Brief review of Protecting Your Practice handout

Available Resources BNDD P.O. Box 570 Jefferson City, MO 65102-0570 (573) 751-6321 Fax (573) 526-2569 www.health.mo.gov/BNDD

DEA—St. Louis 317 S. 16th Street St. Louis, MO 63103 (314) 538-4600

Mo. Veterinary Medical Board P.O. Box 633 Jefferson City, MO 65102-0633 (314) 751-0031 Fax (573) 526-3856 www.pr.mo.gov/veterinarian.asp

DEA—Overland Park, KS 7600 College, Suite 100 Overland Park, KS 66210 (913) 951-4100

www.deadiversion.usdoj.gov

Thank You !! The BNDD thanks the Missouri Veterinary Medical Association for hosting this conference and inviting our Bureau.

Univ. of Missouri Mule Team

503

QUESTIONS & DISCUSSION

504

Special Interest

Carol Ryan, DVM

Practitioner - Troy & Wentzville Veterinary Clinic Wentzville, Missouri

505

506

1/6/2020

Standards for Missouri Veterinary Medical Records

Carol Ryan, DVM President Missouri Veterinary Medical Association

Who establishes the minimum standards for veterinary medical records?

The Missouri Veterinary Medical Board has the power to fix minimum standards for the practice of veterinary medicine. 300.210

Missouri Veterinary Medical Board

Duties of the Board

 The board is composed of four members possessing a license to practice veterinary medicine, one voting public member and the state veterinarian.

 Examine and determine qualifications for

the licensing of veterinarians and technicians

 Issue, renew, deny, suspend, revoke, place

 Board members are appointed by the Governor with the consent of the Senate.

on probation or otherwise discipline licenses, certificates and permits

1 507

1/6/2020

Missouri Veterinary Medical Board

Duties of the Board

The board establishes minimum standards for the following

 Investigate complaints

 Veterinary facilities  Emergency clinics/services  Veterinarian‐client‐patient

 Address complaints through disciplinary

hearings, informal conferences or other legal means if necessary

relationship  Continuing education and medical records

 Establish minimum standards for the

practice of veterinary medicine

Medical Records

2 508

1/6/2020

“Medical Record Jackpot”

Why must our medical records be in tip‐top shape?

Could your veterinary medical records defend your actions in a legal case?

Veterinary Medical Records Our Missouri Veterinary Practice Act requires it. Our Veterinary Oath states it. “I will practice my profession conscientiously, with dignity, and in keeping with the principles of veterinary medical ethics.”

Our patients deserve it! Modern society demands it!

Missouri Veterinary Practice Act

“…when a complaint is filed against a veterinarian with insufficient records it is difficult for a veterinarian to defend his or her actions. You’ve heard the saying, ‘if it’s not in the record, it didn’t happen.’ Even with the most convincing testimony, the medical record is the official recording of the events and procedures.”

0LQLPXP 6WDQGDUGV IRU 0HGLFDO 5HFRUGV

Every veterinarian performing any act requiring a license upon any animal or group of animals shall prepare a legible, written record. The medical record will provide documentation that an adequate physical examination was performed.

Ludwig, High Record‐Keeping Standards are Essential for Quality Practice, Vol. 5, no. 1 State Board Report

3 509

1/6/2020

What should be included in the medical record?

Missouri Veterinary Practice Act Minimum Standards for Medical Records (A) Name, address and telephone number of the animal’s owner or agent. (B)

Name and/or identity of the animal(s), including age, sex, breed, weight and color, where appropriate.

Missouri Veterinary Practice Act Minimum Standards for Medical Records

Minimum Standards for Medical Records (C) A brief history (D) Notations of physical examination (E) Treatments and/or intended treatment plans, including medications, amounts administered, dispensed or prescribed and frequency of use

Missouri Veterinary Practice Act

(F) A diagnosis or tentative diagnosis (G) When pertinent, a prognosis (H) Progress notes and disposition of the case.

Missouri Veterinary Practice Act

Minimum Standards for Medical Records (I) Dates (beginning and ending) of custody of the animal with daily notations (J) In case of vaccination clinics, a certificate including the information may serve as the medical record

Minimum Standards for Medical Records (K) The veterinarian who created the record (L) Name of the veterinarian who orders any radiographs

4 510

1/6/2020

Minimum Standards of Records Computer records are acceptable medical records so long as the security of the computer is maintained. Daily and monthly back‐ups shall be made.

Minimum Standards of Records Keep back‐up data/material off‐site; away from the clinic in case of fire or other disaster. Also, consider keeping old paper files, x‐rays, ultrasounds and other images off‐site.

All records shall be maintained 5 years after the last visit.

How long should medical records be kept?

Minimum Standards of Radiographs

Radiographs are the property of the veterinarian or the facility that ordered it.

Radiographs prepared by a veterinarian are the property of ??????

5 511

1/6/2020

Minimum Standards

How long should radiographs be kept?

Radiographs prepared by a veterinarian are the property of the VETERINARIAN or the facility and, if provided to the client, are to be returned by the client.

R.S. Mo. § 340.264.2(4)

Copies of radiographs will be made available within a reasonable amount time upon request of another treating veterinarian who has the authorization of the owner…or directly to the owner. 20 C.S.R. § 2270-4.041(2)

Minimum Standards

A [veterinarian] shall obtain the informed written consent of the client prior to placing any patient under anesthesia or performing any surgical procedure, or both, except in an emergency.” 20 C.S.R. § 2270‐6.011(19).

