Practitioner Issue 1 2018 by FVMA

Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 1 • 2018

CURRENT UNDERSTANDING OF BACTERIAL BIOFILMS AND LATENT INFECTIONS: A CLINICAL PERSPECTIVE

LYME DISEASE AND BOTULISM IN HORSES – WHAT IS THE CLINICAL RELEVANCE?

RYAN A. FERRIS DVM, MS, DACT

AMY L. JOHNSON DVM, DACVIM (LAIM & Neurology)

ANNUAL PROMOTING EXCELLENCE

SYMPOSIUM

OCTOBER 18-21, 2018

NAPLES GRANDE BEACH RESORT, NAPLES, FLORIDA

Discounted Pre-Registration Ends September 6, 2018

SPORT HORSE LAMENESS TRACY A. TURNER DVM, MS, DACVS, DACVSMR

The President's Line Ruth-Anne Richter, BSc (Hon), DVM, MS - FAEP President Dear Fellow Equine Practitioners, The season is well upon us. After a very successful Ocala Equine Conference in January, we are excited about the upcoming 14th Annual Promoting Excellence Symposium program this coming October: “Insights into equine medicine, lameness and treatment”. This year promises to bring another exciting and unique offering with the return of Dr. Jean-Marie Denoix to headline an informative ultrasound and biomechanics wet lab. In addition, we have several distinctive speakers including Drs. Stephanie Valberg, David Frisbie and Dianne McFarlane, to name a few. Our symposium and wet lab theme brings to the equine practitioner an approach based on the foundation of the horse and will focus on specific areas that challenge the equine veterinary community. The rehabilitation group is taking a more site-specific approach this year, while continuing to develop protocols for returning the equine athlete to performance. Understanding the biomechanics of the injury, treatment and repair only enhances the approach to facilitated rehabilitation and improves case outcome. Later this year, we are also excited to be involved again with the University of Florida in putting on the popular Student Appreciation Day hosted by equine practices in Ocala. We already have facilities and instructors lined up to provide this educational and informative day to equine veterinary students. As always, we would not be able to continue to provide you with the quality CE that you have come to expect without the support of our industry and educational partners, and we thank them whole-heartedly. A big thank you also to the FAEP council members for their dedication to the organization of these events. There are many long hours unselfishly given to bring these events to fruition. I would be remiss if I didn’t acknowledge the efforts of the FVMA staff that help us bring these events to you and for them to run smoothly. We, the FAEP council members, are truly grateful. I would like to take this opportunity to reach out to the FAEP members at large. As the FAEP Council matures and continues to evolve, we are in need of interested members to participate on small committees. These would be a way to broaden our scope and inject new ideas as we continue to strive to provide excellent CE to the equine practitioner. Have a great spring, and we look forward to seeing you again in Naples from October 18-21, 2018, for the 14th Annual Promoting Excellence Symposium.

EXECUTIVE COUNCIL

Dr. Ruth-Anne Richter FAEP Council President

Corey Miller DVM, MS, DACT FAEP COUNCIL PAST PRESIDENT

Anne L. Moretta VMD, MS, CVSMT maroche1@aol.com

cmiller@emcocala.com

Armon Blair DVM abeqdoc@aol.com

Jacqueline S. Shellow DVM, MS REPRESENTATIVE TO FVMA EXECUTIVE BOARD jackie@shellow.com

Adam Cayot DVM adamcayot@hotmail.com

Mr. Philip J. Hinkle EXECUTIVE DIRECTOR phinkle@fvma.org

Amanda M. House DVM, DACVIM housea@ufl.edu

Opinions and statements expressed in The Practitioner reflect the views of the contributors and do not represent the official policy of the Florida Association of Equine Practitioners or the Florida Veterinary Medical Association, unless so stated. Placement of an advertisement does not represent the FAEP’s or FVMA’s endorsement of the product or service. FAEP | 7207 MONETARY DRIVE, ORLANDO, FL 32809 | PH: 800.992.3862 | FAX: 407.240.3710 | EMAIL: INFO@FVMA.ORG | WEBSITE: WWW.FAEP.NET

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CURRENT UNDERSTANDING OF BACTERIAL BIOFILMS AND LATENT INFECTIONS: A CLINICAL PERSPECTIVE RYAN A. FERRIS | DVM, MS, DACT Summary Subfertility in the mare can be frustrating to the clinician. Recent data has suggested that bacteria in either a biofilm or latent state may be responsible for explaining many cases of subfertility. Recent work has identified the pathophysiology for these type of chronic infections in the horse and identified the best methods for therapy. The goal of this discussion is to explain the pathophysiology of biofilm and latent infections, and how the clinician can diagnose and treat these types of infections in clinical practice. Keywords: bacteria, biofilm, latent, chronic, endometritis

Introduction Most encounters between bacteria and the equine endometrium lead to an acute period of subclinical infection and occasionally clinical symptoms. Following an acute infection in the majority of mares, the invading bacteria will be eliminated and the infection resolved. However, in a minority of cases, a small number of bacteria survive and cause persistent infections that can be difficult to eliminate. The development of acute and chronic cases of endometritis is the result of deficiencies in the mare’s ability to eliminate an infection and the causative bacteria’s unique pathogenic properties.

Figure 1: Endometrial biopsy from a mare with a Pseudomonas aeruginosa biofilm adherent to the endometrial surface.

of the reproductive tract will increase the likelihood of bacteria entering the uterus. Consequently, this results in a decrease in pregnancy rates. Once bacteria have reached the uterus, the mare’s innate immune system is activated.

The presence of bacteria within the uterine lumen results in a rapid influx of neutrophils, immunoglobulins and serum proteins. This binding of complement and opsonins to bacteria greatly increase the ability and rate at which neutrophils phagocytize bacteria. Neutrophils from susceptible mares have reduced in vitro ability The mare’s uterine defense mechanisms to bacterial infection to phagocytize bacteria as compared to resistant mares. The are well understood and consist of physical, immunological, inflammation associated with the innate immune system results and mechanical barriers. Bacteria utilize numerous methods to in fluid production into the uterine lumen. survive degradation by the host immune system and antibiotic therapy. One survival tool utilized by bacteria is the production The final defense mechanism against bacterial endometritis of a biofilm. Biofilms allow bacteria to be unrecognized by the is mechanical uterine clearance of bacteria and inflammatory host immune system, prevent exposure to antibiotics, and allow products. Several studies have shown that mares susceptible to for exchange of genetic material leading to antibiotic resistance. uterine infections have decreased clearance of uterine fluid as compared to resistant mares. After intrauterine inoculation with The purpose of this review is to describe how alterations to host bacteria, susceptible and resistant mares have similar uterine defenses, in combination with the pathogenicity of bacteria, myometrial contractions for six to eight hours post inoculation result in chronic cases of bacterial endometritis. but depresses in susceptible mares after eight hours. Failure to clear bacteria and inflammatory products from the uterus results in continued activation of the innate immune system. This results Pathophysiology in a further increase in inflammatory cells, immunoglobulins Host defense mechanisms and serum proteins reaching the uterus that continue to activate The mare has three main defense mechanisms to prevent the innate immune system. bacterial infections in the uterus: physical barriers of the reproductive tract, the innate immune system and mechanical A single alteration to any of the defense mechanisms of a mare uterine clearance. The physical barriers include the vulva, may allow for colonization of the uterus with a bacterial pathogen vagino-vestibular sphincter and cervix. These barriers prevent leading to a chronic infection. feces, air and environmental pathogens from reaching the uterus. A reduction in the pathogenicity and quantity of bacteria occurs from the vulva to the cervix. Any disturbance in conformation 6 The Practitioner

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Bacterial lifestyle Bacteria are capable of living in two different lifestyles: planktonic or biofilm states. Planktonic bacteria are single bacterial cells free flowing in suspension. Bacteria in this lifestyle are utilizing available nutrients for procreation. These individual cells are relatively susceptible to recognition and degradation by the host immune system, susceptible to changes in environment (desiccation, lack of nutrients, etc.), and sensitivity to antibiotics. However, the planktonic cell paradigm does not accurately reflect the growth of bacteria in nature associated with a biofilm. In the last several decades, the biofilm state has been considered to be the more prevalent lifestyle with ~99% of the overall world bacterial biomass living in a biofilm. In natural environments, these biofilms are invariably a multispecies microbial community harboring bacteria that stay and leave with purpose, share their genetic material at high rates, and fill distinct niches within the biofilm. The first step in biofilm formation is migration and adherence to a surface. This is typically performed through the use of flagella and type IV pili in E. coli, P. aeruginosa and K. pneumonia. Strep. equi subsp. zooepidemicus bacteria are non-motile and rely on movement from environmental or host factors. Individual bacteria will migrate (if capable) until other bacteria (same species or other) are encountered and microcolonies start to form. At this point, planktonic and biofilm lifestyles start to diverge. Genes associated with flagella are down regulated, and genes associated with polysaccharide production increase. This exopolysaccaride matrix forms the scaffold for the biofilm community. As the community of bacteria grows in size, the environment within the biofilm becomes heterogeneous with higher concentrations of oxygen and a more neutral pH on the outside of the biofilm as compared to the core which is relatively low in available oxygen with a slightly acidic pH. Bacteria are not randomly distributed within a biofilm but rather organized to best meet the needs of the individual and the group. Intercellular communication or quorum sensing is carried out through the production of bacterial products that are able to diffuse away from one cell and enter another. Signaling between cells is critical in the development of a viable biofilm and in reacting to outside environmental stress. One of the biggest advantages of biofilm living is the ability to acquire transmissible, genetic elements at accelerated rates. Conjugation occurs naturally among bacteria but appears to be accelerated when bacteria are in a biofilm lifestyle. This allows for the rapid horizontal transfer of genetic material making a biofilm a perfect milieu for the emergence of new pathogens by acquisition of antibiotic resistance, virulence factors and environmental survival capabilities.

a biofilm are protected from the host immune system as white blood cells have reduced ability for movement and function, and the thick layer of exopolysaccaride (EPS) prevents antibodies from reaching bacteria deep within the biofilm. Biofilms protect bacteria from antibiotics by providing a diffusion barrier that decreases the amount of antibiotics that reach the protected bacterial colonies and create a microenvironment that slows down the metabolism and, therefore, the replication rate of bacteria. This also makes them more resistant to antimicrobial agents. Ultimately, biofilms are associated with development and maintenance of subpopulations of "persister cells." As antimicrobial agents come in contact with the biofilm, the agents must traverse through a layer of thick EPS, DNA, RNA, lipids and proteins in order to reach bacteria buried deep within this protective barrier. Bacteria in the outer region may be killed, but a decrease in the level of antibiotics reaching the inner layer bacteria contributes to the formation of a nidus for chronic infection. The thick layer of EPS found in biofilms not only prevents antibiotics from penetrating, but it limits the diffusion of oxygen and nutrients. Oxygen and nutrient deprivation, consequently, results in a decrease in metabolic rate as compared to planktonic or free individual bacteria. This reduction in metabolic rate provides additional antimicrobial resistance as antibiotics typically only act upon rapidly multiplying bacteria. A popular theory currently is that growth of bacteria in biofilms produces "persister cells." These cells are unique in that they do not appear to grow and are highly multi-drug resistant to a wide variety antimicrobials. Further work is warranted to understand the role of "persister cells" in chronic infections and biofilms. The innate factors of antimicrobial resistance in bacterial biofilms have led to significant challenges in human medicine. It is estimated that 65% of nosocomial infections are associated with biofilms, and that treatments for biofilm-based infections cost more than $1 billion annually. In equine medicine, we have just started investigating the role of biofilms in chronic infections. Figure 2: Immunohistochemistry of a mare with a Pseudomonas aeruginosa biofilm. The purple spots are areas with bacteria and biofilm components overlaid.

