Practitioner Issue 4 2016

Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 4 • 2016

 REVIEW OF THE MAIN CONDITIONS OF THE HIP IN HORSES

J. M. DENOIX | DVM, AGRÉGÉ, PHD, HDR, CERT. ISELP, ASSOC. ECVDI, DACVSMR

 THE MANY FACES OF UVEITIS ANN E. DWYER | DVM

 EPM: DIAGNOSIS, TREATMENT, AND RELAPSES ROBERT J. MACKAY | BVSC (DIST), PHD, DACVIM

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The President's Line Ruth-Anne Richter, BSc (Hon), DVM, MS - FAEP President

Dear Fellow Equine Practitioners, As we look forward to how 2017 will unfold, I am happy to report that the full program for the 13th Annual Promoting Excellence Symposium has been formulated; and I would like to extend a first invitation from the FAEP for you to join us later this year. We will host our meeting in Naples, Florida at the Naples Grand Beach Resort from October 19 to the 22, 2017. We are proud of this FAEP continuing education offering on the care of the sport horse which is held each year in the fall. I can assure you the 2017 conference will provide an excellent learning and networking opportunity for equine veterinary practitioners and industry professionals from near and far.

Please take a look at the PES program in this issue. Themed 'A Multi-Disciplinary Approach to the Equine Athlete', the 2017 PES will provide you with 39 hours of CE. Attendees will be able to earn a maximum of 27 credit hours from our comprehensive scientific program that will cover topics such as lyme disease, botulism, imaging, compassion fatigue, lameness, neurologic emergencies, equine arrhythmias, joint disease, soft tissue injuries, rehabilitation, and much more.

The Promoting Excellence Symposium has reliably provided equine veterinarians and the equine veterinary supply industry with an excellent meeting ground for valuable learning and exchange of the latest information in the veterinary sciences and from industry. This program is anticipated yearly by equine veterinary professionals who have experienced the FAEP’s flagship CE conference, and this year’s will not disappoint. We hope you will save the date and register to join us when registration opens in March.

We have also begun our planning for the 55th Annual Ocala Equine Conference in January 2018. We should have preliminary information on the Ocala program in our next issue of the Practitioner.

The FAEP welcomes your comments and suggestions, and encourages you to make contact with our council members or the FVMA/FAEP staff, toll free, at 1(800) 992-3862.

EXECUTIVE COUNCIL

Ruth-Anne Richter FAEP Council President 2016

Corey Miller,

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

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Armon Blair, DVM abeqdoc@aol.com

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

Adam Cayot, DVM adamcayot@hotmail.com

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

Jacqueline S. Shellow, DVM, MS jackie@shellow.com

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.

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Review OF THE MAIN CONDITIONS OF THE HIP IN HORSES

J. M. DENOIX | DVM, AGRÉGÉ, PHD, HDR, CERT. ISELP, ASSOC. ECVDI, DACVSMR Abstract:

This paper will review the main conditions of the hip joint in horses. Anatomy, functional anatomy and biomechanics will be covered, allowing a better understanding of the etiopathogenesis and clinical manifestations of equine hip conditions. Diagnostic imaging and documentation will be presented with emphasis on the use of ultrasonography.

Prognosis, management and rehabilitation will be discussed.

Introduction

Hip lamenesses are not commonly diagnosed in horses and identification of the lesions responsible for pain is still a challenge. A specific imaging of the hip area is performed in the following indications: • History of trauma to the pelvis; • Swelling or local deformation of the hip area, identified externally or through transrectal palpation; • Pain to mobilization during protraction, retraction or abduction of the limb; • Hindlimb lameness with positive intraarticular analgesia of the coxofemoral joint and/or negative nerve blocks of the lame hindlimb as well as negative intraarticular analgesia of the stifle joints; • Positive findings on scintigraphic images.

the walk, the horse shows an obvious lameness with typical reduction of the caudal part of the stride.

- Diagnostic imaging: The diagnosis and documentation of this condition is easy with ultrasonography, combining a transrectal approach and an external one. The transrectal approach may image a single fracture plane or a comminuted fracture with multiple fragments. Assessment of the displacement of the fragments, as well as the position of them compared to the obturator vessels, should be done carefully.

Extension of the fracture planes to the ilium, pubis and/or ischium must also be assessed. Complementary information such us the location of the fracture plane(s), the displacement of the fragments, and the severity of the associated coxofemoral synovitis can be obtained using an external approach (Fig. 1).

Because of the presence of strong muscles covering the joint structures, the coxofemoral joint is difficult to examine in the field with portable radiographic machines. Even when adequate radiographic images can be obtained, the use of ultrasonography provides essential information for the diagnosis and management of most of the hip conditions. The purpose of this paper is to present the main clinical conditions Fig. 1: Transverse ultrasound scan performed at the proximal aspect of the hip that can be diagnosed in horses with ultrasonography, of the coxofemoral joint of a 6 month-old French Standardbred used alone or in conjunction with other imaging modalities. Trotter female showing a comminuted fracture of the acetabulum.

Fractures 1- Acetabular fracture

- Cause: traumatic injury: Fall on the side; external trauma; Can be seen in young and adult horses.

- Clinical manifestations: Typical asymmetry of the pelvis at physical examination; muscle atrophy within a few days and elevation of the opposite tuber sacrale; pain and crepitation at mobilization. At transrectal palpation, a hematoma can be felt at the medial aspect of the acetabulum. When moving at

1- Acetabulum; 2- Femoral head; 3- Femoral neck; 4- Physis (growth plate); 5- Gluteus profondus muscle; 6- Gluteus medius muscle.

