MVMA 2022 Proceedings Book

Table of Contents

Note: Abstracts received as of 1/10/2022. Some speakers will provide handouts at their lectures.

Companion Animal Presentations Michael Blackwell, DVM, MPH Access to Veterinary Care: A National Family Crisis…………………………………………………….12 Karen Campbell-Motsinger, DVM, MS, DACVD, DACVIM Cutaneous Manifestations of Systemic Disease…………………………………………………………..16 Hereditary Cutaneous Scaling Disorders………………………………………………………………....28 Topical Therapy…………………………………………………………………………………………..42 Feline Dermatology Updates……………………………………………………………………………..54 Updates in Management of Canine Atopic Dermatitis………………………………………………….64 Sally J. Foote, DVM, CABC-IAABC, Low Stress Handling Certified, Fear Free Elite Certified Feline Body Language …………………………………………………………………………………...74 Canine Body Language…………………………………………………………………………………...76 Feline Ladder of Aggression………………………………………………………………………….…78 Canine Ladder of Aggression…………………………………………………………….……………..80 Jeremy Shomper, MEd, DVM, DACVIM Seizures in Dogs and Cats……………………………………………………………………………….84 The Neurologic Exam and Neurolocalization………………………………………………………..….86 The Vestibular System: Function and Dysfunction……………………………………………………..88

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Food Animal Presentations Pamela Adkins, DVM, PhD, DACVIM Sepsis in Neonatal Beef Calves………………………………………………………………………...….94 Elizabeth Cooksey, DVM Heavy Hitters in Small Ruminant Pregnancy Loss…………………………………………………..….104 Robin Faulkner, DVM Using Systems Perspectives to Reimagine our Practice Mental Models from Animal Health and Production to Broader Constructs of Well-being……………………………………………………….142 Austin Hinds, DVM, MS, DACVIM-LA Anemia in Small Ruminants……………………………………………………………………………150 Rosalie Ierardi, DVM, MS Bovine Disease Trends in Missouri……………………………………………………………………...154 Ron Tessman, DVM Impact of Vaccination with an Inactivated or Modified-Live Viral Vaccine on Reproduction………..164 Kelsey Walker, DVM Beef Cattle Lameness……………………………………………………………………………………172

Equine Presentations Tricia Bailey, DVM, DABVP Acupuncture and Chiropractic Care: Fundamentals……………………………………………………178 Acupuncture and Chiropractic Care: Literature Review and Case Presentation……………………….186 Philip Johnson, BVSc(Hons), MS, DACVIM, DECEIM, MRCVS Intraluminal Obstructions of the Large Colon…………………………………………………………..194 Horse Diseases Resulting from Feeding Errors………………………………………………………….198

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MU CVM Lectures Tim Evans, DVM, MS, PhD, DACT, DABVT Vet ECHO………………………………………………………………………………………………...…206 What Killed the Cow??? Diagnosing Potential Bovine Intoxications……………………………..……208 Sissy (Hsuan-Ping) Hong, DVM, MVM, MS, DACVIM, Neurology Seize the Moment: Management of Status Epilepticus and Cluster Seizures…………………….……212 Charles A. Maitz, DVM, PhD, DACVR, Radiation Oncology Megan A. Mickelson, DVM DACVS-SA, ACVS Fellow, Surgical Oncology Angela McCleary-Wheeler, DVM, PhD, DACVIM, Oncology A Comprehensive Approach to Sarcomas………………………………………………………….……218 Lauren Reeves, DVM, DACVS-SA Wound Management: A Quick Review and Current Recommendations...............................................224 Owen Skinner, BVSc, DECVS, DACVS-SA, MRCVS, ACVS, Fellow-Surgical Oncology Superficial Mass Resection for the General Practitioner…………………………………………..…….228 Aida Vientos-Plotts, DVM, DACVIM (SAIM) Cough: What Does the Gut Have to Do with It?..................................................................................232 Kelly Wiggen, DVM, DACVIM, Cardiology Let the Beat Drop: Understanding ECGs………………………………………………………………240

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Special Interest Presentations Sam Franklin, DVM, MS, PhD, DACVS, DACVSMR New Frontiers: Advances in Canine Orthopedics………………………………………………………250 Advances in Assessment and Treatment of Cranial Cruciate Ligament Rupture……………………...252 Sara Gardhouse, DVM, DABVP (ECM), DACZM Backyard Poultry Medicine – Part 1 and Part 2 ……………………………………………………….256 Pearls of Exotic Animal Medicine – Part 1 and Part 2 ……………………………………………..…260

Wellbeing Presentations Abby Whiting, DVM Disarming the Angry Client: The Imperius Curse……………………………………………………..266 Tapping into our Superhero Skills…………………………………………………………….………..266 Kerry Karaffa, PhD, Licensed Psychologist Tamara Hancock, DVM, PhD, DACVP Cognitive Restructuring: CBT Skills for Everyday Life……………..(Handouts Available at Presentation)

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Companion Animal

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Companion Animal

Michael Blackwell, DVM, MPH Director of the Program for Pet Health Equity at the University of Tennessee Knoxville, TN

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Missouri Veterinary Medical Association Conference January 10, 2021 Michael J. Blackwell, DVM, MPH

Access to Veterinary Care: A National Family Crisis

Pets have become an integral part of our families. Before the COVID-19 pandemic, an estimated 29 million dogs and cats lived in families participating in the Supplemental Nutrition Assistance Program (SNAP), formerly known as food stamps. Qualifying for SNAP indicates limited ability to pay for veterinary care. The pandemic has likely increased the number of pet owners who need assistance.

The Access to Veterinary Care Coalition's report, Access to Veterinary Care: Barriers, Current Practices, and Public Policy, released in December 2018, presents findings from a national study to understand better the barriers to veterinary care experienced by pet owners across the socioeconomic spectrum. More than one out of four pet owners (28%) reported having experienced a barrier to veterinary care, overwhelmingly due to a lack of adequate funds.

We face a paradox: it may be logical that someone should not have a pet if they cannot provide veterinary care, yet denying companionship with pets is difficult to defend. Veterinarians take an oath to use their professional knowledge and skills to benefit society which spans the socioeconomic spectrum.

A One Health healthcare system is critical to improving access to veterinary care. Such a system reflects an understanding that barriers to veterinary care are human factors, primarily associated with low socioeconomics, and that veterinarians alone cannot fix the problem. In this One Health healthcare system, veterinarians understand they provide healthcare to families by focusing on non-human members (i.e., pets). Thus, veterinary services integrate with human healthcare and family support programs.

AlignCare is a novel One Health healthcare system that enables veterinarians to serve families who otherwise would not receive veterinary care. Historically, veterinarians have sought to control costs for those with limited means by not doing all they desire for the patient. Some level of care is better than no care and helps safeguard the quality of life, avoiding not helping or euthanizing the patient. This incremental veterinary care (IVC) is a tiered and dynamic approach to patient management within limited available financial and other resources. The practitioner exercises science-based judgment regarding which patient needs are most critical. IVC helps to control costs, thus keeping pets with their family. Families who qualify for AlignCare participate in a means-tested public assistance program. They are required to pay a copayment. Veterinary service providers offer discounted services and agree to work with a third-party payer, i.e., AlignCare. As a system, AlignCare includes veterinary social workers, human support coordinators, and partnering social service agencies, animal welfare organizations, and funders.

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Companion Animal

Karen Campbell-Motsinger, DVM, MS, DACVD, DACVIM University of Missouri Satellite Specialty Clinic Wentzville, MO

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Hypothyroidism Hypercortisolism Hyperestrogenism Pituitary dwarfism

secondary infections or other complications

 Non-inflammatory unless

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causes of bilaterally symmetrical alopecia

 Endocrinopathies are classical

Alopecia

Karen L. Campbell, DVM, MS Diplomate, ACVIM (SA) and ACVD Professor Emerita, University of Illinois Adjunct Clinical Instructor, University of Missouri Veterinary Dermatologist, CARES LLC, Missouri Veterinary Dermatology Center

Cutaneous Manifestations of Systemic Disease

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Bacteria, protozoa, fungal, immune-mediated, neoplastic

 Cutaneous signs  Thin, dry haircoat, scaling  Failure of hair regrowth after clipping  Secondary infections  Myxedema (thick dermis)  Other signs (variable)  Weight gain or loss  Lethargy  Heat seeking  Infertility, anestrus  Bradycardia  Facial nerve paralysis (rare)  Depression, coma (very rare)

Hypothyroidism

 May be strong relationship  Effects of hormones  Effects of cytokines  Genetic linkages  Other factors

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indicative for a specific systemic disease  May be same etiologic agent or pathogenic process

 Cutaneous manifestations are sometimes highly

 Skin is largest & most visible organ

Cutaneous Manifestations of Internal Disease

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 Common Disorder  Lymphocyctic thyroiditis  Many breed predispositions  Idiopathic thyroid atrophy  Iatrogenic (sulfa antibiotics (reversible), other drugs, surgery)

Hypothyroidism

or administration of a drug or vaccine

 Skin disease develops after an illness

 Poor response to usual treatment

for the dermatological signs

 Patient is atypical (age, breed or sex)

(underlying immune dysfunction)

 Have chronic or recurring skin disease

 The skin disease is unusual

with systemic disease

 Skin disease is present concurrently

Suspect Underlying Endocrine, Metabolic or Other Systemic Disease When:

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Hypercortisolism: Diagnosis

neutrophils,  lymphocytes &  eosinophils Corticosteroid-induced isoenzyme of alkaline phosphatase Hypercholesterolemia Low urine specific gravity Bacteruria

Adrenal function tests Abdominal ultrasonography Abdominal/head CT or MRI

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History, Physical Exam Screening bloodwork & UA

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Mild anemia Hypercholesterolemia  Hypertriglyceridemia  Skin biopsy  May have increased dermal mucin, telogen hairs, vacuoles in arrector pili muscles  Thyroid testing  TT4, fT4, cTSH  Anti-thyroglobulin AB, anti-T3 AB, anti-T4 AB

 Laboratory tests

Hypothyroidism-diagnosis

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Dachshunds, Boxers, Boston Terriers, poodles

 Concurrent disease  Diabetes mellitus (75-80%)

 Signalment  Females predisposed  Middle-age to older

 Etiology  Bilateral adrenal hyperplasia (most common)  Adrenocortical neoplasia  Iatrogenic  Chronic corticosteroid or progesterone treatment

Feline Hypercortisolism

 Causes  Iatrogenic  Bilateral adrenal hyperplasia  Excessive ACTH production from pituitary  Adrenocortical tumor

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uncommon in cats  Predisposed breeds

 Common in dogs,

Hypercortisolism

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PU/PD/PP/Panting Muscle loss Pendulous abdomen many others

Bilaterally symmetric alopecia Thin skin Comedones Phlebectasias Striae Calcinosis cutis Easy bruising Secondary infections Hyperpigmentation Other signs

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Muscle wasting Pendulous abdomen Hepatomegaly Polyphagia Diarrhea Polyuria, polydipsia

 Clinical signs  Truncal alopecia  Variable hyperpigmentation  Thin, fragile skin  Curled ear tips  Secondary infections  Other signs

Feline Hypercortisolism

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Hypercortisolism: Clinical Signs

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Laboratory findings Adrenal function tests Ultrasonography MRI/CT scan

Pituitary Dwarfism

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 Diagnosis

Feline Hypercortisolism

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Autosomal recessive Persistent cysts of Rathke's pouch compress pituitary gland  growth hormone,  TSH, +/ FSH, LH & ACTH

Karelian Bear dogs predisposed

 German shepherd dogs &

Pituitary Dwarfism

Sex Hormone Imbalances

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over time develop alopecia and secondary infections

findings, radiographs show persistence of growth plates in bones, CT or MRI to find pituitary cyst, pituitary function tests

 Diagnose with history, PE

 Proportionate dwarfs  Retain puppy coat and teeth;

Pituitary Dwarfism

 Causes  Sertoli cell (most common in cryptochid dogs)  Ovarian cysts  Clinical signs  Symmetrical alopecia  Variable pigmentation  Seborrhea  Nipple enlargement/ feminization  Linear prepucial dermatosis (erythema or hyperpigmentation)  Diagnosis  Estrogen levels  Ultrasonography (testicular tumor)

Hyperestrogenism

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Feline thymoma-associated exfoliative dermatitis Epitheliotropic/Cutaneous TCell Lymphoma

Alopecia Erythroderma, scales and crusts +/- plaques, nodules +/- leukoderma +/- mucocutaneous lesions

 DX histopathology, IHC

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 Variety of presentations:

Epitheliotrophic/Cutaneous T-Cell Lymphoma

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more scaling than is typical for the endocrinopathies

 Alopecia in conjunction with

Diffuse Alopecia, Scales and Crusts

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New Zealand Veterinary Journal 51(5), 244-247, 2003

Epitheliotrophic/Cutaneous T-Cell Lymphoma

curative

 Surgical removal may be

with thymoma (maybe dyspneic)

 Thoracic radiographs consistent

interface dermatitis

 Skin biopsies show lymphocytic

 Hair coat is unkempt

and scales

 Skin is lichenified with fissures

dermatitis

 Generalized erythematous

Feline Thymoma-Associated Exfoliative Dermatitis

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Discoid lupus erythematosus Systemic lupus erythematosus Exfoliative cutaneous lupus erythematosus

 Lupus erythematosus

 Leishmaniasis

Facial and Dorsal Erythema, Alopecia, Scaling and Crusting

Feline Thymoma

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 “great imitator”  Scaling  Alopecia  Depigmentation  Ulcerations  Skin lesions present in conjunction with other systemic signs that vary depending on organ(s)/tissue(s) affected

cases

 Skin lesions present in 40-50% of

Systemic Lupus Erythematosus

serology, PCR testing

 Diagnose via cytology, biopsy,

 Symptoms may include  Silvery white scaling of head, pinnae, limbs  Periocular alopecia  Nasodigital hyperkeratosis  Onychogryposis  Paronychia  Nasal depigmentation  Nodular lesions  lymphomegaly

Leishmaniasis

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Single nucleotide polymorphism on Chromosome 18 in German Shorthaired Pointers

progressive with lameness, hunched back & lethargy

 Disease may wax & wane, usually

 Painful & pruritic

dorsumgeneralized

 Scaling on face, ears,

 Lesions start 6 mo - 3 yrs

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 Autosomal recessive

Exfoliative Cutaneous Lupus Erythematosus

 Clinical signs  Nose  muzzle, face, ears, lips, occasionally distal limbs, genitalia  Depigmentation, erythema, alopecia, scaling, crusting  loss of cobblestone texture of nasal planum  erosions, ulcers, scars  If nasal turbinates affected epistaxis

 Common disease

Discoid Lupus Erythematosus

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 Vasculitis

 Dermatomyositis  Most common in collies and Shetland Sheepdogs  DM or DM-like disease has been reported in many other breeds

Alopecia, Erythema, Scales & Crusts affecting face, legs and tail

Discoid Lupus Erythematosus

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 Feline Paraneoplastic Alopecia  Often rapid onset of extensive alopecia  Ventral neck, abdomen, legs  Footpads may be dry and scaly  Overgroom if secondary Malassezia infection develops  Underlying pancreatic adenocarcinoma or hepatocellular or biliary carcinomas (grave prognosis)

Alopecia with Shiny Skin of Periocular Region, Ventral Neck, Ventral Abdomen and Legs

 Dermatomyositis  Thought to be autosomal dominant with variable penetrance in collies  Possible linkage to microsatellite marker FH3570 on Canine Chromosome 35 in shelties  Lesions most common on face, lower extremities and tail  Some also have muscle weakness, abnormal gait, dysphagia, megaesophagus

Systemic Diseases with Alopecia, Erythema, Scales & Crusts affecting face, legs and tail

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Paraneoplastic Alopecia

Dermatomyositis

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 Diagnosis  Rule out other diseases (thyroid and adrenal function tests)  Skin biopsies: miniaturization of hair follicles  Abdominal ultrasonography—may find pancreatic or hepatic tumors

Paraneoplastic Alopecia

 Diagnostic plan  complete history  complete physical examination  RO other differentials via skin scrapings, cytology, DTM culture  biopsy of affected skin and muscle  EMG

Canine Familial Dermatomyositis

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Signalment & dietary history Clinical signs Biopsyparakeratosis Serum Zinc levels Response to Tx

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Zinc sulfate 10 mg/kg Zinc methionine 1.7 mg/kg Good diet (avoid excess calcium) Essential fatty acids

 Treatment

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 Diagnosis

Zinc Deficiency/ZincResponsive Dermatitis

Necrosis (Superficial Necrolytic Dermatitis)  Paraneoplastic Pemphigus

 Metabolic Epidermal

 Canine Distemper

(Acrodermatitis)

 Lethal Acral Dermatitis

 Zinc-Responsive Dermatitis

 Diagnostic Clues and Tests  Signalment  Laboratory tests  Imaging/abdominal ultrasonography  Biopsies for histopathology

Erythema, Alopecia, Crusts of Mucocutaneous Junctions and Footpads

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 Median survival ~ 7 months

 Abnormal behavior

 Pneumonia

 Diarrhea

 Growth retardation

 Chronic paronychia

 Chronic pyoderma

 Progressive acrodermatitis

Lethal Acrodermatitis in Bull Terriers

Zinc Deficiency: Type I

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food impacts in the roof of the mouth  Splayed toes  Claws grow fast and are distorted (dystrophy)

 High arched hard palate—

difficulty eating hard foods

 Weak nursing but even more

litter

 Usually, smallest puppies in

Lethal Acrodermatitis in Bull Terriers

Zinc Deficiency: Type II

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Thymic lymphoma Splenic sarcoma

 Clinical signs  Severe ulceration of oral cavity, mucocutaneous junctions, pinnae, clawbed

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with

 Reported in association

 Rare

Vet Pathol. 2005 Jan;42(1):88-91

Paraneoplastic Pemphigus

Lethal Acrodermatitis

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Vet Pathol. 2005 Jan;42(1):88-91

 Grave prognosis

abdominal ultrasound

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characteristic erythematous base under and around the crusts

 Hyperkeratosis and fissuring of f ootpads

Perioral, periocular, legs, feet, perianal, external genitalia

 Lesions have a

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erosions

 Erythema, crusts,

Metabolic Epidermal Necrosis (aka Superficial Necrolytic Dermatitis, Necrolytic Migratory Erythema, Hepatocutaneous Syndrome, Diabetic dermatopathy, Glucagonoma syndrome)

 Thoracic radiographs,

EPL= envoplakin; PPL = periplakin; Dsg3 = desmoglein 3; PNP = paraneoplastic patients; PV= pemphigus vulgaris; PF = pemphigus foliaceus; BP = bullous pemphigoid

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Canine Distemper

 Skin biopsies  Suprabasilar acantholysis  Intraepidermal pustules  Keratinocyte apoptosis

envoplakin and periplakin

 Antibodies against

Paraneoplastic Pemphigus

 Immunological evaluation:  depressed lymphocyte blastogenesis responses

 Clinical pathology  neutrophilia  hypercholesterolemia  Low SAP, ALT  Low plasma zinc

 Autosomal recessive trait

Lethal Acrodermatitis in Bull Terriers

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 Cutaneous lymphoma plaques

 Eosinophilic plaques  Allergies, FHV-1 (?)

 Viral plaques  papillomavirus

 Xanthoma  Abnormal lipid metabolism

 Calcinosis cutis  Hypercortisolism, renal disease, blastomyces, pacecilomycosis, idiopathic

Cutaneous Plaques

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Calcinosis cutis

epidermal protein deficiency and necrolysis  Nutritional or metabolic deficiency of zinc or essential fatty acids  Glucagon induction of inflammatory mediators (derivatives of arachidonic acid)

or another tumors  Generalized malabsorption

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Xanthomas

Honeycomb texture of liver Rare to find tumor

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Diabetes mellitus Hypercortisolism Hypothyroidism Megestrol acetate therapy Extremely high fat diets

hyperlipoproteinemia/ dyslipoproteinemia  Hereditary or due to

 Hypertriglyceridemia/

 Skin biopsies  “red, white & blue”

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 Abdominal ultrasound

 Minimum data base  Hyperglycemia (diabetic cases)  Elevated liver enzymes (inconsistent)  Hypoproteinemia  Hypoalbuminemia  Hypocholesterolemia  Low levels of serum amino acids (often <1/3 of normal)  Elevated serum glucagon levels  CBC: normochromic, normocytic anemia; some poikliocytes, target cells, neutrophilic leukocytosis  ANA weakly positive in some

 Hypoaminoacidemia inducing

 A substance secreted from pancreatic

 Direct action of glucagon in inducing

skin necrolysis

Metabolic Epidermal Necrosis: Diagnosis

Pathophysiology of MEN

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Mutation in folliculin gene

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Fungal, bacterial, algae, oomyces and mycobacterial infections

Nodules

 Infectious/Pyogranulomatous

 Sterile Nodular Panniculitis  Idiopathic  Pancreatitis & pancreatic neoplasia

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 Nodular Dermatofibrosis  German Shepherd Dogs

Cutaneous Nodules

Carlotti DN, Ackermann, Favrot C: Detection of novel papillomavirus in pigmented plaques of four pugs. Vet Derm 2007; 19:21-25

 Tobler K, Lange c,

Viral Plaques—papillomavirus associated

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Mutation of BHD gene on chromosome 5

 Pathogenesis  Tumors may produce growth factors that stimulate nodular growth of collagen fibers

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dominant trait

 Inherited as an autosomal

3-5 years before the renal or uterine tumors

 Dermal nodules may develop

Nodular Dermatofibrosis

Eosinophilic Plaques

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Sterile Nodular Panniculitis & Pancreatic Disease

CTCL Plaques

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 Other symptoms  Diaphragmatic hernia  Perianal hernia  Joint luxations  Subcutaneous hematomas  Periodontal disease

Cutaneous Asthenia

Infectious/Pyogranulomatous Nodules

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Hypercortisolism Corticosteroid tx Progesterone tx Hepatic lipidosis Hepatic neoplasia

 Acquired form

Feline Skin Fragility

Cutaneous asthenia

Skin Fragility

http://www.lbah.com/word/cushings-hyperadrenocorticism/

http://www.fmv.utl.pt/atlas/pele/pages_us/pele055_ing.htm

Feline acquired skin fragility

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Hereditary in Shar Pei

Hypothyroidism

Mucinosis

Thick Skin

Procollagen peptidase ADAMT32 gene mutation Procollagen I N-proteinase gene mutation Cyclophilin B mutation others

Domestic Animal Endocrinology 2007; 32: 43–54

 Progesterone therapy

 GHRH producing tumor

 Pituitary tumor (somatotroph)

Acromegaly

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autosomal dominant or recessive  Defect in collagen synthesis (7 types in humans)

 Maybe several forms—

Cutaneous asthenia

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signs of systemic disease is helpful in making correct diagnosis  Skin biopsies are often helpful in confirming a diagnosis

 Recognition of cutaneous

organ of the body

 Skin is the most visible

Cutaneous Manifestations of Systemic Disease

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Thank Virbac for sponsorship of this session !

10/31/2021

Factors contributing to scale formation

HEREDITARY CUTANEOUS SCALING DISORDERS

• Increased keratinocyte proliferation • Disorders of keratinization • Disorders affecting lipid bilayers (stratum corneum) • Disorders affecting cell cohesion

Karen L. Campbell, DVM, MS Diplomate, ACVIM (SA) and ACVD Professor Emerita, University of Illinois Adjunct Clinical Instructor, University of Missouri Veterinary Dermatologist, CARES LLC, Missouri Veterinary Dermatology Center

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Classification of Keratinization Disorders

Ichythosis

• Primary = Hereditary

• “Accumulation of dead skin cells resulting in thick and dry scales on the skin resembling fish scales” • Congenital ichthyosis – due to primary defects in formation of stratum corneum • Characterized by dry, scaly and/or thickened skin • Diagnosis

• Signs develop early in life • Majority are autosomal recessive (parents phenotypically normal) • Genetic testing available for some disorders

• Secondary = acquired

• • • • • •

• Increased scaling is associated with almost every disorder involving the skin

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Clinical signs Signalment History Detailed dermatologic exam Skin biopsy Genetic testing

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Epidermolytic Canine Ichthyosis

Ichthyosis

• Norfolk Terriers

• Epidermolytic

• Defect in keratin 10 formation

• Light microscopy findings • vacuoles and lysis of keratinocytes in st. spinosum and st. granulosum • Hypergranulosis, hyperkeratosis

• Rhodesian ridgeback • Labrador retriever • Cavalier King Charles spaniels

• Mutation in keratin genes

• Non-epidermolytic • Mutations affecting production of lipids, non-keratin proteins or desquamation of the stratum corneum

British Journal of Dermatology 2005; 153:51–58

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10/31/2021

Norfolk Terriers: Epidermolytic Ichthyosis

Norfolk Terriers: Epidermolytic Ichthyosis

• Autosomal recessive • Skin problems may be evident soon after birth • Superficial epidermis sloughs easily • Epidermal fragility persists into adulthood • Generalized dark grey hyperkeratosis • Intertriginous areas more severely affected • Footpads, claws, hair and teeth are normal

• Skin biopsy • Histopath

• Epidermolysis (st g) • Large keratohyaline granules • Mild hyperkeratosis and mild to moderate epidermal hyperplasia

• IHC: K10 is absent • EM: cytolysis, abnormal tonofilaments

DOI 10.1111/j.1365-2133.2005.06735.x

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Norfolk Terriers: Epidermolytic Ichthyosis

Non-Epidermolytic Canine Ichthyosis • Defect in intercellular lipids, cornified envelop, or desmosomes

• KRT10 mutation • Genetic sequencing identified a single substitution of TT for GT involving intron 5 (exon 5) • Results in production of a truncated form of K10 • Genetic test available

From Vet Pathol 45:2, 2008

Normal dog

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Golden retriever with ichthyosis

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Non-Epidermolytic Canine Ichthyosis

Jack Russell Ichthyosis

Breeds affected

• Loss of function mutation in transglutaminase 1 (TGM1) • LINE-1 element insertion (1980bp insertion) within intron 9 on chromosome CFA8 • Defective formation of cornified envelop

• Jack Russell terrier (Parson Russell) • Low transglutaminase

• • • • • • • •

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Australian terrier Cairn terrier Norfolk terrier American bulldog Golden retriever Great Danes German Shepherd dogs others

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10/31/2021

American Bulldog Ichthyosis

Jack Russell Ichthyosis

• Autosomal recessive • Puppies noted as having a poor haircoat shortly after birth • May have generalized white scales • Skin on ventral abdomen appears thickened with adherent brown scale and mild erythema • Over time footpads become mildly hyperkeratotic • Often have Malassezia overgrowth and maybe pruritic

• Autosomal recessive • Large (0.5-2 cm), thick, adherent white to tan scales • Scaly ear canals • Footpad hyperkeratosis • Onychomalacia • Predisposed to secondary infections (e.g., Malassezia)

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American Bulldog Ichthyosis

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American Bulldog Ichthyosis

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American Bulldog Ichthyosis • Skin biopsies • Histopath: diffuse laminated to compact orthokeratotic hyperkeratosis, hypergranulosis, mild acanthosis; keratinocytes in granular layer may have a perinuclear clear space • EM: discontinuous lipid bilayers, abnormal lamellar bodies, curvilinear membranous material within cytosol of the granular layer and within perinuclear clear spaces

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American Bulldog Ichthyosis • Genetic testing available • Report of testing of 800 American bulldogs • 34.3% carriers • ~5% homozygous affected

• PawPrint Genetics • Animal Genetics (Ich-AB)

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Golden Retriever Ichthyosis

Golden Retriever Ichthyosis

• Autosomal recessive • Puppies may exhibit rough haircoat with hyperpigmentation • “milk crust”

• Scaling may concern owners • Most are mildly affected, primarily a cosmetic disease • Some become subclinical as adults

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Golden Retriever Ichthyosis

Golden Retriever Ichthyosis

• Histopath: • Mild to moderate laminar orthokeratotic hyperkeratosis • Minimal epidermal hyperplasia https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3334879/

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Golden Retriever Ichthyosis

Australian Shepherd Ichthyosis

• Genetic testing has identified mutation of PNPLA1 (patatin-like phospholipase-1) • Prevalence of mutation (carriers) • • • •

France 48.5% Switzerland 56% USA 38.5% Australia 31.5%

• Conflicting reports on penetrance– one study cites 45/48 homozygous dogs as clinically normal, another cites 97% as clinically affected!

