Practitioner Issue 4 2015

Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 4 • 2015

DISORDERS RELATED TO VITAMIN E DEFICIENCY CARRIE J. FINNO | DVM, PHD, DACVIM STEPHANIE J. VALBERG | DVM, PHD, DACVIM, DACVSMR

THE USE OF SEQUENTIAL ULTRASOUND EXAMS IN THE CRITICAL EVALUATION AND FINE TUNING OF HEALING CAROL L. GILLIS | DVM, PHD, DACVSMR

UPDATE ON

INFECTIOUS GASTROINTESTINAL ILLNESS IN HORSES NATHAN M. SLOVIS | DVM, DACVIM

Join us at the

53RD ANNUALOcala

EQUINE CONFERENCE

JANUARY 22-24, 2016 | OCALA, FLORIDA

OSPHOSÂŽ

(clodronate injection) Bisphosphonate For use in horses only.

Brief Summary (For Full Prescribing Information, see package insert) CAUTION: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian.

DESCRIPTION: Clodronate disodium is a non-amino, chlorocontaining bisphosphonate. Chemically, clodronate disodium is (dichloromethylene) diphosphonic acid disodium salt and is manufactured from the tetrahydrate form.

A stride forward

INDICATION: For the control of clinical signs associated with navicular syndrome in horses.

CONTRAINDICATIONS: Horses with hypersensitivity to clodronate disodium should not receive OSPHOS.

for Navicular Syndrome

WARNINGS: Do not use in horses intended for human consumption.

HUMAN WARNINGS: Not for human use. Keep this and all drugs out of the reach of children. Consult a physician in case of accidental human exposure.

Introducing OSPHOS, the new

PRECAUTIONS: As a class, bisphosphonates may be associated with gastrointestinal and renal toxicity. Sensitivity to drug associated adverse reactions varies with the individual patient.

Renal and gastrointestinal adverse reactions may be associated with plasma concentrations of the drug. Bisphosphonates are excreted by the kidney; therefore, conditions causing renal impairment may increase plasma bisphosphonate concentrations resulting in an increased risk for adverse reactions. Concurrent administration of other potentially nephrotoxic drugs should be approached with caution and renal function should be monitored.

Use of bisphosphonates in patients with conditions or diseases affecting renal function is not recommended.

Administration of bisphosphonates has been associated with abdominal pain (colic), discomfort, and agitation in horses. Clinical signs usually occur shortly after drug administration and may be associated with alterations in intestinal motility. In horses treated with OSPHOS these clinical signs usually began within 2 hours of treatment. Horses should be monitored for at least 2 hours following administration of OSPHOS.

FDA approved intramuscular bisphosphonate injection from Dechra Veterinary Products

Easily administered via intramuscular injection

Well tolerated* in clinical trials

Proven efficacy* at 6 months post treatment

No Reconstitution required

OSPHOS contains clodronate disodium, a bisphosphonate indicated for the control of clinical signs associated with navicular syndrome in horses. OSPHOS is the only FDA-approved bisphosphonate for use in horses that is labeled for intramuscular injection.

In a clinical trial evaluating OSPHOS in 86 horses, lameness improved in 74.7% of horses by at least one grade 56 days after treatment. Only 9% of horses displayed clinical signs of being uncomfortable, nervous, colicky and or pawing after receiving OSPHOS. Less than 1% of horses experienced colic requiring treatment.

WITH OSPHOS THE BENEFITS ARE CLEAR . . .

Learn more online

www.dechra-us.com www.equinelameness.com www.osphos.com

Call our 24 hour Tech Support

Bisphosphonates affect plasma concentrations of some minerals and electrolytes such as calcium, magnesium and potassium, immediately post-treatment, with effects lasting up to several hours. Caution should be used when administering bisphosphonates to horses with conditions affecting mineral or electrolyte homeostasis (e.g. hyperkalemic periodic paralysis, hypocalcemia, etc.).

The safe use of OSPHOS has not been evaluated in horses less than 4 years of age. The effect of bisphosphonates on the skeleton of growing horses has not been studied; however, bisphosphonates inhibit osteoclast activity which impacts bone turnover and may affect bone growth.

Bisphosphonates should not be used in pregnant or lactating mares, or mares intended for breeding. The safe use of OSPHOS has not been evaluated in breeding horses or pregnant or lactating mares.

Bisphosphonates are incorporated into the bone matrix, from where they are gradually released over periods of months to years. The extent of bisphosphonate incorporation into adult bone, and hence, the amount available for release back into the systemic circulation, is directly related to the total dose and duration of bisphosphonate use.

Bisphosphonates have been shown to cause fetal developmental abnormalities in laboratory animals. The uptake of bisphosphonates into fetal bone may be greater than into maternal bone creating a possible risk for skeletal or other abnormalities in the fetus. Many drugs, including bisphosphonates, may be excreted in milk and may be absorbed by nursing animals.

Increased bone fragility has been observed in animals treated with bisphosphonates at high doses or for long periods of time.

Bisphosphonates inhibit bone resorption and decrease bone turnover which may lead to an inability to repair micro damage within the bone.

In humans, atypical femur fractures have been reported in patients on long term bisphosphonate therapy; however, a causal relationship has not been established.

ADVERSE REACTIONS: The most common adverse reactions reported in the field study were clinical signs of discomfort or nervousness, colic and/or pawing. Other signs reported were lip licking, yawning, head shaking, injection site swelling, and hives/pruritus.

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As with all drugs, side effects may occur. In field studies, the most common side effects reported were signs of discomfort or nervousness, colic, and/or pawing. OSPHOS should not be used in pregnant or lactating mares, or mares intended for breeding. Use of OSPHOS in patients with conditions affecting renal function or mineral or electrolyte homeostasis is not recommended. Refer to the prescribing information for complete details or visit www.dechra-us.com.

CAUTION: Federal law restricts this drug to use by or on the order of licensed veterinarian. * Freedom of Information Summary, Original New Animal Drug Application, NADA 141-427, for OSPHOS. April 28, 2014.

Distributed by: Dechra Veterinary Products 7015 College Boulevard, Suite 525 Overland Park, KS 66211 866-933-2472 Š 2015 Dechra Ltd. OSPHOS is a registered trademark of Dechra Ltd. All rights reserved.

NADA 141-427, Approved by FDA

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Equine Influenza Virus West Nile-Innovator and Fluvac Innovator MDI Sales Data as of 12/31/14. Zoetis. Dec. 2014.

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Townsend HGG, Penner SJ, Watts TC, Cook A, Bogdan J, Haines DM, Griffin S, Chambers T, Holland RE, Whitaker-Dowling P, Youngner JS, and Sebring RW: Efficacy of cold-adapted, intranasal, equine influenza vaccine: challenge trials.

Chambers TM, Holland RE, Tudor LR, Townsend HGG, Cook A, Bogdan J, Lunn DP, Hussey S, Whitaker-Dowling P, Youngner JS, Sebring RW, Penner SJ and Stiegler GL: A new modified-live equine influenza vaccine: phenotypic stability, restricted spread and efficacy against heterologous virus challenge.

All trademarks are the property of Zoetis Inc., its affiliates and/or its licensors. All other trademarks are the property of their respective owners. ©2015 Zoetis Inc. All rights reserved. FLU-00076

www.faep.net

The Practitioner 3

The President's Line Corey Miller, DVM, MS, Diplomate ACT - FAEP President

I’m honored and privileged to be able to greet you with my personal well wishes as we approach the closing of another successful year for your FAEP. I want to extend season’s greetings to you and yours, on behalf of my fellow Council members and the staff of the FAEP/FVMA. As the equine-exclusive division of the FVMA, the FAEP hosts two major continuing equine education events each year. We are very proud of the outstanding continuing education we provided our members and attendees in 2015. Our Promoting Excellence Symposium (PES) in Naples, FL, set a new record for attendance. We are proud to note that more than 400 equine practitioners from more than 38 states and six countries took advantage of our educational offerings in 2015!

We want to build on this success in 2016 and plan on making it a productive and fruitful year. We invite you to join us for the 53rd Annual Ocala Equine Conference, from January 22 to 24, 2016. This year’s program offers an in-depth ultrasound imaging wet lab, followed by two days of first-rate lectures by some of the foremost clinicians and experts in the field of equine medicine. We encourage you to register soon, and look forward to welcoming you to Ocala, the “Horse Capital of the World.” We are also busy planning our 12th annual PES scheduled for October 2016 at the amazing El Conquistador Resort in Fajardo, Puerto Rico…start planning because, you won’t want to miss this outstanding CE offering in this amazing destination!

The FAEP will be advocating for the veterinary profession at the State Capitol during our annual Legislative Action Days from February 27 to 28, 2016. I encourage you to join us in Tallahassee this year. The opportunity to see and participate in the legislative process of our State is both exciting and a great learning experience. Our efforts in 2014 and 2015 resulted in positive outcomes for our profession. We need to work together in our legislative endeavors to have continued success in 2016.

Make your New Years resolution to become involved in your Association! We are actively seeking members to participate on several committees. Please feel free to contact me, other FAEP Council members, or the FVMA office for information. I am happy to be of service to you and to our great profession.

Warmest season’s greetings,

EXECUTIVE COUNCIL

Corey

Suzan C. Oakley, DVM, MS, Diplomate ABVP(Equine), Cert. ISELP FAEP COUNCIL PAST PRESIDENT oakleyequine@gmail.com

Adam Cayot, DVM adamcayot@hotmail.com

Anne L. Moretta, VMD, MS marochel@aol.com

Amanda M. House, DVM, Diplomate ACVIM REPRESENTATIVE TO FVMA EXECUTIVE BOARD housea@ufl.edu

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

Liane D. Puccia, DVM pucciavet@aol.com

Armon Blair, DVM abeqdoc@aol.com

Ruth-Anne Richter, BSc (Hon), DVM, MS PRESIDENT-ELECT rrichter@surgi-carecenter.com

Jacqueline S. Shellow, DVM, MS docshellow@bellsouth.net

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

A NEW dual ingredient injectable corticosteroid approved by the FDA exclusively for use in horses

The link between FAST-ACTING and

LONG-LASTING relief 1, 2

New BetaVet ® (betamethasone sodium phosphate & betamethasone acetate injectable suspension) is indicated for the control of pain and inflammation associated with osteoarthritis in horses. Learn more at www.betavetequine.com or call 1-800-458-0163.

Please see Brief Summary of Full Prescribing Information on the following page.

From the manufacturer of Adequan® (polysulfated glycosaminoglycan)

INDICATION: BetaVet® is indicated for the control of pain and inflammation associated with osteoarthritis in horses.

IMPORTANT SAFETY INFORMATION For Intra-Articular (I.A.) Use in Horses.

CONTRAINDICATIONS: BetaVet ® is contraindicated in horses with hypersensitivity to betamethasone. Intra-articular injection of corticosteroids for local effect is contraindicated in the presence of septic arthritis.

WARNINGS: Do not use in horses intended for human consumption. Clinical and experimental data have demonstrated that corticosteroids administered orally or parenterally to animals may induce the first stage of parturition when administered during the last trimester of pregnancy and may precipitate premature parturition followed by dystocia, fetal death, retained placenta, and metritis. Additionally, corticosteroids administered to dogs, rabbits and rodents during pregnancy have resulted in cleft palate in offspring and in other congenital anomalies including deformed forelegs, phocomelia and anasarca. Therefore, before use of corticosteroids in pregnant animals, the possible benefits to the pregnant animal should be weighed against potential hazards to its developing embryo or fetus.

Human Warnings: Not for use in humans. For use in animals only. Keep this and all medications out of the reach of children. Consult a physician in the case of accidental human exposure.

PRECAUTIONS: Corticosteroids, including BetaVet , administered intra-articularly are systemically absorbed. Do not use in horses with acute infections. Acute moderate to severe exacerbation of pain, further loss of joint motion, fever, or malaise within several days following intra-articular injection may indicate a septic process. Because of the anti-inflammatory action of corticosteroids, signs of infection in the treated joint may be masked. Due to the potential for exacerbation ®

of clinical signs of laminitis, glucocorticoids should be used with caution in horses with a history of laminitis, or horses otherwise at a higher risk for laminitis. Use with caution in horses with chronic nephritis, equine pituitary pars intermedia dysfunction (PPID), and congestive heart failure. Concurrent use of other anti-inflammatory drugs, such as NSAIDs or other corticosteroids, should be approached with caution. Due to the potential for systemic exposure, concomitant use of NSAIDs and corticosteroids may increase the risk of gastrointestinal, renal, and other toxicity. Consider appropriate wash out times prior to administering additional NSAIDs or corticosteroids.