Radiographs shall be maintained 5 years from the date the radiograph was taken. 33

Every animal shall be given a physical exam within ?? hours prior to the administration of anesthesia. 20CSR2270‐4.031

Client ‐Not Veterinarian ‐Owns

Veterinarian Owns the Records

Privilege

Client Has a Right to Obtain a Copy

Generally, medical records are owned by the veterinary practice and, subject to meeting the requirements of any state veterinarian‐client privilege law, may be sold with a veterinary practice. The client has a right to obtain a copy of its veterinary medical records and can direct that a copy be provided to another veterinarian or person. See R.S. Mo. § 340.264.2(4)(k); 20 C.S.R. § 2270‐4.031(1)(B)

Grounds for Discipline: A veterinarian’s failure to comply with requirements of confidentiality might be grounds for disciplinary action. R.S. Mo. 340.286

Client’s Request for Records: Should a client request copies of records and the veterinarian refuse to release them, this may also be grounds for disciplinary action. R.S. Mo. 340.264.2(4)

6 512

1/6/2020

Consent to Release Information Do not release information or records simply because someone asks for them–even another veterinarian. First obtain the client’s written consent. If prior written consent is not possible (e.g., emergency situation), then directly speak to the client, obtain their verbal consent, document the consent in the file, and promptly send a written consent release form to the client for signature.

Client’s Request / Instruction to Release Records to Another Veterinarian should a client “choose to consult with or utilize the services of another veterinarian, the licensee shall withdraw from the case if so requested. The licensee shall indicate the circumstances for withdrawal on the medical records and shall cooperate fully with the other veterinarian to include the transmittal of a copy of all pertinent medical records upon the request of the other veterinarian or client.” 20 C.S.R. 2270-6.011(9)

Who “Owns” Patient Records Between a Veterinarian‐Employee / Partner and a Practice?

Controlled Substances

Medical records are the property of the practice and the practice owner.”

Bureau of Narcotics & Dangerous Drugs, Missouri Department of Health & Senior Services, Controlled Substance Guidelines for Missouri Veterinarians

Principles of Veterinary Medical Ethics, VII

“ Without the express permission of the practice owner, it is unethical for a veterinarian to remove, copy, or use the medical records or any part of any record.”

‐Available at Missouri Veterinary Medicine Board www.PR.MO.GOV

GET One and READ It! 40

Controlled Substances “Each and every time controlled substances changes hands or is used documentation must be generated and maintained. There should be a paper trail to show the path of a controlled substance dosage unit from the day it was manufactured, though the distributor, to the pharmacy, to a practitioner and then ultimately to the end user.” Controlled Substance Guidelines for Missouri Veterinarians

7 513

1/6/2020

Controlled Substances

“State and federal controlled substance laws require all controlled substance records to be maintained

Controlled substance records must be maintained for 2 years.

These records must be maintained at the registered practice location and must be readily retrievable and open to inspection and copying by the BNDD.” Controlled Substance Guidelines for Missouri Veterinarians

for ?? years. 43

Disciplined Veterinarians

Veterinarian’s medical records on treatment of a 19‐ year old thoroughbred mare did not contain: the owner’s address and telephone number; indicate the mare’s identifying characteristics; nor a medical history.

Controlled substance record‐keeping violations resulting in 3‐years probation by the BNDD and public censure by the veterinary medicine board.

1‐year probation; re‐sit & successfully pass the state board examination; 10 additional CE hours (at least 2‐ hours in recording keeping, professionalism & ethics).

Vol. 6, no. 1 State Board Report, p. 8 (Nov. 2007).

Vol. 6, no. 1 State Board Report, p. 10 (Nov. 2007).

Disciplined Veterinarians Controlled substance record‐keeping and security violations were found by the BNDD. Also, veterinarian did not document drug name, strength and dosages in records. Concurrent 3‐years probation by BNDD and Board. Also, 10 additional CE hours (at least 1‐hour in record keeping and 1‐hour in controlled substances). State Board Report, pp. 8 ‐ 9 (Nov.

2007).

Let’s review!  Name, address and telephone of animal’s owner or agent  Identity, of the animal(s), age, sex, breed, weight and color  A brief history  Notations of physical examination  Treatments or intended treatments, medication, amounts administered, dispensed or prescribed and frequency of use.  A diagnosis or tentative diagnosis.

8 514

1/6/2020

Missouri HAD a five-year statute of limitation for veterinary malpractice.

Let’s review! When pertinent, a prognosis Progress notes Dates (beginning and ending) of custody of the

animal with daily notations

Vaccination clinics, a certificate including this

information may serve as the medical record. The veterinarian who created the record The veterinarian who ordered radiographs

How Long Should You Retain Veterinary Records? Keep veterinary medical records for as long as you might be subject to a lawsuit.

Veterinary records must be kept 5 years after the last visit. Radiographs must be kept for 5 years from the date taken. “State and federal controlled substance laws require all records to be maintained for two years

Continuing Education

Notify the board within 60 days of a name change. Notify the board within 30 days of an address change. If a veterinary facility changes ownership, name or location CONTACT the board office immediately to apply for new permits

•The report period runs from December 1st and

ends November 30th

•Every veterinary licensee shall obtain at least 10 hours and technicians 5 hours yearly. •A licensee who completes more than ten hours may carry over those hours to the next reporting period, not to exceed 10 hours. (Self study hours can not be carried forward.)

9 515

516

MU-CVM Lectures

517

518

MU-CVM Lectures

Karen Campbell-Motsinger, DVM, DACVIM, DACVD Clinical Professor of Dermatology MU-College of Veterinary Medicine Columbia, Missouri

519

520

521

522

523

524

525

526

527

528

529

530

531

532

MU-CVM Lectures

Pamela Adkins, MS, DVM, PhD, DACVIM

Assistant Professor of Food Animal Medicine and Surgery University of Missouri, College of Veterinary Medicine. Columbia, Missouri

533

534

10/30/2019

The Impact of Heat Stress on Cattle

Introduction Heat stress occurs when animals are unable to maintain equilibrium between heat accumulation and heat dissipation Heat stress = significant economic burden Climate change = increased prevalence and intensity

Pamela R. F. Adkins University of Missouri

Heat Stress

Neuro-endocrine responses: ↑ cortisol (stress hormone) ↑ Aldosterone (regulation of water) ↑ ADH (regulation of blood osmolarity) ↑ catecholamines (controlling stress activities)