Adherent scales usually noticed on puppies

https://onlinelibrary.wiley.com/doi/pdf/10.1002/97811186443 17.ch11

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Ichthyosis in Great Danes

Ichthyosis in Great Danes

• Report of 14 affected puppies from 6 litters • Generalized gray to yellow scaling, skin wrinkles on head and legs • Submitted for necropsy (few days to 5 weeks old)

Vet Pathol 2016 May;53(3):614-20. doi: 10.1177/0300985815595516. Epub 2015 Aug 4

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• Histopath

Vet Pathol 2016 May;53(3):614-20. doi: 10.1177/0300985815595516. Epub 2015 Aug 4

• Epidermal and follicular orthokeratotic hyperkeratosis • Enlarged keratohyaline granules • Vacuolated keratinocytes • Hair follicles and sebocytes contained an eosinophilic and alcianophilic, lipid-rich material

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Cavalier King Charles Spaniel

Ichthyosis in Great Danes

https://journals.plos.org/ plosone/article?id=10.13 71/journal.pone.0141514

Congenital Keratoconjunctivitis Sicca and Ichthyosiform Dermatosis (CKCSID)

• Mutation of SLC27A4 gene found on chromosome 9 • Loss of 54 base pairs of one of the proteins involved in fatty acid transport = fatty acid transport protein 4 (FATP4) • FATP4 is an acyl-CoA synthetase required for normal permeability barrier function • Mutation results in uneven distribution of epidermal lipids and abnormal development of the skin

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• Signs of KCS from time of lid opening • “Frizzy coat” • Dorsal scaling • Footpad hyperkeratosis and deformed claws with intermittent sloughing Hartley et al: Vet Ophthal 2012; 15:315-326

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Cavalier King Charles Spaniel

X-linked hypohidrotic ectodermal dysplasia in dachshunds

Congenital Keratoconjunctivitis Sicca and Ichthyosiform Dermatosis (CKCSID)

• Autosomal recessive • FAM83H gene (mutation Exon 5 c.1016delC) • 8-10% of UK CKCS are carriers • Approximately 0.4% are affected • Antagene (France) genetic test

• Congenital hypotrichosis • Missing, malformed teeth • Lack of eccrine glands • X-recessive: clinical signs in 4 male puppies (littermates) • Heterozygous females: mild hypotrichosis (2 littermates), normal dentition

PLoS Genet . 2012 Jan;8(1):e1002462. doi: 10.1371/journal.pgen.1002462. Epub 2012 Jan 12

G3 (Bethesda). 2019 Jan 9;9(1):95-104. doi: 10.1534/g3.118.200814

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Follicular Parakeratosis and Mural Folliculitis in Labradors

X-linked hypohidrotic ectodermal dysplasia in dachshunds

• Labrador retrievers (one black, 3 yellow) • Females; 2.5 mo – 9.5 yrs at onset of lesions • multifocal verrucous papules and plaques, follicular cast formation, hair loss and comedone formation • Haired skin: head (4/4), pinnae (2/4), abdomen (3/4), trunk (2/4), limbs (1/4)

• Mutation of EDA gene (ectodysplasinA) – affected puppies and dam had one base pair deletion in the EDA gene • Has been reported in several breeds • • • • • • • •

miniature poodles Belgian shepherd Labrador retriever Bischon frise German Shepherd dog Whippet Cocker spaniel Mixed breeds (miniature pinscher, Pekingese)

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Follicular Parakeratosis and Mural Folliculitis in Labradors

Hereditary Nasal Parakeratosis

• Thick, tan crusts varied from few mm to 6 cm diameter • Hair shafts encased by keratotic casts forming plaques • Histopathology

• Parakeratotic hyperkeratosis – fills follicles, surrounds hair shafts forming follicular casts • Lymphocytic satellitosis with mild to moderate #s of acidophilic, shrunken keratinocytes in hair follicles • Parakeratotic peaks layered with serous fluid and serocellular crusts

Peters J, Scott DW, Erb HN, Miller WH. Vet Derm 2003; 14: 197-203

• Genetic defect has not yet been identified

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Nasodigital Hyperkeratosis

Familial Pawpad Hyperkeratosis/

Hereditary Footpad Hyperkeratosis

• Dogues de Bordeaux • Irish Terrier (11% carriers) • Kromfohrlander

• May develop in conjunction with other disorders of keratinization • Majority of cases are secondary (rule out underlying diseases) • Idiopathic nasodigital hyperkeratosis

• Severe hyperkeratosis of pads of all feet by 4-9 mo  fissures, lameness, secondary infections • Claws are very hard and fast growing • Haircoat is duller, less wiry and soften (in affected Kromfohrlander dogs) • Autosomal recessive

• Marked hyperkeratosis (ortho- or parakeratotic) • Epidermal hyperplasia

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• Labrador Retrievers • Greyhounds • Mutation in SUV39H2 gene • Results in delayed differentiation of keratinocytes in nasal planum • H&E biopsies show parakeratosis and serum “lakes” • Genetic testing is available

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Familial Pawpad Hyperkeratosis/

Primary Seborrhea

Hereditary Footpad Hyperkeratosis

• Predisposed breeds

• Mutation in FAM83G gene

• • • • • • •

• In mice results in wooly haircoat • Is also mutated in CKCS with CKCSID (dry eye curly coat syndrome) • Mutated in humans with palmoplantar keratoderma

• Delay in terminal differentiation of footpad keratinocytes • Daily soaks in 50% propylene glycol may help lessen cracking of footpads

PLoS Genet 10(5): e1004370. doi:10.1371/journal.pgen.1004370

American Cocker Spaniel English springer spaniel West Highland white terrier Basset hound Golden Retrievers American Bulldogs Persian cats

• Has been reported in many others

www.antagene.com HFH-A DNA test

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Abnormal Epidermal Cell Kinetics

Exfoliative Cutaneous Lupus Erythematosus German Short-Haired Pointers • Cocker Spaniels with primary seborrhea • Epidermal cell renewal time of 8 days (compared to normal of 21 days) • Basal mitotic index may be 3-4X normal • Most hereditary keratinization defects are autosomal recessive (pedigrees document this in Westies)

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• Autosomal recessive • Single nucleotide polymorphism on Chromosome 18

• Lesions start 6 mo-3 yrs • Scaling on face, ears, dorsumgeneralized • Painful & prurutic • May wax & wane, usually progressive with lameness, hunched back & lethargy

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Exfoliative Cutaneous Lupus Erythematosus German Short-Haired Pointers

Exfoliative Cutaneous Lupus Erythematosus German Short-Haired Pointers

• Peripheral lymphadenopathy • Reactive lymphoid hyperplasia

• Secondary pyoderma • Oligospermia • Skin biopsy: interface dermatitis • • • •

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superficial dermal infiltrate basal keratinocyte necrosis DEJ clefts pigmentary incontinence

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Exfoliative Cutaneous Lupus Erythematosus German Short-Haired Pointers

Exfoliative Cutaneous Lupus Erythematosus German Short-Haired Pointers

• Antiseborrheic therapy • Tx 2° pyoderma • Hydrochloroquine 5-10 mg/kg once daily may slow clinical progression in some • Cyclosporine decreases erythema and arthralgia but did not slow overall progression • Mycophenolate mofetil 10 mg/kg q 12  remission for one dog

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• Prognosis is guarded • Bathe q 4-7 days with moisturizers • Omega 3 fatty acids • Carprofen 2.2 mg/kg q 12 hr OR deracoxib 1-2 mg/kg q 24 hr for control of pain • Most are euthanized – try mycophenolate mofetil

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Lethal Acrodermatitis in Bull Terriers

Lethal Acrodermatitis in Bull Terriers • Genome wide association study

• Hereditary in bull terriers and miniature bull terriers • • • • • • • •

• Mapped locus to chromosome 14 • Identified splice region variant of MKLN1 gene

Growth retardation Progressive acrodermatitis Chronic pyoderma Chronic paronychia Diarrhea Pneumonia Abnormal behavior Median survival ~ 7 months

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• MKLN1 gene encodes intracellular protein muskelin 1 – functions in cell adhesion and intracellular transport processes • Antagene (France) genetic test

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Pharaoh Hounds

Zinc Deficiency: Type I • Alaskan malamutes • Siberian huskies • Thought to have decreased intestinal absorption of zinc • Lesions appear in young adults esp. during times of stress • In Northern hemisphere clinical signs most common Sept → Jan

• Severe generalized erythematous crusted papules, footpad hyperkeratosis, pruritus, stunted growth, lethargy • Skin biopsies: severe parakeratotic epidermal hyperkeratosis • Low serum zinc levels • No response to oral zinc • Intravenous zinc (10 mg/kg zinc sulfate) every 3-4 weeks  clinical improvement

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Zinc Deficiency: Type I • Erythema, alopecia, scaling, crusting, pruritus • Mouth, chin, periocular, ears, pressure points, footpads • 2-3 mg/kg elemental zinc (crush tablets and mix with food) • Zn methionine and Zn gluconate bioavailability > Zn sulfate • Phytase to hydrolyze phytates ↑ absorption • Glucocor coids ↑ metallothionine ↑ absorption • If poor response to oral, 10-15 mg/kg IV zinc sulfate weekly x 4 then as needed • Omega 3 and 6 fatty acids may also help

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Zinc Deficiency: Type II • A Zn responsive dermatosis • Seen in rapidly growing dogs fed diets high in phytates or calcium or water high in Fe (interfere with Zn absorption) • Hyperkeratotic plaques over pressure points • Hyperkeratosis of footpads and planum nasale • Secondary skin infections

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Localized Parakeratotic Hyperkeratosis

Zinc Responsive Dermatoses • Diagnosis • • • • • •

Signalment Clinical signs Dietary history Biopsyparakeratosis Serum Zinc levels Response to Tx

• Boston terrier dogs • Scaling affecting face and/or pressure points • Thick, dry, adherent scale, erythema, alopecia • Dorsal muzzle, hocks, elbow, tail

• Median age of onset 3.5 months (1-42 months in a study of 16 affected dogs) • Histopath: moderate to severe parakeratotic hyperkeratosis • Some improved following zinc supplementation, unable to document a zinc deficiency

• Treatment • • • • • •

Elemental zinc 2-3 mg/kg Zinc sulfate 10 mg/kg Zinc methionine or Zinc gluconate Correct diet (avoid excess calcium) Essential fatty acids Moisturize skin

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Vitamin A-Responsive Follicular Hyperkeratosis

Vitamin A-Responsive Dermatosis • Cocker spaniels • Labrador retriever • Miniature schnauzer • Adult-onset • • • • • •

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• DDX: sebaceous adenitis, vit A deficiency or toxicity, demodicosis, follicular dysplasia • BX: marked follicular orthokeratotic hyperkeratosis • DX: response to TX

alopecia/scales/crusts follicular papules/plugs hyperkeratotic plaques ceruminous otitis Hairs epilate easily Rancid odor, pruritic

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Vitamin A-Responsive Follicular Hyperkeratosis • Management • Vitamin A 1000-1200 IU/kg/day given with a fatty meal • Antiseborrheic shampoos • Improvement in 3 weeks • Remission by 8-10 weeks • May need life-long treatment

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Sebaceous Adenitis • Destruction of sebaceous glands— theories: • Genetically inherited developmental defect?

• Abnormality in lipid metabolism?

• Keratinization defect obstructing sebaceous ducts?

• Immune-mediated targeting of sebaceous glands?

• Infiltrations of dendritic antigenpresen ng cells and T cells (→ immune-mediated) • Appears to be autosomal recessive in standard poodles and Akitas

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Sebaceous Adenitis

Sebaceous Adenitis

• Breeds • • • • • • •

• Long-coated dogs

Standard poodle Akita Vizsla Samoyed English springer spaniel Havanese Others (reported in over 50 breeds of dogs, also cats, rabbits, horses and people)

• symmetrical alopecia, scaling, dry coat on dorsum, nose, tail, pinnae, truck • later follicular casts and matting

• Short-coated dogs • “moth-eaten” alopecia • secondary pyoderma • otitis externa

• Age

• young to middle-aged

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Sebaceous adenitis

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Sebaceous adenitis

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Sebaceous adenitis

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Sebaceous adenitis

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Oil treatment for sebaceous adenitis

Sebaceous adenitis: treatment • Topicals

 Sponge or pour mineral oil or baby oil over entire body until skin and hairs are completely saturated  Massage the oil into skin –soak into hair follicles  Let the oil soak on skin 30-60 minutes (as long as possible)  Bathe using a “degreasing” shampoo to remove excess oil from hair coat and skin (may require double lathering, rinsing, lathering, rinsing to remove the excess oil)  Repeat this treatment in one week and then once a month to help keep skin and haircoat healthy  Warn owners not to be surprised if a lot of hair comes out after the first couple of treatments – sebaceous adenitis causes hairs to detach from hair follicles so they come out easily!

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• Follicle flushing shampoos (Ethyl lactate) • Emollients (oils, fatty acids, ceramides, phytosphingosines) • Humectants (propylene glycol)

• Systemics • • • •

Cyclosporine 5 mg/kg Vitamin A (1000 IU/kg) Doxycycline + Niacinamide Isotretinoin (1 mg/kg q 12-24 hr)

• Treat secondary infections • Client Education: goal is to minimize symptoms, no cure, likely hereditary

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Epidermal Dysplasia

Epidermal dysplasia

• Breed • West Highland White Terrier

• Lesions • by one year erythema and pruritus • “amardillo skin”

• Skin colonized with Malasezzia—the dysplasia maybe hypersensitivity reaction to yeast

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Epidermal Dysplasia • Rule out • allergies • parasites • Malassezia hypersensitivity

Epidermal Dysplasia • Management

• Treat secondary infections • Vitamin A 1000 IU/kg • Retinoids • Retin-A topical • Acitretin • Antiseborrheic shampoos

• Biopsy • parakeratotic hyperkeratosis • Basal cell “crowding”/”buds” • Malassezia

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American Hairless Terrier

Autosomal dominant hairlessness

• Hairlessness in this breed is autosomal recessive • Frameshift deletion of SGK3 (serum glucocorticoid regulated kinase family member 3 gene) • Puppies are born with thin coat of hair lost within first months of life (gene involved in postnatal hair follicle development)

• Chinese crested • Mexican Xoloitcuintle • Peruvian Inca Orchid • These breeds have a mutation in FOX13 (forkhead box transcription factor 13) – regulates ectodermal development, post natal hair growth and hair regeneration; hairless dogs may also have problems with dentition and malformed ears • Lethal in homozygous animals

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Schnauzer Comedo Syndrome

Schnauzer Comedo Syndrome

• Dorsal midline • Miniature Schnauzer are affected • Comedones and crusted papules • Hair follicle keratinization defect (developmental dysplasia of hair follicles)

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• Diagnosis • r/o demodex • Skin scrapings

• r/o dermatophytes • Fungal culture

• r/o staph infection • Cytology, culture

• r/o Malassezia • Cytology

• r/o Cushing’s • Endocrine testing

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Schnauzer Comedo Syndrome

Canine Ear Margin Seborrhea • Dachshunds • Other breeds with pendulous pinnae • Follicular casts (“greasy plugs”) • DDx: vasculitis crusting and fissures • Surface and follicular ortho/parakeratosis • TX: sulfur-salicylic acid shampoo followed by moisturizers

• Management • Treat secondary infections • Q 24-48 hr wiping of back with salicylic acid containing pads or cloth soaked in alcohol or Listerine • Q 7-14 day bathing with sulfur and/or benzoyl peroxide shampoo • Refractory cases may respond to isotretinoin 1 mg/kg q 12 hrs

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Summary: Primary Keratinization Disorders

Acanthosis Nigricans • Primary

• Hereditary abnormalities affecting

• Dachshunds

• Secondary (rule out) • • • •

• Epidermal cell proliferation, • Cornification, and/or • Desquamation

Intertrigo Endocrinopathies Hypersensitivities Malassezia

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• Suspect when develop early in life • Suspect when siblings/littermates affected

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Summary: Primary Keratinization Disorders • May be localized or generalized • Often diagnose via skin biopsies and exclusion of differentials • Genetic, IHC or biochemical tests helpful in diagnosing specific disorders

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Thank Virbac for sponsorship of this session !

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TOPICAL THERAPY

Introduction

Karen L. Campbell, DVM, MS Diplomate, ACVIM (SA) and ACVD Professor Emerita, University of Illinois Adjunct Clinical Instructor, University of Missouri Veterinary Dermatologist, CARES LLC, Missouri Veterinary Dermatology Center

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• Advantages of Topical Medications • Directly delivers active ingredients to skin • Minimizes systemic side effects (e.g. corticosteroids) • Decrease dependence on systemic antibiotics and thereby decrease risk of developing antibiotic resistance

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Introduction

Introduction • Types of products

• Indications • • • • • •

• • • • • • • • • •

Cleansing Antibacterial Antifungal Antiparasitic Antipruritic Antiseborrheic • Keratolytic • Keratoplastic • Degreasing

• Otic Agents

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Characteristics of the Ideal Shampoo

Principles of Shampoo Therapy

• Lathers well • Rinses freely • Removes soil/exfoliated cells • No residue • Nonirritating • Client-pleasing fragrance and texture (“elegance”) • Leaves natural oils/moisturizes • Leaves hair soft, shiny, easy to comb

• Proper shampoo selection • Thorough application • Regular application • Appropriate contact time • Thorough rinsing

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Shampoos Powders Rinses Sprays Lotions Creams Ointments Mousses Spot-ons Wipes

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Factors in Shampoo Selection

Preparation of Animal for Bath

• Purpose of shampoo • Species • "Elegance"—color, odor, taste, consistency • Product cost and size of animal • Acceptability to owner • Other treatments being given • Consider that rotation may increase effectiveness of products

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• Clip mats, long hair • Soak 10 to 15 minutes.

• Water temperature 95 to 100 F • Shampoo contact time of 5-15 minutes (read a book chapter, clean pet’s ears, empty anal sacs)

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Differences in Human, Dog and Cat Skin

Dry Shampoos • Absorbent powders • Mild alkali • Static electricity may build-up (negative electrical charges = "flyaway hair”)

• Dog—3 to 5 epidermal layers, 22 day turnover, pH 7.5 • Cat—3 to 5 epidermal layers, pH 6-7 • Human—10 to 15 epidermal layers, 28 (or longer) day turnover, pH 5.5

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Rinse-Free Shampoos

Soap Shampoos

• Apply foam to hair coat soaking hairs • Allow to dry then brush out • Contains cleaning extracts from plants and essential oils to eliminate odors and moisturize skin and hairs

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• Sodium salts—hard soaps • Potassium salts—soft soaps • Require soft water to avoid leaving Ca-Mg deposits on hairs • An acidic rinse is useful to remove residue from hairs

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Detergent Shampoos

“Hypoallergenic Shampoos”

• Salts of lauryl sulfate • Additives combat drying

• Soap free • Moisturizing/cleansing • Examples

• • • •

Glycerol Lanolin Oils Fatty alcohols

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• DermaLyte • Allergroom • Allermyl

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Moisturizers • Humectants • Glycerin • Propylene glycol • Urea

• Emollients • • • • • •

Glycerol esters Lanolin Lanolin derivatives Oils Fatty alcohols Ceramides

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Antibacterial Topicals

Glycotechnology

• • • • • • • • • • • •

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Sulfur Benzoyl peroxide Chlorhexidine Hypochlorous acid Iodophors Hexachlorophene Selenium Triclosan Ethyl lactate Acetic acid Silver Plant Extracts

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Sulfur

Benzoyl Peroxide • Antibacterial • Antiyeast • Keratolytic • Follicular flushing • Antipruritic • Degreasing

• Keratolytic • Keratoplastic • Antifungal • Antibacterial • Antiparasitic • Antipruritic • Odoriferous • Staining

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Chlorhexidine

Hypochlorous Acid

• Antibacterial • Antifungal • Binds to Stratum Corneum

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• Weak acid formed when chlorine dissolves in water • Oxidizers – bleaches, deodorants, disinfectants • Dakin’s solution kills a broad range of microorganisms (bacteria, yeast, viruses)

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Iodophors

Hexachlorophene

• Antibacterial • Antifungal • Staining • Irritating • Sensitizing • Inactivated by organic debris

• Antibacterial • Toxic to cats • Sensitizing • Systemic absorptionseizures • Embryotoxic • Do not use metal buckets or metal dispensers (damages metal)

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Selenium

Triclosan

• Keratolytic • Antibacterial • Anti-yeast • Degreasing/drying • Irritating

• Antibacterial

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Ethyl Lactate

Acetic Acid

• Hydrolyzed to ethanol and lactic acid • Antibacterial • Follicle flushing

• Antibacterial • Antiyeast

Colloidal Silver • Reported to have antibacterial and antifungal properties

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Plant Extracts

Antifungal Shampoos • Miconazole • Sulfur • Chlorhexidine • Benzoyl peroxide (yeast only) • Iodophors • Ketoconazole • Selenium (yeast only) • Acetic acid (yeast only)

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Miconazole

Clotrimazole

• Antifungal • Most effective for yeast

• Topical formulations

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• Malassezia • Microsporum canis

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Ketoconazole

Antiparasitic Shampoos

• Antifungal • Effective for dermatophytes and yeast

• Sulfur • Pyrethrin • Pyrethroids • Carbamates • Lindane

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Colloidal Oatmeal

Antipruritic Shampoos • Moisturizing shampoos • Colloidal oatmeal • Diphenhydramine HCl • Pramoxine HCl • Hydrocortisone • Sulfur • Benzoyl peroxide • Menthol • Aloe Vera • Piroctone olamine

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• Moisturizing • Binds antigens • May have anticyclooxygenase activity (anti-inflammatory)

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Diphenhydramine HCl

Pramoxine HCl

• Antihistamine

• Topical Anesthetic

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Hydrocortisone

Menthol and Witch Hazel

• Corticosteroid • Anti-inflammatory • Short-acting

• Cooling agents • Raise pruritic threshold

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Aloe Vera

Antiseborrheic Shampoos

• Moisturizer • May aide wound healing • Antibacterial • Antifungal

• Keratolytic • Keratoplastic • Degreasing • Moisturizing

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Keratolytic Shampoos

Salicylic Acid

• Sulfur • Salicylic acid • Tars • Retinoids • Benzoyl peroxide • Propylene glycol • Lactic acid

• Keratoplastic • Keratolytic • Antipruritic • Bacteriostatic • Synergistic with sulfur

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Tars

Retinoids

• Toxic to cats!

• Keratolytic • Keratoplastic (antimitotic) • Antipruritic • Antimitotic • Degreasing • Anti-inflammatory • Some may be carcinogenic

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• Available as gels, creams, ointments • Most commonly used is Retin-A • Keratoplastic • Keratolytic • Decrease sebaceous gland secretions • Anti-inflammatory • Activity against some cutaneous tumors

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Propylene Glycol

Lactic Acid

• Humectant • Keratolytic • Ceruminolytic • Nephrotoxic • Irritating

• Keratolytic • Ceruminolytic

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Keratoplastic Agents

Degreasing Shampoos

• Retinoids • Tars • Sulfur • Salicylic acid

• Detergents • Benzoyl peroxide • Selenium sulfide • Ethyl lactate

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Otic Medications

Miscellaneous Products

• Ceruminolytics • TrizEDTA • Antibacterial • Antifungal • Drying agents • Anti-inflammatory agents • Parasiticides

• Oligosaccharides • Chitosanide • Phytosphingosine • EFAs • Zinc gluconate • Vitamin B6 • Hydrolyzed proteins • Topical calcineurin inhibitors • Mupiracin • Silver Sulfadiazine

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Oligosaccharides

Chitosanide • Biopolymer produced from chitosan in crustacean shells • Forms a protective film • Acts as a skin moisturizing agent

• Anti-inflammatory • May decrease bacterial colonization

Allermyl Shampoo L-rhamnose D-mannose D-galactose

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Phytosphingosine

Topical Fatty Acids

• A pro-ceramide • • • • •

• Dermoscent contains 10 essential oils (clove, camphor, gaultheria, rosemary, curcuma, oregano, lavender, peppermint, tea tree and cedar), hemp oil and neem oil, rich in essential fatty acids and vitamin E • improve skin hydration • reinforcing skin barrier function • enhance the shine of the hairs • reduce scales and dandruff • antioxidant activity

Repair of epidermal permeability barrier Facilitates normal structure of epidermis Anti-seborrheic activity Anti-inflammatory activity Anti-microbial effects

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Zinc gluconate

Vitamin B6

• Zinc is co-factor in many enzyme systems • Facilitates normalization of keratinization • May down-regulate sebum production

• Synergistic with zinc in normalizing keratinization • Synergistic with zinc in down-regulating sebum production

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Hydrolyzed proteins

Topical calcineurin inhibitors • Tacrolimus • Picrolimus • Potent anti-inflammatory agents • Block T cell function • Useful in treatment of immune-mediated skin diseases • Have caution label for humans—may predispose to cutaneous tumors

• “Repair split ends” by binding to hair keratins • Moisturizing

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Silver Sulfadiazine

Mupiracin • Topical antibiotic • Blocks the activity of isoleucyl-tRNA synthetase thereby blocking protein synthesis (unique mode of action) • Polyethylene glycol base is nephrotoxic therefore do not use over large areas of body • Not approved for use on cats • Used intranasally to eliminate/reduce carriage of MRSA • Readily penetrates into dermis

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• Topical antimicrobial with activity against many species of bacteria and against yeast • Does not interfere with wound healing • Very popular choice for preventing infections following burns • Dilute 1:1- 1:10 to make otic solution

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Leave-on Formulations

Summary

• Powders • Dips • Sprays • Mousses • Lotions • Creams • Gels • Ointments

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• Wide spectrum of products available for topical use • Understanding goals and mechanisms of action will facilitate product selection • Be sure owners understand the goals and how to use products

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Thank Virbac for sponsorship of this session !

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FELINE DERMATOLOGY UPDATES

Facial Pruritus • Otodectes • Demodicosis • Notedres • Viral/mycoplasma infections • Food allergies • Environmental allergies

Karen L. Campbell, DVM, MS Diplomate, ACVIM (SA) and ACVD Professor Emerita, University of Illinois Adjunct Clinical Instructor, University of Missouri Veterinary Dermatologist, CARES LLC, Missouri Veterinary Dermatology Center

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Feline Viral and Mycoplasma Induced Facial Pruritus

Feline Viral and Mycoplasma Induced Facial Pruritus • Viral: alpha-interferon 100 IU q 12 hrs • Herpes Viral: famciclovir 62.5 mg/cat (1/2 of 125 mg tablet) for 3 weeks • Herpes: lysine 250 mg q 12 hr (little evidence to support use) • Mycoplasma: pradofloxacin 7.5 mg/kg (monitor CBC q 7 days) OR doxycycline 2.5-5 mg/kg q 12 h with water chaser

• PCR testing now readily available • Recent vaccination may cause “false” positive— I treat and retest

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Allergies

Allergies in Cats • Common manifestations include • Pruritus +/- crusts/scales • Feline Miliary Dermatitis • Eosinophilic Granuloma Complex • Feline Symmetrical Alopecia

Food allergy

Flea allergy Feline Atopy (Environmental)

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Allergies

Allergies

Most common Clinical sign is “Overgrooming”

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Pruritus

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Allergies in Cats

Pitfalls which Limit Usefulness of Serum IgE testing

• Atopic Dermatitis-Diagnosis • • • •

• Poor reproducibility • Poor specificity for IgE • Many false positives

R/O ectoparasites R/O food allergies R/O infections Investigate for “offending” allergens

• non-specific binding

• Little distinction between positive tests in normal and allergic cats • Great seasonal variability

• Serum IgE testing • Intradermal testing

• half-life of serum IgE = 2.5 days

• Not all reactions are IgE mediated

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Intradermal allergy testing

Treatment Options for Feline Atopy

• Evaluates antigen-specific IgE and/or IgGd bound to mast cells in skin but not a perfect test (still have false + and false -) • Cat reactions can be more difficult to read (0.2 ml/kg of 2% Evans blue dye IV prior to test)

• Control secondary infections • Eliminate ectoparasites • • • • •

Seresto collar Revolution Plus Advantage Multi Bravecto for cats Lime sulfur (discontinued)

• Allergen-specific immunotherapy • Subcutaneous • oral

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• Skin barrier repair • Omega 3 fatty acids • Antihistamines • Corticosteroids • Cyclosporine • Oral • Injectable

• Oclacitinib • Maropitant • Gabapentin

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Skin Barrier Repair

Omega 3 fatty acids for cats

• Defects in skin barrier allow increased percutaneous absorption of allergens • For repair apply once a week for 4-8 weeks then q 14 days for maintenance

• Reduce production of inflammatory mediators • May take 8-12 weeks for full effect • May be synergistic with other treatments to enable use of lower doses of steroids, antihistamines and CsA

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Antihistamines for cats

Corticosteroids for cats

• Chlorpheniramine

• Prednisolone

• 1.1-2.2 mg/kg q 24 h for first 2 wks then q 48 h and taper to 0.5 mg/kg

• 2 mg/cat q 12-24 h

• Cetirizine (Zyrtec)

• 2.5-5 mg/cat q 24 h

• Dexamethasone

• Hydroxyzine

• 0.1-0.2 mg/kg q 24 h for first 2 wks then q 48-72 h and taper to 0.05 mg/kg

• 5 mg/cat q 12 h

• Loratidine

• If use for > 2 months monitor serum fructosamine

• 5 mg/cat q 12 h

• Amitriptyline

• 2.5-5 mg/cat q 24 h

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Cyclosporine in Cats

Oclacitinib in Cats

• Calcinurin inhibitor • Precautions

• Janus kinase inhibitor

• Decreases production of IL-31 • At higher doses may cause bone marrow suppression

• Do not use in FeLV or FIV + cats • Indoor cats only and avoid feeding raw meats

• Precautions

• Do not use in FeLV or FIV + cats • Indoor cats only and avoid feeding raw meats

• Feline dose for treatment of pruritus is 7 mg/kg PO once daily until itching is controlled and then q 48 h • ?? 2.5 mg/kg SQ once daily (?? q 48 h) • May want to monitor serum concentrations, trough level of 250-500 ng/mL recommended

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• Half-life is shorter in cats than dogs – may require long-term q 12 hour dosing • Published study following K9 protocol

• 5/12 non-flea, non-food allergic cats had good response

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Maropitant

Gabapentin for cats

• Recommended dose for treatment of pruritus in cats is 1-2 mg/kg PO q 24 h • May have increased efficacy when combined with chlorpheniramine 2 mg/cat q 12-24 h

• 10-15 mg/kg q 12 h • ½ 100 mg capsule mixed with canned food • ½ 100 mg capsule opened mix with dry food in ziplock bag “shake and feed” • Liquids – check for xylitol • Reduce dose if too sleepy