ADVERSE REACTIONS: Adverse reactions reported during a field study of 239 horses of various breeds which had been administered either BetaVet ® (n=119) or a saline control (n=120) at five percent (5%) and above were: acute joint effusion and/or local injection site swelling (within 2 days of injection), 15% BetaVet ® and 13% saline control; increased lameness (within the first 5 days), 6.7% BetaVet ® and 8.3% saline control; loose stool, 5.9% BetaVet ® and 8.3% saline control; increased heat in joint, 2.5% BetaVet ® and 5% saline control; and depression, 5.9% BetaVet ® and 1.6% saline control.

DOSAGE AND ADMINISTRATION: Shake well immediately before use.

Use immediately after opening, then discard any remaining contents.

RX ONLY References: 1.Houdeshell, JW. Field trials of a new long-acting corticosteroid on the treatment of equine arthropathies. Vet Med Small Anim Clin. Sept. 1969: 782-784. 2. Trotter GW. Intra-articular corticosteroids. In: McIlwraith CW, Trotter GW, eds. Joint Disease in the Horse.

Philadelphia, PA: W.B. Saunders, 1996;237–256.

BetaVet ® is a registered trademark of Luitpold Pharmaceuticals, Inc. © Luitpold Animal Health, division of Luitpold Pharmaceuticals, Inc. 2015.

BVT003 Iss. 7/2015

LUITPOLD ANIMAL HEALTH

BRIEF SUMMARY OF PRESCRIBING INFORMATION (Betamethasone Sodium Phosphate and Betamethasone Acetate Injectable Suspension) 6 mg betamethasone per mL For Intra-Articular (I.A.) Use in Horses CAUTION: Federal law restricts this drug to use by or on the order of a licensed veterinarian.

DESCRIPTION: BetaVet ® is a sterile aqueous suspension of betamethasone acetate in betamethasone sodium phosphate injection. The combined betamethasone content of the suspension is 6 mg/mL where each mL contains 3.15 mg betamethasone (as betamethasone sodium phosphate); 2.85 mg betamethasone (as betamethasone acetate); 7.1 mg dibasic sodium phosphate; 3.4 mg monobasic sodium phosphate; 0.1 mg edetate disodium; and 0.2 mg benzalkonium chloride, as a preservative in water for injection. The pH is adjusted to between 6.8 and 7.2.

INDICATION: BetaVet ® is indicated for the control of pain and inflammation associated with osteoarthritis in horses.

DOSAGE AND ADMINISTRATION: Shake well immediately before use. Using strict aseptic technique, administer 1.5 mL BetaVet ® (9 mg total betamethasone) per joint by intra-articular injection. BetaVet ® may be administered concurrently in up to 2 joints per horse. Use immediately after opening, then discard any remaining contents.

CONTRAINDICATIONS: BetaVet ® is contraindicated in horses with hypersensitivity to betamethasone. Intra-articular injection of corticosteroids for local effect is contraindicated in the presence of septic arthritis.

WARNINGS: Do not use in horses intended for human consumption.

Clinical and experimental data have demonstrated that corticosteroids administered orally or parenterally to animals may induce the first stage of parturition when administered during the last trimester of pregnancy and may precipitate premature parturition followed by dystocia, fetal death, retained placenta, and metritis. Additionally, corticosteroids administered to dogs, rabbits and rodents during pregnancy have resulted in cleft palate in offspring.

Corticosteroids administered to dogs during pregnancy have also resulted in other congenital anomalies including deformed forelegs, phocomelia and anasarca.

Therefore, before use of corticosteroids in pregnant animals, the possible benefits to the pregnant animal should be weighed against potential hazards to its developing embryo or fetus. Human Warnings: Not for use in humans. For use in animals only. Keep this and all medications out of the reach of children. Consult a physician in the case of accidental human exposure.

PRECAUTIONS: Corticosteroids, including BetaVet ®, administered intra-articularly are systemically absorbed. Do not use in horses with acute infections. Acute moderate to severe exacerbation of pain, further loss of joint motion, fever, or malaise within several days following intra-articular injection may indicate a septic process. Because of the anti-inflammatory action of corticosteroids, signs of infection in the treated joint may be masked. Appropriate examination of joint fluid is necessary to exclude a septic process. If a bacterial infection is present, appropriate antibacterial therapy should be instituted immediately. Additional doses of corticosteroids should not be administered until joint sepsis has been definitively ruled out. Due to the potential for exacerbation of clinical signs of laminitis, glucocorticoids should be used with caution in horses with a history of laminitis, or horses otherwise at a higher risk for laminitis. Use with caution in horses with chronic nephritis, equine pituitary pars intermedia dysfunction (PPID), and congestive heart failure. Concurrent use of other anti-inflammatory drugs, such as NSAIDs or other corticosteroids, should be approached with caution.

Due to the potential for systemic exposure, concomitant use of NSAIDs and corticosteroids may increase the risk of gastrointestinal, renal, and other toxicity.

Consider appropriate wash out times prior to administering additional NSAIDs or corticosteroids.

ADVERSE REACTIONS: Adverse reactions reported during a field study of 239 horses of various breeds which had been administered either BetaVet ® (n=119) or a saline control (n=120) were: acute joint effusion and/or local injection site swelling (within 2 days of injection), 15% BetaVet ® and 13% saline control;

increased lameness (within the first 5 days), 6.7% BetaVet ® and 8.3% saline control; loose stool, 5.9% BetaVet ® and 8.3% saline control; increased heat in joint, 2.5% BetaVet ® and 5% saline control; depression, 5.9% BetaVet ® and 1.6% saline control; agitation/anxiety, 4.2% BetaVet ® and 2.5% saline control; delayed swelling of treated joint (5 or more days after injection), 2.5% BetaVet ® and 3.3% saline control; inappetance, 3.4% BetaVet ® and 2.5% saline control; dry stool, 1.7% BetaVet ® and 0% saline control; excessive sweating, 0.8% BetaVet ® and 0% saline control; acute non-weight bearing lameness, 0.8% BetaVet®and 0% saline control; and laminitis, 0.8% BetaVet® and 0% saline control.

CLINICAL PHARMACOLOGY: Betamethasone is a potent glucocorticoid steroid with anti-inflammatory and immunosuppressive properties. Depending upon their physico-chemical properties, drugs administered intra-articularly may enter the general circulation because the synovial joint cavity is in direct equilibrium with the surrounding blood supply. After the intra-articular administration of 9 mg BetaVet ® in horses, there were quantifiable concentrations of betamethasone (above 1.0 ng/mL) in the plasma.

EFFECTIVENESS: A negative control, randomized, masked field study provided data to evaluate the effectiveness of BetaVet ® administered at 1.5 mL (9 mg betamethasone) once intra-articularly for the control of pain and inflammation associated with osteoarthritis in horses. Clinical success was defined as improvement in one lameness grade according to the AAEP lameness scoring system on Day 5 following treatment. The success rate for horses in the BetaVet ® group was statistically significantly different (p=0.0061) than that in the saline group, with success rates of 75.73% and 52.52%, respectively (back-transformed from the logistic regression).

ANIMAL SAFETY: A 3-week target animal safety (TAS) study was conducted to evaluate the safety of BetaVet ® in mature, healthy horses. Treatment groups included a control (isotonic saline at a volume equivalent to the 4x group); 1X (0.0225 mg betamethasone per pound bodyweight; BetaVet ®); 2X (0.045 mg betamethasone per pound bodyweight; BetaVet ®) and 4X (0.09 mg betamethasone per pound bodyweight; BetaVet ®). Treatments were administered by intra-articular injection into the left middle carpal joint once every 5-days for 3 treatments. Injection site reactions were the most common observations in all treatment groups. Injection site reactions were observed within 1 hour of dosing and included swelling at the injection site, lameness/stiffness of the left front limb, and flexing the left front knee at rest. The injection site reactions ranged from slight swelling (in many horses on multiple days in all treatment groups) to excessive fluid with swelling, pain, and lameness (4x group only). Injection site reactions were observed most commonly on treatment days, and generally decreased in number and severity over subsequent days. The incidence of injection site reactions increased after the second and third injection (number of abnormalities noted on day 10 > day 5 > day 0). In the BetaVet ® treated groups the number and severity of the injection site reactions were dose dependent. The 4X BetaVet ® group had the highest overall incidence of and severity of injection site reactions, which included heat, swelling, pain, bleeding, and holding the limb up at rest.

The control group and 4X group (which received similar injection volumes) had a similar incidence of injection site reactions; however, the severity of reactions was greater in the 4X group. Absolute neutrophils were statistically significantly higher in the BetaVet ® treated groups as compared to the control group. Trends toward a decrease in lymphocytes and eosinophils, and an increase in monocytes were identified in the BetaVet ® treated groups after the initial dose of BetaVet ®. Individual animal values for white blood cells generally remained within the reference range.

BetaVet ® treated horses also had a trend toward increased blood glucose after the initial dose. Some individual animals showed mild increases in blood glucose above the reference range.

STORAGE CONDITIONS Store at 20° to 25°C (68° to 77°F) (See USP Controlled Room Temperature).

Protect from light. Use carton to protect contents from light until used.

HOW SUPPLIED BetaVet ®, One 5 mL vial containing 30 mg betamethasone; packaged in boxes of 1.

SHAKE WELL BEFORE USING NADA 141-418, Approved by FDA

A Division of Luitpold Pharmaceuticals, Inc. One Luitpold Drive | P.O. Box 9001 | Shirley, NY 11967

Vitamin E DEFICIENCY

DISORDERS RELATED TO

CARRIE J. FINNO | DVM, PHD, DACVIM STEPHANIE J. VALBERG | DVM, PHD, DACVIM, DACVSMR INTRODUCTION Vitamin E functions as a biological antioxidant, preventing the oxidation of unsaturated lipids within cellular and subcellular membranes by neutralizing production of free radicals. Through this mechanism, and potentially other mechanisms yet to be elucidated, vitamin E serves to maintain normal neuromuscular function. Several specific equine diseases develop in the face of vitamin E deficiency. These include nutritional myodegeneration, neuroaxonal dystrophy and equine degenerative myeloencephalopathy in young animals. Adult horses deficient in vitamin E may develop a vitamin E deficient myopathy or equine motor neuron disease. Treatment with vitamin E is usually instituted in an attempt to reverse clinical signs. However, selecting the type and amount of vitamin E to supplement can be challenging for veterinarians because the bioavailability and potency varies widely among commercial supplements. Most vitamin E supplements consist of natural or synthetic forms of α-tocopherol because it is the most biologically active and most researched isoform of vitamin E. Vitamin E, however, is a complex nutrient consisting of eight closelyrelated fat-soluble naturally-occurring compounds that form two groups; tocopherols (saturated) and tocotrienols (unsaturated).

Within each group, there are four individual isoforms (α, β, γ and δ). The purpose of these proceedings is to review the equine neuromuscular disorders related to vitamin E deficiency and data on serum and tissue responses to commercial vitamin E supplements.

α-tocopherol deficient horses (serum α-tocopherol <2 μg/mL). A correlation between serum/plasma and CSF α-tocopherol is also evident in deficient horses suffering from neuroaxonal dystrophy/ equine degenerative myeloencephalopathy (Finno, unpublished results) and between serum α-tocopherol and nervous tissue α-tocopherol in equine motor neuron disease.6 This correlation, however, is not consistently evident in horses with vitamin E deficient myopathy. In cases of vitamin E deficient myopathy, a discrepancy between serum and tissue levels of α-tocopherol may indicate that an abnormality exists in uptake of α-tocopherol into muscle tissues.

ASSESSMENT OF Α-TOCOPHEROL DEFICIENCY

Nutritional Myodegeneration (NMD)

Serum or plasma is clearly the most readily available sample for determination of α-tocopherol deficiency. Blood should be chilled as soon as possible after obtaining a sample and protected from light by wrapping in tin foil. Blood samples should be centrifuged at 4°C and plasma/serum separated as soon as possible. If analysis is delayed, serum/plasma samples should be stored frozen (- 21° F, - 70° C) as vitamin E deteriorates rapidly. Reference ranges for plasma/serum concentrations of α-tocopherol in the horse are as follows:1 >2 μg/mL Adequate 1.5-2 μg/mL Marginal <1.5 μg/mL Deficient

Nutritional myodegeneration (NMD), also referred to as white muscle disease, affects skeletal or cardiac muscle of rapidly growing, active foals and is primarily due to a dietary deficiency of selenium beginning in utero.7 In some, but not all cases, there may also be a deficiency of vitamin E.