On a routine basis, radiography examination of the affected hip under general anesthesia is no longer performed on adult horses to avoid the risk of worsening of the lesion or vascular damage; standing radiographs are performed under adequate sedation.

- Prognosis: It is highly dependent on the displacement of the acetabular fragments and correlated cartilage lesions of

6 The Practitioner Issue 4 • 2016

the femoral head. In a retrospective study of 10 acetabular fractures examined in our center, 5 of them went back to compete.

- Management: Box rest; nursing is essential: avoid the horse laying down; the horse can be attached or placed in a sling to avoid laying down from 8 to 10 weeks. If the horse is allowed to lay down, he must be placed in a large box with a very comfortable bedding. The horse should always lay on its sound limb to be able to get up more easily. Human assistance is useful to reduce stress when the horse tries to stand up. Slow walk in hand can be introduced progressively after 3 or 4 months on a firm surface. Introduction of ridden walk and trotting in lunge can be done depending on the clinical evolution of the horse and ultrasound healing of the fracture(s).

3- Fracture of the third trochanter

- Cause: traumatic injury: Fall on the side; sudden stop (e.g. in front of a fence).

- Clinical manifestations: Acute lameness from recent injury, improvement within days or weeks with rest (Bertoni et al. 2013). At palpation, the proximal third of the thigh is painful in acute cases; In old cases, the third trochanter is less prominent.

- Diagnostic Imaging: The diagnosis can be easily done with ultrasonography performing a transverse section in the proximal third of the femur. A gap is identified at the base of the third trochanter and this tuberosity, still attached to the gluteus superficialis tendon, is bent cranially (Fig. 3).

- Prognosis: Excellent, many old fractures are asymptomatic.

- Management: Remove hind shoes if possible, or put light shoes on. On a regular basis: box rest for two weeks, hand 2- Femoral neck fracture walking for 2-4 weeks depending on clinical manifestations.

- Cause and epidemiology: Traumatic injury: bad sliding Then, slow alternate trotting 3 times a week. Slow canter in abduction; young and adult horses can be affected. will be done on the opposite leg (i.e. right canter if left 3rd - Clinical manifestations: Severe lameness when acute; lat- trochanter is affected). eral rotation of the limb, gluteal and femoral muscle atrophy, reduction caudal part of the stride. Mobilisation tests of the proximal hind limb exhibit pain and restriction of motion.

- Diagnostic Imaging: The diagnosis can be done with ultrasonography. Using an external approach of the coxofemoral joint, the lack of connection between the femoral head and neck can be demonstrated; the head is still located in the acetabulum but the neck is displaced proximally (Fig. 2). There is also synovial effusion of the coxofemoral joint.

Documentation of the condition can be done performing standing radiographs.

- Prognosis: Poor in our cases.

- Management: Box rest, but recurrence of lameness occurred after paddock exercise.

Fig. 3: Transverse ultrasound scan performed at the proximal third of the femur of a 6 year-old French Standardbred Trotter gelding showing a displaced fracture (arrowhead) of the third trochanter. 1- Third trochanter; 2- Base of the third trochanter connected to the diaphysis of the femur; 3- Tendon of the gluteus superficialis muscle; 4- Vastus lateralis muscle; 5- Guteofemoralis muscle.

Coxofemoral luxation

Fig. 2: Transverse ultrasound scan performed at the proximal aspect of the coxofemoral joint of a 4 year-old Selle Français male showing a fracture of the femoral neck with proximal displacement of the femur (double arrow).

1- Acetabulum; 2- Femoral head; 3- Femoral neck; 4- Great trochanter; 5- Gluteus profondus muscle; 6- Gluteus medius muscle.

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- Cause: Traumatic injury; upward fixation of the patella seems a predisposing disease in ponies, especially Shetland ponies in our cases.

- Clinical manifestations: Typical ‘shortening’ of the affected limb. In reality this manifestation is the result of a proximal displacement of the whole limb. Gluteal and femoral muscle atrophy will develop quickly. Mobilisation tests of the proximal hind limb exhibit pain and restriction of motion.

- Diagnostic Imaging: At ultrasonographic examination using a proximolateral approach of the hip area, the femoral

FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS | The Practitioner 7

head can be imaged as it is no longer situated in the acetabulum (Fig. 4). It is usually positioned proximally and cranially to the acetabulum margin. There is little or no fluid distension.

Radiographic examination on the standing horse or under recumbency (more easily done on ponies) demonstrates the proximocranial luxation of the femoral head.

- Prognosis: Poor for any kind of use; small ponies can be comfortable at pasture.

- Management: Replacement under general anesthesia if recent (< one week). Resection of the femoral head has been done in few pony cases. In ponies presenting upward fixation of the patella, medial patellar desmotomy is indicated to prevent coxofemoral luxation.

Fig. 4: Transverse ultrasound scan performed at the proximocranial aspect of the coxofemoral joint of an 8 year-old Franche-Montagne gelding presenting a coxofemoral luxation. The proximal profile of the femoral head is completely imaged; there is an osteophyte on the margin of the fovea capitis (arrowhead). 1- Acetabulum; 2- Femoral head; 3- Femoral neck; 4Great trochanter; 5- Gluteus profondus muscle ; 6- Gluteus medius muscle.

Horses affected with severe disease with articular surface eburnation may have trouble to get up.

- Management: Medication of the joint using ultrasonographic guided injection is effective in mild or moderate cases. Progressive warming up and strengthening of the glutei muscles are indicated. Side gates are useful to develop power and proprioception of the deep pelvic muscles which act as stabilizers of the coxofemoral joint.