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Feline Demodicosis

Demodex gatoi

• Demodex cati • Demodex gatoi

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• Short bodied • Found in the stratum corneum • Contagious • Pruritic • May find mites on skin scrapings or fecal flotation

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Demodex gatoi

Demodex gatoi

• Distribution

Therapy • Stop any glucocorticoid or progesterone tx • Treat all in-contact animals • Lime sulfur was traditional treatment of choice

• Head, neck, elbows • Ventral abdomen

• Clinical signs

• improve in 3 weeks • treat for 4-6 weeks minimum

• Alopecia • Scale, erythema • Excessive grooming

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• • • •

Bravecto for cats: one treatment may be curative Revolution Plus: two treatments at 30 day interval Ivermectin: 300 mcg/kg once weekly, variable response Advantage Multi (q 7-14 days, variable response)

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Demodex cati

Demodex cati

Localized follicular demodicosis

Generalized follicular demodicosis • Very rare • Siamese and Burmese at risk • Usually have an underlying condition • FIV, FeLV, Diabetes Mellitus, Bowen’s disease

• Rare condition • Eyelids, periocular, head, neck • Differential for feline acne • Usually responsive to lime sulfur or other mild parasiticides • Often self-limiting

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Feline Symmetrical Alopecia

Demodex cati Treatment: generally much easier than K9 • Manage pyoderma • Lime sulfur dip weekly (discontinued) • Bravecto for cats should be curative • Revolution Plus (q 30 days) • Amitraz at 125 ppm (1/2 strength)

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Feline Symmetrical Alopecia and Dermatitis

Feline Symmetric Alopecia Management

• Differential Diagnoses

• Identify and treat cause Skin scrapings & fecal examination (hair &/or mites) Flea control trial Revolution Plus or Bravecto treatment trial Hypoallergenic Food trial Intradermal allergy test or serum IgE testing and desensitization for environmental allergies • Cone or bodysuit trial • Skin biopsies • Thoracic radiographs + abdominal ultrasound • • • • •

Psychogenic alopecia Allergies - food, flea, environmental (atopy) Ectoparasites – fleas, Demodex gatoi Dermatophytes Endocrinopathies Telogen /Anagen defluxion Feline paraneoplastic alopecia (pancreatic, hepatic or thymic tumor) • Cutaneous T-cell lymphoma

• • • • • • •

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Feline Paraneoplastic Alopecia • Associated with pancreatic adenocarcinoma and less often bile duct or hepatic carcinoma • Older cats • Sudden onset of malaise and hair loss • Marked exfoliation of hair • Shiny appearance to skin and footpads

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Feline Paraneoplastic Alopecia

Feline Paraneoplastic Alopecia

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Neoplastic/paraneoplastic disorders with scaling

Feline Paraneoplastic Alopecia

Feline paraneoplastic alopecia

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Feline Paraneoplastic Alopecia

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Feline Paraneoplastic Alopecia

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Feline Paraneoplastic Alopecia

Feline Paraneoplastic Alopecia

• Differential diagnosis • • • • • • • • •

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Feline hyperadrenocorticism Feline skin fragility syndrome Feline hyperthyroidism Telogen/anagen defluxion Feline thymoma Metabolic epidermal necrosis Alopecia areata Telogen effluvium Self-induced alopecia (feline symmetric alopecia)

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Feline Paraneoplastic Alopecia

Exfoliative dermatitis associated with thymoma

• Diagnosis • Rule out other diseases (thyroid and adrenal function tests) • Skin biopsies: miniaturization of hair follicles • Abdominal ultrasonography—may find pancreatic or hepatic tumors

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Feline Cutaneous T-cell Lymphoma

Feline Thymoma • Reported cases have had generalized erythematous dermatitis • Skin is thickened with cracks and fissures • Hair coat is scurfy and scaly • Skin biopsies show lymphocytic interface dermatitis • Thoracic radiographs consistent with thymoma • Surgical removal usually curative

New Zealand Veterinary Journal 51(5), 244-247, 2003

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Ear disease in cats

Ear disease in cats

• Otodectes • Apocrine gland cystadenomatosis • Nasopharyngeal polyps • Otitis secondary to allergies • Immune-mediated otitis • Proliferative necrotizing otitis • Feline solar dermatitis

• Otodectes • Nasopharyngeal polyps • Apocrine gland cystadenomatosis • Otitis secondary to allergies • Immune-mediated otitis • Proliferative necrotizing otitis • Feline solar dermatitis squamous cell carcinoma

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Bowen’s Disease

Pemphigus foliaceous • Any age • Crusts, pustules, hair loss

• Pre-neoplastic proliferative lesions triggered by papillomavirus • Treatment options

• • • • •

• CO2 laser • Cryosurgery • Topical imiquimod

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• • • •

Ear pinnae Face Clawfolds Footpads Nipples

Cytology Biopsy Treat infections Prednisolone + CsA or chlorambucil

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Feline Plasma Cell Pododermatitis • “Pillow foot” • Test for concurrent FeLV or FIV • Most have increased serum globulins • Bx and/or FNA • TX

Questions?

• Doxycycline 5 mg/kg q 12 hrs • CsA 7 mg/kg q 24 hr • Topical tacrolimus • ? Surgery (CO2 laser)

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Thank Virbac for sponsorship of this session !

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Skin Barrier Dysfunction in AD

Updates in Management of Canine Atopic Dermatitis

Karen L. Campbell, DVM, MS Diplomate, ACVIM (SA) and ACVD Professor Emerita, University of Illinois Adjunct Clinical Instructor, University of Missouri Veterinary Dermatologist, CARES LLC, Missouri Veterinary Dermatology Center

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Avoidance/Elimination of Allergens

Avoidance/Elimination of Allergens • Remove feathers, kapok, wool • Housedust mite control measures

• Use washable curtains • Wet mop floors

• Remove carpets, blinds, plants, upholstered furniture, clutter • Use plastic or micropore covers for mattresses, boxsprings, pillows

• 2 times per week

• use a HEPA air cleaners, furnace filters, vacuum cleaners • Lower the humidity in the house

• Freeze dry food to decrease # of storage mites

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Antihistamines: Mechanisms of Action

Products to Kill HDMs

Block H1 and/or H2 receptors Stabilize mast cells CNS effects Sedation Response for individual antihistamines is < 25% Must be given consistently for effectiveness Two week trials for each product if owner interested in trying • Can be combined with other anti-pruritics to lower doses (steroids, oclacitinib, modified cyclosporine) • • • • • • •

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Antihistamines for Dogs

Amitriptyline HCl

• Diphenhydramine HCl • 1-2 mg/kg bid

• Tricyclic antidepressant • Inhibits serotonin reuptake • Also potent antihistamine • Do not use in dogs with

• Clemastine (Tavist)

• 0.04-0.5 mg/kg bid

• Hydroxyzine HCl or pamoate • 2.2-6.6 mg/kg tid

• Chlorpheniramine

• cardiac disease • renal disease • hepatic disease

• 0.5-2 mg/kg bid

• Cetirizine (Zyrtec)

• 1 mg/kg q 12-24 hr

• Loratadine (Claritin)

• 1-2 mg/kg BID • Should wean off when discontinuing

• 0.25-0.5 mg/kg q 24 hr

• Fexofenadine (Allergra) • 2-5 mg/kg q 12-24 hr

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Fatty Acid Supplements • Gamma-linolenic acid (evening primrose oil): favors production of PGE1 which is antiinflammatory • Omega 3 fatty acids: compete with omega 6 fatty acids in metabolism, result in production of less inflammatory cytokines, may also down regulate inflammation

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Renonyl Ultra Soft Chews (ultra-micro Palmitoylethanolamide)

Products Available • Wide variety of combinations of omega 3 and omega 6 fatty acids in various ratios and quantities • Individual dog responses may vary (varying metabolism) • Ideally try 3-4 different products, each for 8-12 weeks to see which is most beneficial for a given patient

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• Hydrolyzed soy protein • Reported to increase production of the endocannabinoid 2-arachidononylglycerol • Reported to decrease mast cell release of histamine, PGD2 and TNF-alpha • Reported to support keratinocyte health

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Corticosteroids in Treatment of Allergies

Skin barrier repair products

• Very effective • Many side effects: PU/PD/PP, panting, increased risk of infections, weight gain, thinning of skin, hepatomegaly, easy bruising, thromboembolism, adrenal atrophy, diabetes mellitus, pancreatitis, etc. etc.

• Use during flare-ups, if a short allergy season, or if other therapies are not feasible due to owner constraints

Improve skin barrier function by replacement of missing ceramides and other fats in lipid bilayers of epidermis

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Anti-inflammatory Use of Glucocorticoids

Topical treatment of “trouble areas”

• Induction: (5-7 days) • Dog: 0.5-1.0 mg/kg • Cat: 1-2 mg/kg (prednisolone)

• Maintenance: • Dog: 0.2-0.5 mg/kg every other day • Cat: 0.5-1.0 mg/kg every other day

• Should NOT use depo products in treatment of allergies in dogs

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Cyclosporine

Cyclosporine

• Targets T-cells - inhibit cytokines • Langerhans cells

• Effective in treatment of ~80% of dogs with atopic dermatitis • 5 mg/kg/day (attempt to taper to eod after 8 wks; some go into remission) • Expensive, monitor for side effects

 IgE receptor  tissue migration  Antigen processing • Mast Cells  histamine release • Keratinocytes

• Common: GI, gingival hyperplasia, hirsutism • Uncommon: renal, hepatic, bone marrow, cutaneous papillomas, other infections (especially fungal), EM, TEN

 IL-8 receptors

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Cyclosporine

Cyclosporine

• If vomiting is a problem

• If gingival hyperplasia develops

• Give with food and/or freeze the capsules • Premedicate with Cerenia or Reglan

• Try reducing dose • Azithromycin oral paste • Surgical resection if excess tissue

• Cerenia (maropitant citrate) 2 mg/kg PO • Reglan (metoclopramide HCl 0.2-0.5 mg/kg PO)

• To decrease GI side effects and reduce cost give with a cytochrome P-450 inhibitor • Give with ketoconazole 2.5-5 mg/kg PO • Can reduce dose of CsA to 2.5-3 mg/kg PO

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Before and after resection of gingival hyperplasia

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Oclacitinib (Apoquel®)

Topical Calcineurin Inhibitors

• JAK 1 (Janus kinase inhibitor)

• Tacrolimus • Pimecrolimus • Inhibit the activation of T cells and mast cells in the skin • Useful for treating localized lesions • Compound as 0.125% tacrolimus

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• Inhibits production of JAK-1 dependent cytokines involved in allergy • At therapeutic dose blocks production of IL-31 • Also decreases IL-2, IL-4, IL-5, IL-6 and IL13 • Rapid (within hours) decrease in itching • Reduces cutaneous inflammation (not as good for feet or ears as CsA)

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Oclacitinib (Apoquel®)

Oclacitinib (Apoquel®)

• Half-life approximately 5 hours • Recommended dosing • 0.4-0.6 mg/kg q 12 hours for 14 days • 0.4-0.6 mg/kg q 24 hours for maintenance

• NOT for use in dogs < 1 year • NOT for use in breeding animals • NOT for use in dogs with “serious infections” • Monitor CBC +/- chemistry panel and UA q 3 months and also evaluate dogs for “silent infections”

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Caninized Monoclonal Anti-IL-31 Antibody (CytoPoint)

Immunotherapy • Desensitization • Hyposensitization • Allergen-specific immunotherapy • Most specific treatment for atopy

• For most dogs needed as a once per month subcutaneous injection (lasts longer for some) • Binds to and neutralizes IL-31 preventing activation of neuronal itch pathways • Onset of action within 24-48 hrs post-injection • Dose is 2-4 mg/kg subcutaneous injection • Highly specific = minimal side effects • Dog only (caninized) • No direct effect on inflammation

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Immunotherapy

Theories of Hyposensitization

• Methods of administering allergen-specific immunotherapy

• Increased T-suppressor activity • Production of IgG blocking antibody • Decreased number of mast cells • Decreased histamine release

• Subcutaneous injections • Induction: injections initially given every 2-3 days • Maintenance: injections weekly to monthly for maintenance • “Rush Immunotherapy” involves giving injections with increased amount of allergens ~ every 30 minutes in hospital and then starting maintenance injections

• Sublingual (SLIT) – oral allergy drops • Given in mouth once or twice daily (on buccal mucosa)

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Selection of Antigens for Immunotherapy

Management of Side Effects during Immunotherapy • Local Reactions

• Correlate History and IDST • Maximum of 12 antigens per treatment vial • Can use 2 or 3 treatment sets simultaneously for highly allergic dogs • Ideal to have separate vials for molds and other allergens

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• premedicate with antihistamines

• Severe pruritus/exacerbated symptoms • reduce dose administered

• Systemic Reactions (Anaphylaxis) • epinephrine/supportive therapy

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Reported Responses to Hyposensitization

Evaluation of Hyposensitization • Are additional medications required

• 25% complete remission • 25% low level of pruritus, no additional medications • 25% moderate level of pruritus, require other treatment—shorter time than before ASIT • 25% no apparent improvement • CAN IMPROVE IF GOOD CE • (interesting/frustrating that majority of treatments for Atopy are each only effective in 75-80% of patients!)

• antihistamines, corticosteroids, frequency of required use, etc.

• Allow 9 months or longer for maximum benefit

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Supportive Treatments • Flea control is “essential” • Antibiotics for pyoderma • Eliminate/minimize exposure • Frequent bathing decreases antigenic load • Moisturizers as needed

Supportive Treatments • Topical agents • (oatmeal, local anesthetics (Pramoxine), antihistamines, astringents, cooling agents, steroids—hydrocortisone safest) • Skin barrier repair products

• Fatty acid supplements • Redonyl (palmitoyethanolamide) • Antihistamines • Occasional need for steroids, oclacitanib or IL31-mab • especially first 2-4 months of Immunotherapy or in peak season

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Pruritic Threshhold

Cumulative/Additive Effects • Allergen load

• food, fleas, yeast, bacterial products, pollens

• Pruritic factors

• allergens, dry skin, irritants, toxins (bacterial and yeast products, products from WBCs)

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Pruritic Threshold Affected By:

Shampoo Therapy

• Emotional State • Other Diseases • Weather • Altered epidermal barrier

• Relief from cool water • Remove surface debris • Remove bacteria • Remove irritants • Remove allergens

• Irritants, dry skin, trauma

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Antipruritic Shampoos/Other Topicals

Antipruritic Rinses • Colloidal oatmeal

Oatmeal (binds allergens, anti-inflam) Diphenhydramine (antihistamine) Pramoxine (anesthetic) Menthol (cools) Corticosteroids (hydrocortisone, triamcinolone; anti-inflammatory) • Ceramides—repair of barrier defect • Many formulations available: shampoos, rinses, leave-on lotions, creams, sprays • • • • •

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• (1-2 tbls/gal)

• Aluminum acetate • Antihistamines • Anesthetic (pramoxine) • Lime sulfur (2%) 

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Additional Therapies being investigated

Adjunctive Therapy for Contributory Factors

• Antigen modification

• Flea control • Antibiotics • Antifungals (antiyeast) • Water soaks/humectants

• drugs that activate Ts cells, CPG, heat-inactivated Listeria

• Inhibitors of Th2 cell activation • Alafacept • Efalizumab

• if dry skin

• Probiotics (boost Th1 response)

• Restricted allergen diet • if indicated

• Skin barrier repair products

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Client Education

Future Therapies

• Expect partial responses unless underlying causes identified and treated • Discuss potential side effects of all medications • Manage expectations

• Antibody regulation

• antiidiotype antibodies • Anti-IgE antibodies (omalizumab for humans)

• DNA vaccines

• Th subset switching • Blocking antibodies • Immune stimulating sequences

• Antimicrobial peptides

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Thank Virbac for sponsorship of this session !

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Companion Animal

Sally J. Foote, DVM, CABC-IAABC Behavior Consultant Foote and Friends Tuscola, IL

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Feline Ladder of Aggression Progression of Body language signs in response to perceived threat.

Each step escalates up the anxiety scale as fast at .1 second in healthy Cats.

Vocalization will depend on the cat and the setting.

12 11 10 9 8 7 6 5 4 3 2 1

Multiple Bites

Bite

Swat

Stare

Ears Turned Back

Hiding

Body Hunched Down, Head Down

Sitting Still or Grooming Area Touched

Hair Slightly Raised Over Back

Dilated Pupils

Ears Flicking

Laying on Sternum with Legs Tucked Under Body

These signs are common in examinations, shelter settings or where the cat cannot find a way to escaps. A cat can progress as fast as .1 second through each step.

Some cats will skip steps or suppress the body language as they escalate.

Copy write 2017 - Sally J Foote DVM - drsallyjfoote.com

In-clinic Training

Speaker

Publications

Webinars

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The Canine ‘Ladder of Aggression Biting Snapping Growling Stiffening up, stare Lying down, leg up Standing crouched, tail tucked under Creeping, ears back Walking away Turning body away, sitting, pawing Turning head away Yawning, blinking, nose licking © Kendal Shepherd 2004

How a dog reacts to stress or threat

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The Ladder of Aggression The Ladder of Aggression is a depiction of the gestures that any dog will give in response to an escalation of perceived stress and threat, from very mild social interaction and pressure, to which blinking and nose licking are appropriate responses, to severe, when overt aggression may well selected. The purpose of such behaviour is to deflect threat and restore harmony and the presence of appeasing and threat-averting behaviour in the domestic dog’s repertoire is essential to avoid the need for potentially damaging aggression. The dog is a social animal for whom successful appeasement behaviour is highly adaptive and it is used continually and routinely in every-day life.

It is most important to realise that these gestures are simply a context and response-dependant sequence which will culminate in threatened or overt aggression, only if all else fails. Contrary to persistent misinformation, the gestures identified are nothing to do with a purported dominant or submissive state relative to companions. In all dogs, inappropriate social responses to appeasement behaviour will result in its devaluing and the necessity, from a dog’s perspective, to move up the ladder. Aggression is therefore created in any situation where appeasement behaviour is chronically misunderstood and not effective in obtaining the socially expected outcome. Dogs may progress to overt aggression within seconds during a single episode if the perceived threat occurs quickly and at close quarters, or learn to dispense with lower rungs on the ladder over time, if repeated efforts to appease are misunderstood and responded to inappropriately. As a consequence, a so-called ‘unpredictable’ aggressive response, without any obvious preamble, may occur in any context which predicts inescapable threat to the dog, when in reality it was entirely predictable.

(Shepherd, K 2009. BSAVA Manual of Canine and Feline Behaviour, 2nd edition.pages 13 - 16.

Editors Debra F. Horwitz and Daniel S. Mills).

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Companion Animal

Jeremy Shomper, Med, DVM, DACVIM Veterinary Specialty Services Villa Ridge, MO

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Seizures in Dogs and Cats Jeremy Shomper MEd, DVM, DACVIM (neurology/neurosurgery) MVMA Convention 2022

A seizure is the motor manifestation of uncontrolled cortical activity. Seizures are one of the most common neurologic problems in small animals. Seizures consist of multiple phases; the prodrome, aura, ictus, and postictal period. Other disorders such as vestibular events, dyskinesias, and syncope are often mislabeled as seizures, at least according to clients.

Characteristics of seizures include duration (<2 to 3 minutes), stereotypical motor movements, autonomic dysfunction, altered level of consciousness, and an appreciable post-ictal phase.

Notably, not all seizures have all of these characteristics. Since seizures represent cerebral dysfunction, a seizure localizes the problem to the forebrain. There are many types of seizure disorders, though we commonly encounter idiopathic epilepsy, neuroinflammatory diseases, and neoplasia.

There are multiple options to treat seizures in our patients including traditional therapies (phenobarbital, potassium bromide, benzodiazepines) and many newer therapies as well (levetiracetam, zonisamide, gabapentin, pregabalin, topiramate). Anti-epileptic drugs should be prescribed when an animal has had >1 seizure in a 6 month period, an episode of status epilepticus, head trauma within 1 month of seizure onset, or when a structural cause for seizure activity is diagnosed/suspected. Choosing an anti-epileptic depends on many factors including client compliance, cost, monitoring needs, and comorbidities.

Cats develop seizures less commonly than dogs and are also less frequently diagnosed with idiopathic epilepsy. Most anti-epileptic drugs are safe to use in cats though potassium bromide should be avoided. Cats tend to be dosed at a lesser level than dogs (phenobarbital) and there are currently ongoing studies regarding the use of levetiracetam in cats.

Cluster seizure treatment is very variable. In order to help alleviate the cost of repeated hospitalizations cluster prevention protocols are commonly utilized. This most commonly relies on pulse dosing either a maintenance medication or a benzodiazepine.

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The Neurologic Exam and Neurolocalization Jeremy Shomper MEd DVM DACVIM (Neurology/Neurosurgery) MVMA Convention 2022

Performing a complete neurologic exam is absolutely necessary for accurate neurolocalization.

When performed in a sequential and consistent order the neurologic exam is efficient and helps guide empirical therapy, diagnostic recommendations, and a succinct specialist referral (when necessary). There are 6 parts of the neurologic exam; observation, gait analysis, postural reactions, cranial nerve exam, spinal reflexes, and palpation.

Observation – When observing an animal take note of its interactions with the environment. Is this appropriate or inappropriate? Also note the patient’s overall level of consciousness and posture.

Gait analysis – Watch the patient walk both freely and on leash. The most basic question is whether or not the animal is ambulatory. You should assess the regularity or predictability of the gait. Additionally, you can incorporate obstacles and/or utilize stairs or curbs to more readily distinguish subtle abnormalities.

Postural reactions – Postural reactions evaluation the animal’s awareness of limb and body position (proprioception). There are multiple ways to evaluate an animal’s proprioception including proprioceptive placing, hopping, hemi-walking, wheelbarrowing, and visual/tactile placing just to name a few. The goal is to categorize the animal’s proprioception as normal/abnormal as well as identify the body parts that are affected.

Cranial nerve exam – The cranial nerve exam serves to identify function (or dysfunction) of the 12 cranial nerves. Some nerves are evaluated in multiple reflexes and others are much more difficult to accurately assess. Cranial nerve dysfunction helps to identify intracranial disease and also provides a more specific localization with the brain.

Spinal reflexes – Spinal reflexes allow the veterinarian to assess the integrity of a reflex arc. The goal is to categorize the reflex as reduced, normal, or exaggerated. Spinal reflexes are critical for accurate neurolocalization. There are many spinal reflexes to choose from, though patellar reflexes, withdrawals, cutaneous trunci, and perineal reflexes are essential.

Palpation – Palpating the spinal column is helpful in neurolocalization as well as developing a list of differential diagnoses. Additional attention should be paid to palpating the limbs and head in an attempt to identify potentially subtle muscle atrophy.

Generally, there are 8 clinically distinct regions of the central nervous system. They include; forebrain, brainstem, cerebellum, C1-5, C6-T2, T3-L3, L4-S3, and the peripheral nervous system. The information gathered during the neurologic exam allows a lesion to be localized to one (or multiple) of these regions.

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The Vestibular System: Function & Dysfunction Jeremy Shomper MEd, DVM, DACVIM (Neurology/Neurosurgery) MVMA Convention 2022

Vestibular syndrome is relatively common occurrence in small animal practice. In health the vestibular system controls balance and posture with regards to gravity and acceleration/deceleration in multiple planes. In states of dysfunction common clinical signs include head tilt, nystagmus, vestibular ataxia, circling, or positional strabismus. The neurologic exam is very important for differentiating central from peripheral vestibular syndrome as these locations will often have very different differential diagnoses, empirical treatment, and referral recommendations.

Categorizing Vestibular Syndrome

Central Postural reaction deficits Mentation abnormalities possible Cranial nerve deficits (V-XII) possible Any phase (including vertical) nystagmus Variable nystagmus possible

Peripheral Normal postural reactions Normal mentation CN VII & Horner syndrome possible Typically rotary/horizontal nystagmus Fast phase is consistent

Perhaps the most common cause of peripheral vestibular syndrome in both dogs and cats is otitis media/interna. Cranial nerve VII and sympathetic deficits commonly occur and are ipsilateral to the lesion. Empirical antimicrobial therapy is a logical first step with commonly utilized antimicrobials including cephalosporins, amoxicillin/clavulanic acid, or fluoroquinolones. It is important to administer a prolonged course of oral antibiotic (at least 4 weeks). Probiotics can be helpful given the extended duration of antibiotic use. Topical treatments are typically avoided as many are ototoxic and/or vestibulotoxic.

Central vestibular syndrome can be caused by a multitude of problems. These include malformations, degenerative diseases, encephalitis/meningitis, neoplasia, and vascular differentials. The signalment proves helpful in prioritizing these differentials further.

Additionally, MRI is typically of great value allowing for a specific diagnosis, prognosis, and treatment course.

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Food Animal

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Food Animal

Pamela Adkins, DVM, PhD, DACVIM University of Missouri Columbia, MO

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Outline

Sepsis in neonatal beef calves

1. Defining sepsis and bacteremia 2. How often does this happen in beef calves?

- Previous studies - MU research

Pamela R. F. Adkins University of Missouri

3. Practical applications

Definition of sepsis

Definitions Systemic Inflammatory Response Syndrome: Exaggerated host defense response to a noxious stressor (infection, trauma, surgery, etc.)

Sepsis: life threatening organ dysfunction caused by dysregulated host response to infection

Bacteremia: viable bacteria in the blood

Systems evaluated to define sepsis: Respiration – evaluated through PaO2 Coagulation – platelet counts Liver – bilirubin levels Cardiovascular – arterial pressure Central Nervous System – score of neurologic function Renal – creatinine and urine output In humans: scoring systems based on clinical examination and laboratory findings In cattle: No current way to define an animal has sepsis

Boone et al., 1992; Singer et al, 2016

Attempts to define sepsis in cattle Considerations:

Although sepsis is hard to define – It likely plans a major role in poor health outcomes in neonatal calves

- Requirement of blood cultures - Only evaluating CBC

How common is it??

(Fecteau 2009)

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Calf Mortality prior to weaning Missouri DATA

How common is sepsis??

Percent reported cause of death among calves less than 3 weeks of age

Objective: evaluate the prevalence of pathologic findings among neonatal beef calves submitted to the University of Missouri Veterinary Medical Diagnostic Laboratory (VMDL) for necropsy.

Poisoning Theft Other known diseases

Sepsis not a reported cause of death by producers

Other known causes

Retrospective study on necropsy reports from 2015-2020.

Lameness or injury Predators Respiratory problems

Inclusion criteria: bovine, 2–21 days of age, and a nondairy breed.

Digestive problems Unknown causes Weather related causes 0

5

10

15

20

25

30

Diagnoses were categorized based on system and pathologic agent type.

Percent

Statistical analysis was performed to evaluate age of calf related to system affected NAHMS, 2010

SYSTEM MORTALITY CATEGORIES

Calf Mortality prior to weaning Missouri DATA Results

Multisystemic 26 10%

Urogenital disorder 19…

Cardiovascular 14 5%

Central Nervous System 21 8%

1,060 reports were reviewed; 95 calves met the inclusion criteria

Median age of included calves being 9 days (range 2-21) The majority of included calves were mixed breed (45%, 42/95) or Angus (39%; 36/95)

Hemolymphatic 13 5% Other Unknown Reasons 2 1% Other Known Reasons 14 6%

Digestive Disorders 101 40%

255 diagnoses were made with a median of 3 diagnoses per calf (range: 0-7) and 2 different body systems involved per calf (range 0-5).

Respiratory Disorders 32 13%

Musculockeletal Disorders 13; 5%

System findings Most common digestive disorders Enteritis (57%) Rumenitis (14%) Peritonitis (6%) Abomasitis (5%)

Most common respiratory disorders Pneumonia (71%) Bronchopneumonia (28%) Other (29%) Intertitital (19%) Multifocal (19%)

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Study Discussion

Sepsis risk factors

High prevalence of multisystemic disease, mainly sepsis (~10%), that may be contributing to neonatal beef calf mortality.

Depend on colostral antibodies

Bronchopneumonia doe not appear to be the major contributor to pneumonic cases in these animals, but further research is needed.

Lack normal intestinal flora (competitive flora)

CNS disease was more common in younger calves, while cardiovascular disease was more common in older calves.

Primary infections – ex: umbilical infections Source of bacteria – contaminated environment, GI tract

Limitations: retrospective nature of study, necropsy reports not standardized.

Fecteau et al, 2009

Clinical Manifestation

Clinical manifestation: acute sepsis

Sepsis should be include in differential diagnosis for many conditions

Classically affects calves 2 – 6 days of age Early signs:

Whenever multiple organ dysfunction

Alteration in mental status, lack of suckling ability

Abnormal temperature not a consistent sign

Severe cardiorespiratory signs

Scleral injection frequently observed

Progression can be rapid and most often fatal

Hypotension as diseases progresses

Signs can be vague and likely attributed to other disease Diarrhea commonly seen Fecteau et al, 2009

Clinical manifestation: Subacute sepsis

Common hematologic abnormalities Abnormal neutrophil count (↑ or ↓) and presence of immature forms.

Seen in older calves (7 – 28 days) Evidence of localized infection • • • • • •

Fecteau et al, 2009

Evidence of neutrophil toxicity on blood smear.

Arthritis Growth plate infection Hypopyon Meningitis Pneumonia Diarrhea

Increased fibrinogen.

Thrombocytopenia in severe cases.

Abnormal coagulation parameters: aPTT and PT most commonly.