Serum versus tissue α-tocopherol concentrations: Significant correlations exist between serum α-tocopherol concentrations and adipose tissue,2 liver,3 muscle3 and CSF4 in healthy horses.

The normal reference ranges for muscle tissue and cerebrospinal fluid (CSF) α-tocopherol concentrations are reported at 4.2 ± 0.8 µg/g3 and 9.5 ± 5.54 ng/mL,5 respectively; however, the values for CSF concentrations were determined in apparently healthy, but

Diagnosis: Foals with NMD have elevated serum creatine kinase (CK) and aspartate transaminase (AST) activities, whole blood selenium < 0.07 μg/ml and serum vitamin E may or may not be < 2 μg/ml.

www.faep.net

Equine Diseases Associated With Vitamin E Deficiency Vitamin E deficiency may exist in an entire herd of horses, yet only a select few develop clinical signs of neuromuscular disease.

Development of neuromuscular disease appears to depend upon the age of the animal when deficiency develops, the duration of vitamin E deficiency, the genetic make-up of the individual and other concurrent dietary deficiencies or excesses. In many horses, there are no apparent ill effects of vitamin E deficiency.

Therefore, diagnosis of the neuromuscular disorders described below requires not only determination of vitamin E status but also the appropriate clinical signs, supporting clinical pathology and/or muscle biopsy results and elimination of other possible diseases.

Clinical signs: Foals with NMD often present with signs of muscle weakness, difficulty rising, trembling of the limbs, stiffness, prolonged recumbency, firm painful muscles and potentially aspiration pneumonia. Depression, rapid heart rate, difficulty breathing and foamy nasal discharge or sudden death may indicate cardiac involvement.

Treatment: The cardiac form of NMD is usually not compatible with life. Foals with skeletal muscle involvement often show The Practitioner 7

significant improvement within 3 to 5 days of treatment with injectable selenium products as well as general supportive care.

Injectable selenium products contain 50 mg/ml (68 IU) of vitamin E as dl-α-tocopheryl acetate (all-rac-α-tocopheryl acetate) which acts as a preservative for the solution and is, therefore, insufficient for vitamin E supplementation. Therefore, additional oral vitamin E is suggested to quickly increase antioxidant levels (see below for dosages). Foals with prolonged recumbency require significant rehabilitation therapy to regain normal muscle function.

Neuroaxonal Dystrophy / Equine Degenerative Myeloencephalopathy (NAD/EDM) Equine neuroaxonal dystrophy (NAD) and equine degenerative myeloencephalopathy (EDM) are closely related disorders distinguished largely by the location of axonal or neuronal degeneration in the central nervous system. NAD/EDM occurs in multiple breeds with most cases demonstrating clinical signs by six to twelve months of age. Although the pathophysiology is not completely defined, there is strong evidence of a genetic component whose expression is highly influenced by vitamin E deficiency during the first year of life. Low serum α-tocopherol has been described in most, but not all, affected foals.

Diagnosis: The most specific diagnosis of this disease is the histopathologic finding in fresh (not formalin-fixed) sacrocaudalis dorsalis muscle of an abnormal moth eaten mitochondrial staining pattern in the absence of neurogenic angular atrophy of myofibers. In many, but not all cases of VEM, serum α-tocopherol is low. In all affected cases assessed to date, muscle α-tocopherol concentrations have been below normal. This represents an unusual lack of linear correlation between serum and muscle α-tocopherol and may indicate deficient skeletal muscle uptake or excessive muscle consumption.

Treatment: Horses with VEM are remarkably responsive to appropriate vitamin E supplementation (see below for dosages) and show a complete recovery.

Clinical signs: Clinical signs include symmetric ataxia that is often more severe in the pelvic limbs than the thoracic limbs, abnormal base-wide stance at rest, and proprioceptive deficits.

In some reports, hyporeflexia of the cervicofacial and cutaneous trunci is described, in addition to an absent laryngeal adductor reflex. Horses with NAD/EDM that survive to 2-3 years of age commonly exhibit lifelong, stable neurologic deficits.8 Diagnosis: An antemortem diagnosis of NAD/EDM is based solely upon clinical signs, the elimination of other causes of neurologic disease, and a possible association with a low serum α-tocopherol concentration. A definitive diagnosis is only available upon histopathologic evaluation of specific tracts and nuclei within the spinal cord and brainstem tissue at postmortem. There is no treatment for NAD/EDM and there have been no reports of spontaneous resolution.

Treatment: Suspected cases are often treated empirically with vitamin E supplementation (see below for dosages).

Unfortunately, there is strong evidence that vitamin E supplementation of affected horses does not lead to neurologic improvement.9 However, supplementation of dams with vitamin E during pregnancy may lead to a decreased incidence of NAD/ EDM during the next foaling season.10

Vitamin E Deficient Myopathy (VEM) A subset of horses with vitamin E deficiency may develop clinical signs solely related to muscle atrophy and weakness without evidence of damage to motor nerves. These horses, of a wide variety of breeds, have been diagnosed with a vitamin E deficient myopathy (VEM).11 Whether VEM is an entity unto itself or a predecessor to development of equine motor neuron disease is not yet known.

Clinical signs: Horses present with loss of muscle mass, toe dragging, poor performance, weakness and muscle fasciculations.

8 The Practitioner

Before: Belgian draft horse taken when healthy

Equine Motor Neuron Disease (EMND) Equine Motor Neuron Disease (EMND) is an acquired neurodegenerative disorder affecting motor nerves, particularly those supplying highly oxidative type 1 muscle fibers. EMND is associated with low plasma concentrations of α-tocopherol and a dietary deficiency of vitamin E of at least 18 months duration.12 Clinical signs: Horses with EMND show signs of generalized muscle wasting, muscle fasciculations, shifting of weight between hindlimbs, low head carriage in some cases and prolonged recumbency.

Diagnosis: Antemortem diagnosis of EMND is based upon either histopathologic evidence of degeneration of myelinated axons upon biopsy of the ventral branch of the spinal accessory nerve or the finding of neurogenic angular atrophy of predominantly type 1 muscle fibers in sacrocaudalis dorsalis medialis muscle biopsy.13-14 Treatment: Treatment with relatively high doses of 50007000 IU α-tocopherol/day is reported to produce clinical improvement in about 40% of cases within 6 weeks and some Issue 4 • 2015

horses may appear normal within 3 months.15 It should be noted, however, that return to performance may result in deterioration.

(Hercules deficient photo) Same horse several years later who was kept on a dry lot without any vitamin E supplementation.

He developed a vitamin E deficient myopathy with significant generalized muscle atrophy.

Same horse still kept on the dry lot but fed 5000 Units per day of water dispersible alpha tocopherol (Hercules after).

VITAMIN E SUPPLEMENTATION It is important to realize that the absorption and metabolism of vitamin E in healthy horses may differ from horses with vitamin E deficiency. Thus, the choice of the type of vitamin E supplement should differ depending upon whether a maintenance supplement is being selected for a horse with normal serum α-tocopherol or whether there is a need to rapidly increase serum α-tocopherol in a horse with low serum α-tocopherol and clinical signs of vitamin E deficiency.

Vitamin E can be obtained from natural or synthetic sources, but the chemical structure of each is different. Natural vitamin E www.faep.net

is composed of one isomer (d-α-tocopherol [RRR-α-tocopherol]), and it is the most bioactive form in animal tissues. Synthetic vitamin E is a mixture of eight isomers (dl-α-tocopherol [all-rac-α-tocopherol]), of which only one is identical to the natural isomer. These eight isomers vary greatly in relative biopotency. Furthermore, when synthetic or natural vitamin E is formulated as a feed additive, it is manufactured as an esterifed form (α-tocopheryl acetate) to prolong shelf life. In order for α-tocopheryl acetate to be utilized in the body, the ester has to be removed and the α-tocopheryl made water-dispersible by the action of bile salts (micellization). These additional steps may limit α-tocopheryl acetate absorption in the horse.

To account for differences in biopotency, the relative strengths of different forms of vitamin E are expressed as international units (IU) in which 1 mg of synthetic acetate equals 1 IU, 1 mg of natural acetate equals 1.36 IU, and 1 mg of natural alcohol equals 1.49 IU.16 These conversion factors were developed using laboratory animal models. A recent study in horses found that relative to synthetic (dl-α-tocopheryl acetate), natural-source vitamin E acetate (d-α-tocopheryl acetate) had 1.97 and naturalsource vitamin E alcohol (d-α-tocopherol) 2.52 times the potency of synthetic vitamin E.17 To further enhance the bioavailability of α-tocopherol, water dispersible formulations of vitamin E have been developed. When tested, two of the commercially available water dispersible natural vitamin E products had a bioavailability 5.59 (Elevate WS, Kentucky Performance Products LLC, Versailles, KY) and 6.13 (Nano•E, Kentucky Equine Research, Versailles, KY) fold higher than synthetic vitamin E acetate (d-α-tocopheryl acetate).17 The capacity of these compounds to significantly increase serum α-tocopherol concentration in horses has been studied in horses with normal baseline α-tocopherol. Synthetic forms of α-tocopherol produced no significant increase in serum over a range of doses each fed for 14 days. In contrast, the natural acetate form caused a significant increase when fed ≥ 2000 IU/500 kg horse for 14 days and the water dispersible formulation of natural α-tocopherol had a significant and greater increase in serum levels at ≥ 1000 IU/500 kg horse.18

It is important to realize when interpreting these studies that the absorption and metabolism of vitamin E in healthy horses may differ from horses with vitamin E deficiencies. In two studies using horses with a marginal/deficient α-tocopherol status but no clinical signs of deficiency, a serum α-tocopherol concentrations increased with both all-rac-α-tocopheryl acetate (synthetic) and water-dispersible RRR-α-tocopherol (natural; Emcelle, Steward Prodcuts, Bedford, TX) at 10,000 IU/500kg horse/day for 10-14 days, with levels being twice as high in the group on RRR-α-tocopherol. Cerebrospinal fluid concentrations of α-tocopherol increased from baseline (1.3 to 3.5 fold) only in horses supplemented with natural water dispersed RRR α-tocopherol.4 Vitamin E deficiency: Natural-source water-dispersible forms of vitamin E at 10 IU/kg body weight seem like the obvious choice for optimal treatment as they are 5-6 times more bioavailable than synthetic vitamin E acetate, and a 5000-IU dose/horse more than doubles serum vitamin E levels within 12 hr.17 Before implementing supplementation it is important to measure The Practitioner 9

serum α-tocopherol concentrations in order to determine if there is an underlying deficiency and in order to monitor the efficacy of supplementation.

Healthy horses: Current NRC daily recommendations for vitamin E in horses are 1 -2 IU/kg body weight, however, these NRC recommendations do not discriminate between natural or synthetic sources.19 Research-based evidence for the need for additional vitamin E supplementation above 500 IU/day is lacking in healthy young and middle-aged horses receiving adequate dietary vitamin E intake. Synthetic or natural esterified forms of vitamin E are the most costeffective means to provide vitamin E to horses with normal vitamin E status. It is important to periodically check serum α-tocopherol concentrations and, if an adequate response to supplementation does not occur, the dose or formulation of α-tocopherol should be altered. Vitamin E, unlike other fatsoluble vitamins, does not accumulate in the body to a toxic level due to protective mechanisms. Despite these mechanisms, it is important to consider that supplementation with vitamin E may alter drug metabolism and disposition since, in humans, the same cytochrome isoforms that metabolize vitamin E metabolize >50% of therapeutic drugs.20 High levels of supplementation in humans do not enhance plasma concentrations more than 3-4 fold and excess tocopherol is sequestered in the liver, rapidly metabolized and/or excreted.

The NRC has set the upper safe diet concentration at 20 IU/ kg BW based on biopotency of synthetic α-tocopherol (10,000 IU/500 kg horse). Above this level, coagulopathy and impaired bone mineralization have been reported.19 Furthermore, in healthy exercising horses, high dosage of vitamin E supplementation (10x NRC requirements) was shown to be potentially detrimental to beta-carotene absorption and thus not recommended.21

References: Blythe LL, et al. In: Robinson NE,ed. Current Therapy in Equine Medicine 1992;559- 561.