• Combination of temperature, humidity, radiation and wind that produce conditions higher than the animals thermal neutral zone • Temperature humidity index (THI) • Heat load index (HLI)

Metabolic responses: Thyroid hormones ALP NEFA

Heat Load

• Incorporates animal factors and environmental conditions on thermal comfort of animals • • • • • •

Blood biochemical responses: ↑ Haptoglobin ↑ PCV ↑ Hemoglobin ↑ SOD and GPx

Genotype Coat type and color Diet type and composition Body condition – fat coverage Performance – growth and lactation Heath Status

Cellular responses: Heat shock proteins Thyroid hormone receptor gene Prolactin receptor gene

Behavioral responses: Shade seeking Reduced feed intake Increased water intake Increased standing

Physiologic responses: Cutaneous evaporation ↑RR ↑ Rectal temperature ↑ Pulse ↑ Skin temperature

Sullivan et al., 2018

Heat Stress

Sejian et al., 2018

Additional Variable - Fescue

• Most susceptible: Dairy and feedlot cattle

• Endophyte infected fescue -> Summer slump syndrome • Reduced ability to dissipate body heat because of pressor effects of ergot alkaloids

• Clinical heat stress

• Heat waves can result in death of cattle – usually after several days of high temps • June 2017 – 4000-6000 dairy cattle died in California during a heat wave • 1999 – over 5000 feedlot cattle died during extreme heat wave in NE Nebraska

• Results in hyperthermia, ↑ RR, respiratory distress, rough coats, hypersalivation • Peripheral vasoconstriction = reduced dissipation of body heat and reduced evaporative heat loss

• Subclinical heat stress ($$)

• Reduced dry matter intake AND increased maintenance requirements • Impact on immune system and production Lees et al., 2019

1 535

10/30/2019

Clinical Signs of Heat Stress

Multiple stressors

• Respiratory changes are the first visual changes seen during hot conditions

• ≥ 3.5 at extreme risk of dying

Sullivan et al., 2018

Sejian et al., 2018; Lees et al., 2019

Clinical Signs of Heat Stress • Cattle coping with heat stress • • • • • • • • •

Body alignment with solar radiation Shade seeking Increased time spent standing Reduced dry matter intake Crowding over water troughs Body splashing Aditation and restlessness Reduced or stopped rumination Bunching to seek shad from other cattle

Subclinical signs of heat stress

• Cattle NOT coping with heat stress • • • • • •

Open-mouth and labored breathing Excessive salivation Ataxia/inability to move Collapse, convulsion, coma Physiologic failure Death

• Reproduction • Health • Productivity • Growth • Milk production and composition

Sullivan et al., 2018

Subclinical signs of heat stress • Reproductive impacts – Females • • • • •

Conception rates down 20-30% during summer months Altered follicular development and corpus leteum regression Impaired ovarian function and embryonic development Reduced uterine blood flow Reduced expression of estrus behavior

Pennington et al., 1985; Jonsson et al, 1997; Wilson et al., 1998; Wolfenson et al., 2000; Al-Katanani et al., 2002; García-Ispierto et al., 2006; Schüller et al., 2017; Lees et al., 2019

Burke et al., 2001

2 536

10/30/2019

Subclinical signs of heat stress

Subclinical signs of heat stress • Health

• Heat stress associated with increased incidence of disease • Health status influence ability to cope with heat

• Reproductive impacts – Males

• Ex: Previous pneumonia = RR 10.5% higher

• Heat load adversely affects spermatogenesis and/or the viability of stored spermatozoa • Recovery from a single heat-related insult can be as long as 8 weeks

• Productivity and Growth

• Absorbable nutrients are diverted from growth and development to maintaining body temperature

• Milk Production

• Decline in milk yields due to reduced DMI (accounts for 35-50% of reduction) • Negative associated with milk fat and protein composition

Casady et al., 1953; Lees et al., 2019; Sabés-Alsina et al., 2019

Detecting subclinical heat stress

Mitigation opportunities

• Currently based on THI, HLI, etc. • Gene expression markers • Fecal Microbiome – marker for disease?

No single strategy has been found capable of returning performance to thermoneutral levels Environmental modifications ↓ Solar radiation ↑ air movement Evaporative cooling Wetting cows Conductive cooling

Mitigation opportunities

Management Strategy

Nutrition High energy diets Antioxidants Managing the proportion of roughage in the diet Altering feeding time to ↓ metabolic heat loads during hottest hours

Negrón-Pérez et al., 2019

3 537

10/30/2019

References Al-Haidary, A., D. E. Spiers, G. E. Rottinghaus, G. B. Garner, and M. R. Ellersieck. 2001. Thermoregulatory ability of beef heifers following intake of endophyte-infected tall fescue during controlled heat challenge. J Anim Sci 79(7):1780-1788. Al-Katanani, Y. M., F. F. Paula-Lopes, and P. J. Hansen. 2002. Effect of season and exposure to heat stress on oocyte competence in Holstein cows. J Dairy Sci 85(2):390-396.

Questions?