Fecteau et al, 2009

Fecteau et al, 2009

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Common Biochemical abnormalities

Bacteremia

Hypoglycemia commonly but hyperglycemia possible

Thought to be contributor to death in many calves with focal infections

Metabolic acidosis

Previous work has found 31-70% of sick calves to have positive blood cultures

Lactic acidosis: L vs D lactate

Azotemia Plasma IgG < 500 mg/dL consistent with FTPI Total Protein < 5.5 mg/dL Fecteau et al, 2009

Diagnosis of bacteremia

(Hariharan 1992; Aldridge 1993; Fecteau 1997; Lofstedt 1999)

Prevalence of bacteremia

Definitive diagnosis requires an aseptically obtained blood culture Evaluation of 108 dairy calves Two groups: diarrheic or nondiarheic Age: 1-21 days

Critical factors in the optimal recovery of organisms from blood have been identified

Prevalence of bacteremia

Recommendations: minimum of 2 blood cultures but 3 to 4 is preferred.

9.26% in diarrheic calves 14.8% in healthy calves No significant difference

All diarrheic calves had systemic signs, yet a smaller proportion were bacteremic Garcia et al., 2021

Etiology

Bacteremia

E. coli is the most common agent Factors associated with bacteremia Depression Fever (>103.5⁰F) Younger age (<12d)

Other important agents: Salmonella Campylobacter Klebsiella Staphylococcus species Streptococcus dysgalactiae

None of the blood values were associated with bacteremia

OVERALL SUMMARY: Antimicrobial therapy targeting potential bacteremia is not currently justified in cases without signs of depression.

Garcia et al., 2021

Fecteau et al, 2009; Garcia et al., 2021

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Study design

Etiology

Prospective observational study

Most available data is from dairy calves All beef calves ≤ 3 weeks of age

Are beef calves different?

Focal site of infection: omphalitis, septic arthritis, diarrhea, respiratory disease Owner consent

Objective of our study is to determine the prevalence of bacteremia among beef calves that present for veterinary evaluation with focal sites of infection.

Collect blood samples for culture from 3 different veins Follow up data on outcomes (2 weeks and 3 months)

Results to date

Results to date Most common reason for enrollment: Diarrhea

Enrolled 20 calves Many received antimicrobials prior to presentation 3/20 (15%) culture positive based on 2/3 samples being positive To date: all were E. coli positive (plan to look at antimicrobial resistance)

Diagnosis: inflammatory biomarkers Many researched but acute phase proteins, like serum amyloid A (SAA), have shown promise.

SAA has been researched and shown potential to aid in the diagnosis of sepsis in humans, dogs, cats and foals.

SAA has been extensively studies in bovines but not with regards to sepsis.

All blood culture positive calves were either euthanized or died soon after discharge

Treatment Goals: Control the infection Modulate the inflammatory response Support the animal during the critical phase

Hedegaard et al 2015; Troìa et al 2017; Jitpean et al 2014; Stoneham et al 2001

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Antimicrobial Susceptibility patterns

Treatment: control infection Antimicrobials: initially broad spectrum but ideally based on culture and susceptibility results Sodium ampicillin Florfenicol Save for cases that need it based on culture and bacterial susceptibility results 3rd generation cephalosporins (ceftiofur)

Intravenous route preferred (depends on antimicrobial choice) Combination of antimicrobials?

Fecteau et al, 2009

Treatment: Modulate Inflammatory response

Fecteau et al 1997

Treatment: Supportive Care Warmth and good bedding Correct 2nd problems: hypovolemia, hypoglobulinemia, hypoglycemia, metabolic acidosis, electrolyte abnormalities, and hypoxia

NSAIDs Flunixin meglumine: duration limited to 2 – 3 days

IV fluids

Can utilize reduced dosages (0.25-0.5 mg/kg)

Plasma transfusion Oral or parenteral nutrition

Meloxicam

Oxygen administration

Fecteau et al, 2009

Prevention: Colostrum Ensure ingestion of high quality colostrum

Fecteau et al, 2009

Prevention: Environment Ensure calves are born into a clean environment

Assess Transfer of Passive Immunity (IgG, Total Protein, Sodium Sulfide Turbidity)

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Summary

References 1.

Sepsis is difficult to diagnose due to vague clinical signs that can be attributed to other diseases.

Research is focusing on inflammatory biomarkers to aid in the diagnosis of sepsis.

Prompt recognition and aggressive treatment is critical to successful outcomes.

2.

3.

4.

5.

6.

7.

8.

Bacteremia is not common, but should be considered if diarrheic calves are also depressed.

9.

NAHMS U-AV. Beef 2007-08 Part V: Referene of beef cow-calf management practices in the United States, 2007-08. Fort Collins, CO: USDA APHIS VS CEAH, 2010.

Fecteau G, Pare J, Van Metre DC, et al. Use of a clinical sepsis score for predicting bacteremia in neonatal dairy calves on a calf rearing farm. Can Vet J 1997;38:101-104.

Fecteau G, Smith BP, George LW. Septicemia and meningitis in the newborn calf. Vet Clin North Am Food Anim Pract 2009;25:195-208, vii-viii.

Aldridge BM, Garry FB, Adams R. Neonatal septicemia in calves: 25 cases (1985-1990). J Am Vet Med Assoc 1993;203:1324-1329.

Hariharan H, Bryenton J, St Onge J, et al. Blood cultures from calves and foals. Can Vet J 1992;33:56-57.

Lofstedt J, Dohoo IR, Duizer G. Model to predict septicemia in diarrheic calves. J Vet Intern Med 1999;13:8188.

Fecteau G, Van Metre DC, Pare J, et al. Bacteriological culture of blood from critically ill neonatal calves. Can Vet J 1997;38:95-100.

Larson RL, Tyler JW, Schultz LG, et al. Management strategies to decrease calf death losses in beef herds. J Am Vet Med Assoc 2004;224:42-48.

Singer M, Deutschman C, Seymour CW, et al. The third international consensus defitions for sepsis and septic shock (sepsis-3). J Am Med Assoc. 2016

Questions?

Acknowledgements: Luis Rivero (MU) Shuping Zhang (MU VMDL) Loren Schultz (MU)

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Food Animal

Elizabeth Cooksey, DVM University of Missouri Columbia, MO

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Heavy Hitters in Small Ruminant Pregnancy Losses Elizabeth Cooksey, DVM Theriogenology Resident Mentor: Dr. Volkmann 104

Small ruminant pregnancy information ● Gestation length - 150 days ● Cotyledonary syndesmochorial placenta ● Goats are CL dependent for entire pregnancy ● Sheep are CL dependent for ~50 days ○

https://www.iamcountryside.com/

Placenta takes over progesterone production 105

When do we worry? ●

Normal abortion rate ~2% Abortion rate = # animals aborting total # pregnant (or exposed to male)

● Exceeding 5% or cluster happening in a short time frame or location ○ Suggestive of diagnostic investigation needed ● Abortion rate 2-5% - suggestive of endemic infection in herd ● Abortion storms - can exceed 25-50% abortion rate 106

Non-infectious vs.

Infectious

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Non-Infectious causes of pregnancy loss

● Inadvertent hormone administration ● Anthelmintics ● Stress/trauma ● Genetic ● Toxins ● Nutritional deficiencies 108

Infectious causes of pregnancy loss

TODAY’S FOCUS ● ● ● ●

Chlamydiosis Campylobacteriosis Toxoplasmosis Coxiella burnetii

HONORABLE MENTIONS ● ● ● ● ●

Brucellosis Leptospirosis Listeriosis Salmonella Border disease

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SR Abortion Summary from MU VMDL (10/2019 - 10/2021) Sheep 4/13 (31%) No diagnosis 4/13 (31%) Bacterial etiology suspected 2/13 (15%) Toxoplasma gondii 2/13 (15%) Campylobacter spp.

1/13 (8%) Brucella ovis

Goats 10/15 (66%) No diagnosis 2/15 (13%) Bacterial etiology suspected 1/15 (7%) Toxoplasma gondii 1/15 (7%) Enterococcus mundti 1/15 (7%) Possible dystocia 110

Top diagnoses in Missouri - MU VMDL cases ● What is diagnosed most commonly? ○ No diagnosis (50%) ○ Bacterial etiology suspected (21%) ○ Toxoplasmosis (11%) ● How often is a definitive diagnosis actually made? ○ 25% of the time ● Ideal samples to submit ○ Fetal membranes 111

Most infectious agents of abortion are zoonotic!!!

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Chlamydiosis - Etiology ● Chlamydia abortus ● Gram-negative, intracellular organism ● Enzootic Abortion of Ewes (EAE) ● Antigenic Type 1 is responsible for abortions, stillborn or weak lambs at birth ○ Type 2 is associated with polyarthritis and conjunctivitis in adults (L.A. Di Paolo et. al. 2019) 113

Chlamydiosis - Epidemiology and Pathogenesis ● Reservoir hosts - pigeons and sparrows ● Transmission through: ○ Tissues and fluids from aborted fetuses ○ Vaginal discharge from ewes who aborted ○ Fetal membranes of aborted fetuses ○ Persists in feces of infected animals ○ +/- ticks and insects

● Incubation period ~90 days ● Severe placentitis → necrosis of cotyledon → nutrient transfer failure → fetal death 114

Chlamydiosis - Clinical signs and Zoonosis ● Signalment - primiparous or newly introduced animals ● ● ● ●

Minimal to no clinical signs prior to aborting Bloody vaginal discharge a few days before abortion Abort during last month of gestation 30 - 60% of pregnant susceptible animals may abort in a naïve flock

● ZOONOTIC - can cause abortions, premature birth, and life-threatening illness in pregnant women ○

Flu-like symptoms initially which can worsen into serious illness 115

Chlamydiosis - Diagnosis Samples to obtain: ● ●

Placental membranes and at least 3 cotyledons +/- vaginal swabs at time of abortion

Diagnostics: ● ● ●

(L.A. Di Paolo et. al. 2019)

Macroscopically - necrotizing placentitis, reddish brown cotyledons w/ purulent exudate in intercotyledonary space Microscopically - suppurative inflammation, basophilic elementary bodies in trophoblast cells PCR to identify DNA for definitive diagnosis 116

Campylobacteriosis - Etiology ● Major human pathogen ● Gram-negative bacteria ● C. jejuni* ● C. fetus subsp. fetus ● Most commonly isolated cause of abortion in sheep ● Known as epizootic abortion

cdc.gov/campylobacter

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Campylobacteriosis - Epidemiology and Pathogenesis ● Bacteria transmitted via fecal-oral route ○ Or ingestion of fetal membranes and fluids from aborting ewe

● Short incubation period - 14-21 days ● Last trimester abortions ○ Abortion storms in naïve flocks

● Placentitis → fetal infection → fetal death 118

Campylobacteriosis - Clinical Signs and Zoonosis ● ● ● ● ●

Often ewe is asymptomatic +/- diarrhea Mucopurulent vaginal discharge Abortion in last trimester Birth of weak or stillborn lambs Fetus is often autolyzed

ZOONOTIC - diarrhea (bloody), fever, and stomach cramps +/nausea and vomiting, spontaneous abortions in pregnant women, Guillain-Barré syndrome 119

Campylobacteriosis - Diagnosis Samples to obtain: ● Placenta w/ cotyledons ● Whole fetus if possible Diagnostics:

M. Saleh et. al. 2013

● Macroscopically - edematous placenta, necrosis of cotyledons with brown to red exudate, white circular necrotic areas on fetal liver and peritonitis ● Microscopically - inflammation of fetal membranes and fetal tissues ● Culture organism from fetal membranes and/or fetal stomach contents 120

Treatment and control options Chlamydia abortus and Campylobacteriosis: ● Long-acting oxytetracycline 6-8 weeks prior to parturition ● Another injection 4 weeks after parturition ● Vaccinate prior to breeding season with booster 30 days before season ○ Annual booster

● Isolation of aborting ewes/does ● Burn or bury fetal membranes and aborted fetuses if not submitting for diagnostics 121

Toxoplasmosis - Etiology ● Toxoplasma gondii intracellular protozoan parasite ● Domestic and wild Felidae (cats) are definitive hosts ● Present in nearly one third of humans ● Worldwide distribution countryliving. com

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Toxoplasmosis - Epidemiology and Pathogenesis ●

Cats shed unsporulated oocysts in feces

●

Enters maternal blood → spreads to other tissues (muscle, brain, heart, placenta) → invades and multiplies in placental trophoblast cells Degree of effect depends on when maternal infection occurs

●

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Toxoplasmosis - Clinical signs and Zoonosis ● ● ●

Most common maiden ewes/does affected Clinically normal at the time of abortion Asymptomatic after abortion as well

vetwest.com.au

aspca.org

ZOONOTIC - often asymptomatic or mild flu-like symptoms. Pregnant women can pass to baby causing miscarriage, stillborn, or enlargement/smallness of head 124

Toxoplasmosis - Diagnosis Samples to obtain: ● ●

Placenta w/ cotyledons +/- fetus (brain) if present

Diagnostics: ● ● ●

msd-animal-health.ie/

Macroscopically - white foci on placental cotyledons and intercotyledonary space has edema Microscopically - necrotic foci of white matter of fetal brain and cotyledons Detection of T. gondii by immunohistochemistry of fetal tissues or membranes, rtPCR, and serology of fetus and dam for presence of antibodies* 125

Treatment and control options Toxoplasmosis:

● Reduce the exposure of pregnant females to oocysts ○ ○ ○ ○ ○

Remove all cats Spaying all queens to reduce the # of kittens Prevent defecation on foodstuff or near water Top layer of hay should only be fed to non-pregnant animals Store grain in sealed containers

petmd.com

● Intentional exposure to young stock and non-pregnant females ○

Build immunity against reinfection during pregnancy

● No approved treatment or vaccine in US for small ruminants ○

Feed Decoquinate (2mg/kg daily) or Monensin (16.8 mg/head/day) 126

Coxiella burnetii - Etiology ● Obligate intracellular gram-negative rickettsial organism ● Category B potential aerosolized biological weapon ● Q (Query) fever in humans ● Highly infectious

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Coxiella burnetii - Epidemiology and Pathogenesis ● Transmission - cattle, sheep, goat, and wildlife carry organism and shed through: placentas, uterine fluids, colostrum, milk, and feces ○ ○ ○ ○ ○

Direct contact via ingestion or inhalation Contaminated grazing pastures Tick bites Inhalation of contaminated dust from barns Can become aerosolized and spread via wind

● Can survive for months to years in environment ● Naïve pregnant dam → placentitis → decreased O2 and nutrients → fetal death ● Asymptomatic infection is more common than reproductive disease 128

Coxiella burnetii - Clinical signs and Zoonoses ● ● ●

Often no clinical signs in dam Abortion or stillbirth occurs in late gestation In naïve herds up to 70% of susceptible animals may abort

ZOONOTIC - Q-fever can develop in 20% of humans infected resulting in hospitalization +/- long-term disability ● ●

Acute atypical pneumonia, undulant fever, hepatitis, extreme myalgia, chronic fatigue syndrome Most show no or mild signs of illness 129

Coxiella burnetii - Diagnosis Samples to obtain: ● ●

Placenta +/- vaginal swabs Due to zoonotic potential, isolation of organism is rarely feasible in most D-labs

Edmondson, M. et. al. Sheep and Goat Medicine. 2012

Diagnostics: ● ●

Macroscopically: placentitis w/ purulent exudates Microscopically: necrotizing placentitis w/ intracellular basophilic organisms ● ID C. burnetii DNA with rtPCR in placenta, vaginal swabs, milk, or feces

askjpc.org 130

Treatment and control options Coxiella burnetii: ● ●

Infected for life - better to just cull?

Treatment with a tetracycline is controversial - may or may not have any affect on controlling abortions or shedding

Control and prevention ● ● ● ●

Reportable in many states - Missouri Biosecurity measures to reduce spread Good manure management - avoid aerosolizing particles, wear mask Vaccination - NO commercial vaccine available in the US 131

Vaccines available in USA Campylobacter jejuni and fetus subsp. fetus - inactivated ● Vaccinate ewelings and doelings before breeding season ● Booster in 60-90 days ● Annual booster recommended Chlamydia abortus - inactivated ● First dose 60 days prior to breeding ● Booster 30 days later ● Annual booster recommended 132

What still needs to be done?

Need vaccine development for safer (human handling) and more effective vaccines ● ● ● ●

Longer shelf-life, no refrigeration needed Should not be dangerous for the handler to administer Should prevent shedding of the organism Subunit recombinant DNA vaccines promising future in vaccine technology?

Vaccines not available in the USA: ● ● ● ●

Toxovax - attenuated vaccine for T. gondii strain S48 Coxevax - inactivated phase 1 vaccine against Coxiella burnetii Leptoshield/Leptavoid - inactivated multivalent vaccine against L. hardjo and pomona Rev-1 - live-attenuated vaccine against Brucella melitensis (US is free from dz) 133

Generalized diagnostic and clinical approach ● Thorough history ○

Number of aborting animals, number of pregnant animals, time period since first abortion, any fetal malformations?, clinical signs in dams, husbandry changes, transport

● Sampling and testing ○

Placenta w/ at least 3 cotyledons, entire fetus if possible, blood samples from affected animals

● Call your diagnostic lab Immediate management actions ● Separate aborting dams ● Biohazardous waste control - avoid human infection (PPE + disposal) ● Work from healthy to sick and young to old 134

What can be done to prevent pregnancy loss?

pinterest.com

● Proper deworming ● Low stress handling, sheer before breeding ● Avoid pregnancy toxemia w/ proper feeding and management ● Lower impact of infectious causes by...vaccination?

Prophylactic antibiotics?

Biosecurity (control of vectors?)

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Thanks to: Dr. Lauren Delaney, MU VMDL, and Dr. Dietrich Volkmann

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Questions? lazyjvranch.com

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References Borel N, Frey CF, Gottstein B, et. al: Laboratory diagnosis of ruminant abortion in Europe. The Veterinary Journal 2014; 200: 218-229.

CDC.gov Concha-Bermejillo A, Romano J: Pregnancy loss in small ruminants. Clinical Theriogenology 2021; 13:194-205.

Dhama K., Mahendran M. et. al. DNA vaccines and their applications in veterinary practice: current perspectives. Vet Res Commun 2008; 32: 341-356.

DiPaolo LA, Pinedo MFA, Origlia J et al. First report of caprine abortions due to Chlamydia abortus in Argentina.

Veterinary Medicine and Science 2019. 1-6. DOI: 10.1002/vms3.145

Dubey JP: Toxoplasmosis in sheep - The last 20 years. Veterinary Parasitology 2009; 163: 1-14.

Dubey JP, Murata FHA, Cerqueira-Cezar CK, et. al.: Economic and public health importance of Toxoplasma gondii infections in sheep: 2009-2020. Veterinary Parasitology 2020; 286: 109195.

Edmondson MA, Roberts JF, Baird AN, et. al. Chapter 8 - Theriogenology of Sheep and Goats. In: D.G. Pugh, A.N. Baird, Sheep and Goat Medicine (Second Edition). W.B. Saunders: 2012. P.150-230.

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References Menzies PI: Control of Important Causes of Infectious Abortion in Sheep and Goats. Veterinary Clinics: Food Animal Practice 2011; 27:81-93.

Menzies PI: Vaccination programs for reproductive disorders of small ruminants. Animal Reproduction Science 2012; 130: 162-172.

Mobini S: Infectious Causes of Abortion. In: Youngquist RS, Threlfall WR, Current Therapy in Large Animal Theriogenology. 2nd Edition. Saunders Elsevier: 2007. P.575-584.

Plummer PJ, McClure J, et. al. Management of Coxiella burnetii infection in livestock populations and the associated zoonotic risk: A consensus statement. J Vet Intern Med. 2018; 32: 1481-1494.

Saleh M., Harkinezhad M., et. al. An outbreak of abortion in Afshari sheep with probable involvement of Campylobacter fetus. Iranian Journal of Veterinary Medicine. 2013; 7: 51-56.

Wu Z., Yaeger M., Sahin O., et. al. A Homologous Bacterin Protects Sheep against Abortion Induced by a Hypervirulent Campylobacter jejuni Clone. Vaccine (Basel). 2020 Nov. 6; 8(4): 662.

Yadav R., Yadav P., Singh G., et. al. Non-infectious Causes of Abortion in Livestock Animals - A Review. International Journal of Livestock Research 2021; 11(2): 1-13.

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Food Animal

Robin Faulkner, DVM Elanco Animal Health

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Using Systems Perspectives to Reimagine our Practice Mental Models from Animal Health and Production to Broader Constructs of Well-Being T. Robin Falkner D.V.M. Technical Consultant Elanco Animal Health Christiana, TN 37037 Introduction and Overview of Presentations As a veterinarian, I have long viewed myself as a part of the animal health infrastructure. But within my mental models I have struggled to define and manage animal health as meaningful positive outcomes versus as simply the absence of negative (sickness) outcomes. I found my own training lacking in the concepts of wellness or well-being. It is common in many production systems for primarily negative clinical outcomes like morbidity and mortality to be measured, recorded, and managed. These metrics are often interpreted in a false dichotomy where the absence of such clinical failure is conflated with wellness or well-being: usually animals that are not diagnosed and treated for clinical disease are for practical purposes considered “well”.

How might my practice approach change if I took a perspective of well-being as the management of continuous variables of desirable outcomes (well-being metrics and behaviors) instead of as the dichotomous absence of something unwanted (clinical disease)? Another important consideration was a desire to identify proactive variables not compromised by the long delays and randomness often inherent in current metrics like morbidity, mortality, and profitability. Additionally, embracing well-being as the managed output of client systems allows one to better take a broader, positive ownership of animal health. Often, in diseasecentric animal health mental models, it was easy for clients to view themselves as the victims of disease or of “high risk cattle” produced by others. Or as a veterinarian to identify as a savior who rides in to save the day from such villains. I have found that the active ownership of system well-being outcomes provides a superior internal systems perspective from which to better manage outcomes within our control when compared to a disease victim or savior mindset. While it is unpleasant and discouraging to take ownership of negative outcomes viewed as outside of one’s control, it is empowering to take ownership of positive systems outputs seen as within one’s control. Much of the power within a well-being mental model change resides in this empowered ownership.

One of the basic underpinnings of Systems Thinking is that mental models / paradigms exert the highest Leverage Points in a system.1. This is also frequently represented in Goodman’s Iceberg Model2 where the base of the iceberg is Mental Models, described as the values, assumptions, and beliefs that guide and/or constrain one’s perspectives. New or expanded mental models

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can help one see new things, interpret in new ways, and provide new insights that can have tremendous leverage in complex systems. However, changing mental models is also recognized as a difficult undertaking since they tend to be very deeply ingrained frameworks that determine how we understand the world and take action3 As such, one’s mental models are comfortable biases that are hard to overcome or change.

Example: Managing Failure is Managing to Fail A personal example might illustrate the shortcomings of a prevailing management-of-failure animal health mental model: When observing recent feeder cattle placements with a client, I noted that several animals had mild lameness symptoms. Closer observation revealed approximately 10-15% of animals had detectable quality-of-movement issues. When the experienced and capable caretakers were queried, they reported a very low level of lameness with only a couple of animals treated across multiple groups. Further investigation revealed that there were underlying physical injuries resulting from maintenance issues in the processing facilities, which were repaired with immediate observed improvements in the quality-ofmovement observations of new placements.

The individual animal observations and judgement of the caretakers were not inconsistent with my own—none of the mildly affected animals I observed met the current case definition to be pulled for examination and/or treatment. However, the sheer number of mild cases was a potential an early indicator of multiple system problem(s) of serious concern requiring immediate investigation and intervention at the system, not individual animal, level. There was not yet a signal in the animal health metrics that any problem might be arising—few animals had yet required treatment for lameness. There was nothing being measured and recorded that allowed detecting an interim degradation of the wellness outcome of musculoskeletal soundness. Caretakers were obviously not in a mental model of managing systems outcomes unless those outcomes were the simple sum of individual failures. Here is an example of how an approach based on evaluation, management, and metrics of individual animal failure (lameness requiring treatment) lacked the needed sensitivity and utility to proactively manage system-wide positive (or negative) outcomes before failure occurred. In this instance, the presence of mild, easily overlooked symptoms in a large number of recently arrived animals potentially had more significance than a modest increase in clinical lameness. And at an earlier intervention point. The unrecognized slight decrease in quality-of-movement in a large number of animals was potentially the harbinger of a yet to emerge, devastating problem that could impact the ability of the client to maintain market access in an environment where mobility scoring at harvest presentation is a metric used to assess animal welfare.4. In fact, low mobility scores could potentially put the client out of business without access to a market for finished animals.

The example reveals that cattle caretakers (caregivers), including veterinarians, often have mental models tuned to recognize and respond to individual failures (clinical disease) instead of system success (true well-being metrics). We likely do not apply the same “eyes” and mental model for quality-of-movement evaluation in feeder calves that we would use in the pre-

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purchase exam of a work horse for the same client. Nor view an outcome like “soundness at harvest” as a very complex systems output instead of a simple sum of individual outcomes. It would be hard to argue that relatively minor mechanical injuries at processing would not potentially predispose animals to other “causes” of lameness. Or that pulling and treating animals for lameness might not create additional lameness in those animals or pen mates. Or that increasing levels of lameness might result in increased attention and more aggressive pulls and treatment of same. This is potentially creating a vicious, not virtuous, cycle where lameness produces more lameness. Especially if animals are passing back through still defective facilities. In this way, at the Stress—Husbandry—Resource Constraint—Clinical Disease Interface, by treating a symptom we often can create more of the symptom or new symptoms. Conversely, measuring and managing for a wellness behavior (like quality-ofmovement) would be more likely to recognize potential issues early, diagnose key underlying factors accurately, and intervene in a more virtuous manner. In the example scenario, had one waited until an unacceptable incidence of nonresponsive lameness cases accrued and performed diagnostics on them---it is unlikely that the predisposing, underlying cause would have been within diagnostic reach and identified. In the example, few animals required treated for lameness and the potential problem was “nipped in the bud” before it became a system wide issue because a wellness outcome and not a failure outcome was managed.

When I systematically examined many other animal, human, and even non-biological outcomes in beef cattle production systems, from Bovine Respiratory Disease Complex to employee turnover to pen maintenance, I found the false dichotomous management of failure outcomes instead of proactive continuous variable management of success outcomes was common.

Many failure outcomes were likely symptoms of problems and interactions elsewhere in the system. Not uncommonly, the simple, intuitive solutions to one symptom potentially created more problems. Additionally, in many cases, constructs and metrics for scoring system success outcomes did not exist in the mental models of personnel within the systems. (See Figure 1)

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Any system measured and managed at a failure breakpoint will likely eventually fail because it will not detect and react to early signs that a risk of catastrophic failure has increased. When an engine starts smoking and knocking is not the point to intervene, and the underlying “cause” may not be within diagnostic reach. Long delays in system failure metrics are common.

Imagining other examples where “managing failure is likely managing for failure” is not difficult, and the humbling examples where significant animal health investments have not been accompanied by overall reductions in failure outcomes, like Bovine Respiratory Disease Complex (BRDC),5 may represent shortcomings in failure-point-focused animal health mental models. Maybe BRDC is not best managed by focusing on BRDC failure, but instead by focusing

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on overall “well-being” throughout the system. Not just animals, but people, customer relationships, facilities, environment, etc. Might we even view maintaining animal health product efficacy within a construct of system wellness? Or the retention and development of highly engaged employees and loyal clients / customers as “symptoms of systems well-being”?

If we flipped our current mental model and viewed BRDC as an outcome (symptom) of low wellness in the system---instead of viewing wellness as the absence of BRDC---might that have higher potential utility in making progress? Can we in effect expand the boundaries of a preventative medicine philosophy to encompass broader constructs of well-being to be managed (outside of a pathogen/disease centric paradigm)?

In my presentations, I will discuss my own journey in transitioning mental models from “managing to fail less” to “managing towards success” using systems science approaches. The audience will be engaged in discussion on expanding the mental framework of practice to better simultaneously influence multiple meaningful positive outcomes in client systems. The first and difficult obstacle is in clearly defining success as something other than the dichotomous absence of failure, then developing with clients a shared vision and metrics around those new mental models.

Animal Wellness Behaviors There is considerable emerging science underpinning new constructs of animal wellness behaviors and well-being, along with recognition that there is considerable overlap and interaction between stress behaviors and animal sickness behaviors.6 The display of sickness behaviors by stressed animals can confound the timely and accurate identification of disease, leading to mistreatment. There is long held and widespread recognition that physical, nutritional, and/or psychological stress can directly increase the incidence of disease7 and the physiological mechanisms have been extensively studied8. Better managing well-being in production systems can have very high leverage—reducing the stressors underpinning decreased wellness behaviors can not only decrease disease directly, but by increasing wellness behavior expression can improve the sensitivity and specificity of disease diagnosis. This can improve treatment response while also further decreasing the stress on cattle and valuable, limited resources like people and therapeutics when unnecessary treatments are reduced. If these freed up resources are then applied to achieving better wellness outcomes, a virtuous cycle (feedback loop) can be created. Conversely, managing at the failure break point can often result in a vicious cycle (feedback loop) where stressors and limited resource constraints are compounded, resulting in systems collapse. In the presentations I will model and discuss these relationships and complex interactions, wherein managing disease can produce more disease, and managing well-being can produce more well-being. Some might argue that these two approaches are the same, representing the “two sides of the same coin”. However, the mental models underpinning the two approaches are so fundamentally different as to represent a complete paradigm shift—and what is observed, how it is interpreted, and the actions taken will bear little resemblance to each other.

Objective of Presentations

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The objective of my presentations is to give the attending veterinarian some systems insights and tools to better help clients reimagine their management systems into a well-being perspective. I believe there is much potential for redesigned systems---that focus resources on creating broad systems well-being (success) instead of managing disease (failure)---to produce more desirable outcomes for our profession, our clients, their animals, and greater society.