1

Steiss JE, et al. Equine Vet J 1994;26:417-419.

2

Roneus BO, et al. Equine Vet J 1986;18:50-58.

3 4

Pusterla N, et al. Vet Rec 2010;166:366-368.

5

Higgins JK, et al. Am J Vet Res 2008;69:785-790.

6

Divers T, et al. Clin Tech Equine Pract 2006;5:24-29.

7

Perkins G, et al. J Vet Intern Med 1998;12:173-177.

8 9

Blythe LL, et al. Comp Cont Educ Pract Vet 1992;14:1215-1221

Aleman M, et al. J Am Vet Med Assoc 2011;239:823-833.

10

Dill SG, et al. Am J Vet Res 1990;51:1300-1305.

11

Bedford H, et al. J Am Vet Med Assoc in press

12

Divers TJ, et al. Am J Vet Res 2006;67:120-126.

Divers TJ, et al. 42nd Annual Am Assoc Equine Pract Proc 1992;28:215-219 13

10 The Practitioner

Jackson CA, et al. Equine Vet J 1996;28:215-219

14

15

Divers TJ, et al. Equine Vet J 2011;13:63-67

16

Weber P, et al. Nutrition 1997;13:450-460

17

Pagan JD, et al. Nordic Feed Sci Conf Proc 2010;112-115.

18

Pagan JD, et al. Pferdeheilkunde 2005;21:101-1-2

19

NRC National Research Council 2007.

20

Kliewer SA, et.al Endocr Rev 2002;23:587-702

Williams CA, et.al Equine Vet J Suppl 2006;617-621

21

Carrie J. Finno, DVM, PhD, DACVIM Dr. Carrie Finno received her veterinary degree from the University of Minnesota.

Following graduation, she completed a oneyear internship in Large Animal Medicine and Surgery at Minnesota, before coming to UC Davis to complete a three-year residency in Large Animal Medicine and Surgery.

Dr. Finno went on to complete a PhD in Comparative Pathology at UC Davis, and then returned to Minnesota to join their faculty as an Assistant Professor.

After two years on their faculty, she once again returned to UC Davis as a faculty member in genetics and a clinical role with the Equine Medicine Service.

Dr. Finno's research is focused on companion animal genetics, particularly the genetic and environmental risk factors associated with equine neuromuscular disease.

Stephanie Valberg, DVM, PhD Dr. Stephanie Valberg is Mary Anne McPhail Dressage Chair in Equine Sports Medicine at Michigan State University. Prior, she was professor in Large Animal Medicine at the University of Minnesota College of Veterinary Medicine, in St. Paul Minnesota.

Dr. Valberg received her DVM from the Ontario Veterinary College and completed a PhD in equine exercise physiology at the Swedish University of Animal Science. She is a Board certified internal medicine and sports medicine clinician.

Dr. Valberg’s research centers on neuromuscular diseases in horses with a special focus on genetic diseases of skeletal muscle and their nutritional management.

She was inducted into the Equine Research Hall of Fame in 2012 and has received several awards including the British Equine Veterinary Association Clinical Award 2014, University of Minnesota’s Postdoctoral Mentor2013, MVMA outstanding faculty award 2013, The 2012 Milne lecture at AAEP, the 2001 and 2010 Pfizer Award for Research Excellence and the 1999 EquiSci International Award.

Dr. Valberg has over 136 scientific publications and is a frequent speaker at national and international veterinary, nutrition and genetic conferences. She is an avid 3-day eventer with her 5-yr-old Warmblood Cajun.

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The Use of

SEQUENTIAL ULTRASOUND EXAMS IN THE CRITICAL EVALUATION & FINE TUNING OF HEALING CAROL L. GILLIS | DVM, PHD, DACVSMR The initial exam history includes the age, breed and use of the horse as well as any other problems that the horse has concurrently. The important reason to obtain this information is to create a treatment and exercise program that suits each particular patient best. For example, a 2-year-old Thoroughbred racehorse will require different rehabilitation strategies than a 12-year-old hunter, both because they are used to different maintenance and because their ultimate fitness levels need to be different. The initial clinical exam includes a careful assessment of foot balance, particularly of the affected limb but of the other three as well. For the affected limb, supportive shoeing may be required to assist soft tissue healing. The other feet need to be balanced relative to the injured limb foot as well as medial to lateral, with aligned hoof/pastern axes and with adequate support from heel to toe. Maintenance considerations include diet, with restriction of grain, and provision of good quality hay to provide essentials for healing, and appropriate housing.

Controlled exercise is the key element for good healing; however, many horses are unused to confinement and all athletes are unused to restricted exercise. Strategies to minimize stress include ensuring that another horse is in sight at all times and the use of a slow feeder so that feed is present in the stomach at all times. Treatment of concurrent problems should be continued during rehabilitation so that the horse is as sound and healthy as possible upon return to work.

The image shows the ligament after 8 weeks of treatment and controlled exercise. Size has decreased to normal range (or comparable to the paired ligament), lesions are smaller and more echogenic relative to surrounding normal tissue and early linear fiber pattern is evident.

The initial ultrasound exam provides a diagnosis and baseline values for the injured structure(s). Results should include a “map” of the injury, i.e. point of origin to point of termination of damaged fibers, cross-sectional area of the injured structure and of any “core” or circumscribed lesions and assessment of initial fiber pattern.

Initial exercise consists of a period of hand walking; essentially rest. Initial treatment is aimed at modulating inflammation so that optimum healing can occur. This can be achieved through cold therapy, topical and systemic anti-inflammatory agents, and disease modifying agents such as glucosamine and polysulfated glycosaminoglycan. Supportive shoeing should be applied as needed. Repeat clinical and ultrasonographic examinations are scheduled at 6-8-week intervals except for muscle injuries and extensor tendon injuries, which are examined every 4 weeks due to anticipated faster healing.

The image shows an enlarged P2-3 collateral ligament with two tears and a poor fiber pattern.

12 The Practitioner

The second clinical and ultrasound examination should reveal a resolution of inflammation by palpation and gait and improved ultrasound parameters of decreased (ideally normal)

Issue 4 • 2015

The image shows normal healing progress of the P2-3 collateral ligament.

cross-sectional area, improving echogenicity of any lesion or overall echogenicity and stable or slightly improved fiber pattern.

These results correlate with the initial repair of the damaged tissue with Type III collagen.

A positive exam result allows the horse to begin walk with a rider up, which is increased work, not only due to rider/tack weight but to walking at horse rather than human pace and also to being asked to travel at different levels of collection and to do bending exercises. These exercises are meant to stimulate healing of the injured structure and also to keep the entire horse supple, meanwhile strengthening back muscles in preparation for trot work. A negative exam result should prompt a frank discussion of the horse’s treatment, exercise and behavior. Shoeing should be reassessed and corrected if necessary.

The image below shows normal healing progress.

on palpation and sound at the walk and trot in hand and on the lunge line or with a rider up. The ultrasound examination should show normal cross-sectional area, normal echogenicity and a notable improvement in fiber pattern to fair-to good, although likely not yet normal. These results correlate with the presence of predominantly (nearly completely) Type I collagen fibers that are in the process of alignment along stress planes.

A positive examination result prompts the initiation of canter work. After a short period of canter as controlled exercise, the horse may also have free exercise for the first time in the rehabilitation period, as tissues may be judged to have sufficient strength and flexibility to withstand uncontrolled movement.

The third clinical exam should reveal a horse that is painfree on palpation and sound at the walk and brief trot in hand.

The ultrasound examination should show stable or decreased cross-sectional area, normoechoic or slightly hypoechoic areas of damaged tissue relative to normal tissue and a slightly improved fiber pattern. These results correlate with the progressive replacement of initial Type III collagen with normal Type I collagen fibers as repair progresses.

A positive exam result prompts the initiation of trot work.

Variation in pace and collection and bending exercises are continued to improve strength and flexibility. Most horses benefit from a whole horse examination after 2-4 weeks of trot work to detect and treat any lingering source of lameness elsewhere, which likely will be due to joint disease. In fact, these changes may have led to overload and initial injury of the structure(s) currently being treated.

The image below shows a healed P2-3 collateral ligament.

The fourth clinical exam should reveal a horse that is pain-free

www.faep.net

The Practitioner 13

Any supportive shoeing can generally be removed at this time unless foot conformation demands its continued use.

The fifth clinical exam should reveal a horse that is pain-free on palpation and sound at the walk and trot in hand and on the lunge line or with a rider up, with good musculature and evidence of fitness. Foot shape and shoeing should be appropriate for the horse’s conformation and sport. The ultrasound exam should show a structure that is normal in cross-sectional area, echogenicity and fiber pattern. These results correlate with the presence of Type I collagen fibers that are aligned along stress planes and cross-linked for prevention of fiber shearing, providing normal strength range for the structure. A positive exam result allows the initiation of final training for competition.

Careful attention to the clinical and ultrasonographic results for each healing stage with a treatment and controlled exercise plan for the whole horse based upon that information provides a good prognosis for horses with soft tissue injury to return to their sport without re-injury.

Carol Gillis, DVM, PhD, DACVSMR

Selected References Gillis CL, “Soft Tissue injuries”, In Equine Sports Medicine and Surgery 2nd Ed, Hinchcliff KW, Kaneps AJ, eds 2014 Saunders Elsevier, pp 399-419.

Gillis CL, “Rehabilitation of Tendon and Ligament Injuries”. 1997  Vol. 43  AAEP PROCEEDINGS Thomopoulos S, Parks WC, Rifkin DB. “Mechanisms of Tendon Injury and Repair.” J Orthop Res 33:832–839, 2015.

Vos RJ, Weir A, Tol JL. “No effects of PRP on ultrasonographic tendon structure and neovascularisation in chronic midportion Achilles tendinopathy.” Br J Sports Med 2011;45:387–392 Gillis CL, ”Shoulder Injuries” In Current Therapy in Equine Practice 7th Ed, Sprayberry KA, Robinson NE eds 2014 Elsevier, pp 805-809.

Gillis CL, “Diagnosis and Treatment of Equine Supraspinous and Interspinous Ligament Injuries. “ Proc. 8th International Symposium on Veterinary Rehabilitation/ Physical Therapy and Sports Medicine.

Corvallis, OR August 2014:128.

Dakin SG, Jespers K, Warner S. “The relationship between in vivo limb and in vitro tendon mechanics after injury: A potential novel clinical tool for monitoring tendon repair.”.Equine vet. J. (2011) 43 (4) 418-423.

Gillis CL, Meagher DM, Balesdent A. “Suspensory ligament desmitis and associated fractures. Proc. 39Th Ann Conv AAEP Dec 1994:187.

Dr. Carol Gillis is a graduate of UC Davis School of Veterinary Medicine and was one of the first equine veterinarians to perform ultrasound examinations on the musculoskeletal system of horses.

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She undertook an equine surgery residency at UC Davis and obtained a PhD in equine tendon and ligament pathophysiology and concurrently established the equine ultrasound service at UC Davis.

Dr. Gillis has developed many exam protocols for previously unexamined sites on the horse. She has authored numerous scientific publications in journals such as the American Journal of Veterinary Research and the Journal of the American Veterinary Medical Association on the subject of equine soft tissue injury diagnosis and treatment, and recently was an author of “Equine Sports Medicine and Surgery 2014," the definitive reference book on the topic.

Clinically, Dr. Gillis has performed more than 26,000 ultrasound examinations of the horse and guided treatment of problems identified, and currently has a consulting practice in Ultrasound and Sports Medicine in South Carolina.

She is also a charter member of the American College of Veterinary Sports Medicine and Rehabilitation.

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14 The Practitioner

Issue 4 • 2015

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Ultrasound examination of foot can contribute greatly to diagnosis of lameness. The distal ligamentous and tendinous structures of the pastern, podotrochlear apparatus, and distal interphalangeal joint may be imaged.

Palmar pastern, dorsal pastern and solar or “transcunean” views will be demonstrated.

STATION 3: FETLOCK/DISTAL METACARPUS

TARALYN MCCARREL, DVM, DACVS-LA Ultrasound has long been recognized for its utility for evaluation of soft tissue structures of the distal limb. However, more recently the value of ultrasound for evaluation of the joint surface and boney margins has been recognized. This lab will focus on approach to ultrasound of the fetlock joint itself, as well as the digital flexor tendon sheath, and the associated tendon and ligament structures. The normal appearance will be emphasized with examples of lesions presented in the lab notes.