Bagath, M., G. Krishnan, C. Devaraj, V. P. Rashamol, P. Pragna, A. M. Lees, and V. Sejian. 2019. The impact of heat stress on the immune system in dairy cattle: A review. Res Vet Sci 126:94102. Burke, J. M., D. E. Spiers, F. N. Kojima, G. A. Perry, B. E. Salfen, S. L. Wood, D. J. Patterson, M. F. Smith, M. C. Lucy, W. G. Jackson, and E. L. Piper. 2001. Interaction of endophyte-infected fescue and heat stress on ovarian function in the beef heifer. Biol Reprod 65(1):260-268. Casady, R.B., R. M. Myers, J. E. Legates. 1953. The effect of exposure to high ambient temperature on spermatogenesis in the dairy bull. J. Dairy Sci. 36: 14-23. Garcia-Ispierto, I., F. Lopez-Gatius, P. Santolaria, J. L. Yaniz, C. Nogareda, M. Lopez-Bejar, and F. De Rensis. 2006. Relationship between heat stress during the peri-implantation period and early fetal loss in dairy cattle. Theriogenology 65(4):799-807. Gaughan, J. B., T. L. Mader, S. M. Holt, and A. Lisle. 2008. A new heat load index for feedlot cattle. J Anim Sci 86(1):226-234. Jonsson, N. N., M. R. McGowan, K. McGuigan, T. M. Davison, A. M. Hussain, M. Kafi, and A. Matschoss. 1997. Relationships among calving season, heat load, energy balance and postpartum ovulation of dairy cows in a subtropical environment. Anim Reprod Sci 47(4):315-326. Lees, A. M., V. Sejian, A. L. Wallage, C. C. Steel, T. L. Mader, J. C. Lees, and J. B. Gaughan. 2019. The Impact of Heat Load on Cattle. Animals (Basel) 9(6). Negron-Perez, V. M., D. W. Fausnacht, and M. L. Rhoads. 2019. Invited review: Management strategies capable of improving the reproductive performance of heat-stressed dairy cattle. J Dairy Sci. Pennington, J. A., J. L. Albright, M. A. Diekman, and C. J. Callahan. 1985. Sexual activity of Holstein cows: seasonal effects. J Dairy Sci 68(11):3023-3030. Sabes-Alsina, M., N. Lundeheim, A. Johannisson, M. Lopez-Bejar, and J. M. Morrell. 2019. Relationships between climate and sperm quality in dairy bull semen: A retrospective analysis. J Dairy Sci 102(6):5623-5633. Schuller, L. K., I. Michaelis, and W. Heuwieser. 2017. Impact of heat stress on estrus expression and follicle size in estrus under field conditions in dairy cows. Theriogenology 102:48-53. Sejian, V., R. Bhatta, J. B. Gaughan, F. R. Dunshea, and N. Lacetera. 2018. Review: Adaptation of animals to heat stress. Animal 12(s2):s431-s444. Sullivan, K. F. and T. L. Mader. 2018. Managing Heat Stress Episodes in Confined Cattle. Vet Clin North Am Food Anim Pract 34(2):325-339. Wilson, S. J., C. J. Kirby, A. T. Koenigsfeld, D. H. Keisler, and M. C. Lucy. 1998. Effects of controlled heat stress on ovarian function of dairy cattle. 2. Heifers. J Dairy Sci 81(8):2132-2138. Wolfenson, D., Z. Roth, and R. Meidan. 2000. Impaired reproduction in heat-stressed cattle: basic and applied aspects. Anim Reprod Sci 60-61:535-547.

Contact: adkinsp@missouri.edu

4 538

MU-CVM Lectures

Tim Evans, DVM, MS, PhD, DACT, DABVT

Associate Professor, MU Department of Veterinary Pathobiology Toxicology Section Head, MU Veterinary Medical Diagnostic Laboratory Columbia, Missouri

539

540

Free Toxicology Information Resources for Veterinarians Tim J. Evans, DVM, MS, PhD, DACT, DABVT Small, mixed, and large animal practitioners can use a variety of free online/electronic resources to access critical information about potential toxicants. These resources will be discussed and demonstrated during this lecture. General Veterinary Toxicology Electronic Resources:  Lists of potential toxicants/Helpful publications/Links to podcasts and webinars  http://www.petpoisonhelpline.com/separate tabs for pet owners and veterinarians  https://www.aspca.org/pet-care/animal-poison-control for pet owners  http://aspcapro.org/poison for pet professionals  Phone apps available and phone consultations available on a fee for service basis U.S. Government Websites:  http://www.fda.gov/AnimalVeterinary/default.htm ▪ Website for Food and Drug Administration ▪ Go to Animal & Veterinary tab for veterinary drug-specific information ▪ Useful regulatory information on pet food contaminants/recalls ▪ Mechanism for reporting adverse drug reactions/pet food-related incidents ▪ Other helpful information on veterinary medications ▪ Also useful information on human medications  https://www.fda.gov/animal-veterinary/science-research/veterinary-laboratoryinvestigation-and-response-network ▪ Website for Veterinary Laboratory Investigation and Response Network (Vet-LIRN) ▪ Investigates animal illnesses caused by food or drugs ▪ Another potential mechanism for reporting pet food-related incidents  http://www.ncbi.nlm.nih.gov/pubmed/ ▪ PubMed literature search  http://www.niehs.nih.gov/health/topics/index.cfm ▪ Website for National Institute of Environmental Sciences ▪ Information pertaining to environmental health  https://www3.epa.gov/ ▪ Website for U.S. Environmental Protection ▪ Environmental contamination ▪ Superfund sites ▪ Pesticides ▪ Heavy metals ▪ Organic pollutants  http://www.atsdr.cdc.gov/ ▪ Website for Agency for toxic Substances and Disease Registry ▪ Operated by Center for Disease Control ▪ Information on many toxicants of human and veterinary importance ▪ Toxicological Profiles ▪ Tox FAQs™

541

Useful Toxic Plant Electronic Resources:  http://www.aspca.org/pet-care/animal-poison-control/toxic-and-non-toxic-plants ▪ List of toxic and “nontoxic” plants  http://www.ansci.cornell.edu/plants/http://www.petpoisonhelpline.com/  http://www.petpoisonhelpline.com/  http://www.vth.colostate.edu/poisonous_plants/report/search.cfm  https://www.erowid.org/ ▪ Psychoactive plants/drugs Miscellaneous Helpful Websites:  http://www.msds.com/ ▪ Website for free access to material safety data sheets (MSDS)  http://www.snopes.com/ ▪ Useful for urban legends/e-mails forwarded by your mother  http://www.merckvetmanual.com/mvm/index.jsp ▪ Generic animal disease information  http://www.ahc.umn.edu/rar/umnuser/formulary.html ▪ Free veterinary drug formulary  https://www.avma.org/News/Issues/recalls-alerts/Pages/default.aspx ▪ American Veterinary Medical Association website on pet food recalls