Disclosure The views in this abstract and associated presentations represent solely my own. I am currently employed by Elanco Animal Health (EAH) as a Technical Consultant and was sponsored by EAH to present at this meeting. I can identify no potential conflicts of interest in the animal husbandry and systems practice content of this presentation, or other influence, arising from my relationship with EAH. References 1. Meadows, Donella. (1999). Leverage Points: Places to Intervene in a System. The Sustainability Institute. Hartland, VT 2. Goodman, Michael. (2002). The Iceberg Model. Innovation Associates Organizational Learning. Hopkinton, MA. 3. Senge, Peter. (2006) The Fifth Discipline: The Art and Practice of the Learning Organization. Doubleday (A Division of Random House), New York.

4. Edwards-Callaway, LN and MS Calvo-Lorenzo. (2020). Animal welfare in the U.S. slaughter industry—a focus on fed cattle, Journal of Animal Science, Vol 98:4.

5. Vogel,GJ., CD Bokenkroger, SC Rutten-Ramos, and JL Bargen. (2019). A retrospective evaluation of animal mortality in US feedlots: Rate, Timing and Cause of Death. Bovine Practitioner 49:113-122 6. Hart, BL and LA Hart. (2019) Sickness Behavior in Animals: Implications in Health and Wellness. in J Choe et al (ed’s). Encyclopedia of Animal Behavior (2nd ed.). Vol. 1.

Academic Press. Amsterdam. 171-175 7. Williams, Don. (1984) Stress and Its Effects on Cattle. in F Baker and M Miller (ed’s). Beef Cattle Science Handbook (1st ed.). CRC Press. Boca Raton, FL. 8. Verbrugghe, E, F Boyen, W Gaastra, L Bekhuis, B Leyman, A Van Parys, F Haesebrouck, & F Pasmans. (2012). The complex interplay between stress and bacterial infections in animals. Veterinary Microbiology, 155 2-4. 115-27.

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Food Animal

Austin Hinds, DVM, MS, DACVIM_LA University of Missouri Columbia, MO

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ANEMIA AND BLOOD TRANSFUSIONS IN SMALL RUMINANTS C. Austin Hinds DVM, MS, DACVIM-LA University of Missouri Anemia is a common problem in small ruminant medicine. While gastrointestinal parasitism is the primary cause, there are a few other causes worthy of discussion. In this session, we will discuss the best ways to identify anemia, how to identify the underlying cause, and practical treatment strategies. We will also cover non-transfusion treatments of anemia, when to do a blood transfusion, and practical blood transfusion techniques.

Common Causes of Anemia Gastrointestinal parasitism, specifically haemonchosis, is by far the most common cause of anemia in small ruminants. Haemonchosis leads to chronic blood loss anemia. Although blood loss anemias are usually considered regenerative, chronic blood loss results in iron depletion and, therefore, iron deficiency anemia. Iron deficiency leads to a microcytic hypochromic anemia due to decreased production of hemoglobin. The other common cause of non-regenerative anemia is chronic disease in which iron is sequestered in an unusable form in the bone marrow.1 Because copper is necessary for optimal iron absorption and release from body iron stores, copper deficiency also leads to an iron deficiency anemia.2 Acute blood loss is usually associated with trauma. Hemolytic anemia in goats and especially sheep occurs as a result of copper toxicity or other toxins. Clinical signs of hemolytic anemia are icterus, hemoglobinuria, anemia in the face of a normal or high plasma protein, and a strong regenerative response. With acute blood loss or hemolysis a regenerative response will occur within 1-2 days.1 Cutoffs for treatments Animals with chronic anemia are able to adapt well and can become profoundly anemic before clinical signs are apparent to their owners. This tolerance to severe anemia is by two mechanisms. First, with acute blood loss, blood volume is lost and animals can die from shock before they would succumb to hypoxia. Cardiogenic shock occurs when 30% of the circulating blood volume is lost acutely.3 Second, as an animal becomes more anemic, hypoxia leads to the increased concentration of 2,3 DPG. This molecule decreases hemoglobin’s affinity for oxygen, allowing it to offload more readily at the hypoxic tissues. Animals with chronic blood loss can survive severely decreased hematocrits. In general, an animal with chronic blood loss can get to a hematocrit of around 10% before significant weakness or lethargy occurs. Many animals will present with single digit hematocrits and some as low as 3-5% and still survive.

The most important aspect of treating anemia is stopping the loss of red cells. Since haemonchosis is usually the cause of the anemia, using a dewormer that is very likely to kill the worms is of utmost importance. When determining if a patient needs a blood transfusion, it is good to consider hematocrit and clinical signs. When the hematocrit drops below 10%, a blood transfusion is warranted. Animals that have a hematocrit below 10% but are still bright and alert can recover without a transfusion if there are limitations on being able to perform the transfusion. Animals that have a hematocrit of 10-14% but are very weak or are exhibiting signs of shock usually require a blood transfusion. Animals that are alert and still eating and the hematocrit is above 10, can usually be managed without a blood transfusion.

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Methods for transfusions A good blood donor is one that is of significant body size and therefore blood volume, and has a good hematocrit – usually above 30-35%. While many blood groups/types are known in ruminant species, the likelihood of a serious transfusion reaction in a non-sensitized patient is very low. Blood type is not considered when performing most blood transfusions.

Volume of blood to needed can be calculated3: 𝑉𝑜𝑙𝑢𝑚𝑒 𝑡𝑜 𝑏𝑒 𝑖𝑛𝑓𝑢𝑠𝑒𝑑 (𝐿) 𝐷𝑒𝑠𝑖𝑟𝑒𝑑 𝑃𝐶𝑉 − 𝑅𝑒𝑐𝑖𝑝𝑖𝑒𝑛𝑡 𝑃𝐶𝑉 = × (𝑅𝑒𝑐𝑖𝑝𝑖𝑒𝑛𝑡𝑠 𝑏𝑜𝑑𝑦 𝑤𝑒𝑖𝑔ℎ𝑡 (𝑘𝑔) × 0.08) 𝐷𝑜𝑛𝑜𝑟 𝑃𝐶𝑉 A goal hematocrit of 14-16 percent is ideal. A healthy donor can donate up to 20% of its blood volume (10-15 ml/kg). Blood can be collected in commercially available blood collection bags or bottles, depending on availability. Most blood collection systems come with a needle attached. Often inserting an IV catheter into the jugular vein of the donor facilitates easier and more secure blood collection.

Sodium citrate can be used to make anticoagulant blood collection bags, but blood must be used immediately if this is done. Blood products should always be given through an inline filter.

1. Pugh DG. Sheep and Goat Medicine, 2nd ed. Maryland Heights, MO: Elsevier; 2012.

2. Harvey JW. Veterinary Hematology: A Diagnostic Guide and Color Atlas, 1st ed. St. Louis, MO: Elsevier; 2012.

3. Balcomb C, Foster D. Update on the use of Blood and Blood Products in Ruminants. Vet Clin North Am Food Anim Pract 2014;30:455-74, vii.

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Food Animal

Rosalie Ierardi, DVM, MS University of Missouri Columbia, MO

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How it Started

Bovine Disease Trends in Missouri

Veterinary medicine as a career goal ~ University of Illinois VDL ~ B.S. (Animal Science) and D.V.M. at University of Illinois ~ Anatomic Pathology Resident at University of Missouri (2017‐2020) ~ Clinical Instructor at University of Missouri (2020‐Present)

Rosalie Ierardi, DVM, MS, DACVP Veterinary Medical Diagnostic Laboratory

1

2

Diagnostic Data • “Have you been seeing a lot of [X] lately?”

• Contributions to Academy of Veterinary Consultants’ Diagnostic Laboratory Report

3

4

Bovine Disease Trends • Bovine respiratory disease • Bovine viral diarrhea virus

Bovine respiratory disease (BRD)

• Bovine anaplasmosis • Bacillary hemoglobinuria (liver flukes)

5

6

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Bovine Respiratory Disease (BRD)

Data Methods/Case Definition

• Most important cause of morbidity and mortality in beef cattle >3 weeks old

• Includes in‐house and field necropsies

• On cow‐calf operations, 16% of cow deaths and 23% of calf deaths

• Diagnosed by a pathologist *OR* identified as pneumonia by the submitter with recovery of primary pathogen(s) from the lung

• Estimated to cost cow‐calf producers $165 million annually

• May include out‐of‐state submissions

Peel, 2020; Smith, 2021

Dr. Guy Loneragan (top), Doster 2010 (bottom)

7

8

Etiologic Diagnosis in Bovine Pneumonia Cases with Full Workup (Culture + PCR)

Bovine Pneumonia Cases (2019 n = 153; 2020 n = 111) 25

44.4%

20 30.1%

2019

20.3%

15 5.3%

10 56.4%

5

28.7%

2020

13.8% 1.1%

0

Jan

Feb

Mar

Apr

May

Jun

2019

Jul

Aug

Sep

Oct

2020

9

Nov

Dec

Full workup includes aerobic culture of fresh lung; PCR for BRSV, BVD, IBR, and PI3

Identification of primary bacterial pathogen(s) only No primary bacterial or viral pathogens identified Identification of primary bacterial and viral pathogens Detection of virus only

10

Bacterial Isolates in 346 Bovine Pneumonia Cases

2019—2021 Bovine Respiratory PCR Results (n = 308)

Jan. 1 2019—Sep. 30 2021

• Bovine respiratory syncytial virus (BRSV) detected in 12.3% of cases Mycoplasma bovis PCR in 107 cases 54% positive

11

• Bovine viral diarrhea (BVD) virus detected in 7.8% of cases

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A Last Thought on BRD …

• Slow progress on BRD control despite better diagnostics, better therapeutics

Bovine viral diarrhea (BVD)

• Need to consider the whole host‐pathogen‐ environment triad Peel, 2020

13

14

Bovine Viral Diarrhea (BVD)

Bovine Viral Diarrhea (BVD)

• Causes immune suppression, predisposes to secondary infections

• Fetal infection in 1st trimester can result in persistently infected (PI) calves

• Reduced fertility, abortions, congenital defects

• PI calves shed virus constantly • Susceptible to mucosal disease

• Herd outbreak estimated to cost up to $100 per animal Callens, 2016; Lanyon, 2014; Riley, 2019

• About 4% of U.S. herds have at least one PI animal Lanyon, 2014; Riley, 2019

https://www.beefmagazine.com/blog/how‐much‐money‐have‐you‐lost‐bvd

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16

Ear Notches Received 2019‐2020 (n = 2,934)

BVD‐PI Tests Jan. 1 2019—Sep. 30 2021

1000

900

• Ear notches tested via IHC or antigen‐capture ELISA (ACE)

800

700

600

• 13/3,606 = 0.4% PI

500

400

• Large studies of cattle entering feedlots yield BVD‐PI prevalence of 0.3% to 0.4%

300

200

100

0

Jan

Feb

Mar

Apr

May

Jun

Jul

Aug

Sep

Oct

Nov

Dec Riley, 2019

17

18

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“BVD Tracker” from BI

Bovine Anaplasmosis

https://bvdvtracker.com/

19

20

Anaplasma marginale

Anaplasma marginale

• Common tick‐borne pathogen of cattle • Disease associated with severe anemia • Spread primarily by Dermacentor ticks • Can also be spread by biting flies, any equipment contaminated with blood

• Infected cattle become subclinical carriers for life

21

• Carriers detected via antibody testing by (cELISA)

22

Control Strategies

Economic Impact

• Vector control • Avoid sharing needles, etc. between animals • Chlortetracycline (Veterinary Feed Directive) • Experimental vaccine—efficacy not determined

23

• Average cost ~$425 per clinical case • Frustrating to producers!

24

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Bovine Anaplasmosis in Missouri

Bovine Anaplasmosis in Neighboring States

• Contemporary data is limited

• Kansas, herd-level prevalence 52.5% among 925 cow-calf operations sampled 2016—2017

• Past reports from cattle sampled at slaughter • 1972, 32/253 samples positive with CFT = 12.6%

• Illinois, cow-level prevalence 61% among 82 beef herds sampled 2017—2019 Spare M.R., et al, 2020. https://doi.org/10.1016/j.vpoa.2019.100021

• 2013, 19/54 samples positive with cELISA = 35.2%

McCallon, 1973; Whitlock, 2014

25

Spare, 2020; Johnson‐Walker, 2020

26

Sample Submission to VMDL vs. Beef Cow Population

A. marginale cELISA at MU VMDL • Retrospective search of diagnostic records for Anaplasma marginale cELISA, 2010-2019 • 1,647 of 3,781 samples positive (43.6%) • ≥1 positive result in 104 of 114 counties • Highest submissions and detections September—December

27

28

A. marginale cELISA at MU VMDL

Preliminary Conclusions—Anaplasmosis in MO

• Tested cattle* were 82.6% female, 17.4% male

• Bovine anaplasmosis is widespread in Missouri cattle

• Females more frequently positive (43.9%) than males (38.6%)

• Older females may be predisposed

• On average, females older than males • Mean: 58.6 months vs. 36.0 months

• Preliminary results of Bayesian spatiotemporal evaluation of county‐level aggregated data indicate spatial and/or temporal clustering

• On average, positive cattle older than negative cattle • Mean: 63.0 months vs. 47.3 months

29

• This suggests risk factors vary with time and/or geographic location

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Tick‐Borne Diseases on the Rise • Reports of human tick‐borne diseases have been increasing • New pathogens, new ticks • Heartland virus in humans (Missouri) • Theileria orientalis Ikeda genotype in cattle (Pennsylvania, Virginia, West Virginia)

Bacillary Hemoglobinuria

• Asian longhorned tick (Haemaphysalis longicornis) detected in Missouri July 2021

31

32

Bacillary Hemoglobinuria

Bacillary Hemoglobinuria

• Caused by Clostridium haemolyticum (C. novyi type D)

• MU VMDL received seven confirmed cases between December 2020 and May 2021

• Characterized by acute hepatic necrosis and intravascular hemolysis • Typically associated with migration of Fasciola hepatica • Also occurs in cattle without evidence of liver flukes

33

• Seven beef cattle, each from a unique premises, in 3 adjacent counties in north-central Missouri • One 6-month-old heifer, five mature cows, and one mature bull

34

• Focally extensive hepatic necrosis • No evidence of flukes at time of necropsy

Photos courtesy Dr. Luis Rivero

35

Photo courtesy Dr. Renata Mammone

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37

38

Additional Cases

Additional Cases

• Five mature cows, one 6 month old heifer

• In 6 of 7 cases, dark red urine was observed

• Fascioloides magna identified in 2 cases

• In 1 case, hemoglobinuria was identified microscopically

• In 3 cases, fluke ova and/or migration tracts with black pigment

Photo courtesy Dr. Kei Kuroki

Photo courtesy Dr. Dae Young Kim

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40

• In all 7 cases, Clostridium novyi* detected by FAT and IHC • In all 7 cases, C. haemolyticum beta toxin gene detected by PCR

Cases compiled by Lauren Delaney, DVM. Map prepared by Rosalie Ierardi, DVM, MS. Geography shapefiles are from the U.S. Census Bureau (2010).

Locations are approximate to protect client privacy.

Photo courtesy Dr. Francisco Uzal

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Fascioloides magna

Unusual Increase?

• VMDL’s database in 2010‐2021 records only 12 cases of fluke infestation (F. magna) • Three cases of suspected clostridial hepatitis during the same decade • Cases coincided with a period of heavy rainfall in mid‐Missouri • Did something disrupt the host/agent/environment triad?

43

44

The Final Frontier?

Something else we learned: Clients should select multivalent clostridial vaccines carefully!

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“We are drowning in information but starved for knowledge.”

John Naisbitt, 1982

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Acknowledgements • Ram Raghavan, MPH, MS, PhD; PhD Faculty Mentor • MU VMDL Anatomic Pathologists; MU VMDL Anatomic Pathology Residents (Brett Havis, Renata Mammone, Courtney Valerio) • MU VMDL Bacteriology, Molecular, Serology technical staff (too many to list!)

• Dr. Austin Hinds and Dr. Luis Rivero, Food Animal Clinicians (VHC) • Dr. Lauren E. Delaney; Dr. Tamara Gull (Bacteriology); Dr. Wole Odemuyiwa (Molecular); Dr. Michael Zhang (Serology) • Dr. Craig Payne, MU Beef Extension Veterinarian • Dr. Mauricio Navarro, Dr. Francisco Uzal, and technical staff at California Animal Health & Food Safety Lab (CAHFS) • The clients whose support of the VMDL makes this all possible

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Questions? ierardir@missouri.edu

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Food Animal

Ron Tessman, DVM Elanco Animal Health

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Agenda • Data overview • Recent study review • Why is the data important?

Impact of Vaccination with an Inactivated or Modified-Live Viral Vaccine on Reproduction

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What We Know Vaccination with modified-live (MLV) Infectious Bovine Rhinotracheitis (IBR) and Bovine Viral Diarrhea Virus (BVDV) vaccines in immunologically naïve heifers less than 30 days prior to synchronization is not recommended as reproductive performance has been shown to be negatively impacted.

Data Overview

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Infertility, Lower Conception Rates, Ovarian Lesions, cont.

Infertility, Lower Conception Rates, Ovarian Lesions • Infertility in 50% of heifers inoculated by IV with MLV vaccine on post-breeding day 14. N=81 • Naïve heifers vaccinated IM with MLV vaccine at synchronization had lower conception rate vs. controls. N=192 • Ovarian lesions induced in heifers by IV inoculation with MLV vaccine on the day after breeding. N=83

• Naïve heifers vaccinated IV with MLV viral vaccine at time of estrous.

Necrotic oophoritis characterized by multifocal areas of ovarian tissue necrosis, hemorrhage and mononuclear lymphocytic infiltration was observed vs. normal controls. N=221 • Naïve heifers vaccinated at the time of synchronization/breeding with either MLV or inactivated virus vaccine. Pregnancy rates were greater for control heifers (90%; P = 0.02) and heifers given the inactivated virus vaccine (one dose: 86%; P = 0.08; or two: 90%; P < 0.01) than those given the MLV vaccine (48%). N=592

1Miller, J., Van der Maaten, M. et al. 1989. “Infertility in heifers inoculated with modified-live bovine herpesvirus-1 vaccinal strains against infectious bovine rhinotracheitis on post breeding day 14.” Am J Vet Res. 4:551-4.

2Chiang, B., Smith, P., et al. 1990. “The effect of infectious bovine rhinotracheitis vaccine on reproductive efficiency in cattle vaccinated during estrus.”

Theriogeneology. 5:1113-20.

3Van der Maaten, M., Miller, J., et al. 1985. “Ovarian lesions induced in heifers by intravenous inoculation with modified-live infectious bovine rhinotracheitis virus on the day after breeding.” Am J Vet Res. 9:1996-9.

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1Smith, P., Nusbaum, K., et al. Stringfellow and K. Driggers. 1990. “Necrotic oophoritis in heifers vaccinated intravenously with infectious bovine rhinotracheitis virus vaccine during estrus.” Am J Vet Res. 7:969-72.

2Perry, G., Zimmerman,G., et al. 2012. “The effects of vaccination on serum hormone concentrations and conception rates in synchronized naive beef heifers.” Theriogenology. 79: 200-205.

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Cytopathic BVDV • Cytopathic BVDV was isolated from ovaries removed on days 8, 10 and 12 after vaccination. BVDV antigen was detected in ovarian tissue using immunohistochemistry on days 10-30. N=101

Influence of Vaccination with an Inactivated or Modified-Live Viral Reproductive Vaccine on Pregnancy Success in Beef Cows1 1Grooms,

1Perry,

L. et al. 1998. “Detection of Cytopathic Bovine Viral Diarrhea Virus in the Ovaries of Cattle following Immunization with a Modified Live Bovine Viral Diarrhea Virus Vaccine.” J VET Diagn Invest 1998 10: 130.

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G. et al. 2016. "Safety of vaccination with an inactivated or modified live viral reproductive vaccine when compared to sterile saline in beef cows." J Vet Sci Res. 2.1:033.

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Experimental Design

Study Objective

• 9 herds • 1,436 animals

Determine the impact of vaccines on pregnancy success.

• Blocked by age and calving date within each herd

• 3 treatments • MLV; Inactivated; Control

• Some cows were sold prior to calving for non-reproductive reasons (n = 132) • Calving data was calculated on 1,304 animals

1Perry,

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Bovi-Shield® Gold® FP5L5HB Vaccination

GnRH

cows 60 to 66 hours; heifers 52 to 56 hours

CIDR® -30

Vira

-9

Shield® Vaccination -30

Control

-9

• • • •

AI

PG

GnRH

cows 60 to 66 hours; heifers 52 to 56 hours

CIDR® -9

-2

treatment day

AI 0

1Perry,

G. et al. 2016. "Safety of vaccination with an inactivated or modified live viral reproductive vaccine when compared to sterile saline in beef cows." J Vet Sci Res. 2.1:033.

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Had a 6.5% higher artificial insemination (AI) conception rate Had a 4.3% increase in 56-day conception rate Had a 2.8% increase in overall conception rate Had a higher percentage of cows calving in the first 21 days

• Delaying when the animal conceives/calves can have implications on the success of a cow/calf operation, including pounds of calf weaned, rebreeding & longevity in the herd

0 GnRH

Saline injection -30

cows 60 to 66 hours; heifers 52 to 56 hours

-2

treatment day

• Compared to Bovi-Shield®, cows receiving Vira Shield® :

GnRH

PG CIDR®

AI 0

6 L5 HB GnRH

Vaccination

-60

-2

treatment day

10

Key Findings1

PG

GnRH

G. et al. 2016. "Safety of vaccination with an inactivated or modified live viral reproductive vaccine when compared to sterile saline in beef cows." J Vet Sci Res. 2.1:033.

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1Perry,

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G. et al. 2016. "Safety of vaccination with an inactivated or modified live viral reproductive vaccine when compared to sterile saline in beef cows." J Vet Sci Res. 2.1:033.

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Calving by Group Data1

Pregnancy Success Data1 abP

Pregnancy rate, %

< 0.01 b

a

85%

b b

a

ab

70%

98%

88%

93%

95%

75%

= Saline

65%

= Vira Shield ® abP

55%

a

60%

= Bovi-Shield ®

Calving rate, %

abP

95%

= 0.01

= 0.055 ab

b

45% 35%

47%

40%

56 day

= Vira Shield ®

50% 40%

= Saline

*

50%

56% P > 0.15

30%

Early calving improves:

P > 0.41

• Reproductive longevity • Weaning weights • Total ranch profitability

20% 10%

25%

AI

= Bovi-Shield ® *P = 0.09 *

Breeding season

0%

• 7% increase in 1st service conception, Vira Shield® vs. Bovi-Shield®

1 to 12

• 3% increase in final conception rates, Vira Shield® vs. Bovi-Shield®

13 to 30 Day of calving

31 +

1Perry,

G. et al. 2016. "Safety of vaccination with an inactivated or modified live viral reproductive vaccine when compared to sterile saline in beef cows." J Vet Sci Res, 2.1: 033.

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1Perry,

G. et al. 2016. "Safety of vaccination with an inactivated or modified live viral reproductive vaccine when compared to sterile saline in beef cows." J Vet Sci Res, 2.1: 033.

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Influence of Calving Period on Reproductive Weaning Weight1

Influence of Calving Period on Reproductive Longevity1 (B) South Dakota Integrated Resource Management groups.

Commercial beef heifers (n = 2,195) on producer operations that were retained by producers as replacement heifers

• Calf weaning weights based on calving period • Heifers that calved in the first 21 days of their first calving season weaned a heavier calf in each of their first 6 calving seasons (P < 0.05)

*(P < 0.05).

1Cushman, R., Kill, L., et al. 2013. “Heifer calving date positively influences calf weaning weights through six parturitions.” West Central Research and Extension Center, North Platte. Paper 83.

1Cushman,

R., Kill, L., et al. 2013. “Heifer calving date positively influences calf weaning weights through six parturitions.” West Central Research and Extension Center, North Platte. Paper 83.

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Calving Distribution Definition

What This Data Doesn’t Tell Us

• Calving distribution is the number of cows calving in 21-day periods during the calving season

• Does not tell us the mechanism • Does not say that any specific virus (e.g., BVD) is interfering with normal reproductive behaviors

• Standard Production Analysis Guidelines indicate there are two ways to determine when to start the first 21-day calving interval: 1.

2.

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When the third mature cow (3-years-old or older) has calved, or Start the first 21-day calving period 285 days after the start of the breeding season

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Your Vaccine Choice at Pre-breeding Impacts your:

• Profitability • Reproductive efficiency

Why is this Data Important?

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Maintaining Profitability

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Economics

• Reproductive efficiency has a large impact on cow/calf herd profitability • Maintaining basic herd performance measures, such as calves born per cows exposed, is critical to improving profitability

• Conception rates — an increase in open cows of 3% is equal to the loss of 3 calves per 100 cows, a loss of $2,250*

• Implementing industry best practices, such as estrus synchronization and timed artificial insemination, can give you a $50/hd advantage1

• Weaning weights — heifers that calve early the first year produced 350 more pounds of weaning weight by the 6th calf1 • For a 500-lb calf, that is an extra $575 by the 6th calf or nearly $100 per year

J., Bird, S., et al. 2012. “An economic evaluation of estrous synchronization and timed artificial insemination in suckled beef cows.” J Anim Sci. Vol 90(11):4055-62.

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• Your reproductive and respiratory vaccines can impact reproductive performance*

• • • •

PM-US-19-0678

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Your Vaccine Choice: Vira Shield

Maintaining Reproductive Performance

• Compared to Bovi-Shield, cows receiving Vira

*Based on a 500-lb calf at $750.

E., et al. “Effect of heifer calving date on longevity and lifetime productivity.” Driftless Region Beef Conference Proceedings.

1Mousel,

1Rodgers,

PM-US-19-0678

• Establishing lifetime immunity, with both MLV & inactivated vaccines, is critical in setting your herd up to win by preventing reproductive and respiratory diseases that can negatively impact performance

Shield:1

Had a 6.5% higher AI conception rate Had a 4.3% increase in 56-day conception rate Had a 2.8% increase in overall conception rate Had a higher percentage of cows calving in the first 21 days

• ViraShield helps you establish a strong vaccination program by providing a complete line of flexible, safe and powerful inactivated vaccines that protect against up to 13 respiratory, reproductive and leptospirosis diseases

• Your vaccine program may have impacts on estrus synchronization (ES) and timed artificial insemination (TAI), which in turn impact the economic efficiency of your operation *As defined by artificial inception conception rate and calves born alive.

1Perry, G. et al. 2016. "Safety of vaccination with an inactivated or modified live viral reproductive vaccine when compared to sterile saline in beef cows." J Vet Sci Res, 2.1: 033.

PM-US-19-0678

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Impact of Vaccination with an Inactivated or Modified-Live Viral Vaccine on Reproduction Vira Shield, Elanco, and the diagonal bar logo are trademarks of Elanco or its affiliates.

Other company and product names are trademarks of their respective owners. © 2019 Elanco or its affiliates. nchlth 4872-14 PM-US-19-0678

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Food Animal

Kelsey Walker, DVM University of Missouri Columbia, MO

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Kelsey E. Walker, DVM, MS Food Animal Ambulatory Clinical Instructor University of Missouri Veterinary Health Center Beef Cattle Lameness Lameness is an economically important and common disease of cattle that has substantial welfare implications. In addition to the cost of treatment, labor, and facilities, lameness has a direct impact on animal production as it is associated with decreased feed intake, reduced average daily gain, decreased milk production, reduced fertility, and decreased carcass weight. The estimated worldwide prevalence of lameness in cattle ranges from 1.1% to 54.8%. The most common cause of lameness is foot lameness, representing approximately 90% of lameness cases in dairy cattle and 70% in feedlot cattle. According to survey data from the National Animal Health Monitoring System (NAHMS), lameness was the most common reason stated for antimicrobial usage in beef cows and the second most common reason for antimicrobial usage in dairy cattle, second only to mastitis. However, foot lameness lesions are most commonly non-infectious in origin and the primary treatment for non-infectious lesions and sole abscesses in cattle is corrective hoof trim. Antimicrobials are indicated only in cases of primary infectious lesions (such as interdigital phlegmon, digital dermatitis, and heel erosion), or in cases where the deeper soft tissue structures of the foot are infected such as deep sole abscesses where bleeding occurs and DIPJ sepsis.

The results of a recent research study performed at the University of Missouri Veterinary Health Center focusing on bacterial culture and susceptibility of septic foot lesions of adult beef cattle originating from cow-calf operations in Missouri found sole abscesses and DIPJ sepsis are most commonly polymicrobial and due to opportunistic commensal organisms.

Antimicrobial drug resistance to at least one antimicrobial is common, particularly against oxytetracycline. In cases where antimicrobial usage is warranted, culture and antimicrobial susceptibility testing is recommended prior to antimicrobial treatment due to the wide variety of bacteria and resistance patterns demonstrated. If culture and antimicrobial susceptibility testing is not pursued, usage of a lower-index antimicrobial such as ampicillin, sulfadimethoxine, or penicillin is recommended to follow judicious use principles.

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Tricia Bailey, DVM Equine Medical Services Columbia, MO

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Philip Johnson BVSc(Hons), MS, DACVIM, DECEIM, MRCVS University of Missouri Columbia, MO

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Intraluminal obstruction of the large colon Philip Johnson, Veterinary Health Center, University of Missouri Simple digesta (‘feed’) impaction of the ascending colon represents one of the 2 most common causes of colic. In these cases, obstruction results from lodgment of either normal digesta or abnormal digesta (for example: coarse forage, sand, fecoliths, enteroliths) in the lumen (contents of the colon are normally quite fluidic). Anything that results in dehydration of digesta (lack of water) can contribute risk.