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CAROL CLARK, DVM, DACVIM The lab will provide participants with a working knowledge of thoracic ultrasound use in horses. An initial presentation of normal and abnormal cases will be followed by hands on ultrasound exams. Practical evaluation and integration into clinical practice will be stressed.

AMANDA M. HOUSE, DVM, DACVIM A review of the FLASH abdominal ultrasound technique for evaluation of colic, in addition to discussion about a complete abdominal exam of the kidneys, spleen, liver, and GI tract will be performed in this section. Focus will be on the attendee performing the exams.

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STEVEN P. BRINSKO DVM, MS, PhD, DACT

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AMANDA M. HOUSE DVM, DACVIM

TARALYN MCCARREL DVM, DACVS-LA

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RICHARD D. MITCHELL DVM, MRCVS, DACVSMR

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The FAEP strongly recommends an advanced registration for our 53rd Annual Ocala Equine Conference. Registration is required for admission to all aspects of the meeting. Your registration includes all CE sessions (excluding Friday’s Ultrasound Wet Lab), access to the Conference Exhibit Hall, Saturday and Sunday lunch, conference proceedings and all breaks held in the Exhibit Hall. Registrations must be submitted to the FAEP office by Friday, January 10, 2016. There will be a late registration fee of $50.00 charged to all those postmarked or received by fax, phone, email or online after this date. Registrations made at the door will be charged the late fee of $50.00.

Persons with disabilities who plan to attend the FAEP Conference and need auxiliary aids or services are requested to make arrangements by contacting the FAEP office at (800) 992-3862 no later than January 10, 2016.

Each 50-minute lecture qualifies as one continuing education credit. Attendees can earn up to 24 credit hours, including the 7-hour wet lab. For your convenience in recording your CE hours, one certificate will be included in your registration packet. A separate certificate is given at the wet lab on Friday. It is your responsibility to document the sessions you attend and the number of hours you receive.

Confirmation You will receive a confirmation of your registration from the FAEP upon completion of your order. Please contact us if any information in the confirmation is incorrect so we may correct it in a timely manner.

Cancellation Policy

Name Badges Name badges are required and will be checked when attending all conference functions. You must be a registered conference attendee to receive a badge.

Attendees traveling with a spouse/guest who does not want to attend the CE sessions, may purchase a spouse/guest badge for $95.00. This badge allows the spouse/guest to attend all conference food and social events including lunch and dinner.

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REGISTRATION HOURS Saturday, Jan. 23 Sunday, Jan. 24

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If received by January 10, 2016, your registration fee will be refunded, minus a $50 administrative charge. Cancellations not received in writing and acknowledged by the FAEP by the above date will not be eligible for a refund. No-shows will not be refunded.

Proceedings One complimentary 53rd Annual Ocala Equine Conference proceedings CD will be provided to each registered attendee.

Additional copies may be purchased at the FAEP registration desk.

Conference Exhibit Hall The FAEP’s 53 rd Annual Ocala Equine Conference will provide exhibitors and attendees with incredible value Saturday and Sunday during our two-day conference weekend. This is a great opportunity for you to take advantage of face-to-face contact with equine industry representatives.

CONFERENCE EXHIBIT HALL HOURS Saturday, Jan. 23 Sunday, Jan. 24

9:40 a.m. – 6:55 p.m.

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A block of rooms has been reserved for the Ocala Equine Conference at the Hilton Ocala located at 3600 SW 36th Ave., Ocala, FL 34474.

The special room rate is $114.00, Single and Double and $124.00, Triple and Quad; plus applicable taxes. Special extended stay reservations have been set up for the group rate from January 19-27 subject to availability. To reserve your room today, call the Group Reservations Department at Hilton Ocala at (877) 602-4023. When making

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Air Transportation There are two nearby airport destinations for the FAEP’s 53rd Annual Ocala Equine Conference. One is the Gainesville Regional Airport (GNV) in Gainesville, Florida, located only 43 miles from the Hilton Ocala. The other is Orlando International Airport (MCO)

in Orlando, Florida, located 85 miles from the Hilton Ocala.

Airport/Ocala Shuttle Service A special FAEP group rate of $45.00 one-way has been arranged with Shuttleliner of Ocala for those flying into the Orlando International Airport traveling to the Ocala Equine Conference. RESERVATIONS ARE REQUIRED FOR GUARANTEED SERVICE. Please call (352) 237-9900 or visit www. shuttleliner.com to book your discounted conference transportation.

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Richard D. Mitchell, DVM, MRCVS, DACVSMR

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Richard D. Mitchell, DVM, MRCVS, DACVSMR

10:10 a.m. 11:00 a.m.

Timely Topics in Reproduction Steve Brinsko, DVM, MS, PhD, DACT

Reproduction Cases - Common But Not Obvious Conditions Steve Brinsko, DVM, MS, PhD, DACT

11:00 a.m. 11:50 a.m.

Case Series of Lameness Evaluations in Performance Horses Aric Adams, DVM, DACVS 11:50 a.m. - 1:35 p.m. Complimentary Lunch

How to Manage the Challenging Colic When Referral Is Not an Option

Taralyn McCarrell, DVM, DACVS-LA

Facts and Myths About Medical Treatment of Colic

Treatment of the Big 3 Equine Skin Tumors Part 1 Kenneth Sullins, DVM, MS, DACVSMR

Treatment of the Big 3 Equine Skin Tumors Part 2

The Icteric Equine: What Next?

Amanda House, DVM, DACVIM

Creeping Indigo and Other Problematic Pasture Plants Amanda House, DVM, DACVIM

1:20 p.m. 2:10 p.m.

2:10 p.m. 3:00 p.m.

Kenneth Sullins, DVM, MS, DACVSMR

6:30 p.m. -8:40 p.m. Complimentary Dinner for All Attendees Served During the Laws and Rules Session. Service Begins Promptly at 6:30 p.m.

7:50 p.m. 8:40 p.m.

12:10 p.m. - 1:10 p.m. - Complimentary Lunch

Kenneth Sullins, DVM, MS, DACVSMR

5:30 p.m. - 6:30 p.m. Cocktail Reception in the Exhibit Hall

7:00 p.m. 7:50 p.m.

11:20 a.m. 12:10 p.m.

Diagnosis and Treatment of Upper Airway Disease

3:20p.m. - 3:50 p.m. Break - Visit the Exhibit Hall 3:50 p.m. 4:40 p.m.

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

Indications for Bisphosphonates – What Is the Evidence?

David Freeman, MVB, PhD, DACVS

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

8:50 a.m. - 9:40 a.m.

9:40 a.m. - 10:30 a.m. - Break - Visit the Exhibit Hall

David Freeman, MVB, PhD, DACVS 1:35 p.m. 2:25 p.m.

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

Florida Laws and Rules Governing the Practice of Veterinary Medicine Part 1 Bryan Reynolds, BSBA, JD

Florida Laws and Rules Governing the Practice of Veterinary Medicine Part 2

3:00 p.m. - Cover-All Bingo Raffle & Drawing - Must Be Present to Win!

SEE THE PROGRAM DETAILS, INCLUDING SPEAKER BIOGRAPHIES AND LECTURE ABSTRACTS ON THE CONFERENCE WEBSITE:

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Bryan Reynolds, BSBA, JD

A Proud Tradition of Quality Equine Practitioner Education JANUARY 22-24, 2016 • OCALA, FLORIDA

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4

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This program 532-19082 is approved by the AAVSB RACE to offer a total of 24.00 CE Credits (24.00 max) being available to any one veterinarian: and/or 0.00 Veterinary Technician CE Credits (0.00 max). This RACE approval is for the subject matter category(ies) of: Category One: Scientific, using the delivery method(s) 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.

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Musculoskeletal Abnormalities in Foals Aric Adams, DVM, DACVS

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Foot Lameness in the Sport Horse - A Clinical Approach to Diagnosis

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The Practitioner 23

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24 The Practitioner

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Issue 4 • 2015

STOP LOVING their horse to DEATH

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“Food is not love, especially when a horse is prone to EMS. Metabarol is quite useful in managing these horses.”

— Dr. Peter Morresey, Rood & Riddle Equine Hospital, Lexington, KY

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Order copies of “Signs of EMS” for your clients at Equithrive.com or call 866-721-1412 Adams, A. A. (2013). Abstract Title. Journal of Equine Veterinary Science. Abstracts. 33 (321-399). pg. 343.

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The Practitioner 25

UPDATE ON INFECTIOUS GASTROINTESTINAL ILLNESS

IN HORSES

NATHAN M. SLOVIS | DVM, DACVIM CORONAVIRUS Equine Coronavirus (ECoV) is considered an emerging virus in North America that is responsible for fever, depression, anorexia and occasional colic and diarrhea in adult horses. Interestingly, in a study on infectious foal diarrhea in Central Kentucky, the author noted that coronavirus does not appear to be a primary pathogen.

Sporadic cases and outbreaks have been documented with increased frequency since 2010 in the United States and Japan.

Coronaviruses are members of the coronaviridae family all of which are single stranded, positive-sense, non-segmented, enveloped RNA viruses responsible for enteric, respiratory, hepatic and neurologic disease in a variety of mammalian and avian species. A closely-related coronavirus is Bovine Coornavirus (BCoV) known as winter dysentery in cattle. The epidemiologic information at this time is sparse and most of the information is based on BCoV or on published preliminary observations. Since 2010, the number of positive qPCR samples submitted to Cornell, IDEXX and UC Davis has been on a steady rise. These laboratories have noted the majority of the cases are in adult horses, from a wide geographic range across the USA with the number of cases being higher during the colder months of the year (October – April). The majority of the cases/outbreaks appear to be predominately in riding, racing and show horses. There have only been a few cases (published and unpublished) on breeding farms.

It has been speculated that on these breeding farms there are asymptomatic horses spreading the virus conferring protection of clinical disease. Preliminary studies have shown that the fecooral route of transmission has been successful in Japan utilizing three 9 to 10-month Japanese Draft horses. Unlike BCoV that is considered a pneumoenteric virus, ECoV has only been detected by qPCR in 17/2,437 nasal secretions from horses showing signs of fever and/or upper respiratory infections. A French study had similar preliminary findings.

Morbidity can range from 10-83% with mortality rates considered low BUT some published outbreaks were as high as 27% in American Miniature horses. Mortality has been associated with endotoxemia, septicemia and hyperammonemia. The incubation period noted after natural and experimental infection is short with clinical signs developing 48-72 hours after exposure which can last a few days to a week. The illness is usually mild and tends to resolve with minimal supportive care. Shedding of the virus in feces ranged from 10 to 12 days in experimentally unaffected animals while, in one outbreak, fecal shedding was reported to last as long as 25 days. We currently do not know how long ECoV can persist in the environment but it can be speculated from severe acute respiratory syndrome associated virus that it is a short period in warm weather (2-3 days) and longer in colder (4°C) weather (14-17 days).

Clinical presentation collected by 16 outbreaks showed that 26 The Practitioner

30% of the horses showed clinical signs. The primary clinical signs were anorexia (98%), lethargy (89%) and pyrexia (101.5 to 105.8 F: 84%). Colic was observed in 18% of the cases while change in fecal consistency was noted in 25%. A few of the horses showed signs of encephalopathy which has been speculated to be associated with hyperammonemia.

Antemortem diagnosis based primarily on hematological changes is not recommended. Observations noted on the complete blood cell count (CBC) are leucopenia characterized with a neutropenia and/or lymphopenia which tends to resolve in 5 to 7 days. Dr. Nicola Pusterla noted that in 73 diseased horses the CBC was unremarkable in only 11%. Serum biochemistries performed on diseased horses may be unremarkable. Horses that are exhibiting neurological signs should have a blood ammonia level performed as hyperammonemia has been reported in a ECoV case that developed encephalopathy and subsequently died.

For an accurate diagnosis, the presence of ECoV in feces should be determined by qPCR. Interestingly, the viral load measured by qPCR in foals (up to 6 months of age) appears to be lower compared to horses older than 12 months of age, although the difference was not significant.

Horses that died secondary to ECoV had severe diffuse necrotizing enteritis with marked villus attenuation, epithelial necrosis in the tips of the villi, neutrophilic and fibrin extravasation into the small intestinal lumen, as well as crypt necrosis, microthrombi and hemorrhage.