Clinically, biofilms can cause significant difficulty for the clinician to eliminate chronic infections once established. Bacteria within

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It has been proposed that biofilms play an important role in subsequent culturing and exposure to antibiotics resulted in chronic infections in the horse, including chronic uterine continued susceptibility of these previous tolerant colonies. infections resistant to antimicrobials which may be due to biofilm production. Acute and chronic non-healing wounds on the distal Latent bacteria in the horse equine limb contained a significantly greater incidence of biofilmIn the mare, it has been clearly identified that some mares can have producing bacteria as compared to a skin sample near the wound. a population of dormant Streptococcus equi subsp zooepidemicus deep in the uterine glands. This population of bacteria would not Biofilms in the horse be identified on routine culture (not actively dividing bacteria) Evaluation of bacteria isolated from the equine uterus suggests or cause significant inflammation or infection. However, if these that the majority of isolates of Streptococcus equi subsp. bacteria were to leave this dormant stage, the resulting bacterial zooepidemicus, Escherichia coli, Pseudomonas aeruginosa, and growth will result in inflammation and infection leading to Klebsiella pneumonia are capable of producing a biofilm in pregnancy loss. vitro. In the horse using a model of infectious endometritis, a biofilm- involved infection has been clearly identified. The adherent biofilm material is multifocal with the greatest adherent Treatment For Latent Bacteria occurring between the tissue folds and in the uterine horns. The The goal for treating mares with latent or dormant bacteria bacteria are at greater numbers deep in the endometrial glands as is to get the bacteria to move from the dormant state into a compared to the luminal surface. Treatment options may need to metabolically active state in which identification and treatment be able to penetrate deeper into the glands and tissue to effectively can be performed. Recent work by Petersen et al. (2015) has clear these infections. There is an alteration in the host immune shown that dormant Streptococcus zooepidemicus can be activated response with reduced PMNs surrounding areas of adherent by infusing a proprietary media (bActivate) into the uterus. After biofilm as compared to areas free of bacteria. Unfortunately, no the infusion (24 hours), 64% (15/25) of the mares were cultured clinical diagnostic tests are available for the detection of a biofilm- positive for Streptococcus zooepidemicus as compared to 8% (1/12) related infection. In human medicine, a biofilm is suspected if of the mares infused with PBS. The proprietary media is able to appropriate antibiotic therapy is administered and the infection get bacteria to convert from the dormant state to a metabolically is unable to be eliminated. active state and treatment can be initiated. Persister cells and Infections Persister cells represent about 1% of all bacteria in a free-floating state and are characterized by being tolerant to antibiotics with no change in genetic expression. It is often thought that these bacteria are potentially dormant and metabolically inactive. This phenomenon was originally described in the 1940s in that cultures of Staphylococcus aureus exposed to lethal doses of penicillin resulted in less than 1% of the original CFUs surviving penicillin exposure. While this work was conducted before genetic sequencing was available, the authors did not feel the acquired antibiotic resistance was due to a mutation in the bacteria, as

Interestingly, it should be noted that breeding may also result in bacteria being activated from a dormant state. Recent work by Christoffersen et al. (2015) showed that 55% (16 of 29) of mares with a negative culture prior to breeding, but with retained fluid post breeding, were positive for growth of Streptococcus zooepidemicus. The authors conclude that it was more likely to be dormant Streptococcus zooepidemicus that was reactivated as compared to introduction at the time of breeding. The development of post mating fluid in barren mares could be due to both inflammation from breeding but also reactivation of dormant bacteria.

Figure 3: Mare with an induced Pseudomonas aeruginosa biofilm infection. The bacteria had been genetically modified to express a luciferase gene to allow the bacteria to be tracked in the tissue. The image on the left is of the uterus containing a high amount of bacteria. The middle image is the uterus after washing away non-adherent bacteria, leaving only plaques of bacteria in a biofilm state. The image on the right shows that these plaques contain significant bacterial populations.

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Table 1. Antibiotic and Non-Antibiotic Combinations For The Treatment Of Biofilm Associated Bacterial Endometritis In Mares

Tris EDTA- final concentration in the syringe should be 50 mM Tris and 3.5 mM EDTA Note: Tris-EDTA and Tricide are similar; however Tricide is not equivalent to Tris-EDTA in regards to bacterial killing To make Tris-EDTA: 16oz bottle of Dechra Triz-EDTA crystals; add 8 oz of sterile water (this is different than the bottle instructions). The 2x concentration of Tris-EDTA solution will be further diluted by the antibiotics below to the proper final concentration. Antibiotic Drug Amount Tris EDTA QS Final volume Notes: 10 mls of 8.4% sodium bicarbonate 16 mls sterile fluid Amikacin (250 mg/ml) 4 mls (1 gram) 30 mls 60 mls (Saline, LRS, Sterile H2O) should be added to the amikacin Ceftiofur (1 gram reconstituted 10 mls sterile fluid 20 mls (1 gram) 30 mls 60 mls (Sterile H2O) in 20 mls) Ciprofloxacin (10 mg/ml) 40 mls (400 mg) 40 mls 0 80 mls Split between two syringes H2O2- 1% final concentration in the syringe A 3% stock solution is available at many drug stores and veterinary distributors Antibiotic Drug Amount H2O2 QS Final volume Notes: 10 mls of 8.4% sodium bicarbonate 26 mls sterile fluid Amikacin (250 mg/ml) 4 mls (1 gram) 20 mls 60 mls (Saline, LRS, Sterile H2O) should be added to the amikacin Ciprofloxacin (10 mg/ml) 40 mls (400 mg) 20 mls 0 60 mls Ceragyn Infusion Product- >30% final volume in the syringe Antibiotic Drug Amount Ceragyn QS Final volume Notes: Amikacin (250 mg/ml) 10 mls of 8.4% sodium bicarbonate 26 mls sterile fluid 4 mls (1 gram) 20 mls 60 mls (Saline, LRS, Sterile H2O) should be added to the amikacin Ciprofloxacin (10 mg/ml) 40 mls (400 mg) 20 mls 0 60 mls DMSO- 30% final concentration in the syringe 99% stock solution is used for calculations below Antibiotic Drug Amount DMSO QS Final volume Notes: Ceftiofur (1 gram reconstituted 20 mls sterile fluid 20 mls (1 gram) 20 mls 60 mls (Sterile H2O) in 20 mls) Ciprofloxacin (10 mg/ml) 40 mls (400 mg) 20 mls 0 60 mls

2017 Treatment Options For Biofilms Bacteria residing in a biofilm can be up to 1,000 times more resistant to treatment with antibiotics as compared to free-living (planktonic) bacteria. The simple administration of antibiotics has been unable to eliminate chronic infections suspected of involving a biofilm in both human and veterinary medicine. The goal in treating a biofilm-associated infection is to remove the biofilm material and kill the bacteria residing within the biofilm. We have tested various products for efficacy to disrupt a biofilm or kill the bacteria within a preformed biofilm. This is an in vitro assay looking at the effects of these agents, specifically on bacteria residing in a biofilm and the effects observed. N-acetylcysteine. Treatment with 3.3% NAC significantly (p<0.05) reduced the number of CFUs in all P. aeruginosa isolates evaluated, and no significant reduction in biofilm biomass was observed. The E. coli and S. zooepidemicus isolates had a significant reduction in CFUs and biofilm biomass as compared to the untreated control. The MIC for N-acetylcysteine was found to be 3.3% dilution to 1.6% did not disrupt preformed biofilms WWW.FAEP.NET |

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or kill the bacteria within the biofilm. Treatment with NAC did not reduce biofilm biomass or reduced the number of CFUs for K. pneumoniae. Hydrogen Peroxide. Challenge with 1% hydrogen peroxide significantly reduced the number of CFUs for nine of the 10 K. pneumoniae isolates, but it did not reduce the biofilm biomass. E. coli isolates were significantly reduced in biofilm biomass and had a reduction in CFUs following challenge. P. aeruginosa isolates had reduced biofilm biomass in five isolates but no reduction in CFUs following treatment with 1% hydrogen peroxide (Table 1). S. zooepidemicus isolates had significantly reduced biofilm biomass and CFUs as compared to untreated controls. Dilution to 0.5% was found to be just as effective as a 1% concentration. Chelating Agents. No significant difference in biofilm biomass or CFUs was observed following a six-hour challenge with either Tris-EDTA (50 mM and 3.5 mM, respectively) or THAM-EDTA (20 mM and 8 mM, respectively) for isolates of P. aeruginosa, or K. pneumoniae. E. coli had a significant reduction in biofilm biomass following challenge with Tris-EDTA or THAM-EDTA.

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S. zooepidemicus isolates had significantly reduced biofilm biomass and CFUs as compared to untreated controls. Dilution from recommended concentrations failed to disrupt a preformed biofilm or kill the bacteria within the biofilm.

Hypochlorous acid. No significant reduction in biofilm biomass or CFUs was observed following a six-hour challenge with either Vetricyn® (Vetricyn, Riverside Ca) or Omniphase® (Integrated Healing Technologies, Franklin TN) for P. aeruginosa, E. coli, or K. pneumonia. Isolates of S. zooepidemicus had a significant reduction in biofilm biomass and CFUs following challenge with Vetricyn® or Omniphase®. Antimicrobial Peptide Mimic. A significant reduction in biofilm biomass was observed for isolates of E. coli and K. pneumoniae, but no change in CFUs was detected following challenge. In P. aeruginosa, 50% of isolates had reduced biofilm biomass, but none of these isolates had decreased CFUs. Ceragyn® (Ceragyn, Spanish Fork UT) effectively reduced the biofilm biomass and reduced the number of CFUs for isolates of S. zooepidemicus. For K. pneumoniae and E. coli isolates, we were able to dilute this product to 1.5% and 0.5% respectively, and still maintain equal disruption and killing to the recommended concentration. Ozone. No significant changes in biofilm biomass or CFUs was observed following a six-hour challenge with ozone for E. coli, K. pneumonia, P. aeruginosa, and S. zooepidemicus. A series of in vitro studies were conducted to assess biofilm dispersal and/or bacterial killing for antibiotics and non-antibiotic agents alone or in combination against Gram-negative bacteria. Our data indicates that antibiotics and non-antibiotic agents are more effective against biofilm if administered concurrently (i.e. in the same syringe). Table 1 explains how to make up clinical treatments for local infusion into the uterus based on the in vitro data. The amount of either antibiotic or non-antibiotic agent for each infusion are the minimum effective concentrations against E. coli, K. pneumoniae and P. aeruginosa. The treatment period should be at least 72 hours in duration with repeated treatments every 24 hours (i.e. a uterine infusion of the selected combination once every 24 hours for three consecutive days). This treatment protocol resulted in complete biofilm dispersal and bacterial killing in vitro. It is important to note that some non-antibiotic agents and antibiotics should not be combined in the same syringe. For example, the in vitro data indicates that mixing acetylcysteine with antibiotics in the same syringe resulted in reduced activity of the antibiotics. We recommend antibiotic sensitivity testing for all Gramnegative organisms. Bacteria inherently resistant to an antibiotic will still be resistant when that antibiotic is used in combination with a non-antibiotic agent.