542

MU-CVM Lectures

Martha Scharf, DVM, AVBP (Equine)

Equine Ambulatory Veterinarian MU Equine Clinic - College of Veterinary Medicine Columbia, Missouri

543

544

10/28/2019

Equine Parasitism • Result

Equine Fecal Egg Counts

of modern equine management

 Stocking density  Lack of herd migration  Allows for increased contamination and infection

• Has

led to problems with parasitism and overall health

Martha Scharf, DVM, DABVP (Equine Practice)

Equine Parasite Management

Resistance

• Owners

•

Normal mutations occur in nature by chance

•

Inappropriate use of dewormers by owners and veterinarians

and veterinarians have been systematically deworming horses since the 1960s

   

 Most historical protocols lack clinical justification •

Resistance •

Resistance is documented in every major class of dewormers used in horses

•

Cyathostomes

Nielsen, 2014

 Benzamidazoles – most farms, since 1960s Drudge and Lyons 1965

 Pyrantel – many farms (worst in US), since 1996

Kaplan et al, 2004, Traversa et al 2009

 Macrocyclic lactones – isolated reports, decreased ERP

•

Ascarids

von Samson-Himmelstjerna et al 2007, Lyons et al, 2009, 2010, 2011

 Macrocyclic lactones – widely reported worldwide, including farms in KY

 Deworming selects for survival of resistant parasites Excessive frequency Underdosing Off-label use – differing pharmacokinetics Treatment of uninfected horses

Detectable by 25% but uncorrectable by then

 Cessation of use will not alleviate resistance  Exact criteria to prevent resistance are unknown  Need to aim for prevention and detection at low levels

Novel Anthelminthics •

No new medication for equine parasites since the early 1980s; no immanent prospects  Three new drug classes for nematodes

 Emodepside (cyclo-octadepsipeptide) – canine and feline Harder and von Samson Himmelstjerna, 2002  Monepantel (amino-acetonitrile derivatives) – ruminants Kaminsky, 2008  Derquatel (spiroindoles) - sheep Maeder. 2010

 Not yet tested on or not well tolerated in horses, safety or efficacy Neilsen, 2014

Boersema et al 2001, Hearn and Peregrin, 2003, von Samson-Himmelstjerna et al 2007, Schougaard and Neisen 2007, Lind and Christensson 2009, Veronesi et al 2010, Nareaho et al 2001, Laugier et al 2012

•

Tapeworms and Pinworms

 Anecdotal reports, not well documented

545

10/28/2019

Strategy •

Surveillance Programs

Eradication vs Control

Goals:

•

 Want to maintain a low-level, low-threat population

Minimize risk of parasitic disease

 Refugia – remain susceptible to anthelminthics

   

 Breed with resistance parasites  dilute genes and help to maintain susceptibility

 Reduce shedding and contamination •

Identify horses that will shed and contaminate the pastures

 Allow less infected horses to remain untreated for most of the year

Minimize anthelminthic treatment intensity

 Minimize resistance

Adequate control of egg shedding

Fecal Egg Counts

Fecal Egg Counts •

Reported and recommended for almost 30 years

•

Fecal Flotation vs Fecal Egg Count

•

Multiple accepted techniques

•

Gomez and Georgi, 1991; Duncan and Love, 1991

 Qualitative vs quantitative

 Most FEC techniques are sensitive – limits of detection vary from 1 – 100 EPG  Wisconsin technique is the most precise for horses Paras, 2018

Best at detecting strongyle eggs

 Horses carry more different helminth species than any other domestic species of animal 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

•

Differentiation of large and small strongyles  Requires culture of feces, then collection and identification of L3 larvae via intestinal cells  Not difficult but requires training and time  64 species of cyathostomes, not likely all pathogenic Nielsen, 2014

•

Ascarids; Parascaris equorum; Roundworms Bots; Gasterophilus nasalis, intestinalis, hemorrhoidalis Habronema; Habronema muscae, H. microstoma, Draschia megastoma; Summer sores Large Strongyles; Strongylus vulgaris, S. equinus, S. edentates; Blood worms Lungworms, Dictyocalus arnfeldi Onchocercha; Onchocercha cervicalis, O. reticulata Pinworms; Oxyuris equi Small Strongyles; Cyathostome spp.; Encysted strongyles Threadworm; Strongyloides westeri Tapeworms; Anoplocephela perfoliata

Species Specificity

Fecal Egg Counts •

Cyathostomes Large strongyles Tapeworms Ascarids

FEC selective treatment almost exclusively targets luminal cyathostomes

 Migrating and encysted cyathostomes represent up to 80% of the total worm burden  50%+ of horses expel cyathostomes eggs without any clinical signs

Chapman, 2003

von Samson-Himmelstjerna, 2012

•

Large and small strongyles can be most damaging in prepatent stages, before detection

•

False negative rate of ≥15% for Parascaris equorum

Interpretation

 Increased incidence of S. vulgaris in Denmark following dewormer legislation

 In managed horses, >99% of strongyle eggs are cyathostomes

Nielsen, 2012; Pihl, 2017

 In feral horses, 90-95% of strongyle eggs are cyathostomes

 Strongylus vulgaris may be present in up to 5% of selectively dewormed horses Nielsen, 2008

 Unacceptable levels of disease occur at this detection rate Nielsen, 2010

546

10/28/2019

Repeatability •

Consistency

Repeatability is poor

 Individual egg counts are highly variable and poorly repeatable  Variation of ± 50%  Potentially due to distribution in feces

• Reliable

for classifying horses into groups of low, medium, and high shedders Consistent in individual horses over time

•

 Especially in low shedders

Uhlinger, 1993

 Seasonal variation causes a natural peak Feb-May (temperature, rainfall, hypobiosis)

 Even in the absence of anthelminthics

 Best to try to test between 45-85° F

Nielsen, 2014

 90% of horses with a FEC <200 EPG on two consecutive FECs, remained consistently <200 EPG on the third

 Young horses have higher FECs •

Nielsen, 2006

Variation may exist over time, independent of these variables

Wood, 2012

Efficacy - Parasitic Disease

Efficacy - Egg Shedding •

Gomez and Georgi, 1991; Dopfer, 2004; Nielsen, 2006; Becher, 2010; Wood, 2013

Studies have shown good efficacy of surveillance programs in controlling egg shedding  But, no linear relationship between luminal worms versus egg shedding in horses Nielsen, 2014

•

No published studies evaluating the risk of disease in horses with selective versus rotational programs

•

Pathogenic potential  Profound in S. vulgaris, potential for A. perfoliata  Reemergence?