Treatment is usually not necessary for the majority of the cases and horses tend to recover spontaneously in a few days. If pyrexia and depression are noted, then the use of nonsteroidal anti-inflammatory drugs may be warranted for 2 to 3 days.

Horses that suffer from colic, dehydration and diarrhea may require the addition of oral or IV fluid and electrolyte support.

The issue of antimicrobials is under debate with this illness.

Unless the animal is severely neutropenic, broad spectrum antimicrobials are usually not recommended. If the horse has hyperammonemia or signs consistent with hyperammonemia, then the use of lactulose (0.1 to 0.2 ml/kg PO or per rectum) or fecal transfaunation will be recommended.

The epidemiology and pathogenesis of ECoV infection in horses is currently being investigated.

SALMONELLA Salmonella are gram negative, facultative, anaerobic bacteria, which usually can access the intestinal tract via the fecal-oral route. Salmonella commonly infects foals between 12 hours and 4 months of age. Young animals are more susceptible to Salmonella infections maybe because of a less sophisticated or less well-established microflora within the gastrointestinal tract.

Issue 4 • 2015

The most common source of exposure and infection in the foal is another horse. Often, the mare herself is an asymptomatic carrier. Mares have been shown to shed Salmonella at or shortly after parturition despite having as many as 19 negative cultures before foaling. Observations of foalings revealed that all mares defecate during stage 2 labor and that contamination of fetal membranes and the perineum/udder of the mare was possible if Salmonella was in the feces. During udder seeking, foals will have extensive contact with the perineum and therefore may be at risk of Salmonella ingestion.

Most immune-competent adults can be exposed to Salmonella and not succumb to clinical disease. It is not uncommon for a mare with a sick Salmonellosis foal to have no clinical signs of illness and yet be shedding Salmonella in the feces. The exact number of organisms needed to cause clinical disease in an adult animal is unknown because of the multitude of intrinsic and extrinsic factors that are responsible for the overall health and immunity of the animal.

Once Salmonella has overcome the host defense mechanisms (gastric acidity, intestinal flora, peristalsis, intestinal mucus and lactoferrin), the bacteria migrate through the enterocytes and access the lamina propria where they stimulate an inflammatory response. Both phagocytized and free Salmonella organisms travel via the lymphatics to regional lymph nodes where they persist in stimulating an inflammatory response. Salmonella can also reach circulation from efferent lymphatics. The neonate predisposition toward bacteremia and septicemia may be because of factors such as delayed gut closure at birth, immature cellular immune response and decreased complement activity. Salmonella enterotoxins, cytotoxins and generalized inflammation within the bowel induces secretions of fluid from the intestinal epithelium.

Salmonella enterica can be an important factor in healthcareassociated epidemics and zoonotic disease in veterinary hospitals.

Outbreaks associated with multi-drug resistant (MDR) Salmonella among equine patients can result in high case fatality rates and substantial financial cost. As such, routine surveillance to detect this organism among equine patients is commonly performed on targeted high-risk subgroups (e.g., gastrointestinal disease) and upon recognition of epidemic disease, and less commonly performed continuously on all equine inpatients. While there are many reports suggesting patients are more likely to shed Salmonella in their feces at times of stress or systemic compromise, there are no reports that indicate what factors may be important to horses shedding MDR-strains; something that can result in infections that are much more difficult to treat in horses and humans alike. Drs. Paul Morley and Brandy Burgess and myself recently investigated some of the factors associated with the shedding of multidrug resistant Salmonella. The enclosed abstract gives a summary of our findings: Background: Salmonella enterica can be an important factor in healthcare-associated epidemics and zoonotic disease in veterinary hospitals – with outbreaks of multi-drug resistant (MDR) Salmonella among equine patients resulting in high case fatality rates and substantial financial cost.

Hypothesis/Objectives: The objectives of this study were, 1) to determine factors associated with fecal shedding of MDRSalmonella; and 2) to determine what effect Salmonella shedding www.faep.net

may have on health outcomes of previously hospitalized horses and their stablemates.

Materials and methods: Patients eligible for this casecontrol study included those having fecal cultures for S. enterica as part of a surveillance program from January 2011 through December 2012. Data regarding exposures of interest were collected retrospectively from medical records. Information on long-term outcomes was obtained by administering a phone survey to horse owners. Multivariable regression techniques were used to determine factors associated with shedding MDRSalmonella and subsequent health outcomes.

Results: Equine patients enrolled in this study included 94 culture-positive (29 MDR and 65 susceptible) and 279 culturenegative (on at least 3 fecal samples) horses from 199 different farms. Horses experiencing diarrhea during hospitalization were more likely to shed Salmonella (OR 1.88; 95% CI 1.02, 3.45) compared to horses without diarrhea; and horses having decreased feed intake during hospitalization were more likely to shed MDR-strains (OR 5.95; 95% CI 1.21, 29.20) compared to horses with normal feed intake. In general, shedding Salmonella did not increase the long-term risk for non-survival, colic or abnormal feces after discharge of hospitalized horses nor did it increase the risk for hospitalization or abnormal feces in stablemates.

Conclusions and clinical relevance: Horses experiencing diarrhea during hospitalization were less likely to shed MDR-strains; while horses having decreased feed intake during hospitalization were more likely to shed MDRstrains. Interestingly, receiving antimicrobial therapy during hospitalization was not associated with shedding Salmonella, nor was it associated with shedding of MDR-strains. In general, shedding Salmonella did not decrease long-term survival or increase the occurrence of colic or abnormal feces in the hospitalized horse nor increase the risk for hospitalization or abnormal feces in stablemates. Despite these findings, in order to mitigate the exposure risk to other horses and personnel, it is still recommended to manage horses shedding Salmonella separately from other resident horses and to employ rigorous personal and environmental hygiene.

Clinical signs of Salmonellosis are variable and can range from mild enteritis to severe septicemic shock. The diarrhea may be scant or profuse, watery or hemorrhagic. Fevers, if present, are usually > 103° F. Other clinical signs that can be noted are anorexia, tachycardia, tachypnea, and abdominal pain. These signs often related to bacteremia/endotoxemia rather than electrolyte derangements and dehydration. Other signs of bacteremia include the following (Especially in foals): • Green-tinted iris (presumed septicemia-induced uveitis), injected sclera and mucous membranes • Lameness associated with septic arthritis or physitis • Abnormal lung sounds associated with pneumonia of hematogenous origin • Lethargy, stupor, or seizures associated with meningitis (or from severe electrolyte derangements, e.g., hyponatremia) Laboratory findings may be characteristic of a leukopenia as a result of neutropenia. The neutrophils frequently demonstrate The Practitioner 27

toxic changes and may be immature (Bands). Fibrinogen concentration may be elevated. Low platelet count may indicate the presence of disseminated intravascular coagulation.

Hyponatremia, hypochloremia, acidosis, and azotemia are the most common findings in regards to lab work.

• Acidosis may mask life-threatening hypokalemia.

• Low serum potassium may result from a combination of decreased intake, increased loss in diarrheic feces, polyuric acute renal failure.

Diagnosis of Salmonella is conducted by testing fecal samples using bacteriologic procedures in the laboratory. The samples are initially plated to a hektoen agar and inoculated in a selenite broth. However, it can take up to 3 to 5 days to obtain the culture results. Several laboratories have developed PCR tests for detection of Salmonella spp. in fecal and environmental samples but there is evidence of an increased frequency of Salmonella-PCR positive results in horses without clinical signs of salmonellosis that test negative to Salmonella spp. by culture on multiple fecal samples, perhaps due to the use of primers targeting a nonspecific Salmonella spp. gene fragment that may cross-react with other enteric or non-enteric organisms. There is a novel enhanced detection test (Reveal ® 2.0 Salmonella test system)a for the detection of Salmonella spp. in fecal and environmental samples. This test appears to help shorten the time period to obtain laboratory results from our culture samples.

We have had foals present with fevers of unknown origin with no signs of diarrhea that have had positive blood and fecal cultures for Salmonella. Intermittent shedding of Salmonella is common and therefore a minimum of three to five consecutive 1 gram fecal cultures taken 24 hours apart are recommended.

Treatment for Salmonella is non-specific and is aimed at maintaining hydration and electrolyte balance. Antibiotic therapy, even though it does not alter the clinical course of diarrhea or shedding of the organisms, should be initiated in foals to help prevent bacteremia. In adults, the use of antimicrobials is usually not warranted unless the total neutrophil count is < 1000 / ml. Fluid therapy usually consists of polyionic fluids such as lactated Ringers, Normosol-R and Plasma-Lyte because sodium chloride is an acidifying solution. Use hypertonic saline if polyionic fluids do not alleviate hypotension associated with severe disease. It can be administered in 1- to 2-ml/kg boluses at 30- to 60-minute intervals for severe hyponatremia (No more than 2L a day given to an adult horse). Goal for initial correction of severe hyponatremia should be a sodium concentration of 125 to 130 mEq/L, no higher. Potassium chloride should be added to fluids (20 mEq/L) if the animal can urinate properly and serum potassium is ≤ 3.0 mEq/L. Remember Potassium administration should not exceed 0.5 mEq/kg/h. If acidosis remains in the face of adequate fluid therapy, add sodium bicarbonate to fluids. General rule in bicarbonate administration is to give as a bolus half of the calculated deficit and then to correct remaining deficit over 12 to 24 hours. If sodium bicarbonate is used, more potassium supplementation is necessary.

Polymyxin B (6,000 IU/kg IV TID) diluted in 1 L of fluids, flunixin meglumine (0.25mg/kg TID IV) and pentoxifylline (7.5mg/kg PO BID) all have been shown to reduce the effects of endotoxemia. Bismuth subsalicylate (1-3ml/kg PO Q4-8 Hrs)

28 The Practitioner

is also commonly used as a gastroprotectants secondary to its endotoxic and antiprostaglandin properties. J-5 plasma may also be given to aid in decreasing the systemic endotoxin level. The author usually adds 4,000 IU of heparin to each liter of plasma administered in order to activate AT3. Theoretically, you do not want to add more “clotting factors” into an animal already at risk (or has developed) of disseminated intravascular coagulation Prevention of Salmonella consists of proper hygiene. Before the foal is able to nurse, the udder and perineal regions of the mare are to be thoroughly washed with dilute chlorohexidine or ivory soap and water. During an outbreak situation, foals should also be intubated with 6-8 oz of colostrum prior to contact with the mare. A conditionally approved inactivated bacterin (Salmonella typhimurium and Newport) vaccine that is approved in the State of Kentucky has been developed by Hagyard Equine Medical Institute and Dr. John Timmoney at the Gluck Research Center in Lexington KY. We have currently been using this vaccine on endemic farms since 2007. Farms that have incorporated the vaccine into their herd health have not had any cases of clinical salmonellosis.

ENTEROCOCCUS DURANS (GROUP D STREPTOCOCCUS) Enterococcus durans is a gram positive coccus in the alimentary tract that has been implicated as a cause of enteritis in foals, piglets, calves and puppies. The author has documented Enterococcus durans as a cause of diarrhea in 5 of 7 foals that had developed diarrhea during the first 10 days of life. In one study conducted in Australia, E durans (Isolated from a foal that had severe diarrhea) was experimentally infected in 7 foals (Via stomach tube). All 7 foals developed profuse watery diarrhea within 24h of inoculation with varying degrees of depression, anorexia, abdominal tenderness and dehydration. The pathogenesis of diarrhea and enteric disease remains unknown.

Diarrhea induces by E. durans is not associated with enterotoxin production or substantial mucosal injury. However, decreased activity of brush border digestive enzymes such as lactase and alkaline phosphatase suggest that there is a direct mechanical interference with digestion and absorption at the brush border.

Treatment for E. durans has not been adequately investigated, but subjectively, the β-lactams appear to help decrease the duration of the diarrhea (Ampicillin or Penicillin).

The ideal treatment is to improve husbandry on the farm.