Fig. 5: Transverse ultrasound scan performed at the proximal aspect of the coxofemoral joint of an 11 year-old Selle Français female showing dystrophic mineralisation in the joint capsule (arrowhead) and periarticular remodelling of the femoral head (arrow). 1- Acetabulum; 2- Femoral head; 3Femoral neck; 4- Great trochanter; 5- Gluteus profondus muscle; 6- Gluteus medius muscle.

Coxofemoral osteoarthrosis

- Cause: Often secondary to previous traumatic injuries (see above): primary degenerative joint disease of the coxofemoral joint is a difficult condition to diagnose early in adult horses.

- Clinical manifestations: Muscle atrophy, mild to severe lameness, positive flexion test of the affected limb.

- Diagnostic Imaging: Synovial fluid effusion detected at ultrasonography is an indication of coxofemoral joint disease.

Periarticular osteophytes of the acetabular or femoral head margins and or dystrophic mineralisation of the joint capsule can be seen (Fig. 5). On post mortem specimen, there is often a rupture of the capitis ligament. This can be suspected on radiographs performed under general anesthesia when the fovea capitis of the femur is denser than normal.

- Prognosis: tolerance depends on the evolution stage of the disease and especially the degree of cartilage degeneration of the femoral head and lunar surface of the acetabulum. Mild osteoarthrosis is compatible with racing or sport activities.

Fig. 6: Transverse ultrasound scan performed at the proximal aspect of the femur of a 7 year-old Thoroughbred male showing an old trochanteric bursitis with thinning of the gluteus accessorius tendon (arrowhead) and remodelling of the convexity of the great trochanter. 1- Great trochanter, 1a- crest, 1b- convexity; 2- Tendon of the gluteus accessorius muscle; 3- Trochanteric bursa (distended); 4- Gluteus medius muscle.

8 The Practitioner Issue 4 • 2016

Trochanteric bursitis

This is a quite rare condition in our cases.

- Cause: Initiated by a trauma or progressive tendinopathy/ enthesopathy of the gluteus accessorius muscle.

- Clinical manifestations: Clinical incidence was unclear in our cases as the ipsilateral hind limb had other causes of pain.

- Diagnostic Imaging: Mild to marked synovial fluid distension at ultrasonographic examination; tears or fibrillation of the gluteus accessorius tendon (Fig. 6); bone irregularities of the crest (insertion surface) and convexity (gliding surface) of the great trochanter.

- Prognosis: Good tolerance in our cases.

- Management: If required, medication of the bursa using ultrasonographic guided injection is easy.

Selected References: Barone R : Anatomie des Animaux domestiques. Tome 2 : Arthrologie et Myologie, 4éme édition. Vigot éd. Paris, 2000 Bertoni L, Seignour M, Mira MC, Coudry V, Audigié F, Denoix JM. Fractures of the third trochanter in horses: 8 cases (2000–2012) J. Am. Vet. Med. Assoc.

2013;243:261-266.

Denoix J-M. Ultrasonographic examination in the diagnosis of joint disease. In: Mcllwraith WC and Trotter GW ed. Joint Disease in the horse. Philadelphia, Saunders, 1996;165-202.

Jean-Marie Denoix, DVM, PhD, DACVSMR ISELP Certified Instructor Founder and President of ISELP Founder and President of ISELP, France Dr. Denoix of the CIRALE (Center of Imaging and Research on Equine Locomotor Affections) in Normandy, France is considered the world’s foremost equine musculoskeletal system anatomist as well as a leading equine diagnostic ultrasonographer.

Dr. Denoix is a founder and current president of ISELP and was also the 2006 recipient of the Schering Plough Equine Research Award from the World Equine Veterinary Association for outstanding applied research work in Equine Diagnostic Imaging. Jean-Marie has been the invited speaker at many international meetings in more than 30 countries around the world on topics related to clinical examination and imaging of equine locomotor problems.

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THE MANY FACES OF UVEITIS Image courtesy of Wikimedia Commons / Author: OpenStax College

ANN E. DWYER | DVM

Equine Anatomy of the Eye: The uvea (Iris, ciliary body and choroid) is diagrammed as a brown and pink layer inside the eye

Introduction:

Key Clinical Diagnostic Points:

• Recurrent or persistent uveitis is not one disease, but a By definition, uveitis is inflammation of the uvea of whole umbrella of complex of diseases. the eye (iris, ciliary body and choroid). The complex • UVEITIS IS THE LEADING CAUSE OF BLINDNESS of diseases known as “Equine Recurrent Uveitis (ERU) IN HORSES IN THE WORLD. refers to intraocular inflammation that recurs or persists • Recurrent or persistent equine uveitis is immune mediated. causing various degrees of inflammation, scarring, The genetics of a horse’s immune system contribute to degeneration and dysfunction of multiple components individual susceptibility. Pathogenesis of disease includes of the eye. Several classification schemes are used to a Th 1 helper immune response. Etiology may involve differentiate subsets of clinically observed disease. autoantigens and/or microbial infections.

• Systemic leptospiral infection is associated with numerous A: Classification by observed inflammation over time: 1. Primary uveitis: Initial episode of inflammation cases of recurrent classic uveitis.

• Certain lines of Appaloosas, draft horses and European of the uvea. May have inciting cause like a corneal ulcer or blunt trauma. May or may not go on to classic ERU. warmbloods are at risk for persistent, insidious uveitis.

2. Equine recurrent uveitis (ERU): Classic presentation • New therapies aimed at controlling the aberrant immune response are under development. Recent research has where the horse demonstrates repeated bouts of miosis, focused on implanting devices that deliver drugs into severe inflammation and pain in one or both eyes. In between the eye that modify the immune response, and mediating relapses, the eye(s) appear comfortable. A case is not termed disease by removing ocular components that may provoke “recurrent” until two or more classic episodes have occurred.