 Highly correlated in small ruminants

 FECs <500 EPG correspond with lower worm counts

 Significant association found with selective treatment (Denmark & Kentucky) in one study

Nielsen, 2010

Nielsen, 2012

 FECs of <100 EPG found in horses with up to 300,000 luminal worms

 Odds ratio of colic unknown

 Significance of threat is unknown

 Regular use of invermectin reduced incidence of colic compared to non-Ivermectin dewormers

Nielsen, 2013

Uhlinger, 1990

 No research on encysted larvae numbers

 Cyathostomes likely not pathogenic enough to report significant issues •

Acceptable loss percentage  Companion animals vs production animals

Efficacy – Reducing Resistance •

Reducing treatment intensity and increasing parasite refugia should decrease resistance

•

Must factor in cost of FECs

•

Farms performing FECs three times yearly and deworming at >200 EPG saved an average of $21.26 per horse per year over rotational deworming (herds of 10-50)

•

Large farms may be able to pool samples by age group

Van Wyk, 2011

 Shown in sheep

Martin, 1981; Waghnorn, 2008; Lethwick, 2012

 No specific evidence for equine parasites

•

Cost Gomez and Georgi, 1991; Duncan and Love, 1991; Krecek, 1994; Matthee and McGee, 2004

Weak evidence due to lower levels of resistance in Denmark

 Many other confounding factors to consider  Higher treatment of younger horses in other countries historically

 Won’t save money on every horse  But, cost effective when compared to treating every horse at intervals

Lester, 2013

 Examine groups over 100 EPG individually

Eysker, 2008

547

10/28/2019

Overall Efficacy

Current Implementation

•

Highly effective herd management

•

20% of horses carry and shed 80% of gastrointestinal parasite population  Treatment of horses at >200 EPG with a 99% effective product will decrease the worm burden of a herd by 95%

•

USA – 22% of farms use FECs, only 10% routinely

•

Denmark – 97% of owners use FECs

•

Europe – 50-60% FEC

 Most deworm 2-3 times per year with Ivermectin

Nielsen et al, 2018

 Leaves 50% of herd untreated Kaplan and Nielsen 2010, Relf et al 2013

 41% perform larval cultures. 11% FECRT  Ivermectin is preferred treatment Nielsen et al, 2006

Nielsen et al, 2018

Fecal Egg Count - Classification

Fecal Egg Counts •

Sampling

Class

 Only need a few grams – 1 “road-apple”  Can be obtained from the ground or the rectum  As fresh as possible (<12 hours)

 Avoid diarrhea •

Storage  Air-tight, leak-proof  Store in refrigerator after collection  Anaerobic, room temperature also prevents the majority of eggs from hatching  Works better for wet feces than dry

EPG

% of Population

Low Contaminators

< 200 EPG

50-70%

Moderate Contaminators

200-500 EPG

10-20%

Heavy Contaminators

> 500 EPG

20-30%

 Avoid freezing

 Test within 7 days

AAEP Parasite Control Guidelines, 2019

Deworming Recommendations Class

Frequency of Deworming

EPG

Low Contaminators

< 200 EPG

2x/year

Moderate Contaminators

200-500 EPG

4x/year

High Contaminators

> 500 EPG

6x/year

Fecal Egg Count - Frequency • Lack

of consensus

Nielsen et al, 2006

•

Current recommendations are 3 FECs, every 6 months

•

Recheck every 1-3 years

 Look for consistency

 Some continue q 6 months  Or, as clinical signs arise AAEP Parasite Control Guidelines, 2019

All Horses:

Spring: Avermectin Fall: Avermectin + Praziquantel AAEP Parasite Control Guidelines, 2019

548

10/28/2019

Egg Reappearance Period •

Time interval between last Anthelminthic Old ERP effective anthelminthic treatment and the Fenbendazole/ 6 weeks resumption of significant Oxibendazole strongyle egg shedding  When shedding is reduced below cut-offs, posttreatment:

 Measured by performing FECRTs until egg reappearance is seen  Shortening ERP is a sign of developing resistance

4-5 weeks

ERP on Farms with Resistance *

Timing •

Cyathostomes shedding is more reliable during grazing season  Encysted cyathostomes accumulate in autumn and winter months  Adult female worms shed fewer eggs in the non-grazing season  Cyathostomes survive best in hot dry or cold moist conditions

 80% for benzamidazoles and Pyrantel pyrantel  90% for ivermectin and moxidectin

Current ERP

5-6 weeks

4-5 weeks

Ivermectin

9-13 weeks

6-8 weeks

3-5 weeks

Moxidectin

16-22 weeks

10-12 weeks

4-6 weeks

Eysker, 1990 Poynter, 1954

 Avoid treatment during these times

 Slower to develop resistance when treating in winter and early spring

Nielsen, 2007

 Lower rates of egg development, resistant worms make smaller pasture contribution and most likely to be replaced  Less effective in climates with year round warm weather

Nielsen, 2019

Deworming Recommendations •

Frequent, prophylactic treatments to all horses is still the norm for control world-wide

•

Decreasing deworming to twice yearly is most effective at preventing resistance  May even be better to selectively deworm in spring and universally deworm in fall