CLOSTRIDIUM DIFFICILE Clostridium difficile is the agent that causes pseudomembranous colitis associated with antibiotics in humans. It is now being identified in recent years as a significant nosocomial pathogen for equine as well as human patients. First described in 1935 by Hall and O’Toole, this gram-positive anaerobic bacillus was named “the difficult clostridium” because it resisted early attempts at isolation and grew very slowly. The organisms were found in stool specimens from healthy human neonates (up to 50%) which led to its classification as a commensal and was subsequently ignored as a potential pathogen. In the 1960’s and 1970’s, antibioticassociated pseudomembranous colitis became a major clinical problem, which was attributed to mucosal ischemia or viral

Issue 4 • 2015

infection. In 1977, Larson et al. reported that stool specimens commonness of fever, depression and decreased appetite. This from affected patients contained a toxin that produced cytopathic is consistent with recognition in humans that CDI is not always changes in tissue culture cells. C. difficile was identified as accompanied by overt diarrhea, as discussed above. The high the source of the cytotoxin. It is now clear that C. difficile is rate of CDI in 2014 at HEMI neonatal unit resulted in a suspicion responsible for virtually all cases of human pseudomembranous of hospital-associated infection, but preliminary investigation colitis and 20% of the cases of antibiotic-induced colitis. has revealed 7 different ribotypes from nine clinically-affected Pathogenesis of antibiotic-associated diarrhea/colitis begins foals that were tested, something that is consistent with multiple with a disruption of colonization resistance (disruption of the community sources rather than a hospital focus. Farms in Central normal colonic flora) of C. difficile. Colonization occurs by the Kentucky have also experienced outbreaks (>10% incidence) of C. oral-fecal route. C. difficile forms heat-resistant spores that can difficile neonatal enterocolitis within their foaling barns. persist in the environment for years. These spores can survive Diagnosis of C. difficile infection depends on the demonstration the acid environment of the stomach and convert to vegetative of C. difficile toxins in the stool. The cytotoxin assay that uses forms in the colon. Environment contamination by C. difficile tissue cell culture had been the gold standard for diagnosis. It is particularly common in human hospitals that have reported is the most sensitive test (sensitivity 94-100% and specificity isolation rates of 11.7% to 29%. Health care personnel may carry 90%), detecting as little as 10pg of toxin B (This test is not used bacteria on their hands, under rings, or on stethoscopes, but fecal commonly because it is time consuming and expensive). A stool carriage by staff is rare. High rates of infection can be isolated culture of C. difficile is a less efficient method of establishing from stalls (hospital rooms), scales, thermometers and surgical a laboratory diagnosis, since some strains of C. difficile are preparation room. Clostridium difficile has also been implicated nontoxigenic (approximately 25%). Two enzyme immunoassays in an outbreak of colitis among horses at veterinary teaching have been introduced that 1) detect toxin A/toxin B (Clostridium hospitals. difficile TOX A/B test, Techlab®, Blacksburg VA USA ) or 2) detect When established in the colon, pathogenic strains of C. difficile antigen of Clostridium difficile and toxin A (TRIAGE® Micro; produce toxins that cause diarrhea and colitis. Strains that do BIOSITE, San Diego CA 1-888-BIOSITE). These tests have a good not produce toxins are not pathogenic. Two large exotoxins, sensitivity (69-87%) and specificity (99 to 100%). Clostridium toxin A (enterotoxin) and toxin B (cytotoxin) are produced by C. difficile TOX A/B test, Techlab® has been validated for use in feces difficile. Toxins A and B appear to act synergistically which cause of horses. The C. difficile toxins have been found to be stable in fluid secretion, mucosal damage, and intestinal inflammation. fecal samples which were refrigerated at 4˚C for 60 days. DO Toxin A is also a chemoattractant for human neutrophils in vitro. NOT USE STYROFOAM CUPS to submit a fecal sample because Recently, a third toxin, an actin-specific ADP-ribosyltransferase they can bind the toxins. PCR techniques can also be used to (binary toxin), has been identified in certain strains of C. difficile differentiate toxigenic strains from nontoxigenic strains in isolated from human patients. The role and the pathogenesis of feces or among bacterial isolates. However, PCR methods can binary toxin is unclear, but it may act synergistically with toxins detect toxigenic C. difficile organisms that are present in low A and B. The toxic effects appear to follow binding of toxins to and clinically irrelevant levels. A related issue is the accuracy membrane receptors. After binding to its intestinal receptor, of testing in foals. The author has noted an increased number Toxin A enters the cell and alters the actin cytoskeleton, leading of C. difficile enterocolitis cases that have tested positive for the to cell rounding. Toxin B causes the identical rounding.

C. difficile glutamate dehydrogenase antigen (a highly sensitive Clinical presentation of C. difficile in foals range from anorexia test that detects the organism) and negative for Toxins A and and pyrexia to fulminate colitis with ileus. The foals with severe B utilizing a commercially available Rapid Membrane Enzyme colitis become anorexic and dehydrated. In addition to the Immunoassay. Results from 2013 and 2014 at HEMI revealed diarrhea, foals become tachypneic, which may be secondary 11.6% (34/291) and 15.6% (71/454), respectively, samples that to discomfort associated with the enteritis, pyrexia, metabolic were antigen positive but toxin negative. This could be caused by acidosis or the anxiety of being in the hospital. Hypoproteinemia a few different reasons, each with different clinical implications. is also a feature of C. difficile secondary to the effects of toxins It could indicate the presence of C. difficile in the absence of A and B leading to extravasation of plasma proteins. Metabolic relevant toxin production. It could also result from sub-optimal acidosis is also consistent with clostridial enterocolitis and sensitivity of the assay. Another possible cause is presence of hypovolemia or gastrointestinal tract loss of bicarbonate. high levels of toxin in the proximal intestinal tract with disease Hyponatremia may also be attributable to the gastrointestinal at that location (e.g. accounting for fever and colic) but little toxin tract losses, as well as to an excess of free water associated with in feces. It could also result from the presence of strains that are water consumption by these foals. nontoxigenic (and therefore clinically irrelevant). Understanding In Kentucky, there has been recognition of an increased which of these occur is critical because of the marked differences incidence of C. difficile infection (CDI) in the equine community in clinical relevance of test results in those situations. Pilot over the past several years, with increased disease on farms study of discrepant results has been performed. In 10 antigen and an increase in the number of foals arriving to a hospital positive, toxin negative cases, enrichment culture for C. difficile setting without enteric disease that later develop clinical disease was performed, and C. difficile that possessed genes encoding (e.g. pyrexia, leucopenia and colic) usually after 48 hours of toxins A and B genes were isolated in 9 (90%). A separate subset hospitalization. CDI is often subtle initially and not consistent of 30 antigen-positive/toxin-negative samples were submitted for with classical CDI, with a lower incidence of overt diarrhea but commercial PCR for Toxin A and B genes, with 74% (22/30) being

www.faep.net

The Practitioner 29

positive. Clearly, much remains to be understood about diagnosis of CDI and the relative performance of different tests. Accurate detection of potentially pathogenic Clostridium difficile shedders and individuals with CDI is imperative for adequate disease control and biosecurity measures. Prompt and accurate diagnosis of CDI is needed for prompt treatment and understanding of the epidemiology and pathophysiology of equine CDI. Hence, further evaluation of the efficacy of these test methods is warranted.

Treatment in managing diarrhea and colitis with confirmed or suspected C. difficile infection is to discontinue antibiotic therapy, if possible. Specific therapy is aimed at eradicating C. difficile from the intestinal tract. Oral metronidazole is the drug of first choice. Adult horses are dosed at 15mg/kg PO TID-QID and foals less than 6 months of age are dosed at 10-15mg/kg BID-TID. The response rate for C. difficile in patients (humans) taking metronidazole is 98%. Patients who cannot tolerate oral medication because of an ileus may either receive the same dose per rectum or can be effectively treated with intravenous metronidazole at 10mg/kg TID to QID. Excretion of the drug into bile and exudation from the inflamed colon results in bactericidal levels in the feces.3 Metronidazole-resistant strains of C. difficile have been isolated, and there are even reports of metronidazole inducing colitis. For resistant strains of C. difficile, the use of vancomycin orally is indicated. The dose is 4mg/kg PO loading dose then 2mg/kg PO Q6h. When oral vancomycin is prescribed, I recommend the use of the parenteral solution because of the expense. It is recommended that treatment be continued for 5 days past the resolution date of the diarrhea. A substantial number of human patients, 10 to 20%, will have a relapse of C. difficile diarrhea. Various other approaches have been suggested for the management of relapses, including slow tapering of metronidazole therapy, bacteriotherapy with the use of nasogastric fecal transfaunation or fecal enemas, oral

2 day old TB Foal with Necrotizing Enteritis from Clostridium perfringens. The foal survived with the use of Oral and IV metronidazole and supportive care including TPN nutrition.

administration of nontoxigenic C. difficile, and treatment with the yeast Saccharomyces boulardii (may compete with C. difficile toxin 30 The Practitioner

A for binding sites on the intestinal epithelium). Saccharomyces boulardii anecdotally can be given to a foal at dose rate of 5 billion colony-forming units orally 2x a day. One novel treatment plan currently used as an adjunctive treatment for both viral and bacterial causes of diarrhea is the use of Bentonite clay. Bentonite is effective because it bonds to a variety of toxins and prevents the absorption of toxins by coating the intestinal wall. Not all bentonite clay is created equally and currently there is an ultrapurified bentonite clay that is available for use in our equine patients.a There is a hyperimmunized Clostridium difficile Toxin A and B plasma that is currently available.b The efficacy of the plasma in resolving diarrhea/toxic insult is currently anecdotal.

CLOSTRIDIUM PERFRINGENS Clostridium perfringens is a relatively ubiquitous bacterium that has been associated with enteric diseases in a number of diverse species. It is widespread in the soil and is found in the alimentary tract of nearly all warm-blooded species. Clostridium perfringens is a frequent postmortem invader in the alimentary tract’s tissues of bloating cadavers. Therefore, one must be cautious about drawing conclusions based on the presence of the organisms in the tissues of these animals. Types of C. perfringens are differentiated (5 major types A, B, C, D and E) based on the production of 4 major toxins; alpha, beta, epsilon and iota. In addition, isolates may have the gene known as C. perfringens enterotoxin (CPE). Toxins are produced by sporulating cells in an alkaline environment and is released upon LYSIS of these cells. It is resistant to proteolytic enzymes and will bind and insert on the brush border membrane causing pore formation in cells leading ultimately to cell lysis.

Enterotoxin can be produced by all types of Clostridium perfringens but is most commonly associated with type A. Many factors are involved in the production of enterotoxin by C. perfringens. In one study, the prevalence of CPE in feces of adult horses with diarrhea was 16% and detected in only 10% of the horses with colic regardless of whether or not they had diarrhea. Studies investigating CPE in feces of adult horses and foals with diarrhea have produced variable results. CPE has been detected in the feces of 7% to 33 % of adult horses with diarrhea and 28% of the foals with diarrhea. Furthermore, out of 843 C. perfringens type A isolates from dogs, people, and horses that were genotyped, only 62 (7.3%) contained the CPE gene.

An unassigned type of C. perfringens that produces alpha-toxin and a β2-toxin was described. It was isolated from piglets with necrotic enterocolitis and was also found in horses with enterocolitis. Since the alpha toxin, which is produced by all types of C. perfringens including non-pathogenic type A strains, is not considered a primary cause of digestive lesions, it was suggested that the β2-toxin, which is present in this type of C. perfringens, is responsible for the lesions. A recent study found that β2-toxin was detected in 52% of the horses with typical and atypical typhlocolitis. To a lesser extent, they were also isolated from horses with other intestinal disorders, in which they represented 37% of the isolates. No β2-toxinigenic C. perfringens has been found in healthy horses or in horses hospitalized for reasons other than intestinal problems. Recently, the group at Guelph has identified toxin genes encoding proteins related to the pore-forming Leukocidin/Hemolysin Superfamily; these Issue 4 • 2015

were designated netE, netF, and netG. netF is a new toxin that has been documented to cause hemorrhagic diarrhea in dogs and horses.

Pathogenesis of C. perfringens is based on their production of one or more of the 4 major exotoxins or enterotoxin. The factors that lead to the development of disease are not clear, but it is believed that there is an alteration of the normal flora that allows overgrowth of the clostridia. Proposed causes include diet changes, antibiotic therapy, stress, or concurrent infection. In adult ponies, enterocolitis has been produced when antibiotics (clindamycin or lincomycin) were given to the animals orally with a fecal cocktail containing clostridium. However, fecal cocktail alone did not cause disease. Other factors that may play a role in the development are host factors such as age, immunity, and the presence or absence of intestinal receptors for the perfringens toxins. Beta toxin-producing types of C. perfringens (Type C) appear to cause enterocolitis in neonatal animals only. The digestive enzyme trypsin is produced by older animals and can inactivate the toxin. Neonatal animals have a less developed digestive enzyme production, thus may be more susceptible to disease caused by this toxin. Most of the affected foals in one study had serum IgG concentrations of >800mg/dl, indicating adequate passive transfer. This finding helps support a theory that trypsin inhibitor in the dam’s colostrum, which protects immunoglobulins from gastrointestinal breakdown, may potentially allow C. perfringens type C β-toxin to persist in foals with adequate passive transfer and may allow type C bacteria to overgrow.