3. Insidious uveitis: Horse appears normal to the owner recurrence. Response to treatment is variable, and long and the animal exhibits little to no overt ocular pain. term visual prognosis remains guarded.

Examination of the globe with a direct ophthalmoscope

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Acute uveitis: Circumlimbal corneal edema and neovascularization, severe miosis, blepharospasm and lacrimation.

or slit lamp shows deterioration of numerous ocular structures that is progressive over time. Pupils may be slightly miotic. Other subtle signs include corneal haze, slight aqueous flare, muddy iris color, iris rim and/or corpora nigrans atrophy, cataract, low-grade vitreous haze and chorioretinal scarring. Insidious uveitis is most often seen in Appaloosas, draft horses and European warmbloods. ****Miosis is a hallmark of acute ERU. Miosis is a component of persistent insidious uveitis as well, but usually to a milder degree.

B. Classification by region of ocular involvement 1. Panuveitis: Cases where the entire uveal tract is inflamed.

Most cases of ERU and insidious uveitis involve a panuveitis.

2. Posterior uveitis: Inflammation is predominantly observable in the posterior segment (vitreous, retina and optic nerve). Most often seen in draft horses and European warmbloods.

C . . Classification by stage of disease at time of examination: 1. Active, or acute cases are horses suffering from a flareup of classic uveitis. Signs of an acute bout vary but include pain, lacrimation, photophobia, chemosis, conjunctival hyperemia, corneal edema, corneal vascularization, dotlike keratic precipitates on the corneal endothelium, aqueous flare, hyphema or hypopyon, miosis, vitritis, and ocular hypotension (pressure of 10-12 mm Hg).

2. Quiescent cases are horses in a “calm” time of their cycle of repeat inflammation. Slit lamp examination will show subtle flare in the anterior chamber, indicating low grade but persistent inflammation. Ocular examination may reveal “footprints” of previous disease including chronic corneal edema, iris atrophy, iris color change, synechiae

(adherence of the iris to the lens or cornea), pigment rests on the anterior lens capsule, cataract, densities or haze in the vitreous, or scarring around the optic disc. Chorioretinal scarring from previous inflammatory episodes is evidenced by either a “bullet hole” pattern, where numerous tiny, pale ring-shaped scars with hyperpigmentated centers occur in a geographic pattern in the peripapillary region, or as alar scarring, where islands of retinal depigmentation flank the optic disc in a pattern resembling butterfly wings.

3. End-stage cases are horses with longstanding, chronic ERU that have undergone severe degeneration. The affected eye(s) may show extensive corneal scarring, circumferential synechiae, dense cataract, lens luxation or subluxation, secondary glaucoma, retinal detachment or phthisis bulbi.

End-stage uveitis is associated with vision loss.

Diagnosis of uveitis is simplified by understanding that a horse may present anywhere along the spectrum from acute to end stage, and as either a recurrent or insidious case.

Horses that present with three or more signs of intraocular inflammation and a history that is suggestive of either recurrent disease or breed-associated insidious disease can be given a presumptive diagnosis of ERU or persistent uveitis.

Examination of these horses may reveal some signs reflecting acute or recent inflammation and other signs representing chronic ocular scars from previous episodes. Inflammation is always present on a cellular basis in both quiescent and insidious cases, so sequential examination may discover progressive ocular deterioration in horses that have seemed “normal” to their owners.

NOTE: Care must be taken to assure that there is not another primary problem in any eye that is demonstrating intraocular inflammation. The cornea must be examined closely for signs of corneal ulcer, stromal abscess, foreign body, neoplasia and immune mediated or idiopathic keratitis. The globe should be examined for neoplasia. Ruling out concurrent ocular disease

Chronic uveitis: Corneal edema, pupil iris atrophy, luxated lens with dense cataract.

12 The Practitioner Issue 4 • 2016

is critical, as the corticosteroid therapy that is indicated for treatment of recurrent uveitis is contraindicated in many of these conditions.

Key Etiologic and Pathophysiologic Points:

Pathophysiology: Normal horses have a blood ocular barrier that functions to keep the aqueous and vitreous ocular media clear. Tight fenestrations between ocular capillary cell walls prevent circulating cells and large molecules from passing through the blood vessels of the iris, ciliary body and choroid into the surrounding stroma. The blood ocular barrier also serves to isolate intraocular structures from the normal cellular immune surveillance traffic, making the tissue of the inside of the eye an immune privileged site.

Uveitis begins with compromise of the blood ocular barrier. The blood vessels in the iris, ciliary body and choroid thicken and become congested. Soon, these vessels become “leaky”, allowing cells and inflammatory mediators to cross the compromised blood ocular barrier and enter the inside of the eye. Most of the cells that initially cross the barrier are neutrophils. The invading cells may be seen grossly as hypopyon, aqueous flare, and vitreous haze. Neutrophils that enter the eye are soon replaced by large numbers of lymphocytes, some of which infiltrate the connective tissues of the ciliary body and iris, forming spherical organized follicles within the stroma of various regions of the uvea. The lymphocytes produce antibodies and inflammatory cytokines that are detectable in the ocular media and within ocular tissues. These substances react with host and (in some cases) infective factors to contribute to ongoing pathologic changes. Numerous heavy exudates appear on intraocular tissue surfaces, most notably on the epithelium of the iris and ciliary body, on the capsule of the lens, and in the layer between the retinal pigmented epithelium (RPE) and the photoreceptors of the retina. The exudates interfere with the function of adjacent ocular tissue. Cytokine activity mediates additional tissue destruction. With repeated or persistent inflammation, chronic changes occur within the ocular tissues, affecting, variably, the cornea, uvea, lens and retina. Vision loss results when dense cataract and synechiae obscure acuity, when the retina detaches or degenerates and no longer can transmit processed light signals to the brain, or when glaucoma causes ischemic damage and degeneration of the axonal processes of the retinal ganglion cells and optic nerve.