Deworming Recommendations •

Do not deworm when FEC is < 200 EPG  Cut off may need further research

Nielsen, 2013

 Apparent consensus based on poll of laboratories Uhlinger, 1993

 Some support shown for 100-500 EPG in post-mortem, luminal worm study

Nielsen, 2019

Nielsen, 2010

 Reinforced by majority of subsequent studies  Solidified by AAEP Guidelines

Deworming Recommendations •

Legislation

If treatment interval is shorter than the pre-patent period, susceptible worms don’t reach maturity

Kelly et al 1981, Uhlinger 1991, Herd 1993, Herd and Coles 1995

•

Rotating anthelminthics does not appear to delay resistance and may mask use of an ineffective medication

•

Dewormers are available by prescription only in Denmark, Sweden, Finland, Netherlands, Italy, and some parts of the UK

•

May be slowing resistance

•

May necessitate better diagnostics

Uhlinger and Kristula, 1992

 May even select for greater resistance than exclusive use of one medication

Kaplan, 2002

•

Use of moxidectin against encysted cyathostomes may increase resistance pressure

Kaplan and Nielsen 2010

549

10/28/2019

Future Detection and Treatment

550

•

FECs lack ideal diagnostic power and repeatability

•

The future will likely bring better diagnostics and hopefully new dewormers

•

Prescription restrictions

•

For now, must endorse responsible stewardship

 May still slow resistance and aid in control of symptoms  Prepatent testing (before damage has occurred)  Better correlation with worm numbers or disease severity  Blood, feces, saliva

Questions?

MU-CVM Lectures

Leon Tu, DVM Faculty - University of Missouri Shelter Medicine Program Columbia, Missouri

551

552

Overview

Current Practices in Spay/Neuter of Dogs and Cats Leon Tu, DVM University of Missouri Shelter Medicine Program

Surgical sterilization of dogs and cats is often regarded as a hallmark of responsible pet ownership both for the benefit of individual animal health and to address the plight of unwanted companion animals in this country. The following are primary motivations for this message: •

Although shelter euthanasia rates are declining nationally, healthy, behaviorally normal animals are still at risk of shelter euthanasia due to overpopulation

•

Intact animals are more likely to be surrendered to animal shelters

•

Compliance with sterilization contracts post-adoption is <60%

•

Some risk factors for shelter surrender may be addressed through altering

Why have new/alternative techniques emerged? •

In part, veterinarians working in shelter and high-volume settings face a higher surgical caseload, where even small improvements in efficiency can have large impacts when multiplied across many, many patients.

•

Similarly, by performing a large number of procedures, a naturally occurring rate of complications will result in additional rechecks and opportunities to reflect and refine protocols. There is a natural inclination to pursue techniques that may be safer and less traumatic.

•

Nationally, ASPCA Humane Alliance has propagated techniques via available on-site training in Asheville, NC, instructional videos, and establishment of clinic models.

Current techniques Pedicle ligation:

553

•

In cats, autoligation of the ovarian pedicle has been shown to be a safe alternative to traditional double ligation with suture. A study out of the Oregon Humane Society used the technique in 2136 cats and observed a hemorrhage-related complication in six of those (0.281%). This was deemed to be an acceptably low rate, in line with or lower than studies evaluating traditional suture ligation.

•

Cats that were in heat, post-partum, or pregnant were not excluded from the sample size of 2136, demonstrating that the technique is safe regardless of estrus and pregnancy status.

•

The primary benefit was increased efficiency: Surgical times were significantly shorter (nearly a 30% reduction) when the pedicle tie was employed, as opposed to double ligation with suture.

•

To our knowledge, this technique is used exclusively in the feline due to the scant amount of fat surrounding the pedicle, resulting in excellent visibility of the structures involved.

Choice of knots for ligation and closure: •

ASPCA Humane Alliance stresses the principle that double ligation is not universally required: “Two ligatures will not be effective if they are poorly placed or insecure… what is needed for effective ligation is a single, secure ligature.”

•

An in vitro study has shown that the choice of technique in the first throw of a knot used as a ligature may affect its holding power. The miller’s knot, strangle knot, and constrictor knot were found to have excellent knot security, only permitting leakage at 2-3 times physiologic pressures.

•

A mechanical study has demonstrated that the traditional wisdom of requiring 5-7 throws for the beginning knot of a simple continuous pattern may be misguided; for all suture types tested, knot security was sufficient after 4 throws and minimally affected by additional throws.

Scrotal vs. pre-scrotal castration in canines:

554

•

Despite scrotal castration being performed in virtually every other species, pre-scrotal castration in the dog has largely been the norm. This has been the result of convention as well as a belief that scrotal incisions may result in a greater rate of self-trauma.

•

A study which tracked self-trauma, hemorrhage, swelling, and pain found no significant difference in complication rates between pre-scrotal and scrotal castrations. The scrotal approach offered a 30% reduction in surgical time.

•

In addition to improved efficiency, benefits to the scrotal approach may include reduced use of suture, smaller incision, eliminating the risk of urethral trauma, and reduced risk of scrotal hematoma/seroma.

•

To reduce the risk of self-trauma, it is recommended to avoid the placement of skin sutures and overzealous clipping of scrotal hair. A splash block with a mixture of lidocaine and epinephrine may reduce discomfort and hemorrhage. An e-collar and activity restriction are ideally recommended as for any other castration.

•

There is no broad consensus on the optimal closure technique; currently ASPCA Humane Alliance recommends a single buried simple interrupted in the subcutaneous layer, leaving the skin incision open to drain. Owners/guardians should be advised that mild serosanguinous incisional drainage post-op would be expected. Other options include closure of the skin with skin glue and no closure at all.

•

Despite numerous advantages, adoption of scrotal castration may be hampered by custom and preconceived notions. Because complications will still occur with either technique, it may be prudent to advise colleagues and local ER staff that you are performing this technique and educate them on what concerns owners may have. In my experience, post-op scrotal wall edema may be quite pronounced in some large-breed scrotal neuters and mimic the appearance of a hematoma or abscess; unlike the latter conditions, this has invariably resolved relatively rapidly (typically within 1 week) without additional treatment.