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Suggested Reading

Costerton JW, Stewart PS, Greenberg EP. Bacterial biofilms: a common cause of persistent infections. Science. 1999;284:1318–22. Ferris RA, McCue PM, Borlee GI, Loncar KD, Hennet ML, Borlee BR. In Vitro Efficacy of Nonantibiotic Treatments on Biofilm Disruption of Gram-Negative Pathogens and an In Vivo Model of Infectious Endometritis Utilizing Isolates from the Equine Uterus. J Clin Microbiol. 2016;54:631–9. LeBlanc MM. Advances in the diagnosis and treatment of chronic infectious and post-mating-induced endometritis in the mare. Reprod Domest Anim. 2010;45:21–7. Lindsay D, Holy von A. Bacterial biofilms within the clinical setting: what healthcare professionals should know. Journal of Hospital Infection. 2006;64:313–25. Loncar KD, Ferris RA, McCue PM, Borlee GI, Hennet ML, Borlee BR In Vitro Biofilm Disruption and Bacterial Killing Using NonAntibiotic Compounds Against Gram-Negative Equine Uterine Pathogens. J Eq Vet Sci 2017:accepted Petersen MR, Skive B, Christoffersen M, Lu K, Nielsen JM, Troedsson MHT, et al. Activation of persistent Streptococcus equi subspecies zooepidemicus in mares with subclinical endometritis. Vet Microbiol. 2015;179:119–25. Petersen MR, Nielsen JM, Lehn-Jensen H, Bojesen AM. Streptococcus equi subspecies zooepidemicus resides deep in the chronically infected endometrium of mares. Clinical Theriogenology. 2009;1:161–5.

Ryan A. Ferris DVM, MS, DACT Owner, Summit Equine, Inc. Newberg Oregon Dr. Ferris graduated from veterinary school at Washington State University in 2007. Ryan completed an internship in equine surgery, medicine and reproduction at the Equine Medical Center of Ocala in 2008, followed by a residency in Equine Reproduction at Colorado State University. He received a MS in Clinical Science from Colorado State University, passed the board examinations for the College of Theriogenologists and was an assistant professor at Colorado State University from 2010-2017. In 2018, Dr. Ferris and his family moved to Newberg, Oregon and established Summit Equine, Inc. Summit Equine is a referral equine reproduction practice for mares and stallions. They offer services in breeding management (fresh, cooled or frozen); embryo transfer; problem mares; oocyte aspiration; stallion collections for fresh, cooled or frozen semen; international shipment of semen; and stallion evaluations. Interests: Bacterial and fungal endometritis, biofilm, post mating induced endometritis, and embryo transfer.

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LYME DISEASE AND BOTULISM IN HORSES – WHAT IS THE CLINICAL RELEVANCE? AMY L. JOHNSON | DVM, DACVIM (LAIM & NEUROLOGY)

Introduction Lyme disease and botulism are important diseases of horses. The diagnosis and treatment of equine Lyme disease can be difficult, and, in some respects, the disease is very poorly understood.

Botulism is uncommon but occasionally devastating, and practitioners must be prepared to identify and treat cases quickly to prevent massive losses. Current understanding of these two diseases will be summarized here with particular attention to recent advances in their diagnosis, treatment and prevention.

LYME DISEASE Horses are frequently infected with Borrelia burgdorferi, the Gram-negative spirochete that causes Lyme disease. One of the major problems in diagnosing Lyme disease is that many horses have been exposed to B. burgdorferi but do not show clinical signs. Exposure occurs when the horse is bitten by an Ixodes spp. tick carrying B. burgdorferi, and the organism infects the horse. Some horses eliminate the infection on their own. Some become chronically infected but asymptomatic. Yet, some are chronically infected and symptomatic. Documented syndromes attributed to B. burgdorferi infection in horses include neuroborreliosis,1-4 uveitis5 and cutaneous pseudolymphoma.6 Many practitioners attribute other clinical signs, such as sporadic lameness, arthritis, and muscle soreness, to infection. However, these syndromes are not as well-documented.

Diagnosis:

Diagnosis of Lyme disease is complicated. Positive serology is not sufficient for definitive diagnosis, even in the presence of compatible clinical signs. Positive serology in the absence of compelling clinical signs has very poor predictive value for disease. Suggestive clinical signs depend on the organ system involved. Neurlogic sequelae - Lyme Neuroborreliosis (LNB) to infection might include behavioral changes (especially hyperesthesia or hyper-reactivity), gait abnormalities, cranial nerve deficits, neck stiffness, muscle atrophy, and muscle tremors or fasciculations (Figure 1). Additional systemic signs might occur concurrently, including weight loss, uveitis, cardiac arrhythmias and dermal masses at the sites of tick bites (pseudolymphoma). Antemortem diagnosis of Lyme disease is best achieved by fulfilling several criteria, which include potential B. burgdorferi exposure (via residence in or travel to an endemic area); presence of neurologic signs, uveitis, or cutaneous skin masses at the site of tick bites; diagnostic testing to rule out other potential diseases; documentation of abnormal CSF, ocular fluids, or dermal histopathology; and identification of the organism or immunologic evidence of infection. Cytological analysis of CSF is strongly recommended for horses with suspected neuroborreliosis, as results are often abnormal with neutrophilic or lymphocytic pleocytosis and increased total protein concentration.4 Although identification of the organism via culture, immunohistochemistry, or PCR in tissue, CSF, or ocular samples from the patient provides strong evidence for active infection, positive results are uncommon in horses with confirmed neuroborreliosis, and immunologic testing remains the mainstay of laboratory diagnosis.

Figure 1: Shows masseter muscle atrophy due to trigeminal nerve damage.

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Commercially available tests for B. burgdorferi include ELISA, IFAT, WB, C6 ELISA SNAP test, and fluorescent bead-based multiplex assay (Multiplex). The SNAP test can be performed in-clinic or stall-side, while the other tests are performed at

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- Continued from page 13

BOTULISM

Botulism is a disease of people and animals exposed to the neurotoxin of Clostridium botulinum (BoNT), which causes progressive flaccid paresis and cranial nerve deficits. C. botulinum is a spore-forming, anaerobic, Gram-positive bacterium with eight different serotypes (A-G, with C-α and C-β subgroups), each of which is distinguished by the unique properties of its toxin. These toxins are antigenically different and act specifically on various parts of the synaptic vesicle docking and fusion apparatus at the motor end plate to prevent release of acetylcholine. BoNT is widely regarded as the most potent and lethal toxin known to humankind. Figure 2: Shows decreased lip tone due to bilateral facial nerve Botulism in horses can be categorized in two ways: either by the dysfunction as well as evidence of dysphagia (feed material at naC. botulinum serotype involved or by the route of acquisition of res) due to dysfunction of the glossopharyngeal and vagus nerves. disease. Certain serotypes are prevalent in certain geographic regions. In the United States, type B is endemic in the mid- or tongue stress test, (Figure 3) where the examiner gently Atlantic states and Kentucky, while type A is reported primarily in withdraws the tongue from the horse’s mouth and assesses the the western United States (California, Idaho, Montana, Oregon, ability of the horse to pull it back while holding the jaw closed. Nebraska, Washington and Wyoming).12,13 Type C is seen The second is known as the grain test and involves feeding the sporadically across the United States, whereas confirmed cases horse eight ounces of grain in a bucket while timing how long it of types D-G have not been reported in horses. Both type B and takes for the horse to consume the feed. Normal horses finish type A are associated with soil, while type C is associated with in less than two minutes, whereas horses with dysphagia do not. carrion. Equine type B cases are most common and are estimated to account for over 85% of equine cases diagnosed in the United States. Horses with botulism almost always acquire the disease Although clinical diagnosis by experienced practitioners is in one of three ways: ingestion of preformed toxin with food probably reasonably accurate in predicting botulism, and (“food-borne” botulism in adults), ingestion of C. botulinum serotype may be predicted based upon known serotype spores that subsequently germinate in the gastrointestinal tract prevalence in a geographic region and likely means of exposure, and elaborate toxin (“toxicoinfectious” botulism in foals), or confirmation of serotype must be made in the diagnostic contamination of wounds with C. botulinum and subsequent laboratory. For suspected equine cases or outbreaks, the most bacterial growth with toxin release (“wound” botulism). Foodappropriate samples to submit include forage, gastrointestinal borne botulism in adults and toxicoinfectious botulism in foals contents and feces. As aforementioned, the gold standard for are more common than wound botulism. Considering both laboratory diagnosis is the mouse bioassay, which detects BoNT. serotype and route of acquisition, several trends are evident: toxicoinfectious botulism due to type B is common in foals in the mid-Atlantic region and Kentucky; food-borne botulism in adult horses most commonly results from spoiled forage contaminated with type B (in the eastern part of the country) or type A (in the western part); and food-borne botulism due to type C is occasionally seen when carrion contaminates forage.

Laboratory diagnosis:

Clinical diagnosis: The gold standard of botulism diagnosis is identification of BoNT in serum samples from patients with compatible signs by using the mouse bioassay test. However, diagnosis is often based on compatible history and clinical signs, since laboratory confirmation with the mouse bioassay can be difficult. Historical details that increase suspicion of botulism include consumption of fermented forages or large-bale hay and lack of adequate vaccination. Regardless of botulinum toxin type, the clinical signs of intoxication are the same: progressive flaccid paresis or paralysis and cranial nerve deficits such as dysphagia, (Figure 2) weak tongue tone, weak eyelid tone, and slow pupillary light reflexes. Two clinical tests have been described to diagnose botulism in the horse.14 The first is known as the tongue tone 20 The Practitioner

Figure 3: Horse with botulism showing recumbency and weak tongue tone.

Issue 1 • 2018

TO THE

You are Invited

INSIGHTS INTO EQUINE MEDICINE, BIOMECHANICS AND ULTRASOUND WET LAB SATURDAY, OCTOBER 20, 2018

FEATURED WET LAB INSTRUCTOR

PROFESSOR

JEAN-MARIE DENOIX

DVM, PhD, Assoc. LA-ECVDI, DACVSMR, ISELP Certified Instructor

rn EaC E 6 urs Ho

Internationally renowned professor of veterinary anatomy and equine lamenesses at the École Nationale Vétérinaire d’Alfort, France. Dr. Denoix is considered the world’s foremost equine musculoskeletal system anatomist. He will present his “Demonstration of Focused Physical Examination & Biomechanical Evaluation of the Live Horse.” He will also offer four hours of lectures during the symposium.