Etiology: Decades of research have substantiated that recurrent uveitis is an immune mediated disease. However some bacterial, viral and parasitic infections, as well certain host conditions have been associated as triggering events for the syndrome. These factors include: • Bacterial infections: Leptospirosis, Borrelia burgdorferi (Lyme Disease), brucellosis, Streptococcus, Rhodococcus equi (foals), generalized septicemia

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Differential diagnosis: : Always inspect eyes showing pain and miosis for other diagnoses of intraocular inflammation. This eye has a stromal abscess at 7:00. Steroid therapy is contraindicated.

• Viruses: Influenza, equine viral arteritis, parainfluenza, herpes viruses • Parasites: Onchocerciasis, Strongylus, Toxoplasmosis • Host conditions: Tooth root abscess, septicemia, severe trauma Of all possible infectious triggers, leptospirosis is the most significant worldwide. Leptospiral associated ERU cases account for at least 60% of the cases seen in the Genesee River Valley where the author practices. This temperate river valley is in western New York, in the northeastern part of the United States directly south of Toronto, Canada.

Leptospirosis and Uveitis: The most significant serovars associated with disease are L. interrogans serovar Pomona (seen often in the USA) and L. interrogans serovar Grippotyphosa (seen often in Germany and central Europe). Factors that increase the risk of leptospirosis in horses include: • Pasture access to cows, pigs, deer or raccoons • Close proximity to streams or ponds frequented by the same • Access to ponds or other non-flowing water sources • Rat infestation in the stable • Rainy season with persistence of ground water Horses become infected when they drink water contaminated by the urine of a carrier animal (often a cow, deer, raccoon, pig or rat). The spirochete gains access to the horse’s bloodstream by mechanical penetration of mucous membranes. Bacteremia results in clinical illness, manifested by anemia, fever and flu-like symptoms. Acute clinical disease is mild and self-limiting, thus rarely diagnosed as a leptospiral infection. Resolution of signs occurs in a few days to a few weeks. However, the spiral organisms colonize the kidneys of the horse during the acute phase, and may persist for a

FLORIDA-ASSOCIATION -OF-EQUINE-PRACTITIONERS | The Practitioner 13

End stage uveitis: Blind eye with posterior synechia and dense cataract.

few months, being shed in the urine. L. pomona has also been associated with late term abortion in mares, as well as placentitis, stillbirth and neonatal illness.

Ocular signs of leptospiral associated uveitis (LAU) do not occur during the acute infection; they begin months later. The ocular inflammation observed during the initial episode of LAU is variable but often severe. Inflammation usually subsides with or without therapy but then may recur at unpredictable intervals. Subsequent episodes of ocular inflammation may be more or less severe than the initial one.

Inflammation and damage to ocular tissues associated with repeat episodes eventually compounds and creates visual deficits. Blindness is a common final outcome.

The pathogenesis of the “lepto link” with equine recurrent uveitis has been the subject of much research and debate.

Key findings: 1. Antibodies to pathogenic serovars can be found in the sera, aqueous and vitreous of horses with LAU. Research studies have supported the hypothesis that intraocular antibody synthesis is occurring.

2. Leptospiral organisms have occasionally been cultured from the ocular media of horses with uveitis.

3. Molecular homology has been demonstrated between certain equine corneal proteins and unique proteins in pathogenic strains of leptospira.

4. Pineal inflammation has been shown to accompany LAU in horses similar to models of experimental autoimmune uveitis (EAU) in laboratory animals.

5. MHC II immune reactivity has been demonstrated on resident and infiltrating cells of horses with both natural and experimental LAU. 6. Seroreactivity to equine retinal proteins has been found in horses with LAU. A unified theory is yet to appear to explain all the ocular

events that accompany LAU, but three questions can be considered: • Does LAU stem from a direct toxicity of intraocular infection with the spirochete?

• Is LAU an autoimmune disease triggered by molecular mimicry between leptospira and host tissue?

• In LAU, are leptospiral organisms somehow modulating the immune response of the eye?

These questions continue to challenge researchers. Although systemic infection with pathogenic strains of leptospirosis is clearly a common trigger for vision threatening ERU, the genetic makeup of an affected horse, specifically the genes that determine the MHC complex and ELA (equine lymphocyte antigen) profile of that individual, probably play a major role in determining both susceptibility to leptospirosis as an inciting trigger, and severity of subsequent inflammatory episodes.

Testing horses for exposure to leptospirosis: The author routinely submits serum from horses diagnosed with uveitis to the diagnostic laboratory at Cornell University for MAT analysis against a panel of leptospiral serovars (https://ahdc. vet.cornell.edu/ ). Many non-uveitic horses will show low titers to the bratislava, autumnalis, hardjo or canicola serovars; these findings are judged to be insignificant in the author’s practice geography. Titers above 1:400 to L. interrogans serovar Pomona or L. interrogans, serovar Grippotyphosa are judged to be significant in horses with ERU and are a likely indicator of leptospiral associated etiology. Seroreactivity to L. interrogans serovar Icterohemmorhagica is often paired with reactivity to L. interrogans serovar Pomona but the titer levels to the Icterohemmorhagica serovar are consistently much lower than those reported for serovar Pomona.