•

For pediatric dogs, many veterinarians have recognized that the smaller size of the spermatic cord lends itself well to effective autoligation, analogous to feline castration. A scrotal approach is also used. A study conducted at the Oregon Humane Society has documented the safety and efficiency of this technique in dogs 2-5 months old.

Minimum age/weight for sterilization •

Traditionally the minimum weight and age for patients accepted for sterilization surgery has been two pounds and two months (8 weeks), respectively. While widely accepted in sheltering, there does not appear to be discrete evidence behind this requirement. Scientific literature has established safe anesthetic and surgical protocols for animals as young as 6 weeks.

•

Within the last few years, there has been movement in a segment of the shelter community toward shifting that requirement downward to 1.5 pounds and 1.5 months (6 weeks), specifically in kittens. The primary argument in favor of this shift is that by sterilizing these animals earlier, they can be adopted out earlier. The advantages are twofold: first, by reducing the time a kitten spends in the shelter, one can reduce the exposure risk to infectious diseases during this particularly susceptible period of life.

•

Second, adopting out kittens at 6 weeks of age allows that pet to spend at least some time with its adoptive family during its critical socialization window (2-7 weeks in cats, 3-16 weeks in dogs). Animals that are appropriately exposed to a variety of stimuli during this time period are less fearful and more affectionate with people.

•

While pediatric surgery is clearly demonstrated to be a safe practice, caution is always prudent, especially for those accustomed to operating on older patients. In terms of surgery, the pertinent structures are exactly the same, simply smaller and sometimes friable. In terms of anesthesia, the primary concerns are preventing hypoglycemia and hypothermia. Hypoglycemia risk can be reduced by feeding a small snack 1-2 hours prior to anesthesia and feeding immediately upon recovery. Hypothermia can be prevented by reducing contact with cold surfaces, minimizing clipping, providing supplemental warmth, and minimizing surgical time.

Identification of altered animals

555

•

In the Association of Shelter Veterinarians 2016 Veterinary Medical Care Guidelines for SpayNeuter Programs, a strong recommendation is made for all providers of spay-neuter services to select a consistent, permanent means of visually identifying animals that have been altered. A linear green tattoo is recommended due to its visibility and ease of distinguishing the mark from naturally occurring structures.

•

The resulting tattoo is inconspicuous and well-accepted by pet owners. In many cases it has prevented unnecessary abdominal surgery for stray animals that end up in shelters, and animals that have changed owners. Conversely, animals that have been altered but not tattooed may occasionally have surgical scars that are too small to be detected; unfortunately, these animals may undergo an invasive, and preventable, negative exploratory surgery.

•

For female animals, the tattoo should be applied lateral to the ventral midline incision. For male dogs, the tattoo should be applied on the caudoventral abdomen, or alternatively, lateral to the

prepuce. For male cats, the tattoo should be applied in the area where a ventral midline incision would be (where a surgery may be attempted if it is inaccurately sexed or if abdominal cryptorchidism is suspected). References: Griffin B, Bushby PA, McCobb E, White SC, et al. The Association of Shelter Veterinarians 2016 Veterinary medical Care Guidelines for Spay-Neuter Programs. JAVMA, 2016 Jul 15, Vol. 249 No. 2. Hazenfield KM, Smeak DD. In vitro holding security of six friction knots used as a first throw in the creation of a vascular ligation.J Am Vet Med Assoc. 2014 Sep 1;245(5):571-7. doi: 10.2460/javma.245.5.571. Marturello DM1, McFadden MS, Bennett RA, Ragetly GR, Horn G. Knot security and tensile strength of suture materials. Vet Surg. 2014 Jan;43(1):73-9. doi: 10.1111/j.1532-950X.2013.12076.x. Epub 2013 Nov 19. Miller KP, Rekers W, Ellis K, Ellingsen K, Milovancev M. Pedicle ties provide a rapid and safe method for feline ovariohysterectomy.J Feline Med Surg. 2016 Feb;18(2):160-4. doi: 10.1177/1098612X15576589. Epub 2015 Mar 13. Miller KP, Rekers WL, DeTar LG, Blanchette JM, Milovancev M. Evaluation of sutureless scrotal castration for pediatric and juvenile dogs. J Am Vet Med Assoc. 2018 Dec 15;253(12):1589-1593. doi: 10.2460/javma.253.12.1589. Woodruff K, Bushby PA, et al. Scrotal castration versus prescrotal castration in dogs. 2015 May 11. http://veterinarymedicine.dvm360.com/scrotal-castration-versus-prescrotal-castration-dogs http://blog.millioncatchallenge.org/case-for-spayingneutering-at-6-weeks1-5-pounds/

556

Partners for Progress Presentations

557

558

Partners for Progress Presentations

Keith VanHoy, MS, CPA Stopp & VanHoy CPAs

St. Louis, Missouri

559

560

TOPIC: Questions you wished your CPA would ask you – Five tax ideas to discuss with your CPA this year Description: One question we often hear from new clients is “Are there any deductions that I may be eligible for that I don’t know about? I don’t even know what to ask!” Communication is key to successful advisor/client relationship in order to ensure compliance as well as reduce your tax burden. In this session, we will discuss the most asked tax questions we receive from our veterinary practices so that you can be prepared to get the most at tax time! Topics include: •What is the 20% tax deduction for veterinary practices and how do I make sure I qualify? •How can I get the most deduction for the mileage I incur or vehicle I use in my practice? •Can I still deduct travel costs and what if part of the costs is for personal/vacation travel? •Deductions for meals and entertainment has changed significantly. What are the new laws and how I can I make sure I get the most from it? •What’s an accountable plan and how can it be beneficial to both my practice and my employees? •(Bonus) – The hiring environment in the vet industry is COMPETITIVE. What fringe benefits can I offer tax free to my employees and what benefits that you might be offering now will get you in trouble with the IRS!

NOTES ________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ _________________________________________________________________________________ 561

562