Specific locations along the ascending colon that are most commonly implicated (narrowing is part of the normal anatomy at these locations): Pelvic flexure Transverse colon Alternatively, colonic impaction may occur at an area of the colon that is narrowed by a disease process (scar/stenosis) [good example is right dorsal colitis – often, significant fibrosis occurs as a complication of the condition and leads to significant reduction of the luminal diameter]. However, MOST ascending colon impactions are ‘simple’ and result from coarse dietary fiber loading into the large intestine.

Predisposing factors to colon impaction include: Coarse food (straw bedding, late-cutting fibrous hay) Consumption of bedding (e.g. straw, shavings) Insufficient access to water (ice in winter) Too much distance to water source for old horses affected with OA Mastication failure (bad teeth, painful teeth) Dehydration (all causes)(colonic water is an important reservoir for the whole body) Protracted inappropriate recumbency (neurological disease, lameness, musculoskeletal injury, etc) Insufficient exercise Abnormal nerve function/structure in the enteric nervous system – there is some evidence that some colicprone horses have an abnormally low number of enteric nerve plexus nerves Drugs that interfere with normal motility – NSAIDs are included in this regard (e.g. phenylbutazone) Debilitation and emaciation Obesity Other diseases (abdominal tumor) There is a need for sufficient intestinal force (peristalsis) to “push” digesta through points of normal (or abnormal) narrowing. There is an optimal viscosity for colonic digesta. Viscosity may be increased by reduced fluid content (insufficient water or dehydration) or an increase in particle size (inadequate mastication, food type). Any factor that results in delay or inhibition of normal motility may promote additional water resorption from the digesta and increase its physical bulk (and viscosity).

Once lodged (‘stuck’), the surrounding gut muscle will struggle to try to move the impaction in an aboral direction – in so doing, it causes the fluid component of the offending bolus to be squeezed out and to cause the impaction to become even drier and harder!

The first response of the colon to the presence of dry digesta is to increase motility in an attempt to promote movement of the “clog”. This increased activity (pushing against the clog) results in signs of pain. Some gas and fluid transit may continue (the obstruction is not always complete). Therefore, colonic tympany does not necessarily develop, especially in early cases. The affected horse may continue to pass some manure. Signs of systemic inflammation/endotoxemia are unlikely with simple (early) colonic impaction.

Significant systemic dehydration is also unlikely (unless the impaction occurred as a result of dehydration).

Other signs (aside from pain and reduced passage of manure) include hypophagia, muscle fasciculations, altered facial expression (grimacing - orbital (eye) tightening, tension above the eyes, and stiff, turned back ears), and sweating (sometimes). Passage of manure gradually decreases and fecal balls become rounded and hard, sometimes covered with yellow mucus (a feature of intestinal stasis).

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Left untreated, an obstruction may eventually become complete and result in tympany (with distention of the abdomen). Pressure at the site of impaction may lead to necrosis of the adherent mucosa that could cause endotoxemia. Protracted anorexia may lead to significant dehydration (worsening the situation in the colon). Unrecognized or untreated, colonic displacement may occur (especially right displacement).

Similarly, unrecognized or untreated, colonic rupture is a possibility.

Physical examination findings: Lethargy, hypophagia, and pain (initially intermittent) Reduced borborygmi (percussion may elicit local tympany) Reduced passage of manure (becoming drier) Dehydration and darkening membranes (endotoxemia) – in the later stages, if unresolved.

Abdominal distention (‘bloat’) – in the later stages, if unresolved.

NG reflux – usually negative Per rectum abdominal palpation: Impaction can often (but not always) be detected Quantity of manure in rectal lumen is decreased (or absent) Manure may be small in quantity (+ hard and covered with mucus) It is not always possible to detect colonic impaction on palpation Abdominocentesis: PF is usually normal Increased protein concentration and evidence of inflammation may be present in advanced (protracted) cases.

Routine labs: PCV and plasma total solids may increase as a result of dehydration (and pain, in the case of PCV).

Mature leukocytosis (mature neutrophilia) occurs because of stress.

Might see degenerative changes and leucopenia in advanced cases if there is disruption of the mucosal lining Elevated blood lactate concentration may be detected if there is bodily dehydration.

Treatment: • NPO (if the horse is not inappetent, small meals might help promote GI motility)(failure to provide any food leads to diminishment of motility). Important to NOT feed horse much until the obstruction has been relieved (especially following administration of analgesics) – otherwise the obstruction simply gets bigger!

• Analgesia – as needed. The two most commonly used drugs include flunixin meglumine (Banamine™) and xylazine hydrochloride (Rompun™). Other analgesic drugs may be employed sometimes.

• Laxative/stool softening strategies.

• Walking or light exercise during treatment.

Recommend enteral fluid therapy to restore hydration, stimulate peristalsis (gastro-colic reflex) and promote rehydration of impacted colonic digesta.

Recommend employment of an enteral electrolyte solution [49 g of sodium chloride; 37.8 g of sodium bicarbonate; 7.4 g of Lite Salt™; 10 liters of water].

Can run the enteral fluid therapy as a CRI [5 – 10 ml/kg/h for 2 h, then increase rate to 10 - 15 ml/kg/h].

Check to make sure that no more than 1-2 liters can be retrieved from the stomach via the NG tube at 30 minutes following stopping CRI. If there is >2 l, stop flow and reduce the rate.

Consider IV fluid therapy More expensive.

Not as ‘effective’ as the enteral method for rehydrating impacted digesta.

Restores hydration and promotes hydration of the colonic digesta (does NOT stimulate peristalsis directly but promotes colonic perfusion).

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Must use IV route (or per rectum route) whenever reflux is present (but reflux is not typical for a simple colon impaction).

If necessary for systemic circulatory therapy, fluids can also be administered per rectum (that method will not directly rehydrate colon impaction, however).

Surgical treatment is not usually required.

Surgical treatment should be considered for refractory cases, in the face of developing tympany, and in those cases in which structural failure may be occurring (follow up PF).

Consider surgical treatment when the conservative approach has not resolved the problem within 48 h.

Surgical intervention may also be considered for extremely large-sized impactions (thus staving off the risk of GIT rupture).

Observe carefully for resolution – usually requires 24-48 h: Signs of improvement include increasing borborygmi, softening of impaction (based on results of palpation), increased passage of manure (passing softer manure), comfortable facial expression, and reduced/absent signs of pain (especially when pain relieving medication effect has diminished). If needed for dehydration/hypovolemia, positive results of fluid therapy may include improvement in mucous membranes, strength of peripheral arterial pulses, urination, and resolution of hyperlactatemia.

Feeding the patient?

It is important to NOT allow the patient to eat too much during management of colic. Holding the patient NPO for a while is a common treatment, allowing time for fluids and stool softeners to relieve the impaction. Treatment with analgesic drugs (such as Banamine™) will relieve pain and the patient’s appetite usually returns. However, if the patient is allowed to eat under the influence of Banamine™, new ingesta may ADD to the size of the obstruction and further pain will resume when the effect of Banamine™ wears off. Also, the size of the impaction will be much bigger!

Following a period of NPO during the early stages of an impaction treatment, some small quantities of food may be allowed. Such small feedings may be helpful by stimulating colonic peristalsis (gastro-colic reflex).

We usually allow the patients to graze a little grass for a few bites or they may be offered a small volume (handful) of grain/Senior ration. Alternatively, a hay net is sometimes ‘hung’ on the outside of the bars of the stall – it serves to remind the patient about food, stimulate appetite and allow a small amount of ingestion through the stall bars. Some people like to spread a few handfuls of hay on the stall bedding and let the horse ‘work’ to find and eat it.

Prognosis for ascending colon impaction: Favorable.

Note that recurrence is possible, even likely, in an individual patient (idiosyncratic predisposition).

Some contend that there exists an initial predisposition associated with either damage to the gut (idiopathic) or an idiosyncratic abnormality in the enteric nerve plexuses.

Others suggest that the presence of one impaction that resolved may cause some damage to the enteric nerve plexuses that serves to increase the risk for recurrence.

It is important to identify risk factors and, through client education, and to do one’s best to eliminate those risk factors.

Commonly encountered risk factors (listed above) include insufficient water access (ice in winter), dental issues, rough/coarse forage, change of forage source, insufficient exercise, drug treatments for osteoarthritis/laminitis (phenylbutazone), protracted recumbency (neurological comorbidity), geosediment, parasites, etc.

OTHER If a case of colonic impaction does not appear to be responding to conservative treatment, consider other causes of colonic (intra-luminal) obstruction or causes of extra-luminal colonic obstruction (such as displacements, volvulus, etc).

Other underlying causes of colonic (intra-luminal) obstruction include: geosediment (sand), foreign body, enterolith, fecolith, etc.

Consider:

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Simple colonic impaction is a common (frequent) cause of colic.

Other less common causes of large intestinal colic (example = non-strangulating displacement) often ARISSE as a complication of a primary colonic impaction.

Some preventive strategies to discuss with owner based on local circumstances: Assurance of access to water. Make sure water is available in winter (ice). Provision of a greater number of water sources (especially for older horses if affected with OA). Adding salt to the daily food intake (~2 tablespoons, daily) and providing salt blocks. Soaking the hay (feeding it before it becomes moldy).

Provide ‘sweet tea’ as water source option. Promote exercise and self-motivated mobility (reduce times of confinement). Routine dental prophylaxis. Careful attention to GIT helminth parasitism. Client education and strategies to offset known risks associated with sand/geosediment, enterolith formation, diet changes, NSAID treatments, etc. Use of complete pelleted food sources instead of long stem hay (reduced fiber load). Role of probiotics (yeast?)? A change in food type/source or hay batch within the antecedent two weeks is very commonly identified when presented with colic. An abundance of our patients have developed some degree of obesity – improved client awareness regarding cause and effect may lead to reduced colic risk associated with lipoma development.

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Horse diseases resulting from feeding errors Dr. Philip Johnson In this presentation, examples of feeding errors that can adversely affect equine health will be presented.

Equine motor neuron disease (EMND) – a result of insufficient vitamin E in the diet.

EMND is a neurodegenerative disease that results from dietary insufficiency of vitamin E. It is uncommonly encountered in Missouri because most horses have plentiful access to grass and/or fresh (green) hay. In most instances, EMND is seen in horses that have no access to grass pastures, no fresh (green) hay, and no dietary vitamin E supplements in their management. There’s some indication that excess dietary copper intake might also predispose to EMND. Copper is a ‘transition’ metal and, if present in tissues to an excessive degree, can promote oxidative stress. EMND tends to arise when horses are being managed with these risk factors over the course of at least 18 months. The age range for affected horses is quite broad (2 – 25 years of age) and there are no known inherited predispositions. In some respects, EMND has been likened to Lou Gehrig disease (amyotrophic lateral sclerosis or ALS) in people. This condition results from the loss of nerves in the spinal cord that are important for bodily muscle function and support. Normal function of these nerves is characterized by a very high oxidative capacity and, in the healthy state, plentiful access to vitamin E (a food-derived antioxidant) is critical for normal nerve maintenance. In the absence of vitamin E, nerve cells are degraded by their normal oxidative processes leading to loss of nerve control over muscles. Without normal nerve control (innervation), the affected muscles also undergo degradation leading to weakness and atrophy (shrinkage). The clinical picture for EMND is generally regarded as virtually pathognomonic, meaning that veterinarians can make the diagnosis by simply observing the patient. The symptoms include symmetrical loss of muscle (weight loss, thin), trembling, muscle fasciculations, fidgeting, sweating, increased time spent lying down, shifting body weight to the pelvic limbs, unable to ‘lock’ stifles, low head carriage, abnormal tail carriage, and a preference for walking rather than standing in one position (EMND patients will sometimes lie or fall down when ‘asked’ to stand in one location). Veterinary diagnosis of EMND is further corroborated by measuring the blood vitamin E level (very low in EMND) and looking at affected muscle (a muscle that is present on the top of the tail is usually examined) via biopsy. Not surprisingly, the treatment for EMND is to restore the body’s vitamin E levels through supplementation with natural vitamin E. However, the prognosis is guarded at best – only approximately 40% of EMND-affected horses will respond to treatment and the outcome is one of ‘improvement’ and stabilization rather than resolution (the damage has been done).

Botulism – often a result of spoiled food.

Fortunately, we do not commonly encounter botulism in Missouri horses, but we encountered a number of (suspected) outbreaks this past summer. In its most common manifestation, botulism results from the ingestion of a neurotoxin that is produced by bacteria (Clostridium botulinum) that normally exist in both the soil and in the intestinal tracts of animals. Given the right conditions, these bacteria can become active and start to produce botulinum toxin, one of the most potent toxins that are known. We see botulism when horses have been fed with soil-contaminated forage (as when hay is fed at pasture and becomes trampled into the soil under horses’ feet).

Botulism is also associated with feeding silage, haylage, chaff, and bagged hay (when plastic bags have been torn).

Botulism that results from soil-contaminated and/or improperly prepared (silage, haylage) forage is commonly known as forage poisoning (type B botulism). When ingested, this toxin is absorbed into the body and blocks the nerves that control muscles. All resulting clinical signs are a result of muscle weakness or paralysis. Disease severity depends on the quantity of ingested toxin. It should be noted that botulism can also result from some other circumstances: toxin contamination of forage as a result of the death of a small field animal (such as a mouse); gemination of bacterial spores and toxin production in the intestine of foals, typically aged between 7 days and 3 months (‘shaker foal syndrome’); wound botulism (a wound is contaminated by the bacteria); dead animal in water source; iatrogenic (veterinarian using botulinum toxin for treatment). Botulism can affect groups of horses (forage poisoning) or single animals. In its most severe form, the intoxicated horse (or horses) is (are) simply found dead. Veterinarians consider botulism when presented with horses showing signs of weakness. Although the bacterial that cause botulism are regarded as ubiquitous, clinical disease is more common in certain areas (type B botulism is seen more commonly in horses in Kentucky, the Atlantic seaboard states, and in the northeast). Milder cases of botulism are characterized by difficulties with picking up feed, chewing, and swallowing (dysphagia); there

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is decreased eyelid tone, dilated pupils, a slippery tongue (excess saliva), nasal discharge (saliva and food), abnormal gait (short-strided, weak, stiff-looking movements), tail and anal sphincter weakness, and muscle trembling. Botulism tends to be progressive (especially if weakened horses are being forced to move around a lot). In its more severe forms, affected horses exhibit generalized weakness, falling, increased recumbency, inability to stand up, development of decubital ulcers (skin injury or bed sores), and difficulty with breathing (risk of aspiration pneumonia, paralysis of respiratory muscles). Despite all these bodily dysfunctions, the brain is not affected, and horses retain normal mental faculties. In most instances, the diagnosis of botulism is made presumptively based on the circumstances and clinical signs (including ruling out other possible explanations). Laboratory confirmation of the presence of botulinum toxin can be attempted (gastrointestinal contents, contaminated food, wound tissue) but this testing approach lacks for sensitivity (a lot of false negatives).

A clinical test (“botulism test”) is to offer the patient ~8 ounces of grain in the bottom of a dish – botulism-affected horses exhibit difficulty eating the grain and leave some of it in the container (normal horses should consume it effectively within 2 minutes). The most important early treatment if botulism is suspected in the early stages is to administer antiserum (antibodies against the toxin). The VHC pharmacy holds botulism antiserum in its freezer.

Approximately 70% of affected horses will eventually recover if botulism antiserum can be administered when the patient is still able to stand up. The prognosis is significantly less favorable for horses that have lost the ability to stand up. Symptomatic and supportive care for affected animals must include maintenance of hydration and food intake (inability to swallow) and antimicrobials (risk of pneumonia). Preventive strategies include not feeding hay on grass (where hay may be trampled into the soil), not feeding bagged hay or haylage if the bags have been punctured, not feeding silage to horses (unless the quality of its preparation can be assured), and not feeding hay when a dead animal is identified in the bale. There exists a safe, effective, and inexpensive vaccine for type B botulism.

Problems associated with feeding too much – the mesenteric lipoma.

Through the process of evolution, horses evolved to be at their best (healthiest) when they are grazing native (prairie) pasture grasses and needing to walk over some considerable distances to satisfy their daily nutritional requirements. As has become widely appreciated in recent years, modern horses are commonly accommodated under restrictive conditions that preclude the need to travel far in search of food and they are typically surrounded by (or provided with) modern forage that is characterized by a very high sugar and starch content (non-structural carbohydrates NSC). In contrast, native (prairie) grasses tend to have relatively lower NSC content. Modern forage has been developed through artificial selection. It is very robust and grows readily, generating a higher NSC content that is ideal for food producing farm animal species. Modern forage (Fescue, Kentucky Bluegrass, etc) is almost ubiquitous on Missouri farms and it capably outcompetes native grasses. In addition to a relatively inactive lifestyle (limited exercise, minimal need to avoid predators), the forage component of contemporary horses is often supplemented with grains and/or pellets that further serves to add calories into a daily dietary energy intake that already exceeds the need. Dietary energy excess is all too quickly converted into obesity. There are some clear genetic predispositions and those horses (and ponies) that develop obesity quickly are sometimes referred to as ‘easy keepers’ or ‘good doers’. Although there are a number of potentially adverse health issues that result from obesity in horses, one of the more common complications of obesity that we encounter in mature-to-older obese horses is the mesenteric lipoma, a fatty tumor. Unlike obese dogs that often develop lipomas under their skin, lipoma development in obese horses usually occurs within the animal’s abdomen. Some affected horses develop solitary lipomas and others develop numerous lipomas. In most instances, these lipomas do not cause a problem and are ‘unknown’ to both the horse and the horse’s caregiver. Unfortunately, in some cases, lipomas can predispose to colic. Whereas mesenteric lipomas are a risk factor for mild recurrent colic episodes (by virtue of their obstructive presence, pushing on the intestine), they also sometimes become ‘pedunculated’. A pedunculated mesenteric lipoma arises when the lipoma starts to grow away from its attachment and effectively becomes a ‘ball on a string’. When a lipoma develops pedunculation, it has the potential to wrap around a part of the intestine and cause both obstruction (severe colic) and strangulation (death of affected bowel). This scenario represents a ‘ticking time bomb’ – horses can have pedunculated mesenteric lipomas with anyone knowing – until it wraps the intestine and causes an emergency. Mesenteric lipomas are effectively dormant and unrecognized until severe colic occurs. Severe colic as a result of pedunculated lipomas is the most common reason for which we treat small intestinal colic in Missouri horses. As veterinarians, we are typically suspicious of lipoma when mature horses in relatively high body condition are presented to us for the emergency treatment of small intestinal colic

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with evidence of strangulation. Lipomas are (eventually) positively identified during surgery (or during a postmortem examination). Treatment usually requires removal of both the lipoma (and its attachment) and affected intestine. Small intestinal surgeries such as this are quite complicated and often require a prolonged period of post-operative care in the hospital. The only logical preventive strategy for lipoma development is to proactively guard against obesity.

Persimmons Each year, in the Fall season, we typically see a number of horses and ponies that have ‘overindulged’ on fallen persimmon fruits. A surprisingly high number of our clients are oblivious to the risk associated with persimmons.

Affected animals develop colic, usually as a result of pyloric outflow obstruction by one or more phytobezoars (persimmon associated phytobezoars are also known as diospyrobezoars). In some cases, pieces of the offending bezoar break away and cause (more) serious colic as a result of small intestinal obstruction. Diospyrobezoar formation is a result of the interaction between the flesh of the fruit (contains tannins), seeds, and gastric acid.

Interestingly, persimmon intake also represents a common reason for phytobezoar formation in people. Resulting colic is usually recognized in the fall/winter part of the year. In some cases, affected animals may be presented with spontaneous reflux (yellow-colored acidic fluid draining from the nostrils). Diagnosis of gastric bezoar obstruction is usually confirmed endoscopically – the obstructing structure is seen in the pyloric antrum (along with ulceration). Positive recognition is aided by recognition of persimmon seeds at the surface of the bezoar.

Some bezoars are quite hard/firm and others are more fibrous, presumably a result of the incorporation of forage from the diet. Hard obstructing diospyrobezoars may require surgical removal via gastrotomy, a surgical procedure that is neither routine nor easily accomplished in equids. In some cases, it is possible to ‘crush’ an obstructing bezoar without need to enter the gut lumen. Thus dismantled, offending material may be ‘milked’ to the large intestine. It has been suggested that diospyrobezoars can be ‘dissolved’ using carbonated soda products (such as Coke™), evidence of which originated from the human medical perspective. Our own success with this treatment has been disappointing. Horses and persimmon trees should be kept apart.

Refeeding syndrome Refeeding syndrome was probably first recognized/described by Hippocrates. Later, The Roman historian Flavius Josephus (first century) also reported typical features of refeeding syndrome among survivors of the siege of Jerusalem. He described the death of those who overindulged in food after the famine, whereas those who ate at a more conservative pace survived. More recently, a number of Polish prisoners who had been freed from Soviet camps in 1941–1942 died after they had been given food while in a state of starvation. Refeeding syndrome has also been recognized in horses. It is characterized by critical fluid and electrolyte imbalances, especially hypophosphatemia, with neurologic, pulmonary, cardiac, neuromuscular, and hematologic complications following the reintroduction of food following a period of starvation (minimal nutrient intake). It is also recognized following the re-introduction of food intake for individuals that have been metabolically stressed by critical illness or major surgery. Evidence of re-feeding is typically seen within ~4 days of feeding. Refeeding syndrome is fatal if not recognized and treated properly. Awareness of the condition and a clinical suspicion are needed in order to recognize the condition and to provide effective treatment. Refeeding syndrome results from the provision of food into the body after it has adapted to a period of significant food deprivation (when, in order to survive, principal cellular energy sources are switched from carbohydrates to adipose tissue, fatty acids and amino acids). Central to these fasting/starvation adaptations, insulin secretion is inhibited while glucagon secretion is increased.

Intracellular minerals are severely depleted during fasting/starvation (circulating plasma levels remain may be normal). During fasting/starvation, splenic degradation of erythrocytes is reduced to maintain oxygen carrying capacity. Insulin secretion resumes following refeeding (response to post-prandial hyperglycemia) and leads to increased glycogen, fat, and protein synthesis. The basal metabolic rate is also increased. These processes accelerate the utilization of phosphate, magnesium and potassium (already depleted by fasting/starvation), and reserves are rapidly depleted. Stimulated generation of phosphorylated carbohydrates depletes intracellular ATP levels in liver and skeletal muscle and 2,3-diphosphoglycerate is depleted in erythrocytes. Cellular dysfunction and inadequate oxygen delivery are serious consequences of these metabolic adjustments. Movement of electrolytes from the extracellular to the intracellular compartment occurs (with parallel decreases in plasma levels), especially for phosphate and magnesium (also calcium and potassium). Circulating plasma glucose concentration is elevated and thiamin levels fall. The most common cause of death from refeeding syndrome is acute heart failure (fatal

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cardiac arrhythmia). Regarding the management of refeeding syndrome in people, caloric intake is intentionally reduced when hypophosphatemia arises in patients being reintroduced to enteral (or parenteral) nutrition. During a period of reduced caloric intake, replacement electrolytes, thiamin, vitamin B complex, and multivitamin/mineral preparations are administered. Plasma biochemistry is monitored regularly until abnormalities have been resolved and stabilized.

As veterinarians facing the question about how best to start refeeding starved/emaciated horses, the natural inclination can be to provide plenty of rich food. However, death associated with refeeding occurs in emaciated/starved horses and a more careful approach should be adopted. Feeding exclusively alfalfa has been shown to be the most effective feeding strategy in these situations. Although there is a paucity of information regarding refeeding starved horses, excellent and helpful information has been provided by Dr. Carolyn Stull at the University of California-Davis: UC Davis Refeeding Program: *A hay scale is necessary to implement a refeeding program* Days 1 to 3: Feed one pound (approximately 1/6 of a flake) of high quality, leafy alfalfa every four hours (total of 6 lb per day in 6 feedings).

Have a veterinarian evaluate the horse’s medical status.

Days 4 to 10: Slowly increase the amount of alfalfa and decrease the number of feeding so that, by Day 6, you are feeding just of 4 lb of hay every 8 hours (total of 13 lb per day in 3 feedings).

Day 10 to several months: Feed as much alfalfa as the horse will eat and decrease the feeding to twice a day. Provide access to a salt block. Do not feed grain or any supplemental material until the horse is well along in its recovery – early feeding of grain/supplemental material can complicate the return to normal metabolic function and result in death. **Provide clean, fresh water at all times.

For more information about unwanted horses please visit the Unwanted Horse Coalition: http://www.unwantedhorsecoalition.org/

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MU-CVM Lectures

Tim Evans, DVM, MS, PhD, DACT, DABVT MU-College of Veterinary Medicine Columbia, Missouri

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What is ECHO? ECHO (Extension for Community Healthcare Outcomes) is an educational program that uses videoconferencing technology to create communities of learning focused on specialists sharing their expertise with community providers who can give their patients improved care in their own communities.

Extension for Community Healthcare Outcomes

Veterinary Education Training (VET) Starting March 9, 2021

Telementoring project that creates communities of learning.

ECHO is Extension for Community Healthcare Outcomes

The VET ECHO will be held on zoom, 2nd Tuesday of Every Month 12:00 pm to 1:00 pm

Goal The goal of the VET ECHO is to create a collaborative and inclusive community to support veterinarians through case‐based learning opportunities and evidence‐based education, therefore working to improve outcomes for Missouri producers.

Objectives 1. To share accurate, evidence‐based knowledge and build a community for discussion of important topics in livestock medicine (including beef, dairy, swine, small ruminants, poultry).

2. To facilitate collegial consultation on herd health and individual livestock animal health concerns.

3. To provide virtual opportunities for continuing education credit for practicing veterinarians.

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Target Audience • Veterinarians Treating Food Animals • Mixed Animal Veterinarians • Rural Veterinarians • Veterinary Technicians • Veterinary Students

Curriculum Topics DATE

TOPIC

PRESENTER

3/9/2021

Forage-related livestock morbidity in the “fescue belt”

Tim Evans (MU)

4/13/2021

Lameness in cow/calf operations

Pamela Adkins (MU)

5/11/2021

Swine vaccination: commercial vs pet

Corinne Bromfield (MU)

6/8/2021

TBD

Craig Payne (MU)

7/13/2021

Antimicrobial Stewardship

Tamara Gull (MU)

8/10/2021

Pain management in beef calves

9/14/2021

Calf diarrhea

Mike Kleinhenz (Kansas State) Dusty Nagy (Texas A&M)

10/12/2021

Backyard poultry medicine

Rachel Oman (MU)

11/9/2021

Bovine orthopedics – practice tips

Joseph Lozier (Ohio State)

12/14/2021

Anaplasmosis in cattle

Emily Reppert (Kansas State)

Multidisciplinary Hub Team • • • • • •

Pamela Adkins, DVM, PhD, DACVIM, Food Animal Internist, University of Missouri Tim Evans, DVM, MS, PhD, DACT, DABVT, Toxicologist / Theriogenologist, University of Missouri Corinne Bromfield, DVM, Extension Veterinarian – Swine, University of Missouri Craig Payne, DVM, MS, Extension Veterinarian – Beef, University of Missouri Scott Poock, DVM, DABVP (Dairy), Extension Veterinarian – Dairy, University of Missouri Brian Shoemake, DVM, MS, DACVIM (LAIM), Food Animal Internist / Herd Health, University of Missouri • Tamara Gull, DVM, PhD, DACVIM, DACVPM, DACVM, Food Animal Internist / Microbiologist, University of Missouri • Christopher Baughman, DVM, State Extension Specialist – Small Ruminants, Lincoln University • Cody Secrest, DVM, Rural Large Animal Practitioner, Countryside Veterinary Clinic

Register for the ECHO at www.showmeecho.org/register

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WHAT KILLED THE COW??? Diagnosing Potential Bovine Intoxications Tim J. Evans, DVM, MS, PhD, DACT, DABVT The goal of this lecture is to outline a practical diagnostic approach to cattle intoxications, ESPECIALLY WHEN IT IS NOT THE VACCINE OR FEED!!! Dr. Williams will be providing additional info in his Food Animal lecture on Friday January 28, 2022 from 2:40 to 3:30 PM. OVERVIEW OF BASIC DIAGNOSTIC APPROACH TO SUSPECTED INTOXICATIONS:  SIGNALMENT + EVIDENCE OF EXPOSURE TO TOXICANT/CONSISTENT CLINICAL SIGNS ▪ WHICH ANIMALS (locations, breeds, ages+)?

▪ EVIDENCE OF EXPOSURE TO “TOXICANT X”→≈HOW MUCH?/WHEN?/WHERE? (How reliable???)

▪ WHAT CLINICAL SIGNS??? (video?/digital images?)  PROBLEM LIST ▪ WHAT’S WRONG?/SOME CLINICAL SIGNS “TOXICANT X” SPECIFIC/SOME GENERIC ▪ Physical examination and STAT laboratory testing, IF proximate to patient  “BIG PICTURE” PROBLEMS ▪ SUMMARY OF CRITICAL LIFE-THREATENING ISSUES AND TARGET SYSTEMS/ORGANS • TREAT THE PATIENT NOT THE POISON, UNLESS TOXIC EXPOSURE OBSERVED!!!