Clinical appearance of the disease is usually associated with foals < 5 days of age with a history of being obtunded, colicky and /or diarrhea for less than 24 hours. The animals usually present dehydrated with a severe colitis. Some of the animals may develop an ileus with evidence of colonic distention. In adults, the author has documented cases of chronic colic associated with low-grade clostridial enterocolitis. Clinical pathology work-up for a majority of these cases reveals that the animal is acidotic (HCO3 10-15 Meq/L), azotemic and occasionally hypoglycemic. The complete white blood cell count is characterized as a leukopenia with a toxic left shift. Some of these animals may develop a protein-losing colitis secondary to severe intestinal inflammation.

Specific diagnosis and definitive diagnosis of equine clostridial enterocolitis requires both identification of toxins and isolation of the organism from intestinal contents. Isolation of the organism without the analysis for toxins is considered inappropriate because of the possibility of isolating a non-enterotoxigenic C. perfrigens type A which can be isolated from normal horses’ manure. In a population study of fecal shedding of C. perfringens in 128 broodmares and foals C. perfringens was isolated from 90% of the normal 3-day-old foals. 85% were identified as type A; 12% of the samples had type A with the β2-toxin gene isolated, C. perfringens with the enterotoxin gene was identified in 2.1 % of samples and C. perfringens type C was identified in < 1 % of the samples. A presumptive diagnosis may be made (until culture and toxin analysis) by demonstration of abundant grampositive bacteria in a fecal smear. However, this test did not appear to be sensitive because C. perfringens was isolated from 59% of samples in which no gram-positive rods were seen. The www.faep.net

diagnosis is supported by culture of fecal clostridia and further verify the isolates as C. perfringens by the use of a polymerase chain reaction method that incorporated primers that allowed for classification of C. perfringens types A, B, C, D and E, as well as genes for β2-toxin, enterotoxin (CPE) and recently netF. Toxin detection kits are commercially available for identification of C. perfringens enterotoxin (C. perfringens enterotoxin test, ELISA, Techlab®, Blacksburg, VA USA).

Treatment for neonatal C. perfringens is considered a medical emergency. Even with the best care, many foals can die if infected with C. perfringens type C. Neonates with clostridiosis are at a higher risk for the development of peritonitis. When there is a large volume of peritoneal exudate, the prognosis is grave and euthanasia would be recommended. If attempted, the treatment plan should be aggressive and aimed at the following areas: abdominal pain, septic shock, clostridial infection and toxin production, and maintenance of nutrition. The use of oral metronidazole 10-15mg/kg 3-4x daily (dose depends on severity) for foals and 15mg/kg 3-4x daily for adults. If the animal has an ileus and is intolerant of oral feeding, then the use of intravenous metronidazole is recommended at a dose of 10mg/ kg IV 4x daily. Should the foal develop an ileus with marked colonic distention, we have used neostigmine 1-2mg (2mg for foals greater than 250 pounds) SQ with good clinical response.

The author will administer 2-3 doses at 1-hour intervals and then use it as needed. Oral and IV administration of C. perfringens type A, C and D hyperimmunized plasma may be given to the neonate.d The oral dosage would range from 50-100cc every 6 hours for 48-72 hours. If the animal is severely ill, the author would nasogastrically intubate the foal with 250-500ml of the hyperimmunized plasma. So far, subjectively, foals given the hyperimmunized plasma appeared to have their manure become formed faster than the patients not treated with the plasma.

Bentonite clay can also be used for treatment since it has been shown to adsorb Clostridium perfringens alpha, beta and beta-2 exotoxins without interfering with absorption equine colostral

7 Month Old Weanling with chronic Salmonellosis. The weanling was placed on enrofloxacin and subsequently recovered.

The Practitioner 31

antibodies.

Numerous prophylactic measures can be instituted on farms with a history of C. perfringens-associated enterocolitis in foals. Optimal hygiene efforts to ensure cleanliness of the foaling stall and the mare (clean udder before and after birth, clean the perineal and hind limb region) at parturition should be undertaken to decrease the degree of exposure of the foal to pathogens in the feces. Some farms have stopped their outbreak of foal diarrhea by foaling the mares out in pasture. Oral administration of lactobacillus acidophilus (found in yogurt and commercial probiotics) have been successfully used in chickens to minimize the overgrowth of C. perfringens. Prophylactic use of metronidazole (10mg/kg PO BID) has also been instituted after birth. In mares that have a good history of milk production, a ration containing low to moderate amounts of digestible energy should be fed beginning 1 week before parturition and 1 week after parturition to aid in the prevention of excessive milk production and, thus excessive milk intake by the foal.

Specific preventative methods addressing C. perfringens include immunization of mares with the use of a toxoid vaccine (Aluminum hydroxide adsorbed culture supernatant PLUS recombinant β2-toxoid. Vaccine strain is Clostridium perfringens Type A and carries genes for Alpha, β2 and CPE) that has recently been developed (2007) by Hagyard Equine Medical Institute (www.hagyardpharmacy.com). We have currently been using this vaccine on endemic farms since 2007. There is a vaccine that has been developed by the group at Guelph against netF with preliminary data that is very encouraging. Other oral enteric protectants include the oral and/or administration of hyperimmunized plasma which was previously mentioned.

Specific immune treatments for C. perfringens types C and D do

provide some protection against alpha-toxin, but it is generally believed that this protection would be inadequate against C. perfringens type-A organisms. a Resolvet Relieve, Hagyard Pharmacy, Lexington KY 40511 USA, www.hagyardpharmacy.com b Lake Immunogenics Clostridium difficle Toxin a and B Antibody Select HI Plasma, Ontario NY 14519 USA

References and Footnote: Nicola Pusterla UC Davis, Personal Communication August 2015 Coronavirus Pusterla N, Mapes S, Wademan C, White A et al. Emerging outbreaks associated with equine coronavirus in adult horses. Vet Microbiol.

2013; 162:228-231 Oue Y, Morito Y, Kondo T, Nemoto M. Epidemic of equine coronavirus at Abihiro Racecourse, Hokkaido , Japan in 2012. J Vet Med Sci. 2013; 75:1261-1265 Fielding CL, Higgins JK, Higgin JC, McIntosh S et al. Disease associated with equine coronavirus infection and high case fatality rate. J. Vet Intern. Med. 29, 307-310 Tzipori S, Hayes J and et al. Streptococcus durans: an unexpected enteropathogen of foals Jones JM, Adney WS, Alexander AF, et al. Hemorrhagic necrotizing enterocolitis associated with Clostridium difficile infection in four foals. J Am Vet Med Assoc 1988;193:76-79.

Magdesian KG, Hirsh DC, Jang SS, et al. Characterization of Clostridium difficile isolates from foals with diarrhea: 28 cases (19931997). J Am Vet Med Assoc 2002;220:67-73.

Weese JS, Staempfli HR, Prescott JF. A prospective study of the roles of Clostridium difficile and enterotoxigenic Clostridium perfringens in equine diarrhoea. Equine Vet J 2001;33:403-409.

Nathan Marc Slovis, DVM, Diplomate ACVIM, CHT

Pepin J, Alary M-E, Valiquette L, et al. Increasing risk of relapse after treatment of Clostridium difficile colitis in Quebec, Canada. Clin Infect Dis 2005;40:1591-1597.

Dr. Nathan Slovis is the Director of the McGee Medical and Critical Care Center at the Hagyard Equine Medical Institute located in Lexington, Kentucky. He is a native of Annapolis, Maryland. He received his Bachelor of Science from Radford University, Doctor of Veterinary Medicine from Purdue University, interned at Arizona Equine Center and completed his residency in Internal Medicine at the University of California, Davis.

Pépin J, Valiquette L, Alary M-E, et al. Clostridium difficile-associated diarrhea in a region of Quebec from 1991 to 2003: a changing pattern of disease severity. CMAJ 2004;171:466-472.

Dr. Slovis has published over 40 manuscripts in both national and international peer reviewed veterinary journals. He is the Editor of both the Atlas of Equine Endoscopy and The Atlas of Diseases/ Disorders of the Foal, both distributed by Elsevier. He implemented the current Infectious Disease and Equine Emergency Response Programs at Hagyard Equine Medical Institute and holds the position of Infectious Disease Officer and Equine Emergency Response Director. He is also a Certified Hyperbaric Technologist and a Member of the Veterinary Infectious Disease Society.

He maintains strong interests in infectious diseases, neonatology, neurology, cardiology, dermatology, critical care medicine and hyperbaric medicine.

32 The Practitioner

Mulvey MR, Boyd DA, Gravel D, et al. Hypervirulent Clostridium difficile strains in hospitalized patients, Canada. Emerging Infect Dis 2010;16:678-681.

Pépin J, Valiquette L, Gagnon S, et al. Outcomes of Clostridium difficile-associated disease treated with metronidazole or vancomycin before and after the emergence of NAP1/027. Am J Gastroenterol 2007;102:2781-2788.

Vohra P, Poxton IR. Comparison of toxin and spore production in clinically relevant strains of Clostridium difficile. Microbiology (Reading, Engl) 2011;157:1343-1353.

Medina-Torres CE, Weese JS, Staempfli HR. Prevalence of Clostridium difficile in horses. Veterinary Microbiology 2011.

Schoster A, Staempfli HR, Arroyo LG, et al. Longitudinal study of Clostridium difficile and antimicrobial susceptibility of Escherichia coli in healthy horses in a community setting. Veterinary Microbiology 2012.

Songer JG, Trinh HT, Dial SM, et al. Equine colitis X associated with infection by Clostridium difficile NAP1/027. J Vet Diagn Invest 2009;21:377-380.

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Rodriguez C, Taminiau B, Avesani V, et al. Multilocus sequence typing analysis and antibiotic resistance of Clostridium difficile strains isolated from retail meat and humans in Belgium. Food microbiology 2014;42:166-171.

Magdesian KG, Leutenegger CM. Real-time PCR and typing of Clostridium difficile isolates colonizing mare-foal pairs. Veterinary journal (London, England : 1997) 2011;190:119-123.

Medina-Torres CE, Weese JS, Staempfli HR. Validation of a Commercial Enzyme Immunoassay for Detection of Clostridium difficile Toxins in Feces of Horses with Acute Diarrhea. J Vet Intern Med 2010.

Schoster A, Arroyo LG, Staempfli HR, et al. Longitudinal study of Clostridium difficile, Clostridium perfringens, Salmonella and Escherichia coli in healthy horses. Annual Forum of the American College of Veterinary Internal Medicine. Denver, CO, 2011.

Weese JS, Staempfli HR, Prescott JF. Isolation of environmental Clostridium difficile from a veterinary teaching hospital. J Vet Diagn Invest 2000;12:449-52.

Madewell BR, Tang YJ, Jang S, et al. Apparent outbreaks of Clostridium difficile-associated diarrhea in horses in a veterinary medical teaching hospital. J Vet Diagn Invest 1995;7:343-6.

Kelly CP, Pothoulakis C, LaMont JT. Clostridium difficile colitis. N Engl J Med 1994;330:257-62.

Magdesian G, Hirsh D, Jang S, et al. Clostridium difficile and horses: a review. Reviews in Medical Microbiology 1997;8:S46-S48 Weese JS, Parsons DA, Staempfli H : Association of Clostridium difficile with enterocolitis and lactose intolerance in a foal. J Am Vet Med Assoc. 214;2:229232, 1999 Magdesian G, Hirsh D, Jang S, et al. Charcaterization of Clostridium difficile isolates from foals with diarrhea: 28 cases (1993-1997).

JAVMA 2002;220:67-73.

Gohari IM, Parreira VR, Nowell VJ, Nicholson VM, Oliphant K, Prescott JF. A Novel Pore-Forming Toxin in Type A Clostridium perfringens Is Associated with Both Fatal Canine Hemorrhagic Gastroenteritis and Fatal Foal Necrotizing Enterocolitis. 2015 PLoS ONE 10(4): e0122684. doi:10.1371/journal.pone.0122684

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