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LAMENESS AND TREATMENT NINE NATIONALLY AND INTERNATIONALLY ACCLAIMED SPEAKERS PRESENTING 37 HOURS OF CUTTING-EDGE CONTINUING EDUCATION

TIMOTHY FLYNN PT, PhD

LAURA RIGGS DVM, PhD, DACVS-LA, DACVSMR (Equine)

DAVID FRISBIE DVM, PhD, DACVS, DACVSMR

CHRIS SANCHEZ DVM, PhD, DACVIM

SARAH LE JEUNE DVM, DACVS, DACVSMR, CVA, Cert. Vet. Chiro

SHEILA SCHILS MS, PhD

DIANNE MCFARLANE DVM, PhD, DACVIM

STEPHANIE VALBERG DVM, PhD, DACVIM, ACVSMR

PRE-REGISTRATION & HOTEL RESERVATIONS DEADLINE IS SEPTEMBER 6, 2018

O NA L PA RT N E R S I T A C U D E 19 2018-20

EQUINE DIVISION

DISTINGUISHED SPEAKERS

JEAN-MARIE DENOIX DVM, Phd, Assoc. LA-ECVDI, DACVSMR, ISELP Certified Instructor

PRE-REGISTRATION & HOTEL RESERVAT

PRELIMINARY SCHED Friday, October 19

Rehabilitation CASE STUDIES

Time

8:00 a.m. 8:50 a.m.

8:55 a.m. 9:45 a.m.

Case studies presented by each speaker will follow the progression from diagnosis through the rehabilitation process. The focus will be on the following: 1. Preventing injury and improving poor performance 2. Science-based rehabilitation protocols when injury occurs

Room 1

Diagnostic Techniques: Specificity and Sensitivity for Stifle Disease Including How Standing Stifle Arthroscopy Fits In Dr. Frisbie

Video Gait Analysis of Runners Focusing on the Relationship of the Spine and Lower Limb in Creating Dysfunction in Knee Mechanics Dr. Flynn

Intra-articular Biologics

Video Gait Analysis of the Horse: Common Problems of the Stifle

Dr. Frisbie

Time

10:30 a.m. 11:20 a.m.

11:25 a.m. 12:15 p.m.

Room 1

Navicular Bursa Dr. Riggs

PRP in Acute Injury Dr. Riggs

Pain Recognition and Management: What’s New?

2:40 p.m. 3:30 p.m.

Case-Based Approach to Pain Management

Dr. Sanchez

1:45 p.m. 2:35 p.m.

2:40 p.m. 3:30 p.m.

Dr. Sanchez 3:30 p.m. - 4:00 p.m. Break

Dr. le Jeune Exercise Treatment Strategies and Functional Integration Focusing on the Knee Dr. Flynn

Nonexertional Rhabdomyolysis and Immune-Mediated Myositis

Exercise and Treatment Strategies Focusing on the Stifle in the Horse

Dr. Valberg

Dr. Schills

Genetic Testing: What Tests Are Available and When to Use Them

Integrative Rehabilitation Protocols for Stifle Dysfunction

Dr. Valberg

Dr. le Jeune

3:30 p.m. - 4:00 p.m. Break - Visit the Exhibit Hall

Working up Stifle Abnormalities, the Clinical Side Dr. Frisbie

4:00 p.m. 4:50 p.m.

Ocular Manifestations of Systemic Disease and Systemic Manifestations of Ocular Disease Dr. Sanchez

4:55 p.m. 5:45 p.m.

Integrative Rehabilitation Protocols for the Postoperative Stifle Patient

12:15 p.m. - 1:45 p.m. Complimentary Lunch in the Exhibit Hall

1:45 p.m. 2:35 p.m.

4:00 p.m. 4:50 p.m.

Dr. Schills

9:45 a.m. - 10:30 a.m. Break - Visit the Exhibit Hall

Attendees will leave with some solid ideas on protocols that can be used in their practices!

Thursday, October 18

Room 2

Specific Surgical Treatments to be Aware of in the Stifle Dr. Frisbie

Drs. Schils, le Jeune & Flynn Rehabilitation Cases

4:55 p.m. 5:45 p.m.

5:45 p.m. - 7:00 p.m. Reception - Exhibit Hall

Rehabilitation Cases

Drs. Schils, le Jeune & Flynn 5:45 p.m. - 7:00 p.m. Reception - Exhibit Hall

CONTINUING EDUCATION CREDITS RACE Approved By:

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This program 532-33238 is approved by the AAVSB RACE to offer a total of 37.00 CE Credits (24.00 max) being available to any one veterinarian: and/or 37.00 Veterinary Technician CE Credits (24.00 max). This RACE approval is for the subject matter categories of: Category One: Scientific | Category Two: Non-Scientific-Clinical | Category Three: Non-Scientific-Practice Management/Professional Development using the delivery method of Seminar/LectureLab/Wet Lab. This approval is valid in jurisdictions which recognize AAVSB RACE; however, participants are responsible for ascertaining each board's CE requirements. RACE does not "accredit" or "endorse" or "certify" any program or person, nor does RACE approval validate the content of the program.

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DULE AT-A-GLANCE

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Saturday, October 20 Time

8:00 a.m. 8:50 a.m.

Room 1

Sunday, October 21

Offsite Location

Biomechanics & Ultrasound Wet Lab

Endocrine Disease in the Horse: Is it EMS, ID or PPID? Dr. McFarlane

Dr. Jean-Marie Denoix 8:00 a.m. - 5:30 p.m.

8:55 a.m. 9:45 a.m.

Understanding the Diagnostic Tests for Equine Endocrine Disease Dr. McFarlane 9:45 a.m. - 10:30 a.m. Break - Visit the Exhibit Hall

10:30 a.m. 11:20 a.m.

11:25 a.m. 12:15 p.m.

Clinical Applications of Laminitis Research

2:30 p.m. 3:20 p.m.

5:15 p.m. 6:05 p.m.

7:00 a.m. 7:50 a.m.

BASIC: 3 cases: Diagnosis, Management and Outcome (P3 Fracture, Biceps Brachii Trauma, and Laceration to the SDFT of Hind Limb) Dr. Denoix

8:00 a.m. 8:50 a.m.

BASIC: 3 cases: Diagnosis, Management and Outcome (P3 Fracture, Biceps Brachii Trauma, and Laceration to the SDFT of Hind Limb) Dr. Denoix

9:20 a.m. 10:10 a.m.

General Assembly: 8:00 a.m. – 10:30 a.m.

Dr. Riggs Electrophysical Rehabilitation Modalities: EvidenceBased Medicine Dr. Riggs

Hands-on (Group 1): 10:30 a.m. – 1:45 p.m.

10:15 a.m. 11:05 a.m.

Lunch: 1:45 p.m. – 2:30 p.m. Hands-on (Group 2): 2:30 p.m. – 5:45 p.m.

REHABILITATION (1) Lowering of the Neck: Biomechanics and Indications. (2) Back Up: Biomechanics and Indications (3) Muscle Injuries: Ultrasound Diagnosis and Rehabilitation Dr. Denoix REHABILITATION (1) Lowering of the Neck: Biomechanics and Indications. (2) Back Up: Biomechanics and Indications (3) Muscle Injuries: Ultrasound Diagnosis and Rehabilitation Dr. Denoix

Sunday Featured Speaker: Dr. Jean-Marie Denoix,

Managing Endocrine Disease in the Horse

Equine Musculoskeletal System Anatomist

Dr. McFarlane

Dr. Jean-Marie Denoix (Normandy, France) will be teaching lectures on Sunday, October 21 at PES 2018. Dr. Denoix is known for drawing crowds for his lectures about clinical examination and imaging of locomotor problems. His lectures will include the following case study topics:

An Update on Polysaccharide Storage Myopathy and Myofibrillar Myopathy in Warmblood Horses Dr. Valberg

• The diagnosis, management and outcome of main conditions of the hip in horses • Rehabilitation: ▶ reviewing the biomechanics and indication of lowering the neck and back up ▶ ultrasound diagnosis and rehabilitation of muscle injuries

3:20 p.m. - 4:20 p.m. Break - Visit the Exhibit Hall 4:20 p.m. 5:10 p.m.

Room 1

8:50 a.m. - 9:20 a.m. Break

Wet Lab Schedule -

12:15 p.m. - 1:35 p.m. Complimentary Lunch in the Exhibit Hall 1:35 p.m. 2:25 p.m.

Naples Therapeutic Riding Center

Time

Exertional Rhabdomyolysis in Endurance Horses Dr. Valberg

We are offering four hours of CE on Sunday taught by Dr. Denoix. Don’t miss out on your chance to attend CE classes from the leading equine diagnostic ultrasonographer!

Medicine Case Studies Drs. Valberg & McFarlane

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OCTOBER 18-21, 2018

reference laboratories. These tests detect antibody production by the host but differ in test methodology and which specific antibodies are detected. For example, the Multiplex assay detects antibodies against three outer surface proteins (Osps) of B. burgdorferi. Antibodies directed against OspA can indicate vaccination or natural infection, antibodies against OspC are considered to indicate recent infection, and antibodies against OspF are considered to indicate chronic infection. Although the pattern of antibody production might help elucidate the chronicity of the horse’s infection, none of these tests will tell you whether the infection is significant and related to the horse’s clinical signs. Some general rules for test interpretation follow: • A positive test usually indicates past or present infection with B. burgdorferi, although vaccination can also cause positive results for some tests. There are four canine vaccines that are occasionally used in horses. Three (LymeVax, Zoetis; Duramune Lyme, Boehringer-Ingelheim; Nobivac Lyme, Merck) are two-strain bacterins that could induce antibody production against multiple antigens, including OspA and OspC (to varying degrees). One (Recombitek Lyme, Merial) is a recombinant pure non-adjuvanted protein that only includes the OspA antigen. • Regardless of test utilized, clinical Lyme disease cannot be confirmed, and there is no gold standard test. Horses living in an endemic area are frequently seropositive, so positive results will have a low positive predictive value of disease. None of the tests prove causation of clinical signs or predict whether disease is likely to develop in the future. There is no known correlation between magnitude of titer and likelihood of disease. It is unclear how well tests that predict stage of infection perform with horses that have had repeated exposures. • Although in theory, documentation of intrathecal antibody production is recommended for the diagnosis of neuroborreliosis, in practice it becomes difficult. There is no established optimal cutoff for neuroborreliosis using a serum:CSF antibody ratio. Horses with neuroborreliosis frequently have abnormal CSF cytology and, hence, might have an abnormal blood-brain barrier, confounding results. Sample dilution can complicate interpretation of results (e.g., the Multiplex assay tests serum at a dilution of 1:400 whereas CSF is generally run undiluted, and these dilution factors are not reported with results). • Finally, at least for the diagnosis of neuroborreliosis, the Lyme Multiplex shows poor discriminatory ability. Recent retrospective analysis of Lyme Multiplex values for neurologic horses with post-mortem diagnoses shows similar results for horses with and without neuroborreliosis. Horses with neuroborreliosis can have negative Multiplex results, and horses without neuroborreliosis can have positive Multiplex results (on serum, CSF, and CSF:serum ratios).7 • Negative test results usually have a high negative predictive value for disease. However, “false” negative results are possible in horses with acute infection, WWW.FAEP.NET |

FLAEP |

immune-compromise, or infection in immune-privileged sites (central nervous system or eyes). The author’s current approach to diagnosing neuroborreliosis is to “back into” the diagnosis by testing for and ruling out all other plausible causes of the horse’s neurologic signs. Abnormal CSF cytology, either neutrophilic or lymphocytic pleocytosis, is supportive. Lyme Multiplex results are considered, but negative results do not exclude the diagnosis and positive results do not confirm it.