• STABILIZATION OF THE PATIENT IS NUMBER ONE PRIORITY!!!  D.A.M.N.I.T. ▪ D = Degenerative ▪ A = Anomaly ▪ M = Metabolic ▪ N = Nutritional/Neoplastic ▪ I = Infectious/Inflammatory/Idiopathic ▪ T = Traumatic/Toxic  POISONING SHOULD BE SUSPECTED WHEN: ▪ DIRECTLY OBSERVED TOXIC” EXPOSURE/”TOXICANT X” IN GI TRACT ▪ Sudden death/Similar clinical signs in MULTIPLE animals ▪ Signs of unknown etiology/Other causes ruled out ▪ Recent change in diet or environment ▪ Neighborhood feuds/Love gone bad/Owner often certain of “CULPRIT” ▪ Very small, young, and/or stupid animals!!!

▪ Might be a “Darwinian phenomenon” OR “aliens”, “bikers”, “local meth labs” ▪ Might need to seek out the individual really in the know OR the “CULPRIT”!!!  A GOOD PHYSICAL EXAMINATION IS CRITICAL AND MAY NEED TO BE REPEATED!!!

▪ It is perfectly ok to use a stethoscope and a thermometer if there are live animals!!!

▪ A NECROPSY IS ANOTHER FORM OF PHYSICAL EXAMINATION!!!

▪ DEAD CATTLE HAVE BEEN KNOWN TO “TELL TALES”!!!  CAREFUL OBSERVATION OF EVIDENCE OF EXPOSURE TO TOXICANT IS ALSO CRITICAL!!!

▪ Direct repeated observation of environment might yield different information!!!!

▪ Impacted by scheduling/ lighting/finances/crowds/decomposition/”karma”!!!

▪ THINGS CAN LOOK VERY DIFFERENT WHEN THE SUN IS SHINING!!!  ARRIVE AT MOST LIKELY FINAL “TOXIC” DIAGNOSIS AND WHY IS IT “TOXICOSIS X” ▪ Not always possible to CONFIRM Dx/Looking and acting like “Dx” might be sufficient.

▪ HOWEVER, THERE ARE INSTANCES WHEN IT IS NECESSARY TO GO FURTHER!!!

▪ THIS IS ESPECIALLY TRUE WHEN DEATH IS THE ONLY CLINICAL SIGN!!!

CONFIRMING DIAGNOSIS OF SUSPECTED INTOXICATIONS WHEN DEATH IS THE ONLY SIGN  DIRECT OBSERVATION OF “TOXIC” EXPOSURE/”TOXICANT X” IN RUMEN OR GI TRACT 208

   

PRETTY MUCH TRUMPS EVERYTHING ELSE IF “TOXICANT X” IS IDENTIFIABLE BRING IN CONTAINERS/LABELING/MSDS/ANY AVAILABLE DOCUMENTATION MIGHT BE ALL DONE WITH Dx/EXCEPT ”LEGAL” CASES REQUIRING Dx CONFIRMATION IF PRECEDING DOESN’T HAPPEN OR “LEGAL” OR REGULATORY OFFICIALS INVOLVED ▪ AGAIN, YOU ALWAYS NEED A DETAILED AND ACCURATE HISTORY!!!

▪ Usually 1st stage of assessing/reassessing clinical signs and circumstances ▪ Possible analyses of potential sources of “poisons”  GUESS WHAT THE NEXT STEP IS???

▪ Physical examination of VERY DEAD ANIMAL!!!

▪ Usually 2nd stage of clinical signs/clinical circumstances assessment/reassessment.  NECROPSY EXAM/HISTOPATHOLOGY ±TOXICOLOGY TESTING IF DEAD ▪ A TOXICOLOGIC NECROPSY IS NO DIFFERENT THAN ANY OTHER NECROPSY!!!

▪ Collect appropriate samples for histopathology IN FORMALIN!!!

▪ Collect appropriate samples for toxicologic analyses NOT IN FORMALIN!!!

▪ CAREFULLY labeled and separated samples/COC?/Refrigerated or frozen (best) ▪ SUSPECT FEED/PLANT/WATER/”SOURCE”/”JUNK” ▪ RUMEN CONTENTS/OCULAR FLUID/LIVER/KIDNEY/BRAIN (IF NEURO or ???)

▪ Fat is ideal for “older” pesticides/access to “old” junk piles and “old” barns/sheds.

▪ Whole blood and urine might also be very useful, if that is what they really are.

▪ A variety of useful screening/confirmatory analyses for metals/organic toxicants ▪ IDEALLY, histopath/analytical results agree with one another AND “Toxicosis X” Dx. ▪ HOWEVER, GARBAGE IN = GARBAGE OUT!!!

• “Rotten” tissues tell no tales!!!/Pathognomonic lesions might be MIA!!!

• Can’t analyze for “Toxicant X” IF appropriate tissue samples/source not collected • JUST ONE SAMPLE MIGHT JUST MEAN ONLY ONE DIAGNOSIS RULED-OUT!!!

SPECIFIC EXAMPLES OF TOXIC BOVINE DEATH AND MAYHEM  HEAVY METALS AND METALLOIDS • Lead • Arsenic  PESTICIDES • OPs and Carbamates • Organochlorine Pesticides  TOXIC PLANTS • Neurotoxic and Hepatotoxic Blue-green Algae • Cardiotoxic Plants • Other Neurotoxic Plants  “LIGHTNING”  GUNSHOT  CARBOHYDRATE OVERLOAD

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MU-CVM Lectures

Sissy (Hsuan-Ping) Hong, DVM, MVM, MS, DACVIM, Neurology MU-College of Veterinary Medicine Columbia, Missouri

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12/10/2021

Outline • Definition • Treatment

Seize the moment: Management of Status Epilepticus and Cluster Seizures

• Emergency benzodiazepine • Maintenance anti-convulsant • Cluster protocol

• Other Consideration

Sissy (Hsuan-Ping) Hong, DVM, MVM, MS, DACVIM (Neurology) Assistant Teaching Professor, Veterinary Neurology & Neurosurgery Department of Veterinary Medicine and Surgery College of Veterinary Medicine University of Missouri

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2

Definition

Treatment – why treat?

• Status Epilepticus

• Goal of treatment = reduce the frequency and severity of seizures

• Single seizure lasting > 5 mins • >3 seizures without return to normal consciousness

• Maintenance anticonvulsant RARELY stops seizures from happening again !!!

• Cluster Seizures

• Short Term goal: STOP the seizures • Long Term goal : decrease the frequency and severity

• > 2 seizures in 24 hours

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4

Treatment - Case Example

Treatment Baseline Value

• 3 YO FS Border Collie • Status epilepticus STOP immediate seizure activity

• What do you do?

5

START Maintenance Anti-convulsant

Other Consideration

6

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12/10/2021

Treatment

STOP immediate seizure activity

Treatment

• IV catheter • Check blood work • BG, electrolytes, calcium, PCV/TP • Cat – FeLV/FIV

YES catheter

No catheter

Baseline Value

• Midazolam: • 0.3-0.5 mg/kg intranasal, IM • Diazepam: • 0.5 mg/kg – 1 mg/kg per rectum

• Oxygen • Temperature • Treat hyperthermia • Blood pressure assessment

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• Midazolam: • 0.3-0.5 mg/kg IV • Diazepam: • 0.5 mg/kg – 1 mg/kg IV

If NOT working after 2- 3 doses • Midazolam: • 0.3 mg/kg/hr CRI • Diazepam: • 0.5 mg/kg/hr CRI

**To START**

8

START Maintenance Anti-convulsant

Treatment

Treatment – Timeline (phenobarbital) Midazolam: 0.3 mg/kg IV single dose (or repeat)

How do we choose?

OR +/- Midazolam: 0.3 mg/kg/hr CRI 4 hr

0 hr

*Phenobarbital* OR * Bromide * OR *Keppra*

Phenobarbital: 16 mg/kg loading dose divided into 4 doses given q4h IV

Phenobarbital: 4 mg/kg IV

Phenobarbital: 4 mg/kg IV

24 hr

Phenobarbital: 4 mg/kg IV Phenobarbital: 2.5-3mg/kg IV

** May use oral phenobarbital if IV not available **

*To START*

9

12 hr

8 hr

10

Treatment - Timeline

Treatment – How to taper CRI ?

Midazolam: 0.3 mg/kg/hr CRI

Midazolam: 0.3 mg/kg/hr CRI

BOLUS Midazolam: 0.3 mg/kg IV single dose

Midazolam: 0.2 mg/kg/hr CRI Midazolam: 0.1 mg/kg/hr CRI

+/- ↑ Midazolam: 0.4 mg/kg/hr CRI 0 hr

4 hr

2 hr

Phenobarbital: 4 mg/kg IV

Phenobarbital: 4 mg/kg IV

Phenobarbital: 4 m/kg IV

11

8 hr

20 hr

0 hr

Phenobarbital: 4 mg/kg IV

Phenobarbital: 4 mg/kg IV

**↓ Interval between phenobarbital loading doses if more seizure(s) occur**

Phenobarbital: 2.5-3mg/kg IV

4 hr

Phenobarbital: 4 mg/kg IV

8 hr

Phenobarbital: 4 mg/kg IV

12 hr

18 hr

24 hr

Phenobarbital: 4 mg/kg IV

Phenobarbital: 2.5-3mg/kg IV or PO

*ONLY consider tapering (every 4-6 hr in 0.1mg/kg/hr interval) once FINISHED with phenobarbital loading *

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Treatment – When to send home?

Treatment – Timeline (phenobarbital)  Phenobarbital loading at home, if hospitalization is not possible  12-16 mg/kg loading dose, divided into 6-8 doses over 48 hrs

Midazolam: 0.3 mg/kg/hr CRI Midazolam: 0.2 mg/kg/hr CRI Midazolam: 0.1 mg/kg/hr CRI 0 hr

Phenobarbital: 4 mg/kg IV

4 hr

8 hr

Phenobarbital: 4 mg/kg IV

12 hr

Phenobarbital: 4 mg/kg IV

18 hr

24 hr

Day 1

0 hr

6 hr

12 hr

18 hr

Phenobarbital: 2 mg/kg PO

Phenobarbital: 2 mg/kg PO

Phenobarbital: 2 mg/kg PO

Phenobarbital: 2 mg/kg PO

36 + hr

Phenobarbital: 4 mg/kg IV

Day 2

24 hr

32 hr

40 hr

Phenobarbital: 2 mg/kg PO

Phenobarbital: 2 mg/kg PO

Phenobarbital: 2 mg/kg PO

Phenobarbital: 2.5-3mg/kg IV or PO

*IDEALLY 12-24 hrs seizure free on oral maintenance anti-convulsant ONLY*

GO HOME !!

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Phenobarbital: 2 mg/kg PO

12 hr

Phenobarbital: 2.5-3 mg/kg PO

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Treatment – Timeline (Keppra)

Treatment – Timeline (Bromide)

Midazolam: 0.3 mg/kg IV single dose (or repeat)

Midazolam: 0.3 mg/kg IV single dose (or repeat)

OR +/- Midazolam: 0.3 mg/kg/hr CRI

OR +/- Midazolam: 0.3 mg/kg/hr CRI

0 hr

8 hr

16 hr

Keppra: 60 mg/kg IV loading dose

Keppra: 30-40 mg/kg IV maintenance

Keppra: 30-40 mg/kg IV maintenance

*Elderly OR suspected PSS patients **

24 hr

0 hr

Keppra: 30-40 mg/kg IV maintenance

24 hr

Sodium Bromide: 450 mg/kg – 600 mg/kg loading dose IV infusion over 24 hrs

Potassium Bromide: 30-40 mg/kg PO q24h maintenance

*If seizure is poorly controlled, may still need to add on phenobarbital loading *

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Treatment – Timeline (Bromide)

Treatment – Cluster seizure at home

 Example: 15 kg FS Beagle

Potassium Bromide: 450 mg/kg – 600 mg/kg loading dose PO over 5 days or more Day 1

KBR: 120 mg/kg PO q24h

Day 2

KBR: 120 mg/kg PO q24h

Day 3

KBR: 120 mg/kg PO q24h

Day 4

KBR: 120 mg/kg PO q24h

**If too sedate during loading, may consider dropping to maintenance dose earlier **

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START MAINTANCE

48 hr

 

**Pulse therapy length is dependent on cluster Currently on Phenobarbital 64.8 mg BID PO st characteristics** Pulse therapy with Keppra after 1 seizure for 48-72 hrs

8 AM

8 PM

Phenobarbital

Phenobarbital

Day 6

Day 5

KBR: 120 mg/kg PO q24h

10 AM

6 PM

2 AM

Keppra

Keppra

KBR: 30-40 mg/kg PO q24h

Keppra: 25-30 mg/kg PO q8h

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12/10/2021

Treatment – Cluster seizure at home  Example: 15 kg FS Beagle 

Currently on Keppra 750 mg TID PO

8 AM

Keppra

10 AM

EXTRA Keppra

4 PM

Keppra

Treatment – Cluster seizure at home

6 PM

EXTRA Keppra

Keppra

 

12 AM

Currently on Phenobarbital 64.8 mg BID PO Currently on Keppra 750 mg TID PO

8 AM

Keppra

Keppra

Keppra

8 AM

Need Phenobarbital !!

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**No more than 2 extra doses of phenobarbital in 24 hrs; No more than 2 doses of phenobarbital in 1 hr **

 Example: 15 kg FS Beagle

**If still clusters at high dose of Keppra, phenobarbital need to be initiated **

Phenobarbital

10 AM

EXTRA Keppra

Keppra

10 AM

Keppra

EXTRA Phenobarbital

6 PM

4 PM

12 AM

EXTRA Keppra 6 PM

EXTRA Phenobarbital

Keppra 8 PM

Keppra

Phenobarbital

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Treatment – Cluster seizure at home

Other consideration – profound systemic effects

 Example: 15 kg FS Beagle  

• Early sympathetic overdrive

Currently on Phenobarbital 64.8 mg BID PO  2 extra phenobarbital already in 24 hrs Currently on Keppra 750 mg TID PO  double doses already for 24 hr

**EMERGENCY

TO ER OR Call VET **

• Respiratory compromise • Hypertension • Major cause for death: • Inadequate ventilation • Tachycardia • Pulmonary edema • Arrhythmias • Ventricular arrythmia • Aspiration • Respiratory compromise • Hyperglycemia • Renal Failure • Hyperthermia • Exacerbates neuronal • Acidosis damage • Myoglobinuria

1) Consider if midazolam/diazepam is warranted 2) Check Phenobarbital level (target 25-30 ug/ml) 3) Add on another anti-convulsant: - Zonisamide: 5-10 mg/kg BID PO - KBR -

• Other

Loading: 450-600 mg/kg PO div over 5 days Maintenance: 30-40 mg/kg PO q24h

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Take home message • Status epilepticus and cluster seizures are common neurological emergencies

Thank you!!

• Maintenance anticonvulsant should be initiated along with emergency benzodiazepine treatment • Cluster seizure protocol should be tailored to individual patient and seizure characteristics

Questions?

• Systemic complications need to be considered during prolonged seizure activity

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215

MU-CVM Lectures

Charles A. Maitz, DVM, PhD, DACVR Megan A. Mickelson, DVM DACVS-SA, Angela McCleary-Wheeler, DVM, PhD, DACVIM, MU-College of Veterinary Medicine Columbia, Missouri

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A Comprehensive Approach to Sarcomas Charles A. Maitz, DVM, PhD, DACVR (Radiation Oncology) Megan A. Mickelson, DVM, DACVS-SA, ACVS Fellow, Surgical Oncology Angela McCleary-Wheeler, DVM, PhD, DACVIM (Oncology) Background: Soft tissue sarcomas (STSs) are very common skin and subcutaneous tumors in dogs. These tumors can be subclassified based upon the tissue of origin, including fibrosarcoma, perivascular wall tumors, peripheral nerve sheath tumors, liposarcomas, myxosarcomas, rhabdomyosarcomas, undifferentiated sarcomas, etc. Majority have a similar behavior, which is dependent upon the histopathologic grade (I, II, or III). Metastasis occurs in 0-13% of Grade I, 7-27% of Grade II, and 22-45% of Grade III STSs. Metastasis is most commonly to the lungs, lymph nodes, and rarely other organs. Poor prognostic indicators include size (> 5cm), infiltrative tumors, locations other than limbs (at or below elbow or stifle), high grade, certain histopathologic subtypes, and incomplete surgical margins.

Diagnostics recommended for work-up include fine needle aspirate for cytology to confirm the diagnosis. Additional recommended diagnostics for clinical staging include minimum database with CBC, Chemistry, and Urinalysis, assessment of regional lymph node(s) via cytology, and 3view thoracic radiographs. Depending upon the tumor location, advanced imaging may be required via CT or MRI for surgery and/or RT planning.

Locoregional control is the main goal of treating STSs. Surgery with wide excision is considered the treatment of choice. However, there are many instances when radiation is used in combination or instead of surgery. Electrochemotherapy is another local treatment option available in cases where surgery and/or RT are declined. Survival times are variable by choice of treatment and tumor grade. Median survival time ranges from 940-2270 days with definitive-intent treatment (wide excision with or without RT). It is estimated that a minority of patients will die of their STS (up to 33%). Lower MSTs are reported for high grade tumors, certain tumor subtypes, and those with higher mitotic indices on histopathology.

Chemotherapy/Electrochemotherapy Pending the grade of the soft tissue sarcoma, adjuvant chemotherapy should be considered (i.e., Grade III). The most commonly used injectable chemotherapy is Doxorubicin. Current literature is mixed as far as response to chemotherapy for STSs. Another study with incompletely excised STS and metronomic chemotherapy showed a prolonged disease-free interval using Piroxicam and lowdose cyclophosphamide postoperatively. Some have used intralesional chemotherapy; however, this is not recommended in the author’s opinion given unclear advantages and high rates of wound complications.

Electrochemotherapy can be used as an adjuvant therapy for incompletely excised STSs. Bleomycin administered intravenously or directly into the tumor bed and electrical pulses are stimulated at the tumor site. Minimal literature exists to-date, but it may decrease the risk of local recurrence and prolong the disease-free interval.

Surgery: Common considerations include feasibility of wide resection, risks/complications, wound healing, location of the mass, underlying comorbidities, and behavior of the tumor. For example,a firm, fixed tumor likely requires advanced imaging (CT or MRI) depending upon its location to help guide the surgeon for appropriate resection planes. A good surgeon is prepared with plan A and 218

plan B for surgical removal, as well as closure. The main principle of surgical oncology is to obtain clean, wide margins even if that means being unable to close the wound versus sacrificing margins for wound closure. Surgical dose is the aggressiveness of surgical resection applied to a particular tumor. “Curative intent surgery” includes wide and radical resections, as well as planned marginal resection with adjuvant radiation therapy. Wide excision is surgical removal with en bloc resection of the lesion including a margin of normal-appearing tissue. Radical excision is removal of an entire tissue compartment (ex: limb amputation for appendicular tumors or splenectomy for splenic hemangiosarcoma).

Determining surgical margins is complex. Overall, margin recommendations are truly unknown in veterinary medicine and extrapolated from some human studies and clinical experience.

Recommendations vary with tumor type and location. Fascial planes that are considered appropriate include muscle, muscle fascia, bone, and cartilage. Adipose is NOT sufficient for a fascial plane. Typically, we assume 2-3 cm lateral margins and one fascial plane deep for majority of malignant skin tumors. However, there are situations that require more aggressive margins, such as feline injection site sarcomas (FISS). The current recommendations for this are 5cm lateral margins and 2-3 fascial planes deep, essentially always requiring a radical excision. The tumors are also best assessed preoperatively with advanced imaging, such as CT or MRI. Given these margin recommendations, it is best to vaccinate cats in the tail as distally as possible. These cases are also best served with referral to a surgical oncologist for radical excision and adjuvant radiation therapy +/- chemotherapy.

The purpose of surgical oncology is to take all of this into consideration for each individual patient. For example, a dog with a large soft tissue sarcoma on the limb can be treated with clean margins via limb amputation. However, this is obviously a radical choice many owners would not be interested in pursuing and/or the patient may not be a good candidate for limb amputation.

Another option is planned marginal resection of the tumor with adjuvant radiation therapy, marginal resection with adjuvant electrochemotherapy, or primary radiation therapy.

Local recurrence rates for completely excised tumors are low (0-5%). For incompletely excised masses, local recurrence is related to the grade, with 7% in Grade I STSs and 34% in Grade II STSs recurring locally.

Radiation therapy: Definitive-intent radiation therapy can be performed with small fractions of radiation delivered over 15-20 treatments to a margin around the scar with very effective local tumor control, especially for low grade soft tissue sarcomas. Coarsely fractionated radiation therapy, typically delivered once weekly for 4 weeks, can be considered after surgery in a small number of cases, but is not expected to provide as good of control as standard fractionated radiation therapy.

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In some cases, where the primary tumor is too large to remove with clean margins, the owner is averse to surgery, or the patient may already have evidence of metastasis, primary radiation therapy may be indicated rather than surgical treatment. Options could include “definitive” treatment with stereotactic body radiation therapy (SBRT) or palliative radiation therapy. SBRT aims to maximally shrink (or get rid of) the primary tumor using high doses of radiation therapy given over 1-5 treatments. Palliative radiation therapy aims to keep the patient comfortable for as long as possible, while minimizing side effects of radiation therapy. It may shrink the tumor, but more likely it could prevent further growth for some unknown period of time. As a generality, macroscopic tumors will have ~50% tumor control at 10-12 months with SBRT and generally less time with palliative radiation therapy. Palliative radiation protocols vary greatly depending upon the tumor location, safety of the radiation dose,owner convenience, and radiation oncologist’s preference.

References: Liptak JM and Christensen NI. 2020. Soft Tissue Sarcomas. In Withrow and MacEwen’s Small Animal Clinical Oncology, 6th ed. (Ed: Vail DM, Thamm DH, and Liptak JM). St. Louis, Elsevier, pp.404-431.

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MU-CVM Lectures

Lauren Reeves, DVM, DACVSSA

MU-College of Veterinary Medicine Columbia, Missouri

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Wound Management: A Quick Review and Current Recommendations MVMA Conference 2022 Lauren Reeves, DVM, DACVS-SA University of Missouri Veterinary Health Center

Wound Physiology •

•

Phases of Wound Healing o Inflammatory phase  Days 1-3  Leukocyte migration o Proliferative phase  Days 4-12  Granulation formation and epithelialization o Remodeling/Maturation phase  Up to 12 months depending on tissue  Collagen remodeling, reach peak tissue strength Impediments to Wound healing o Local factors: perfusion, tissue viability, infection o System factors: impaired immune function, cancer, age

Open Wound Management •

•

•

Immediate treatment o Assess stability of patient (ie. triage exam), implement appropriate treatment/diagnostic tests as indicated o Irrigation o Antimicrobial treatment (systemic and/or topical) o Place temporary bandage Definitive Treatment o Sedate or place under general anesthesia o Clip and clean wound o Aseptic skin prep o Sterile gloves, instruments, surgical drape o Explore all wounds (especially punctures) and assess tissue viability o Layered surgical debridement and/or drain placement o Lavage o +/- Culture wound bed o Apply topical dressing o Bandage Topical Dressings o Goal: to achieve moist wound healing environment  Optimizes fibroblast proliferation and epithelial migration

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Manuka Honey: antibacterial, reduces inflammation, stimulates lymphocyte proliferation  Ex. MediHoney or unpasteurized  Change daily  Used during inflammatory phase of healing o Calcium Alginate: Absorbs exudate, enhances autolytic debridement, promotes granulation tissue formation  Ex. Aligcel +/- silver  Change every 2-3 days  Use during later inflammatory and proliferative phase of healing o Hydrocolloid: attracts and absorbs water/exudate to create moist healing environment  Ex. Xtrasorb • Hydrogel colloid sheet (HCS): use with dry to moderately exudative wounds • Foam: moderate to heavily exudative wounds • Classic: heavily exudate wounds  Change every 1-7 days depending on amount of exudate produced.  Use during inflammatory and proliferative phase of healing o Non-occlusive dressings  Adaptic and Telfa pads  Only use when epithelium is present  Can dry granulation tissue Negative Pressure Wound Therapy o Local application of sub-atmospheric pressure o Functions: Increases perfusion, decreases edema, removed exudate, stimulates granulation tissue formation, reduces bacterial colonization o

•

Please do not hesitate to contact the MU VHC Soft Tissue Surgery Service with questions or referrals.

Thank you.

Lauren Reeves, DVM, DACVS-SA Assistant Teaching Professor Small Animal Soft Tissue Surgery Veterinary Health Center University of Missouri 573-882-7821

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MU-CVM Lectures

Owen Skinner, BVSc, DECVS,

DACVS-SA, MRCVS, ACVS

MU-College of Veterinary Medicine Columbia, Missouri

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SUPERFICIAL MASS RESECTION FOR THE GENERAL PRACTITIONER Owen Skinner, BVSc DECVS DACVS-SA MRCVS, ACVS Fellow - Surgical Oncology Surgical oncology is the use of surgical intervention in the diagnosis or treatment of patients with cancer. Surgical oncology is performed throughout the veterinary profession, whether in general practice or specialty centers. While most dogs (and humans) cured of cancer are treated with surgery, not all patients have disease that is treatable surgically.

Furthermore, not all surgeries are equivalent. A strong understanding of cancer behavior and an understanding of cancer biology are critical to effective planning and management.

Pre-Operative Evaluation Diagnosis - Ideally all confirmed or suspected neoplasms should be diagnosed before surgical intervention. On occasion this may not be possible, for example in the context of hemoperitoneum due to rupture of a splenic mass; however, every effort should be made to ensure that sufficient information has been gathered before committing to a management strategy. For superficial masses, fine needle aspirates and cytology will almost invariably represent the first step. If aspirates do not provide a diagnosis or if the information is insufficiently detailed (e.g. broad categories such as “sarcoma” or “malignant neoplasm”), biopsy and histopathology is indicated.

Biopsies may be categorized as incision or excisional in nature. Incisional biopsies remove a piece of the mass but leave the remainder of the lesion in place. Excisional biopsies remove the gross lesion. While an excisional biopsy may seem appealing from the perspective of efficiency, if a diagnosis has not been obtained, it may not be possible to effectively plan surgical margins. This can risk undertreating due to an inadequate surgery or overtreating due to an excessively aggressive surgery or performing surgery in a patient that would not benefit from that intervention. If the clinical team is considering an excisional biopsy, all differential diagnoses should be considered. The treatment options and expected outcomes associated with those differential diagnoses should then be reviewed prior to committing to excisional biopsy.

Staging – Before any major management decisions are made, a patient’s disease stage must be considered. While a patient is staged as a whole, this process can be broken into local staging, where the extent of the primary tumor is assessed, regional staging, which involves assessing draining lymph nodes for metastasis, and distant staging, where remote sites such as the lungs or liver are evaluated for evidence of cancer. Local staging may be performed via physical examination in cases with well-defined, superficial cancers. If lesions are ill-defined, deep, or fixed, cross-sectional imaging such as CT or MRI is often recommended.

The importance of regional staging depends on the behavior of the disease involved. Benign tumors or tumors that very rarely metastasize to lymph nodes, such as soft tissue sarcomas, do not typically warrant detailed regional staging.

Conversely, tumors such as mast cell tumors, squamous cell carcinoma, and melanoma that metastasize commonly to lymph nodes must have regional staging to fully assess the extent of disease. Multiple options are available for regional staging, with associated pros and cons. Palpation is neither sensitive nor specific and so should not be relied on for lymph node staging. Fine needle aspirates of regional lymph nodes may be helpful but approximately a third of metastatic lymph nodes may not be identified on aspirates. In addition, patterns of lymphatic flow vary between patients and the nearest anatomic lymph node is not always the draining lymph node. Sentinel lymph node techniques may be used to try to identify the first node draining a site. A variety of sentinel techniques have been reported, including radiographic or CT lymphography, lymphoscintigraphy, and the use of dyes such as methylene blue. While promising, these techniques have yet to be fully validated in veterinary medicine. Elective lymphadenectomy may also be considered, where the regional lymph node/nodes are excised regardless of appearance based on a moderate to high risk of lymphatic spread. Ultimately, the limitations of staging the nearest anatomic lymph node(s) alone should not prevent staging if more selective techniques are not available; pretty good is rather better than nothing!

Distant staging should be targeted based on the primary tumor diagnosis. Pulmonary staging with 3-view thoracic radiographs or CT is often necessary for distant staging given the high number of tumors that may develop pulmonary metastasis. This approach will not be applicable for all tumors, however. Mast cell tumors, for example, very rarely metastasize to lungs, with liver and splenic involvement most common for distant metastasis of mast cell tumors in dogs and cats.

Surgical Intent/Dose If surgery is to be used for therapeutic purposes in dogs and cats with cancer, surgery can be considered either curativeintent or palliative. Diagnosis and staging are essential to determine an appropriate intent. Excessively aggressive surgery in a patient with advanced disease will cause undue morbidity, while assuming that only palliative options exist when disease can still be controlled can inappropriately eliminate viable treatment routes. Owner goals must be considered

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when determining intent, although owners should be provided with appropriate prognostic information to ensure that these goals are realistic.

The dose of surgery for tumor resection has been previously classified within the following categories: -

Intracapsular resection: Dissection enters the tumor and is often likely to leave gross disease with an associated high risk of regrowth.

Marginal resection: The gross disease is excised at its margins with no or minimal normal tissue surrounding the mass. This may be sufficient for anatomically encapsulated, benign or low-grade lesions but may frequently be inadequate for aggressive masses.

Wide resection: The gross disease is excised with a barrier of normal tissue. For superficial masses, wide margins are often considered as 2-3 cm of tissue laterally and a fascial plane of dense collagenous tissue deep to the mass.

Radical resection: Resection of the entire compartment containing the mass.