Research has shown that horses with uveitis can be seronegative for antibodies to leptospira and still have leptospiral DNA or live organisms that can be cultured from the eye.

A negative leptospira titer thus does not fully rule out leptospirosis as an etiologic factor. However, a positive titer to either serovar L. Pomona or L. Grippotyphosa is a strong cause for concern. The “gold standard” for diagnosing LAU is a positive “C value”, that is, an aqueous to serum leptospiral MAT ratio that is greater than 3 or 4. Determining a C value requires an anterior chamber tap to sample aqueous humor. This is an invasive procedure not often performed in the field. However, the author has performed C value testing on several eyes from enucleated or deceased horses with ERU where previous serologic testing has suggested LAU. In every case to date, the testing has confirmed LAU (C value higher than 4).

Breed and Uveitis: Recent work has also shown that cer-

Continued on Page 19 14 The Practitioner Issue 4 • 2016

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Continued from Page 14 tain breeds are at risk for uveitis, most notably Appaloosas, European warmbloods and draft horses. A survey done by the author found the Appaloosa breed to be 8.3x more at risk than other breeds for uveitis. Appaloosas that have insidious disease often have overall roan or light coat colors rather than dark coats with a rump blanket. The skin around the lids of affected Appaloosas is often mottled or pink in pigmentation.

Mane and tail hair may be sparse. Recent studies performed at the University of California Davis and at the University of Saskatchewan have found that affected individuals have a genetic proclivity to uveitis due to aberrations in the Major Histocompatibility Complex, specifically in their Equine Lymphocyte Antigen subtype. Recent research from Germany has supported this concept in German warmbloods susceptible to disease. Substantial research in this subject is ongoing in many universities, and genetic testing for mutations associated with uveitis may be available in the future.

Unilateral vs Bilateral disease: Little work has been done to document the incidence of ocular involvement in horses, but recurrent uveitis can be a unilateral or bilateral disease.

In a study of 160 cases reviewed by the author: • 50%of horses seropositive for a pathogenic strain of leptospira had unilateral disease and 50% had bilateral disease • Over 80% of the Appaloosas had bilateral disease • 62% of the non-Appaloosa horses that were seronegative for pathogenic strains of leptospira had unilateral disease Uveitis may begin in one eye and later occur in the fellow eye. However, if a case is unilateral and no attacks are seen in the other eye for two years after the initial attack, it is uncommon for uveitis to occur in the contralateral eye.

EDTA chelation.

• Secondary corneal ulcers are discovered in 25% of horses with ERU or persistent uveitissome point in their disease course (statistics compiled by author). This fact is not surprising given the pain associated with uveitis and the propensity of horses to suffer self trauma. Corticosteroids are contraindicated in these cases. Systemic NSAIDs can be used to treat pain, and the ulcer should be treated topically with anti-infectives and anti-collagenases.

• Acupuncture therapy may help moderate the frequency or severity of episodes.

• Insidious, persistent uveitis is a challenging condition that is common in Appaloosas, some draft horses and many Warmbloods. Therapy does little to alter the progression of disease in affected horses.

• Secondary glaucoma is a complication seen in many horses, particularly Appaloosas suffering from insidious disease. Glaucoma therapy is often unrewarding in the long term, but topical timolol maleate, dorzolamide or a combination of these two drugs may be tried. Judicious topical steroids and/or mydriatic therapy may help as well.

• Suprachoroidal cyclosporine implant surgery may reduce the frequency and/or severity of ERU and persistent insidious uveitis. The best candidates for this referral procedure are early ERU cases that have only experienced a few “attacks” who show little or no permanent ocular scarring.

• Pars plana vitrectomy is frequently performed on ERU horses in central Europe with reported good results. The procedure is not often performed in the United States.

Key Prognostic Points:

Visual prognosis for horses suffering from multiple acute attacks of uveitis or insidious chronic disease is always guarded. Data on the statistical incidence of blindness in uveitic horses is lacking, but it is clear that uveitis is the Key Therapeutic Points: leading cause of blindness in horses worldwide. The author • Mydriasis is essential therapy for all cases of acute uve- has observed ocular inflammation serious enough to threaten itis. Initial application of atropine should be BID until vision in at least 1-2% of her practice population. Analysis pupil is fully dilated, then reduced to SID with frequent of the visual outcome of 160 cases followed over 11 years monitoring to assure that the pupil stays dilated. Severe revealed the following trends: cases may show poor response to the action of mydriatics. • 56% of the case series ((89/160) lost vision in one or • Topical corticosteroids and systemic NSAIDS are the both eyes. core elements of anti-inflammatory field therapy for acute • 20% of the cases (32/160) became completely blind. attacks. Therapy should be intense for about two weeks • 36% (57/160) lost vision in one eye. and may be tapered over another two to four weeks depending on response. Subconjunctival and/or systemic Breaking the cases down further into those that were corticosteroids are indicated in severe cases. seropositive or seronegative to L. interrogans serovar Pomona, • Corticosteroid topical therapy may induce calcific band and those that were Appaloosas or “non-Appaloosas”, the keratopathy, especially in horses with leptospiral associ- following trends were seen: ated uveitis. The troublesome calcium deposits should Horses that were seropositive to L. pomona and also be treated wi†h diamond burr debridement followed by Appaloosas had a very poor visual prognosis: 100% lost vision

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in at least one eye and 50% went completely blind (n=14).

• Horses that were Appaloosas and seronegative had substantial occurrence of blindness: 72% lost vision in at least one eye and 29% went completely blind (n=28).