Treatment: The ideal treatment regimen for equine LNB is unknown. Investigation is hampered by lack of a disease model as well as lack of a reliable antemortem diagnostic test. Only one study using a small number of experimentally infected ponies has assessed efficacy of treatment against Borrelia.8 Based on this experimental study, many practitioners began treating suspected equine Lyme disease cases with seven to 30 days of intravenous oxytetracycline (often 6.6 mg/kg IV q 24 h), occasionally followed by oral doxycycline (usually 10 mg/ kg PO q 12 h). In cases where intravenous treatment is not feasible, oral doxycycline is often used exclusively. More recently, minocycline has been used (4 mg/kg PO q 12 h). Anecdotally, horses often improve with these therapies, though it is very difficult to ascertain whether the response is due to specific killing of B. burgdorferi or to non-specific anti-inflammatory effects, as tetracycline drugs are known to have potent anti-inflammatory properties via their inhibition of matrix metalloproteases.9 For cases with suspected CNS infection, treatment recommendations based on human medicine include parenteral regimens of high-dose penicillin (44,000 U/kg IV q 4-6h), cefotaxime (25-50 mg/kg IV q 6-8h), or ceftazidime (20-40 mg/kg IV q 6-12h).10 If these options are cost-prohibitive, minocycline (4 mg/kg PO q 12h) is likely to be more effective than doxycycline or oxytetracycline due to more favorable bioavailability and blood-brain barrier penetration, respectively.

Vaccination: There are no Lyme vaccines labeled for horses. However, based on evidence from horses and other species, we believe that appropriate vaccination would prevent infection in horses. Adequate vaccination protocols have not yet been clearly defined for horses. The protective OspA antibody titer is unknown, and the required frequency of vaccination is also unknown. Data from one study show that increased antibody levels only persist for four to five months after vaccination with canine Lyme vaccines.11

FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS

- Continued on page 20 | The Practitioner 13

Unfortunately, detection of BoNT in equine samples is difficult. When compared to other species, horses are highly sensitive to BoNT and develop clinical signs after exposure to smaller amounts of toxin. Any circulating toxin is quickly bound to receptors and internalized in motor endplates, becoming undetectable. Furthermore, toxin remaining in the gastrointestinal tract is degraded by microbial organisms and their enzymes. Although preformed toxin may be detected by the mouse bioassay in a small number of foal cases (approximately 20%), it is rarely detected in adult cases. Therefore, toxin testing is generally performed or repeated after culture enrichment which allows any spores in the original sample to germinate and elaborate toxin, thus increasing the diagnostic yield of the assay. These culture-enriched samples are positive in approximately 53% of suspected foal cases and 32% of suspected adult cases.15 The identification of C. botulinum spores in the original sample is considered presumptive evidence of botulism in animals with compatible clinical signs as this organism is not part of the normal gastrointestinal flora. As can be intuited, the mouse bioassay has a high positive predictive value (100% for foals and 89% for adults) but lower negative predictive value (51% for foals and 67% for adults).15 Additionally, it requires live animal use, is performed at a limited number of facilities and has an extended lag time for results. Due to the issues with the mouse bioassay, PCR technology has been investigated to improve diagnostic accuracy and speed while reducing live animal use. This modality is particularly appropriate for equine samples, which more commonly contain C. botulinum spores than preformed toxin. Our laboratory first optimized and validated a quantitative real-time PCR assay for the detection of the neurotoxin gene of C. botulinum type B in equine diagnostic samples; this assay is faster, more sensitive, and more economical than the mouse bioassay.16 Subsequently, PCR capabilities were expanded to a multiplex assay for types A and B, as well as a singleplex assay for type C.17 Results indicate that both the A/B multiplex assay and the C singleplex assay are highly specific and more sensitive than the mouse bioassay for detecting C. botulinum in equine samples. Information on samples submission can be found at the following link: http://www.vet.upenn.edu/veterinary-hospitals/NBC-hospital/ diagnostic-laboratories/national-botulism-reference-laboratory

Treatment: Antitoxin administration is considered a mainstay of therapy and should be administered as soon as possible, as it greatly increases odds of survival.18 Currently, there are two commercially available antitoxins: a trivalent antitoxin against types A, B, and C (Lake Immunogenics, Ontario, NY; http://www.lakeimmunogenics.com/ index.php/product/antigen-select-botulism-a-b-c-toxins/) and a monovalent antitoxin against type B (Plasvacc, Templeton, CA; http://plasvaccusa.com/products/equiplas#equiplas-b). Antitoxin will only bind circulating toxin, not toxin bound at motor end plates or internalized, so clinical signs can continue to progress for 24 hours after administration. Since toxin is irreversibly bound and regrowth of motor end plates is required for recovery, administration of antitoxin will not reverse clinical signs.

WWW.FAEP.NET |

FLAEP |

Supportive care is an essential component of therapy. Dysphagic horses require their hydration and nutritional requirements to be met through enteral (preferred) or parenteral administration. Horses with moderate to severe myasthenia require thick bedding and/or padding to prevent complications associated with excessive recumbency. Even horses receiving high-quality nursing care will develop necrosis of skin and underlying muscle over pressure points if recumbency is prolonged. Horses should not be forced to rise frequently or stand for prolonged periods, as depletion of acetylcholine stores will increase weakness and lead to progression of signs. Therefore, the use of sling support is generally not recommended during initial treatment (first one to three days). However, after antitoxin treatment and stabilization of signs, some severely affected horses will benefit from use of a sling to assist them to rise. Evacuation of the bladder and rectum may be necessary. Complications will occur in severely affected, hospitalized horses. These may include decubital ulcers, cellulitis, myositis, colic, cystitis, pneumonia and salmonellosis, yet development of complications has not been associated with nonsurvival.18

Prognosis: A dataset of 30 foals treated for botulism at New Bolton Center showed an overall 96% survival rate among treated foals with an 88% survival rate among the eight treated foals requiring mechanical ventilation.19,20 Based on laboratory confirmation (when available) and characteristics of the referral area, these foals likely all had type B botulism. A similar retrospective study of adult horses treated for botulism at New Bolton Center showed an overall survival rate of 48%.18 This survival rate was substantially higher than that reported in outbreak situations, which had survival rates of 10-30%. Horses that maintained the ability to rise without assistance were more likely to survive than those that could not rise unassisted. Survival rate for horses that arrived at the hospital with the ability to rise was 67%, and if they maintained the ability to rise throughout hospitalization their survival rate was 95%. Conversely, horses that could not rise had a survival rate of only 18%, even with aggressive hospital treatment.18

Prevention: Only one USDA-approved vaccine against equine botulism is available in the United States (BotVaxÂŽ B, Neogen Corporation; http://animalsafety.neogen.com/en/neogenvet-botvax-b).This product is a killed (toxoid) vaccine directed against C. botulinum type B. The initial series consists of three doses administered at four week intervals with subsequent yearly boosters. Pregnant mares should receive their primary series and then be revaccinated four to six weeks prior to foaling. Passively acquired maternal antibodies do not appear to interfere with the foalâ&#x20AC;&#x2122;s serologic response, so foals may have their primary series started as early as two weeks of age, although it is more commonly started at one to three months of age.

FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS | The Practitionerâ&#x20AC;&#x201A; 21

Unfortunately, there are no licensed vaccines available for preventing types A or C botulism, and there is no cross-protection between types. Horses affected by botulism may not develop protective immunity, as the amount of toxin required for intoxication is less than that required to stimulate an immune response. Therefore, affected horses should be vaccinated during or after recovery assuming that C. botulinum type B is the serotype of concern.

References

1. Hahn CN, Mayhew IG, Whitwell KE, et al. A possible case of Lyme borreliosis in a horse in the UK. Equine Vet J 1996;28:84-88. 2. James FM, Engiles JB, Beech J. Meningitis, cranial neuritis, and radiculoneuritis associated with Borrelia burgdorferi infection in a horse. J Am Vet Med Assoc 2010;237:1180-1185. 3. Imai DM, Barr BC, Daft B, et al. Lyme neuroborreliosis in 2 horses. Vet Pathol 2011;48:1151-1157. 4. Johnstone LK, Engiles JB, Aceto H, et al. Retrospective evaluation of horses diagnosed with neuroborreliosis on postmortem examination: 16 cases (2004-2015). J Vet Intern Med 2016;30:1305-1312. 5. Priest HL, Irby NL, Schlafer DH, et al. Diagnosis of Borreliaassociated uveitis in two horses. Vet Ophthalmol 2012;15:398-405. 6. Sears KP, Divers TJ, Neff RT, et al. A case of Borreliaassociated cutaneous pseudolymphoma in a horse. Vet Dermatol 2012;23:153-156. 7. Johnson AL, Johnstone LK, Stefanovski D. Serum and CSF Lyme Multiplex results for neurologic horses with and without neuroborreliosis. Proceedings of the American College of Veterinary Internal Medicine Forum, 2016. 8. Chang Y-F, Ku Y-W, Chang C-F, et al. Antibiotic treatment of experimentally Borrelia burgdorferi-infected ponies. Vet Microbiol 2005;107:285-294. 9. Sapadin AN, Fleischmajer R. Tetracyclines: nonantibiotic properties and their clinical implications. J Am Acad Dermatol 2006;54:258-265. 10. Johnson AL, Johnstone L. Equine Lyme neuroborreliosis: perceptions and reality. Proceedings of the American College of Veterinary Internal Medicine Forum, 2014. 11. Guarino C, Asbie S, Rohde J, et al. Vaccination of horses with Lyme vaccines for dogs induces short-lasting antibody responses. Vaccine 2017;35:4140-4147. 12. Johnson AL, McAdams SC, Whitlock RH. Type A botulism in horses in the United States: A review of the past ten years (1998– 2008). J Vet Diagn Invest 2010;22:165–173. 13. Ostrowski SR, Kubiski SV, Palmero J, et al. An outbreak of equine botulism type A associated with feeding grass clippings. J Vet Diagn Invest 2012;24:601-603. 14. Whitlock RH, McAdams S. Equine botulism. Clin Tech Equine Pract 2006;5:37–42. 15. Johnson AL, McAdams-Gallagher SC, Aceto H. Accuracy of a mouse bioassay for the diagnosis of botulism in horses. J Vet Intern Med 2016;30:1293-1299. 16. Johnson AL, Sweeney RW, McAdams SC, et al. Quantitative realtime PCR for detection of the neurotoxin gene of Clostridium botulinum type B in equine and bovine samples. Vet J 2012;194:118-120. 17. Johnson AL, McAdams-Gallagher SC, Sweeney RW. Quantitative real-time PCR for detection of neurotoxin genes of Clostridium botulinum types A, B, and C in equine samples. Vet J 2014;199:157-161. 18. Johnson AL, McAdams-Gallagher SC, Aceto H. Outcome of adult horses with botulism treated at a veterinary hospital: 92 cases (1989-2013). J Vet Intern Med 2015;29:311-319. 19. Wilkins PA, Palmer JE. Botulism in foals less than 6 months of age: 30 cases (1989–2002). J Vet Intern Med 2003;17:702–707. 20. Wilkins PA, Palmer JE. Mechanical ventilation in foals with botulism: 9 cases (1989–2002). J Vet Intern Med 2003;17:708–712.6. Feary DJ, Magdesian KG, Aleman MA, et al. Traumatic brain injury in horses: 34 cases (1994-2004). J Am Vet Med Assoc 2007;231:259-266.