Surgery can also be combined with additional treatment such as radiotherapy to allow a reduced dose of surgery to provide long-term control. If the clinical team has a suspicion of needing multimodal therapy, this should be communicated to owners prior to treatment to effectively manage expectations. While revision surgery may be possible at some sites, the first surgery always represents the best chance of control; as a result, a careful diagnostic approach and thoughtful decision-making will give patients the highest likelihood of a successful outcome.

Perioperative Considerations Contingency plans are important to allow flexibility in surgery. Anticipating potential challenges can allow preparation and prevent these challenges becoming more major issues. For example, if a superficial mass is to be resected, Plan A may be to close the site primarily. If this is not possible and the clinical team has not anticipated this challenge, options may be more limited or decisions may be made in a more stressful situation. Planning for the eventuality that primary closure may not be straightforward or feasible could allow the patient to have a wide clip and alternative management methods, such as tension-relief techniques, flaps, or second-intention healing to be considered.

Tumor cells remaining at a surgery site can regrow. If margins are incomplete or if recurrence develops, the entirety of a surgical site must be revised. Keeping the surgical site as limited in size as possible within the bounds of the intended margins can limit unnecessary spread. If drains are used, they should exit close to the primary incision to avoid seeding cancer cells along the drain tract. Tumor cells can also be spread to other sites via contaminated gloves or instruments. If a tumor is diagnosed or suspected, clean gloves and instruments should be used at each surgical site to prevent spread.

Sample Handling Almost all specimens should be submitted for histopathology following tumor resection. If it is worth removing, it is worth finding out for sure what it is. If a curative-intent resection has been attempted, cut surfaces should be marked using tissue ink, which should then be allowed to dry completely before formalin is added. Inking allows the pathologist to identify surgical margins more easily. If ink is seen to be covering cancer cells, the pathologist can be confident the resection is incomplete. Conversely, if ink is a long way from the cancer cells, that provides greater confidence that the resection is complete. Sufficient formalin must be added to allow effective tissue fixation (typically 10 times the volume of tissue). Larger specimens can benefit from incisions to allow penetration of the formalin. If the entire specimen cannot be sent out, keeping the remaining tissue in a bucket (or buckets) with formalin allows the clinical team to submit additional sections, if necessary.

Framing is the context provided to a pathologist by the submitting clinical team. Framing for tumor submission should include previous diagnostic tests such as aspirate or biopsy results and clinical staging results. Describing tumor behavior, precise location, and surgical management can all provide invaluable information to a pathologist and can improve the quality of information sent back.

Postoperative Considerations The histopathology report should be reviewed to assess whether sufficient margins were achieved to provide local control of the tumor. If margins were not sufficient, additional treatment such as revision surgery or radiotherapy may be recommended based on risk and owner goals. The type and grade of tumor should also be assessed to determine the risk of metastasis and whether additional systemic treatment such as chemotherapy would be indicated.

Final Comments Surgery for superficial masses affords the opportunity to provide an owner with answers, control potentially lifethreatening disease, and improve or preserve quality of life. The principles used in surgical oncology are typically not complicated but being systematic and thorough can make an enormous difference in the quality of medicine provided.

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MU-CVM Lectures

Aida Vientos-Plotts, DVM, DACVIM (SAIM)

MU-College of Veterinary Medicine Columbia, Missouri

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1/11/2022

Not respiratory

Cough: what does the gut have to do with it?

Cough

Aspiration related disorders

Compression

LN enlargement

AIDA VIENTÓS-PLOTTS, DVM, DACVIM (SAIM)

Respiratory

Mediastinal mass

Not respiratory

Cardiac Cardiac enlargement enlargement

Not Respiratory

Respiratory

Aspiration related disorders

Compression

Cough •

REFLEX

•

PROTECTIVE MECHANISM

Upper Airways Extrathoracic tracheal collapse

Tracheitis

Infectious (bacterial, parasitic) Noninfectious (post anesthesia)

Lower Airways Post-nasal drip Infectious (fungal, parasitic, viral)

Intrathoracic tracheal collapse Inflammatory airway disease

Idiopathic chronic rhinitis

Infectious bronchitis (parasitic, bacterial)

Neoplasia

Bronchiolar disease

Pulmonary Parenchyma Interstitial lung diseases Eosinophilic

Pulmonary Fibrosis Immune mediated

Neoplasia

Upper airways Pneumonia

Infectious (bacterial, viral, fungal, protozoal)

Oral preparatory defects

Laryngeal dysfunction

Cranial nerve defects

Post – nasal drip

Periodontal disease

Pharyngeal swallow defects Cricopharyngeal achalasia Cricopharyngeal dyssynchrony Myopathy/neuro pathy

Esophageal swallow defects Esophageal hypomotility LES - achalasia like syndrome Megaesophagus

Hiatal hernia

GERD

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COUGH - HISTORY

COUGH – PE

 Characterize

the cough long has it been going on?  What is the pet’s environment (include potential irritants (incense, “dusty” hobbies) travel history, vaccination and use preventatives, other clinical signs?  Other pets in the household sick?



 How



COUGH - HISTORY

COUGH - INITIAL DIAGNOSTICS

 Is

the cough associated with any of the following activities:  Eating

or drinking  Excitement  Exercise  Time of the day? Seasonality?  Do

they have a video?

Wood burning fireplaces?

In cats: what kind of litter do they use?



THORACIC RADIOGRAPHS

Can you elicit a cough on PE? Is the cough productive or non-productive?

Thoracic auscultation  Murmur  Abnormal

 

lung sounds



R/O



Increase suspicion for



External compression



Airway disease



Congestive heart failure





Tracheal collapse?

Pulmonary parenchymal disease



Metastatic disease

Nasal discharge? Characterize? Airflow?

Dental disease?

 Minimum

data base

 4DX  Thoracic radiographs Inspiratory and

expiratory

Most common diagnostics performed in general practice

Challenge: Change your diagnostic approach to coughing patients

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TAKING INITIAL DIAGNOSTICS A STEP FURTHER

ASPIRATION IS COMMON  Over



50% healthy adults aspirate during sleep In a recent report of VFSS, ~40% of healthy dogs had documented reflux

VIDEOFLUOROSCOPIC SWALLOW STUDIES (VFSS)

 Echocardiogram  Are

 Inclusion

criteria (n=32 dogs): cough, thoracic radiographs, VFSS and no GI signs

 Thoracic

radiographs normal (n=11); aspiration pneumonia (n=4) 

– even when there is no murmur

Natural

 Pulmonary hypertension

CANINE AERODIGESTIVE DISORDERS CAN OCCUR WITHOUT OBVIOUS GI SIGNS

 Abnormal

Imaging

 VFSS

VFSS in 30 dogs (94%)

 No

medications indicated?

VIDEOFLUOROSCOPIC SWALLOW STUDIES (VFSS)

Grobman M, et al 2018 JVIM

need for force feeding

12

hour fast recommended

GERD 

Clinical signs 

Cough**

 Lip

licking

 Repetitive

dry swallowing



Regurgitation Nasal discharge



Neck extension



Pharyngeal and esophageal hypomotility (n=14 each); large volume reflux (n=13); ME (n=4), macroaspiration (n=4)

in real time

positioning and bolus size

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GERD

GERD - MANAGEMENT

 Predisposing

factors

 Can

cause secondary

 Obesity

 Tonsilitis

 High

 Pharyngitis

fat diet

 Delayed gastric

emptying (Ileus)

 Hiatal hernia

 Rhinitis  Laryngitis

SELF-PERPETUATING CYCLE  GERD

induces cough, cough induces GERD

 Pressure

gradient differential

 Increased number

of LES relaxation events

 Low

fat diet

 Who

 Antacids  Omeprazole SID

vs Famotidine

VS BID

 Prokinetics  Metoclopramide  Cisapride

dog with AP

 ALL

Brachycephalic dogs

K Tolbert 1, S Bissett, A King, G Davidson, M Papich, E Peters, L Degernes Affiliations •PMID: 21143305 •DOI: 10.1111/j.1939‐1676.2010.0651.x Free article

3

episodes of “aspiration pneumonia” and lethargy

 Treated

should be screened?

 Any

Efficacy of oral famotidine and 2 omeprazole formulations for the control of intragastric pH in dogs

“PENELOPE” 11 MO FS MBD

 Fever

HIATAL HERNIA

with antibiotics and supportive care – improved within 24 hours each time

HIATAL HERNIA  Brachycephalic  Correlation

disease

 88%

dogs are predisposed

between GI signs and severity of respiratory

of dogs with BOAS treated for their GI signs has better outcome after airway surgery

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TAKE AWAY POINTS Can I look for a hiatal hernia without a VFSS?

YES

 All

dogs with BOAS should be screened for GERD, HH and esophageal dysmotility

 Aspiration

All you need is a wooden spoon

related disorders should be considered a differential for any dog with cough (particularly with eating or drinking, recurrent aspiration)

TAKE AWAY POINTS  Not

every case that presents with ”typical” respiratory signs has primary respiratory disease

 History  VFSS

is a crucial part of any work up

has revolutionized the diagnostic approach for coughing dogs

Questions AIDA VIENTOS-PLOTTS, DVM, DACVIM ASSISTANT PROFESSOR, SMALL ANIMAL INTERNAL MEDICINE

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MU-CVM Lectures

Kelly Wiggen, DVM, DACVIM, Cardiology

MU-College of Veterinary Medicine Columbia, Missouri

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Most reactions to ECGs:

Let the beat drop: understanding ECGs Kelly Wiggen, DVM, DACVIM (Cardiology) Assistant Teaching Professor of Cardiology University of Missouri Veterinary Health Center

You are not alone!

Reviewing the basics Q-wave: The first negative deflection of the QRS complex May or may not be present in the dog R-wave: The first positive deflection of the QRS complex S-wave: The negative deflection following the R-wave QRS complex: ventricular depolarization

R-wave

Atrial depolarization

T-wave

P-wave

Q-wave T-wave: ventricular repolarization S-wave

The conduction system

Steps for interpretation 1.

Don’t panic!

2.

What is the heart rate?

3.

Is the rhythm originating from the atria (supraventricular) or the ventricles?

4.

Is the sinus node in control of the rhythm?

What is the relationship between the P waves and the QRS complexes?

5.

Is there ectopy present?

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Average heart rate

Instantaneous heart rate

50 mm/sec •

One tiny box = 1 mm; one big box = 5 mm

•

Note the paper speed (25 mm/s or 50 mm/s)

•

Note the paper speed (25 mm/s or 50 mm/s)

•

Average heart rate – Bic pen method!

•

Instantaneous rate  At 25 mm/s, HR is 1500/# tiny boxes  At 50 mm/s, HR is 3000/# tiny boxes

 150 mm long (30 big boxes long)  6 seconds at 25 mm/s – multiply complexes by 10 for bpm  3 seconds at 50 mm/s – multiple complexes by 20 for bpm

Supraventricular vs ventricular in origin •

Narrow QRS complexes = supraventricular •

•

Depolarize ventricles using the fast His-Purkinje system

Is the sinus node in charge?

•

Key findings:    

There is a P wave for every QRS complex The P waves are positive in lead II There is a QRS complex for every P wave The heart rate is reasonable for the sinus node

Wide and bizarre QRS complexes = CANNOT use the fast His-Purkinje system • •

Depolarize cell-by-cell  takes longer Ventricular in origin OR bundle branch block

What if there are no visible P waves?

What if there are no visible P waves?

• Atrial

• Atrial

fibrillation

 No P waves  Irregular  Tall + narrow QRS complexes  Fast heart rate

standstill

 Permanent – atrial cardiomyopathy  Transient – hyperkalemia  Blocked cat  Aortic thromboembolism cat with reperfusion injury  Dog in Addisonian crisis

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What is the relationship between the P waves and QRS complexes?

•

First degree AV block • Prolonged

First degree AV block

PR interval

 Prolongation of the PR interval •

Second degree AV block

Physiologic

 Mobitz type I  Progressive PR interval prolongation, then block  Aka Wenckebach: “Longer, longer, longer, drop. Then, you have a Wenckebach…”

 Mobitz type II  No change to PR interval before block

•

Third degree AV block

Pathologic

 AV dissociation

Second degree AV block •

Occasionally an impulse originating from the atria is blocked before it reaches the ventricles

•

P wave without a QRS complex

•

Need to differentiate Mobitz type I vs type II

Is there ectopy present?

•

Atrial premature complexes (APCs)

Third degree AV block •

Complete atrioventricular dissociation  Underlying sinus rhythm but no impulses reach the ventricles  Ventricular escape rhythm

How concerned should I be?

Criteria

Not so scary

Scary

Uniform

Pleomorphic/polymorphic

Single

Couplets, triplets, runs

<160 bpm

>180-200 bpm

Morphology •

Ventricular premature complexes (VPCs)

Repetitiveness

Rate

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Accelerated idioventricular rhythm

6 seconds

Differentials for ventricular arrhythmias • Heart

Criteria

Accelerated idioventricular rhythm (AIVR)

Ventricular tachycardia (VT)

Compared to sinus

About the same

Faster

Rate

Typically < 180 bpm

>180 bpm

Hemodynamic compromise?

Typically no

Yes

Treatment

Typically no – address underlying disease

YES!

Ventricular escape vs premature beats

disease/Hypoxia

• Electrolyte

abnormalities

 Ca/Mg/K • Autonomics/Algesia • Drugs • Stuff

(and toxins)

surgeons cut

Another differential for wide QRS complexes: bundle branch block •

Bundle branch block ≠ arrhythmia!

•

Bundle branch block = conduction disturbance

Artifact • Respiratory • Muscle

• Electrical • Errors

motion

twitching interference

in lead placement

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Undulating baseline – respiratory artifact

•

Can you see the QRS complexes?

Tips    

Acquire in right lateral recumbency Look for QRS complexes (tall spikes) marching through the artifact Palpate apex beat and/or peripheral pulses to help identify QRS complexes Move leads more distally on the leg (point of elbow and distal to the knee)  Baseline movement is usually due to chest excursions causing excessive lead motion

 Prevent patient from panting

Fine oscillations – muscle tremors

•

Tips     

Alternating current artifact (aka 60 cycle interference)

Acquire in right lateral recumbency Look for QRS complexes marching through the artifact Place towels between patient’s legs to support the upper legs Apply gentle pressure to proximal legs to minimize motion Move the leads slightly more proximal

Incorrect lead placement

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Good veterinary resources:

Lastly, don’t forget you can always…

Call your friendly neighborhood cardiologist!

University of Missouri Veterinary Health Center Address: 900 East Campus Drive, Columbia, MO 65211 Phone number: (573) 882-7821 Email: mucvmcardiology@missouri.edu

Thank you for listening!

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Special Interest

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Special Interest

Sam Franklin, DVM, MS, PhD, DACVS, DACVSMR Kansas City Canine Orthopedics Overland Park, KS

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Samuel P. Franklin, MS, DVM, PhD Kansas City Canine Orthopedics, www.kck9ortho.com Diplomate, American College of Veterinary Surgeons (Small Animal) Diplomate, American College of Veterinary Sports Medicine and Rehabilitation (Canine) ACVS Founding Fellow, Minimally Invasive Orthopedic Surgery

New Frontiers: Advances in Canine Orthopedics Numerous advances have been made in small animal orthopedics over the last 10-15 years, largely due to greater availability and improvements in technology. Arthroscopy continues to advance in both the procedures and equipment available and is now used in lieu of arthrotomy on a routine basis by those surgeons that are skilled in arthroscopy and that seek to provide less invasive surgery for their patients.

Examples include performing arthroscopic assessment of the stifle in all patients undergoing surgery for cranial cruciate ligament rupture. Arthroscopy is also now the standard for assessment of the canine elbow and treatment of shoulder osteochondritis dissecans or assessment of biceps pathologic change.

Furthermore, an increasing array of entirely arthroscopic or arthroscopic-assisted procedures are being employed including arthroscopic stabilization of shoulder instability, arthroscopic or arthroscopicassisted treatment of coxofemoral luxation, and arthroscopic-assisted fracture repair.

Just as traditional arthroscopy has advanced, the technical improvements in needle arthroscopy are opening doors for new treatment and diagnostic options. Needle arthroscopes are smaller arthroscopes on the order of large hypodermic needles. Although these have been available for several years, the image quality has not been comparable to traditional arthroscopy until recently. Now image quality of these usually disposable units is comparable to a traditional arthroscope with less equipment and lower cost. Furthermore, and most importantly, these arthroscopic procedures can now be performed with the patient just sedated, minimal patient preparation, and minimal time. For example, evaluation of the shoulder to assess for medial shoulder instability or biceps pathology can occur in less than 5 minutes with a sedated patient and provide high resolution images and video of the joint. It is no longer as if doing a diagnostic arthroscopy requires general anesthesia, an operating room, lots of equipment, and a $2,000 price tag. This author loves using the nanoscope for diagnostic shoulder arthroscopy in dogs with elusive/puzzling forelimb lameness where the shoulder is the suspected source.

While minimally invasive joint surgery (ie arthroscopy) has progressed, so too has minimally invasive fracture repair. More readily available and high-quality fluoroscopic units and improvements in locking implants, such as locking bone plates and angle-stable interlocking nails, enable minimally invasive stabilization of long bone fractures. Specifically, these implants can be placed through a small skin incision away from the fractures site and applied with great strength and stiffness of the repair. The fracture alignment, and the application of the implants, can be assessed intra-operatively using fluoroscopy, thus precluding the need to perform an “open” approach.

Corrections in limb deformities has grown by leaps and bounds thanks to wider availability of high resolution and rapid CT scanning. These data can now be quickly imported into numerous software programs, many that are free on the internet, to create 3D models and perform detailed assessments of the limbs and perform “virtual surgery”. Furthermore, since 3D printing is so widely available it is very easy to print replicas of the bone, print individual specific guides to dictate osteotomy performance and re-alignment, and 3D printing even enables printing of patient-specific bone plates for stabilizing the bone segments. Further, when I say these things are available, they are actually available to surgeons

250

anywhere thanks to ease of electronic imaging and data sharing. CT information can be sent to surgical and printing services around the world for planning surgery and designing and printing implants.

The other big area that has progressed, also attributable to imaging and manufacturing advancements, are individual-specific joint replacement or joint resurfacing implants. Off-the-shelf joint replacements are still more commonly used. But, for some patients and some joints there just aren’t off-the-shelf options that will fit. It is increasingly easy to have individual-specific partial or total joint replacements, along with the associated, individual-specific instrumentation manufactured for an unusual case.

Since the advancements require specialized skills, and because veterinary surgery is becoming increasingly complex, the American College of Veterinary Surgeons has created fellowships and fellowship status to help spur the training of surgeons in these fields. These fellowships include the areas of Oncological Surgery, Oral-Maxillofacial Surgery, Minimally Invasive Soft Tissue Surgery, Minimal Invasive Orthopedic Surgery, and Joint Replacement Surgery. The two that most apply/pertain to orthopedic surgery are Minimally Invasive Orthopedic Surgery and Joint Replacement Surgery.

The major take home message is that there are options for virtually every orthopedic patient these days with many options being advanced but not exorbitant. Arthroscopy, CT, and 3D printing are all improved, less expensive, and more widely available. As one example, with a combination or free software on the internet and a 3D printer that can be as little as $250, or can be free to use at your local library, one can print models of bones, cutting guides, and reduction guides for just a few dollars in material cost. Really the limitation is in the time, interest, and expertise of the veterinarians involved.

Veterinarians can advise their clients to seek some of these “advanced” options. Fellowship status or fellowship training is one avenue to seek out surgeons who have experience and skills in these areas.

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Samuel P. Franklin, MS, DVM, PhD Kansas City Canine Orthopedics, www.kck9ortho.com Diplomate, American College of Veterinary Surgeons (Small Animal) Diplomate, American College of Veterinary Sports Medicine and Rehabilitation (Canine) ACVS Founding Fellow, Minimally Invasive Orthopedic Surgery

Advances in Assessment and Treatment of Cranial Cruciate Ligament Rupture Most veterinarians are aware of lateral sutures, Tightrope, tibial tuberosity advancement, and tibial plateau leveling osteotomy for surgical treatment of cranial cruciate ligament disease and/or rupture.

However, in the last 5-10 years the field of veterinary surgery has amassed a truly remarkable amount of data on these procedures which provides answers to old questions and creates new questions. These advances are large attributable to technology as are most advances in the area of veterinary or human orthopedic surgery. With regards to CCL disease specifically, a major break through came about 5 years ago when 2 or 3 different groups began performing in vivo assessment of stifle biomechanics (ie stability and instability) in dogs with CCL rupture that had been treated with a number of these procedures and particularly lateral suture, TTA, and TPLO. This technology and technique included performing CT scans of dogs, then having dogs walk on treadmills while recording their gait with fluoroscopy, and then taking those video images and “shape-matching” the bones to the CT data of their limbs. What this enables is then basically replicating the movement of the skeleton and the tibial and femur in particular, and measuring their motions relative to one and other. This is essentially a way to assess stability.

Surprisingly, and disappointingly, all patients with nylon lateral fabello-tibial suture had persistent femoral subluxation (ie 100% are still unstable even when performed by a board-certified faculty member with decades of experience). Over 66% of TTA patients are unstable. Up to 33% of TPLO patients were unstable. The questions that came from these studies are why and what can be done to improve things? With regard to lateral sutures, there is only a little information to add. We know from a cadaveric studies that use of fibertape (part of Tightrope) provide better strength and stability ex vivo.

However, no studies have assessed Tightrope patients in vivo using fluoroscopy (yet). As for TTA, there continue to be efforts to look at things like should the tuberosity be advanced more, but no real answers have been identified and so the majority of surgeons prefer TPLO over TTA. As for TPLO, there have been answers obtained. One answer is that dogs with slightly higher tibial plateau angles are more likely to have subluxation (ie be unstable) than those that are fully leveled. Further, although previous cadaveric studies suggested that we should be aiming for 5-7 degrees post op of TPA, a follow-up study showed that in another group of dogs if the TPA was rotated to about 3 degrees 95% of cases were stable. What this indicates is that not all TPLOs are the same (a TPLO is not a TPLO). Minor differences in surgical execution have an impact on outcome.

The other area or aspect that we learned about TPLO from these in vivo studies is that in the dogs that had persistent subluxation following TPLO (ie were unstable), they had significantly more internal rotation of the stifle than those that were stable. This has prompted some surgeons to add extracapsular stabilization (ie lateral suture, Tightrope, or “internal brace”) in addition to the TPLO in patients that appear to “need it”. The enormous unanswered question right now is, how do you tell when a patient “needs” the extracapsular in addition to the TPLO? Many surgeons are performing a tibial compression test immediately following the TPLO (while still in surgery) and simultaneously internally rotating the tibia. If the tibia is stable when “straight” but then “pops” (ie subluxates) when internally rotated, many surgeons are using this as 1 guideline to indicate that adding a lateral suture

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should be performed. This is imperfect science because that test may not be a great predictor of which dogs do and do not have the internal rotation and subluxation in vivo.

Finally, and related to the aforementioned discussion of stability and instability following surgery, there are some other pieces of information we now have answers to and relate to the timing of surgery versus conservative management. One clinically relevant question is, when do you perform surgery if you have a patient with mild lameness, effusion, and no notable instability on physical exam? Should you do surgery now, and if so, which surgery? Alternatively, should you give the dog time and see how they do.

In the interest of incentivizing, you to come to this talk, we do have answers for these questions based on data. However, rather than give you the short version here in writing, we will discuss this and answer this question during the presentation. A teaser hint is that the considerations include what can be done and the success rate of non-surgical management, complications and likelihood of progression to CCL rupture in dogs managed non-surgically, likelihood of CCL preservation if “surgery” is performed, stability of the stifle in dogs with partial versus complete rupture, and likelihood of meniscal damage if the CCL is completely or partially ruptured. We hope to see you at the presentation!

253

Special Interest

Sara Gardhouse, DVM, DABVP (ECM), DACZM

Kansas State University – College of Veterinary Medicine Manhattan, KS

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Backyard Poultry Medicine – Part 1 and Part 2 Over the past ten years, keeping backyard chickens as pets, has seen a dramatic increase in popularity in both the urban and suburban setting. An overall awareness of how these birds are housed, fed, and raised safely, in conjunction with an understanding of the key aspects of their anatomy, and physiology is critical to veterinarians being able to properly care for these birds as patients and make appropriate husbandry recommendations. Of critical importance, since the eggs, and sometimes the meat of these birds is consumed, there are significant considerations when it comes to the treatment and management of these birds, many of which are limited by laws. Pet chickens are a very unique pet bird that require specific management and treatment that require a solid knowledge base from their veterinarian. This lecture series of talks will cover laws and regulations, basic knowledge, housing and management, nutrition, history taking, restraint, physical examination, common presenting complaints, and a multitude of infectious and non infectious diseases.

Talk Outline Part 1 • Laws and regulations o Homeowner and neighborhood level o City/town level o Municipality o State o Country • Purchasing chickens o National Poultry Improvement Plan (NPIP) • Designation as a food-producing species even when kept as pets o Forbidden drug classes • Housing and management o Ventilation o Temperature o Lighting o Bedding o Diet o Water o Space o Predators • Nutrition o Requirements o Deficiencies • History • Restraint • Physical examination • Diagnostics and sample collection o Blood sampling – jugular vein, ulnar/brachial vein, medial metatarsal o Swabs – conjunctival, choanal, cloacal

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o Parasite sampling o Cultures o Molecular testing Vaccination Common presenting complaints o Trauma o Reproductive tract disease

Part 2 • Diseases o Parasitic  Toxoplasmosis  Baylisascaris  Trichomonosis  Coccidiosis o Significant diseases  Avian influenza  Newcastle disease o Respiratory  Mycoplasmosis  Fowl cholera  Infectious laryngotracheitis o Musculoskeletal  Marek’s disease  Avian leukosis virus o Dermatological  Marek’s  Fowl pox  Ectoparasites • Lice • Mites o Reproductive  Oviduct prolapse/cloacal prolapse  Oviduct impaction  Egg binding  Egg yolk coelomitis  Paratyphoid oophoritis  Egg problems o Gastrointestinal and hepatic  Fowl pox  Candida albicans  Crop enlargement • Normal • Stasis • Pendulous • Impaction • Candidiasis • Capillariasis

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Intestinal • Salmonella pullorum • Salmonella gallinarum • Coccidiosis • Round worms (Ascaridia galli) • Tapeworms • Capillariasis • Clostridium perfringens type A (necrotic enteritis) • Mycobacteria Hepatic • Hemorrhagic liver syndrome Cardiovascular • Ascites/pulmonary hypertension in broilers • Nutritional • Toxic • Atherosclerosis

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Pearls of Exotic Animal Medicine – Part 1 and Part 2 Exotic animal medicine is a discipline that requires a broad and extensive depth of knowledge beyond that of domestic species. Exotic animal patients are delicate, unique, and require a whole different set of considerations when they are being seen by a veterinary hospital. The anatomy, physiology, behavior, diagnostics, and treatments are very different and present a unique set of challenges that are not commonly encountered in the domestic dog and cat. Over the last decade, the demand and keeping of exotic pets has increased dramatically, meaning the need for veterinary care for these patients has also increased. The purpose of this two hour lecture series to provide a broad overview of important components of exotic animal medicine that will help you to see them on a daily basis in your practice.

Talk Outline Part 1 •

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Exotic animal appointments o Husbandry assessment o Basic equipment for physical examination Exotic companion mammals o History o Physical exam for each species – rabbits, ferrets, chinchillas, guinea pigs, hedgehogs, sugar gliders Avian o Physical exam and handling Reptile o Physical exam and handling Clinical techniques o Intramuscular injections o Subcutaneous injections

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Basic principles of triage and CPR o Preparation o CPR  Airway  Breathing  Circulation  Drugs Common presentations on emergency by species Triage Euthanasia o How to determine if a reptile is alive Venipuncture tips and tricks

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Wellbeing Presentations

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Wellbeing

Abby Whiting, DVM Veterinary Specialty Services St. Louis, MO

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Abby Whiting DVM MVMA Convention January 2022 Disarming the Angry Client: The Imperius Curse in Practice Useful Strategies for managing unmanaged human behavior.

The Imperius Curse: “When cast successfully it places the victim completely under the caster’s control: though a person of exceptional strength will be able to resist it.”

Wouldn’t it be great to feel really proficient in disarming angry clients, disgruntled staff?

Were you adequately trained to handle difficult communication situations?

Are you aware of your personal triggers that serve as barriers to successful communication?

Are you a good team leader: are all your messages received and understood?

In this 50 min lecture we will explore communication tricks and tips for our ever-changing veterinary practice landscape.

Tapping into our Superhero skills.

Resilience Strategies for practices in the here and now: Navigating the changing landscape of the post pandemic veterinary world.

Veterinary medicine faces many challenges: Increasing demand for services Staff Turnover Trouble recruiting staff Costs associated with human resources, supplies, and operational costs.

Need to increase staff compensation Increasing emotionally intense human interactions Threats, disgruntled clients, angry staff.

Origin Story: You know how every superhero has their “origins story”. The event or experience that propels them into their superpowers? (Batman had his encounter with the bats and his PTSD, Spiderman had his spider bite) Well maybe COVID is ours? Perhaps by working together and proactively problem solving we can lead our profession into more success and greater satisfaction.

In this 50 min lecture we will explore idea sharing for leveraging our strengths.

Leveraging the appointment schedule to maximize efficiency and prevent burnout of staff and attrition of clientele.

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Leveraging support staff to maximize efficiency inside the clinic.

Navigating the staffing shortage How Private practice can help keep ER facilities remain open and able to operate.

Utilization of a client code of conduct Development of a violence prevention plan Wellness initiatives and ideas to improve resilience: The Science of Happy

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