• Horses that were seropositive to L. pomona and nonAppaloosas had a slightly lower rate of blindness, but 50% loss vision in at least one eye and 17% went completely blind (n=86).

• Horses that were seronegative and non-Appaloosas had the best visual prognosis: 34% lost vision in at least one eye, and just 6% went completely blind. (n=32).

Secondary complications and degeneration of ocular tissues are common sequellae of uveitis. Several interesting findings were noted in this series that are representative of sequellae seen in ERU horses in other geographic regions of the world: • Cornea: Focal scars, folds, calcium deposits and other corneal opacities were common. The seropositive horses experienced a high rate of calcific band keratopathy. Striae and dense corneal folds were common in Appaloosas and were highly correlated with blindness.

• Iris: Iris atrophy and color change were common, especially in Appaloosas and seropositive horses.

Anterior synechiae were rare unless phthisis bulbi was present, but posterior synechia occurred in nearly one third of all cases and 40% of Appaloosas.

• Lens: Diffuse cataract(s) developed in 41% of all cases, and affected nearly 75% of the Appaloosas. These cataracts were a common cause of blindness. Lens luxation was very common in Appaloosas (29%).

• Posterior segment: Severe vitritis was observed in nearly one third of the cases. Peripapillary scarring (focal or alar) was also present in about one third of the horses. Cataracts and synechiae often obstructed posterior segment evaluation, so inflammatory changes were probably underreported.

• Glaucoma and phthisis bulbi: Appaloosas had a high rate of glaucoma (21%). Phthisical eyes developed most often in Appaloosas and seropositive horses.

Owners are concerned that horses with ERU will need enucleation. In the above series, only 4% (6/160) were enucleated for complications from corneal infection or glaucoma. Of more concern is the fact that 43 of the 160 horses (27%) were treated for corneal ulcers over the observation period. Clinicians should stress that horses with ERU are at risk for ulcers, as owners often choose to treat horses with painful eyes with medications that have been dispensed for previous problems. They may potentiate serious infections by applying corticosteroids and delaying proper diagnosis. An additional ten horses suffered from calcific band keratopathy. This is a troublesome complication that limits therapeutic options for ERU.

Posterior uveitis: Common in Appaloosas, draft horses and warmbloods. Posterior segment shows vitritis (yellow haze) and diffuse cortical cataract.

References/Suggested Reading Barnett, KC et al. Color Atlas and Text of Equine Ophthalmology, 2nd edition London, Mosby-Wolfe, 2004.(note: A new color atlas for equine ophthalmology is currently in production from Wiley Blackwell publishing. It is due to be released in 2017 or 2018).

Brooks, D. Ophthalmology for the Equine Practitioner, 2nd ed. Jackson, Wyoming, Teton NewMedia, 2009.

D eeg CA, Marti E, Gaillard C, et al. Equine recurrent uveitis is strongly associated with the MHC class I haplotype ELA-A9. Equine Vet J, 36:73-75, 2004.

Deeg CA. Ocular immunology in equine recurrent uveitis.

Vet Ophthalmol 11 (Suppl 1): 61-65, 2008.

Dick AD. Understanding uveitis through the eyes of a horse: relevance of models of ocular inflammation to human disease. Ocul Immunol Inflamm; 6:211-214, 1998.

D wyer, AE et al. Association of leptospiral seroreactivity and breed with uveitis and blindness in horses: 372 cases (1986-1993). JAVMA, 207 (10): 1327-1331, 1995.

Gilger, BG and Hollingsworth, SR. Equine recurrent uveitis: new methods of management. in Veterinary Clinics of North America, Equine Practice 20 (2), p. 417428. Updates in Equine Ophthalmology. Philadelphia, Saunders, 2004.

G ilger, B and Deeg, C. Diseases of the uvea, uveitis and recurrent uveitis. In Gilger, B, (ed.) Equine Ophthalmology, 3rd Ed. 369-415. Ames, Wiley Blackwell, 2017.

G elatt, KN, Spiess, B and Gilger, B. Vitreoretinal Surgery.

In Gelatt KN and Gellatt JP, Veterinary Ophthalmic Surgery. 369-370. Philadelphia, Elsevier, 2011.

Jones T. Equine periodic ophthalmia. Am J Vet Res 3:45-70,1942.

P aglia, D et al. James Wardrop and Equine Recurrent Uveitis. Arch Ophth, 122: 1218-1223, 2004.

R ebhun, WC. Diagnosis and treatment of equine uveitis.

JAVMA 175: 803-808, 1979.

R oberts SR, York C, Robinson J. An outbreak of leptospirosis in horses on a small farm. J Am Vet Med Assoc;121:237-242, 1952.

20 The Practitioner Issue 4 • 2016

Schwink, K. Equine uveitis. Veterinary Clinics of North America, Equine Practice 8, 557-574, Philadelphia, Saunders, 1992.

Williams RD, Morter RL, Freeman MJ, et al. Experimental chronic uveitis. Ophthalmic signs following equine leptospirosis. Invest Ophthalmol;10:948-954, 1971.

Website for owners of horses that are blind: www.blindhorses.org

Resources for clinicians with a special interest in equine ophthalmology: h ttp://www.equineophtho.org/ Website for the International Equine Ophthalmology Consortium, an international professional organization that welcomes practitioner members. Dues are $125 per year and there is one meeting per year, held early in June. In 2017 the meeting is in Saratoga Springs, NY (USA). In 2018 the meeting will be held in Reykjavik, Iceland. http://www.wiley.com/WileyCDA/WileyTitle/productCdVOP2.html Website for Veterinary Ophthalmology, the journal that is devoted to research on animal eye issues.