22 The Practitioner

Amy L. Johnson DVM, DACVIM (LAIM & Neurology) Dr. Johnson received her DVM from Cornell University in 2003. Following an internship at B.W. Furlong and Associates, Dr. Johnson went back to Cornell for a residency in large animal internal medicine. In 2007, she began working as a clinician at New Bolton Center while concurrently completing a residency in neurology at the University of Pennsylvania. In 2011, Dr. Johnson became the third veterinarian in the world to obtain board-certification in neurology as well as large animal internal medicine. She currently works at New Bolton Center as Assistant Professor of Large Animal Medicine and Neurology. Her research efforts focus on improving diagnosis of neurologic disease in the living horse, and she has special interests in equine protozoal myeloencephalitis (EPM), Lyme neuroborreliosis and botulism.

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TRACY A. TURNER | DVM, MS, DACVS, DACVSMR Introduction: Lameness is an indication of a structural or functional disorder in one or more limbs that is manifested in progression or in the standing position.1 Lameness can be classified in several different ways. A supporting-leg lameness is seen when the horse is supporting weight on the foot or when the horse lands on the leg. Swinging-leg lameness is seen when limb is in motion. Mixed lameness is seen when the leg is moving and when it is supporting weight. A complementary lameness is seen when pain in a limb causes uneven distribution of weight on another limb or limbs, which can produce lameness or the perception of lameness in a previously sound limb. Lameness can also be graded to help define the severity of the problem. However, lameness of the sport horse often manifests itself not as a noticeable gait anomaly, but as a decrease in performance or change in attitude toward performance. Because of this, the diagnosis of these problems can be very difficult. The purpose of this presentation is to discuss the systematic steps that the author has found useful in the evaluation of these horses. Any evaluation begins with a good history. We will discuss the pertinent information and how and why it is helpful. The second stage is physical examination. Discussion will center on process and key points to evaluate. The third component of evaluating the sore performance horse is imaging. Usually in these cases, it is difficult to pin point an area to evaluate with imaging. Our discussion will center on determining which imaging modality is most appropriate. We will discuss anatomic imaging versus physiologic imaging and the value of each.

History:

An anamnesis (an accurate history) should be obtained in every case.1 Information obtained from a careful history not only will help determine where lameness is, which is especially important for subtle lameness, but it may also provide you with valuable therapeutic or prognostic information. Unfortunately, you will also find that most horsemen speak a foreign language. Questions that I have found to be useful to ask are: How long has the horse been lame? Does the owner know what caused the lameness? Does the horse warm out of the lameness? Does the horse stumble? What other signs does the horse show? When was the horse shod? For racing horses, what times has the horse ran? How well has the horse run since the onset of the problem (i.e. is the horse making money)? Finally, what treatments have been done and were they helpful? In my experience, the veterinarian needs to get the owner to talk freely, once that happens the important details will flow. Otherwise, the owner, trainer and/or rider may remain guarded. 24 The Practitioner

There are breed variations of lameness. For the Thoroughbred, what is the horse used for? Racing? Hunting? For racing horses, does the horse move toward or away from the rail? This breed is most commonly afflicted with carpitis, carpal fractures, injury to metacarpophalangeal joint, tendon and suspensory ligament injury, and sesamoid injury (racing). In hunters/jumpers, look for forelimb feet problems, tarsitis, or back and quadriceps problems. Standardbreds are typically used for racing, so you want to ask is the horse worse in the straights or turns? Does the horse move toward or away from the rail? Is the horse on one line? Is the horse on one shaft? Has there been a recent change in shoeing (Borium, trailers, etc.)? These horses are most commonly afflicted with tarsal and stifle problems. Quarter Horses may be used for any number of things, such as racing, gaming or pleasure. Does the horse point a foot? Is the horse reluctant to take a lead? Has the horse lost suppleness? Has there been recent changes in the horse's attitude toward work? The gaming or working horse is most commonly afflicted with "ringbone," fractures of the phalanges, "bone spavin" and "navicular disease." With ponies and draft breeds, one should look for signs of founder (laminitis) and question the owner accordingly (i.e. access to feed and feed changes, etc.). Ask if the horse works in a team. Most importantly, I have learned to develop an understanding of what the owner expects. What do they think is wrong? Because no matter what else happens during the examination, the practitioner must show them what is wrong.

Visual Examination:

The next step is to perform a visual examination. It is most important to be systematic and do the exam the same way every time.1 One will not only be quicker but less likely to miss something. The author is a firm believer in the adage “you will miss more things by not looking than not knowing.” The visual examination begins the second you see the horse. Look for clues to the location of the problem. Look for obvious swellings or enlargements. Observe the horse's posture or how it stands. Constantly pointing or flexing one leg is a good clue that the leg is in pain. Look for conformational defects that may predispose to lameness. Asymmetry of anatomical parts is often a clue to many problems. Look at hoof size, pectoral or shoulder muscles, or the gluteal muscles. Following the initial observation, one needs to determine if the horse is lame and where. Watch the horse move coming toward you, going away and from the side. It is easiest to detect lameness at the trot, but you should always observe the horse at a walk. There are some breeds that you may find it difficult to get them to Issue 1 • 2018

trot. The Tennessee Walking Horse, Standardbred, Paso Fino and Icelandic have a natural pace and tend to look like they "waddle" when they move. Typical forelimb lameness is characterized by the "head nod." It is caused by the horse moving its head up and down to shift its center of gravity (weight) toward its hindquarters. The head rises when the lame leg hits the ground. Conversely, the head lowers when sound leg hits the ground. These movements are most easily seen when the horse is coming toward you. A typical hind limb lameness is characterized by the "hip hike." This is caused by the horse shifting its pelvis to accommodate leg movement and weight bearing pain. It is most easily observed with the horse moving away from you. The observer must concentrate on the movement of the tuber coxae. This movement is symmetrical in the normal horse. Lameness is noted when one side moves more than the other. The side that moves the most is the lame side. Reluctance of the horse to flex the joints of the hind leg causes the horse to tilt the affected side of its pelvis up as the lame leg is moved forward. As the horse begins to place weight on the limb, the horse tilts the affected side down to avoid putting full weight on that leg. Observations of the horse from the side are necessary to fully evaluate limb function. The normal horse should land on its hoof either flat or heel first. Landing on the toe usually indicates pain in the caudal hoof. The length of stride should be evaluated and is symmetrical in the normal horse. Shortening usually indicates pain but may also represent a quick step to relieve the other leg, so do not jump to conclusions. The arc of the stride should also be symmetrical. A decrease in arc of foot flight usually indicates a reluctance to flex joints in that leg. Some lameness problems can be completely characterized by the changes in stride (these include stringhalt, fibrotic myopathy, upward fixation of the patella).

Figure 1: Wedge tests are important methods of placing stress on the soft tissues of the distal limb. From top to bottom: toe wedge, frog wedge and abaxial wedge.

There are aids to help visualize a lameness. Working the horse on a hard surface, such as pavement, is probably the best one. Working the horse on a lounge (i.e. small circles) is also very helpful especially for forelimb problems. Some horses need to be seen under saddle or being driven. Cinematography can be used to see the horse in faster gaits and to be able to slow the motion.

Palpation:

Palpation is a crucial part of every examination. It is the systematic evaluation of the limb by touch (i.e. feel for structural changes and pain).1 The examination needs to look at all portions of the limb, but should be gauged so the most time is spent in examining the most common areas of injury (i.e. in the front limb concentrate on structures from the carpus distally and in the hind limb concentrate on the hock and stifle). To begin, the author checks the horseâ&#x20AC;&#x2122;s teeth and mouth. This is done by palpation by inserting the hand and arm into the mouth. By placing the hand in the space between the tongue and teeth, the tongue can be pushed to the opposite side and the teeth can be digitally palpated to the last molar. This must be done quickly and certainly does not replace a speculum examination, but it is a quick way to determine if the mouth or teeth may be an issue. Examination of the foot involves evaluating hoof wall texture. The coronary band should be elastic and fit over the hoof like a cuff.2 The alar cartilages should be easily palpable and flexible. WWW.FAEP.NET |

FLAEP |

Examination of the pastern should involve checking for increased digital pulse. The tendons should be assessed as to their relative size, which normally should be about two-thirds the width of the bones. The long and short pastern bones form the pastern joint. There is usually a slightly raised area on the dorsal surface of the pastern that is palpable and is roughly the location of the pastern joint. Palpating proximal to distal the pastern begins to narrow

FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS | The Practitionerâ&#x20AC;&#x201A; 25

Figure 2: Hoof testers are excellent for superficial pain in the hoof capsule. However, hoof testers probably do not test deep pain very well. Top: note arrows showing where pressure would be applied. Bottom: note arrows from sulcus to wall do not get near applying pressure to the navicular area (N).

then flares out, and this also roughly corresponds to the pastern joint. Cases of ringbone or exostosis usually have either obvious enlargements or distinct enlargements of the normal structures, so it's important to always check symmetry when in doubt. Examination of the fetlock starts by looking for distension of the fetlock which is most easily detected by palpation of the volar pouches (between the suspensory ligament and MCIII/MTIII).1 The presence of a firm, movable nodule underneath the skin and joint capsule of the dorsal fetlock is indicative of a villonodular lesion. A pain response, elicited by firm palpation over the sesamoids, may indicate a fractured sesamoid or sesamoiditis. Pain elicited over the most proximal sesamoid, where the suspensory ligament inserts, is often seen in cases of suspensory desmitis. Examination of the metacarpus/metatarsus regions requires that the bone, tendons and suspensory ligament is all that should be palpated. Careful palpation between MCIII and MCII or MCIV should reveal a shallow groove. Disappearance of this groove is indicative of a "splint." The suspensory ligament 26 The Practitioner

and flexor tendons should feel taut, be of uniform thickness and easily palpated in the normal horse. Squeezing the suspensory ligament will cause a pain response in any horse and should not be mistaken for an indicator of injury. To check the suspensory, one should firmly press the ligament against the caudal aspect of MC/MT III. Any thickenings, or areas where the tendons cannot be separated from each other, indicate disease. Palpation of the distal tendon sheath often indicates a slight amount of effusion, which is normal. A common mistake is to think the "puffiness" caused by the digital veins is effusion in the tendon sheath. Only two of the three joints of the carpus are easily palpable: the antebrachiocarpal (formerly radio carpal) and the middle carpal (formerly intercarpal). Distension of these joints can be determined by pressing over the medial or lateral aspect of the joint and feel fluid move to the opposite side. When these joints are flexed, the dorsal margins of each of the bones is easily palpated. The muscles and tendons of the antebrachium (forearm) are readily palpable and identifiable. The main thing to check is for swelling. Distension of the elbow is very difficult to determine. The main item to check is the olecranon. Little can be felt over the humerus, yet an effort needs to be made to check the surrounding musculature for pain. Palpate the right and left scapula simultaneously to check for atrophy, swelling, etc. Gentle pressure over the bicipital bursa will usually result in a pain response. If the area is truly affected, the response is very pronounced. Shoulder distension is difficult to determine. Pressure over the brachiocephelicus muscle, followed by a pain response by the horse, often indicates that is the lame leg. The reason being that the horse begins to use that muscle differently causing soreness. The examination of the distal rear limb is the same as the forelimb. Examination of the tarsus reveals that only the tibiotarsal joint is easily palpable.1 The trochlea of the talus should be easily palpable. The saphenous vein on the dorsomedial aspect of the joint can be mistaken for joint distension. Firm palpation over the head of MTII (insertion of the cunean tendon) followed by a pain response by the horse often indicates inflammation of the distal tarsal joints (Churchill's test). The gaskin (tibia region) is simple to examine, palpate for swelling. Stifle distension can be determined by palpating the patellar ligaments. In the normal horse, these ligaments are readily palpable. In the presence of stifle distension, they become more difficult to feel. In most cases, the patella is easily palpable and portions of the trochlea are palpable. While examining the hip region, apply firm pressure over the greater trochanter. If this is followed by a pain response, it is circumstantial evidence for trochanteric bursitis or gluteal tendon problems. Palpation over the semimembranosus/ semitendinosus, which reveals either a hard or tense mass in the muscle, is supportive evidence for fibrotic myopathy. Palpation over the quadriceps should reveal a firm tone. Muscle that feels “flabby” and lacks tone can predispose the horse to "loose patella syndrome." Examination should include a rectal examination to assess pelvic symmetry and muscular tone. A walking rectal is helpful to check for crepitus in the pelvis or sacroiliac region. A common mistake when examining the horse's back is to squeeze the horse's back. This will invariably cause a pain response. The proper way to test is to place firm pressure across the musculature. Issue 1 • 2018

A pain response produced by this test is reliable. Palpate the spinous processes for pain, then palpate the tuber sacrale for pain or asymmetry.

Manipulation:

Manipulative tests or flexion tests are important adjunct to a lameness exam and can often give an important lead to establish the cause(s) of lameness.1-3 In many cases, the pain caused by manipulation is so severe that the horse will retract the limb. In more subtle cases, the only satisfactory way of evaluating the effect of manipulation is to trot the horse immediately and note any exacerbation of a problem. Distal limb flexion is the same for both forelimbs and hind limbs. It is performed by picking the leg up; keeping the upper leg as straight as possible; grasping the toe of the hoof; and flexing the coffin, pastern and fetlock. Keep firm pressure on the flexion for 30-60 seconds. Attempts by the horse to retract the limb, to get away or distinct behavior change indicates pain caused by the test. Exacerbation of the lameness by the test is also a positive indicator of pain. The fetlock can be flexed alone by grasping around the pastern instead of the toe of the hoof. Normal range of motion for the fetlock is about 90 degrees. Range of motion for the coffin and pastern joints is difficult to assess. Carpal flexion is performed by picking a leg up and completely flexing the knee. Keep firm pressure on flexion for one to two minutes. Normal range of motion is nearly 180 degrees. One should be able to touch the palmar fetlock to the palmar forearm without difficulty and without causing the horse pain. Elbow flexion is performed by holding the leg at the level of the forearm and flexing the leg to its fullest. Keep flexed for one to two minutes. Shoulder flexion/extension/abduction is difficult, if not impossible, to manipulate without manipulating the elbow. Flexion of the shoulder is achieved by grasping the leg at the forearm and pulling the leg back. You should pull hard enough to allow the front hoof to touch the gaskin. Needless to say, it is difficult to hold this portion for any length of time. Extension of the shoulder is achieved by holding the leg at the pastern and pulling the leg up as far as possible. Normally, a horse will tolerate this quite well. A positive response usually causes the horse to walk backwards in an attempt to get away from you. Abduction of the shoulder is achieved by holding the leg in flexion, grasping the horse's knee and rotating it away from the horse. A positive response is seen either by the horse moving away from you (he is trying to get away from pain) or the horse may even try to go down. This is an excellent test for OCD of the shoulder. The spavin test (tarsal flexion) is performed by picking the leg up and completely flexing the hock for one to two minutes. These manipulations also cause flexion of the distal limb and stifle. A positive response is seen as an exacerbation of lameness. Be careful. This test is definitely not pathognomonic for hock problems; however, hock problems tend to have a very positive response to this test. Several stifle manipulations can be performed. The patellar ligament test is performed by placing firm pressure on the base of the patella and pushing. Normally, slight movement should be encountered. Crepitus, excessive movement or "locking" of the stifle are abnormal responses. The "drawer" test is done by placing hands around the horse's tibia and placing your knee behind the point of the horse's hock. Firmly pull back on the tibia. Crepitus or excessive movement is abnormal. Be careful. You could get seriously hurt performing WWW.FAEP.NET |

FLAEP |

this test. The collateral ligament test is performed by placing hands around the horse's tibia and placing your foot outside the horse's hoof. Firmly pull the tibia toward you. Crepitus is abnormal. Be careful. A lot of horses do not appreciate this test either. Stifle rotation starts by abducting the horse's distal hind leg and grasping the hoof or pastern with one hand. With your other hand, grasp the calcaneus and rotate it outward. Normally, you will get very little rotation. Excessive rotation has been associated with ligamentous injuries. Hip manipulation is difficult, but abducting the leg as far as the horse will tolerate can give you some idea of soreness in the hip.

Foot Examination:

Foot examination is extremely important because it is the most common site of lameness.2 It cannot be performed well without the foot being properly prepared (sole pared and shoes may need to be removed). Hoof testers (Figure 2) are used to squeeze between the hoof wall and sole to check for areas of pain. Be systematic. Generally, I check the sole first and move left to right. I then check the "navicular area": medial sulcus to lateral wall, lateral sulcus to medial wall, central sulcus to toe, and heel to heel. Percussion is performed by tapping the hoof wall with a hammer. If an area of pain is encountered, the horse will flinch. It is also an excellent idea to tap on the nail heads if a horse has shoes. This test is to see if any of the nails are causing pain. Wedge tests (Figure 1) are performed by standing the horse on a small block of wood.3 The hoof extension test is performed by elevating the toe with a block, holding up the opposite limb and trotting the horse away after 60 seconds. The block the author uses is an old hoof knife wrapped in tape to protect from the blade. The palmar hoof wedge test is performed in a similar fashion except the block is placed under the palmar two-thirds of the frog and forcing the horse to stand on that foot. The opposite limb is held up for 60 seconds and the horse is trotted off. The test can be further modified so that the wedge can be placed under either the medial or lateral wall to determine if the pressure or hoof imbalance caused by the wedge exacerbates the lameness. As before, the opposite limb is held up for 60 seconds before the horse is trotted in hand. A positive test is, once again, noted if the manipulation causes lameness or lameness is exacerbated.

Saddle Fit:

Saddle position should be assessed with the horse standing squarely.4 The rider should be allowed to position the saddle and pads as he or she would normally on the horse. Many riders place the saddle too far forward, which interferes with movement of the scapula and may tip the balance of weight distribution in the saddle caudally. The pads may not extend the full length of the saddle, resulting in an area of focal pressure under the rider’s seat. After the saddle has been positioned, the examiner should grab the pommel of the saddle and give it a sharp tug down and back. If the saddle moves and "locks in" further back, the saddle was not positioned correctly. On the other hand, if the saddle does not move, it is positioned correctly. The saddle should next be placed on the horse’s back without pads or girth to visually inspect the balance of the saddle, withers clearance at the pommel, evenness of the panel contact along the epaxial muscles, and width of the channel or gullet

FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS | The Practitioner 27

between the panels at the rear of the saddle.4 With the saddle correctly positioned in relation to the shoulder, the lowest part of the seat is identified. This point can easily be found by placing a cylindrical object, such as a pencil, crossway on the seat, and the pencil will roll to the lowest point. This point should be centered between the pommel and cantle. Otherwise, balance and weight distribution of the rider is problematic because it is shifted toward the lower side. Next, placing fingers between the pommel and saddle checks, the clearance between the pommel and the withers should be 2.5 - 3 fingers wide without being cramped. The angle of the points of the saddletree should be checked next. Ideally, the "points" of the saddle (the projections at the front and sides of the saddle tree) should be far enough behind the back edge of the scapula so that the saddle does not interfere with the range of motion of the scapula. The points also determine the ideal width of the saddle because the angle they form must also conform to the shape of the withers. The angle is determined either by visualizing the points of the saddle and back together or, more objectively, by molding a malleable ruler over the horse’s back at the most forward spot where the saddle should sit. This curved angle can then be compared with the gullet of the saddle off the horse. The angles of the back and points should be parallel to within 10 degrees. It is important to note that many horses are asymmetric through the withers and may have different angles or shapes between right and left sides of the withers. This asymmetry can also be appreciated by observing the horse’s withers and shoulders when standing a safe distance behind the horse, usually on a stool or mounting block. All of these fit parameters should be assessed again after the girth is fastened and tightened.

Imaging: There are several different methods of imaging the horse. Imaging is of utmost importance because it will provide pathologic and physiologic information necessary to treat the specific condition. Imaging can be divided into anatomic and physiologic imaging methods. Anatomic imaging modalities include radiology, ultrasonography, computer-aided tomography and magnetic resonance imaging. Physiologic imaging modalities include scintigraphy and thermography. Radiologic techniques are the most commonly used to evaluate the horse for lameness.6 Utilizing radiography requires multiple projections to evaluate any area. Radiography provides the most information about bone, but with digital radiography one does get a gross evaluation of soft tissues. Essentially, the practitioner must attempt to draw conclusions about a three-dimensional object utilizing two-dimensional pictures. Occasionally, it becomes necessary to utilize radiographic techniques that

With the saddle correctly positioned and the horse standing squarely, a hand should be placed on the center of the seat and a light downward pressure applied.4 The other hand is used to run the length of the angle of the points and then under the panels of the saddle in a front to back manner. The examiner should feel for points of pressure or gaps in pressure or contact (bridging). The hand on the seat should then move forward and backward to check for "rocking" of the saddle. Pressure points, bridging and rocking are all indicators of saddle fit problems. The examiner should now step back and look at the position of the saddle on the horse’s back. The length of the saddle should fit between the withers and last rib. If it extends farther back, the saddle fits poorly. As the examiner walks around the horse and observes the saddle from the back, the gullet clearance can be assessed. The gullet should clear the spine and associated ligaments along the entire length of the saddle. Pressure on the seat should not change this parameter. Another potential source of discomfort is if the gullet width is too narrow and the saddle contacts the spine region, particularly in large horses or those with heavy riders.

Regional Analgesia:

Local nerve blocks or intra-articular blocks are extremely important.5 The blocks provide indisputable evidence of the general location of lameness. But they are not 100% due to migration of local anesthetic or insufficient desensitization due to aberrant nerves. Regardless, the results should be assessed in light of the physical examination findings. 28 The Practitioner

Figure 3: Muscle injuries are probably underdiagnosed because they may be difficult to detect. Thermal imaging can show inflammation associated with such an injury. Top: shows thermal imaging with increased heat in the semitendinosus area. Bottom: shows an ultrasonographic examination of that area showing type 2 muscle tear (arrow).

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provide more information. Contrast radiography is one such technique that provides information about the articular cartilage and surfaces. It is of particular value in determining whether subchondral cysts communicate with the joint or in delineating a subcutaneous tract. Generally, five to 10 ml of contrast injected into the joint is adequate, but this depends on the size of the joint or synovial structure. Pathologic diagnoses are usually made by radiography in conjunction with clinical examination. The future of radiography lies in digital radiography. There are two types: computed radiography (CR) and digital radiography (DR). CR utilizes a special plate that is read by the computer. The advantage of CR is that there will be fewer retakes, less radiation is necessary and post processing of the film can eliminate contrast problems. DR utilizes a special plate but the radiation is directly read from the cassette to the computer where an image is produced. It has the same advantages as CR, plus it has the advantage of being more rapid.

Skin overlying muscle is also subject to temperature increase during muscle activity. Injured or diseased tissues will invariably have an altered circulation (Figure 3). One of the cardinal signs of inflammation is heat which is due to increased circulation. Thermographically, the "hot spot" associated with the localized inflammation, will generally be seen in the skin directly overlying the injury. However, diseased tissues may in fact have a reduced blood supply either due to swelling, thrombosis of vessels or infarction of tissues. With such lesions, the area of decreased heat is usually surrounded by increased thermal emissions, probably due to shunting of blood.

Physiologic imaging techniques would be those techniques that provide the evaluator with an image that reflects physiologic processes. Unlike anatomical imaging that reflects structure, these images give insight into metabolism or circulation. Thermography and scintigraphy provide the examiner with the opportunity to examine the entire horse. When combined with a thorough clinical examination, these methods are extremely useful in identifying injuries that may have otherwise gone undetected.

Scintigraphy utilizes polyphosphonate radiopharmaceuticals administered by intravenous injection and is followed by measurement of the distribution of the pharmaceutical by a gamma camera.11 Concentrations of the pharmaceutical can be detected as the polyphosphonates bind rapidly to exposed hydroxyapatite crystal. This is generally in areas where bone is actively remodeling. This is the basis of the bone scan, yet prior to this, the distribution of the drug goes through two other phases. It is these phases that can be useful to evaluate soft tissue changes. There are three phases: the vascular phase, the soft tissue phase and the bone phase.11 The vascular phase or blood pool phase begins immediately after injection of the pharmaceutical. This phase is dependent on local variations in vascular supply. The most common clinical application for vascular phase scintigraphy is the determination of patency of blood vessels. In the second phase, or soft tissue phase, scintigraphy is performed while most of the pharmaceutical is in the extracellular fluid (ECF). This usually begins one to two minutes post-pharmaceutical injection and lasts until significant uptake of the polyphosphonate by bone, which takes usually one to two hours. The distribution of the radiopharmaceutical during this phase is due to local blood flow, capillary density, capillary permeability and regional ECF volume. Because inflammation causes an increase in blood flow, capillary permeability and ECF volume, inflamed tissues accumulate high levels of radiopharmaceutical. This is the basic principle behind evaluation of soft tissue injuries by scintigraphy. The bone phase is the most useful in that the uptake of the radiopharmaceutical always increases around areas of increased remodeling or vascularity. Since injured bone is undergoing more rapid remodeling, this is the basis for using bone phase to detect injuries. Scintigraphy has been most useful for the detection of lesions in bone and ligaments. Scintigraphy has been particularly useful in the identification of enthesopathy (damage to the insertions of tendons and ligaments on bone).

Thermography is the pictorial representation of the surface temperature of an object. It is a noninvasive technique that measures emitted heat. A medical thermogram represents the surface temperatures of skin making thermography useful for the detection of inflammation.10 This ability to noninvasively assess inflammatory change makes thermography an ideal imaging tool to aid in the diagnosis of certain lameness conditions in the horse. The circulatory pattern and the relative blood flow dictate the thermal pattern which is the basis for thermographic interpretation. The normal thermal pattern of any area can be predicted on the basis of its vascularity and surface contour.

The purpose of any lameness examination is to be able to narrow the problem to a regional diagnosis. Once a regional diagnosis has been made, it is possible to assess the area utilizing some type of anatomical imaging modality. Assessment of those anatomical changes serves as the basis for any pathologic diagnosis that may be made, as well as being important in determining prognosis. For these purposes, radiography and ultrasonography are complimentary. Radiography provides information regarding the boney tissues. Radiographs reflect change that has happened. Ultrasonography provides information about boney contour, but it more importantly, provides insight to the soft tissues that

Ultrasonographic examination can be used to assess any soft tissue in the horseâ&#x20AC;&#x2122;s body. The deeper the tissue that needs to be evaluated, the lower wavelength probe needs to be used. The tissues are examined for changes in echogenicity and fiber alignment. Changes in echogenicity and fiber alignment correspond to changes in the tissue.7 Ultrasonography is most useful in the evaluation of tendons and ligaments, but it also can be used to evaluate muscle and cartilage. Magnetic resonance imaging and computer-aided tomography are both interesting and high-detail anatomic imaging tools.8,9 They provide the best information regarding pathology, but due to their expense, its use is limited to referral centers and universities. It is the authorâ&#x20AC;&#x2122;s opinion that the sport horse practitioner must be adept at reading and interpreting these modalities because they have the most insight into the patient and physical findings and, therefore, can make a more informed interpretation of the results of imaging.

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connect bone or provide support. Sonography can give much better insight into the activity of a lesion. That is, is the lesion active or not? Do the soft tissue changes reflect an ongoing process or is it a chronic process? In addition, sonography can provide information about joint capsule, collateral ligaments, the consistency of joint fluid and provide insight into the articular cartilage. However, the pursuit of a regional diagnosis can be difficult. There are three instances where this can be frustrating: when diagnostic analgesia has failed to eliminate the lameness; when the lameness is too subtle to avail itself to diagnostic analgesic techniques; and when the patient is not amenable to handling or injection. In these cases, other methods must be used to evaluate the patient. This is where physiologic imaging modalities can be so useful. By providing insight into physiologic changes in the tissues, this can lead the examiner to evaluate those areas utilizing anatomic imaging methods. Another area in lameness evaluation where imaging can be useful is in preventing injury. This requires the early detection of the physiologic change of injury. Although the frequent use of an anatomical imaging modality can discover change in one region, physiologic imaging allows the assessment of the entire animal on a routine basis. The utilization of imaging modalities in the diagnosis and treatment of equine lameness is absolutely necessary. This is the only reliable method to assess the type and severity of the injury. In addition, the routine use of any method can provide insight into the stresses and strains of the athlete.

Conclusion:

Sport horse lameness is no different than any other lameness with the exception that they are probably more subtle. In fact, these issues may be as simple as perceived loss of speed or other performance factors. The sensitivity of the rider, driver or trainer to notice issues much sooner is, thus, extremely crucial. The examination is critical and must be systematic and thorough.

References

1. Baxter GM, Stashak TS: History, Visual Exam, Palpation and Manipulation in Baxter GM(ed) Adams and Stashak’s Lameness in Horses. West Sussex, Wiley-Blackwell, 2011, pp109-150. 2. Turner TA: Examination of the equine foot. Vet Clin NA: Eq Prac, 19(2): 309-332, 2003. 3. Turner TA: How to Use Manipulative Tests to Diagnose and Manage Equine Foot Pain in 60th Annual Meeting Am Assoc Eq Practnr, 2014:59-61. 4. Turner TA, Waldsmith JK, Wilson JH: How to assess saddle fit in horses. 50th Annual Meeting Am Assoc Eq Practnr, 2004: 196-201. 5. Baxter GM, Stashak TS: Perineural and Intrasynovial Anesthesia in Baxter GM(ed) Adams and Stashak’s Lameness in Horses. West Sussex, Wiley-Blackwell, 2011, 173-202. 6. Valdes-Martinez A, Park RD: Radiology in Baxter GM(ed) Adams and Stashak’s Lameness in Horses. West Sussex, Wiley-Blackwell, 2011, 207-337.

30 The Practitioner

7. Redding WR: Ultrasonoraphy in Baxter GM(ed) Adams and Stashak’s Lameness in Horses. West Sussex, Wiley-Blackwell, 2011, 338-376. 8. Schramme M, Redding WR: Magnetic Resonance Imaging in Baxter GM(ed) Adams and Stashak’s Lameness in Horses. West Sussex, Wiley-Blackwell, 2011, 416-450. 9. Pease AP, Redding WR: Computed Tomography in Baxter GM(ed) Adams and Stashak’s Lameness in Horses. West Sussex, WileyBlackwell, 2011, 451-459. 10. Turner TA: Diagnostic thermography,Vet Clin N.A.: Equine Pract. 17(1): 2001, 95-114. 11. Dyson SJ, Pilsworth RC, Twardock AR, Martinellin MJ: Equine Scintigraphy, Newmarket, EqVetJ; 2003.

Tracy A. Turner DVM, MS, DACVS, DACVSMR Dr. Tracy Turner received his DVM degree from Colorado State University in 1978 and interned at the University of Georgia. He completed a surgical residency and Master's degree at Purdue University. He has served on the faculties of the University of Illinois, University of Florida and the University of Minnesota. He joined Anoka Equine Clinic in Elk River, MN in 2004, where he practices in sports medicine, lameness and surgery. Dr. Turner's primary area of research interests has focused on equine lameness with particular interest in equine podiatry and thermography. He has spoken nationally and internationally on lameness topics. He has written more than 100 peer reviewed manuscripts, more than 250 non-peer reviewed papers, and more than 30 book chapters on equine lameness, podiatry and thermography. He is board certified by the American College of Veterinary Surgeons and the American College of Veterinary Sports Medicine and Rehabilitation. Dr. Turner is a Diplomate of the American College of Veterinary Surgeons, a Diplomate of the American College of Sports Medicine and Rehabilitation, and is a Fellow of the American Academy of Thermology. He is an active member of the AVMA, AAEP, and the American Horse Council, and he is currently the vice president of the Minnesota Horse Council.

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