The journal is now published online and a subscription purchase permits access to previous issues. h ttp://www.equineeyeclinic.co.uk/how-to.html Website from a specialty practice in England that has many “how-to” resources for the equine patient.

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Ann E. Dwyer, DVM Co-Owner, Genesee Valley Equine Scottsville, New York Dr. Ann Dwyer is co-owner of the Genesee Valley Equine Clinic, PLLC, and has worked at the practice since graduating from Cornell in 1983. She has a special interest in equine ophthalmology and practice management and has lectured widely on these topics. Dr. Dwyer’s field research has focused on equine ophthalmology, particularly uveitis, leptospirosis, and blindness in horses. As a result, she has authored several book chapters on field ophthalmology for ambulatory clinicians as well as blindness.

In 2011, Dr. Dwyer was named an honorary member of the American College of Veterinary Ophthalmology. She holds an appointment as a clinical associate at the Flaum Eye Institute (the ophthalmology arm of the medical school at the University of Rochester). Dr. Dwyer was a member of the board of directors at the AAEP from 2006 through 2008; she then became an officer of the AAEP in 2011, serving as VP that year, as president-elect in 2012, and as president in 2013. Additionally, she served as the program chair for the AAEP 2012 Anaheim convention and organized the first Focus on Equine Ophthalmology meeting that the AAEP staged in 2009.

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Relax, you’ve got To learn more, contact a Vétoquinol sales representative or call 800-267-5707.

Zylkene is a registered trademark of Vétoquinol. ©2015 Vétoquinol 7/2015

3146 Zylkene FAEP Ad.indd 1

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EPM: DIAGNOSIS, TREATMENT, AND RELAPSES ROBERT J. MACKAY | BVSC (DIST), PHD, DACVIM

E

quine protozoal myeloencephalitis (EPM) is the most that have no travel history to the Americas and the nature common infectious neurological disease of horses of infection in these cases remains unclear.9,10 Horses of all in the US and Sarcocystis neurona is the usual cause, breeds can be affected by EPM and there is no gender bias.11 with sporadic cases caused by Neospora hughesi.1,2 Species of There is only one report of EPM in a pony and one describSarcocystis have an obligatory predator-prey 2-host life cycle.3 ing N. hughesi in a mule, suggesting that these equids may Sexual reproduction occurs in the lining of the small intestine be less susceptible to EPM than are horses. Ages at onset of the definitive host, the opossum (Didelphis virginiana in have ranged from 2 months to at least 30 years although it North America and D. albiventris in South America), while is rare in horses less than 2 years old. One study identified asexual proliferation occurs in the intermediate host and an increased risk of EPM in horses aged 1â&#x20AC;&#x201C;4 years and >14 culminates in the formation of sarcocysts in muscle. The years. EPM typically occurs as individual cases, but clusters 9-banded armadillo, the striped skunk, the raccoon, and of cases have occasionally been reported.12 the domestic cat are natural intermediate hosts that cover The reported prevalence of S. neurona infection as evi4-7 the geographic range in which EPM occurs. The hosts for denced by S. neurona antibodies in horses in various locations N. hughesi are not known. The horse usually functions as an throughout the USA varies from 0% to 89.2%.13,14 Generally aberrant dead-end intermediate host. With the exception high rates are found in areas with dense human populations, of a single foal with S. neurona muscle sarcocysts,8 only abundant water sources, and moderate rainfalls; low seroprecystic stages (i.e., merozoites and schizonts) have been positivity rates are found in arid sparsely populated regions. found in the CNS of horses with EPM. The geographic variation in prevalence is accounted for by the still-expanding range of the definitive host, the opossum.

Pathogenesis Despite the high rate of infection by S. neurona, there is The pathophysiology and immunology of S. neurona infec- probably only about a 1% lifetime risk of a horse develoption in horses is not completely understood. Horses ingest the ing EPM in these areas (estimated from the mean 0.14% infective sporocyst stage of S. neurona in food and water that one- year incidence reported in the NAHMS 1998 survey15). has been contaminated by opossum feces. The mechanism of The factors that influence the relationship between infecentry into the CNS of the horse is likely related to leukocyte- tion with S. neurona and development of EPM are not well associated parasitemia. Once in the CNS, S. neurona can understood. Although S. neurona lacks the genetic diversity localize and replicate in any region, from cerebrum to spinal found among Toxoplasma gondii isolates it may still be cacord (and including the optic nerves). Peripheral nerves pable of T. gondii-like clonal expansion of virulent strains16 (other than cranial nerves I and II which are actually part of although conclusive evidence for this in strains that have the CNS) and nerve roots are not infected. The location and infected horses has not yet been found. Results of risk factor extent of the lesions determine the character and severity of analysis for EPM vary by study, but factors likely to increase clinical signs. Histologically, protozoa are usually associated exposure to opossums, their environment, and their feces with mixed inflammatory cellular responses and neuronal are consistently identified.11,17-19 Other risk factors include destruction. Schizonts (multicellular proliferative bodies) previous diagnosis of EPM on the premises, primary use of or free merozoites are seen commonly in the cytoplasm of the horse, with show horses and race horses at increased risk, neurons or mononuclear phagocytes and in capillary endo- recent transport, and recent adverse health events, including thelial cells or rarely in other inflammatory or CNS cells.3 medical problems, parturition, and management changes.

Both cellular and humoral immunity are thought to be Collectively, these risk factors indicate that physiological important for control of infection by S. neurona. Because stress may play an important role in the onset of EPM. of the intracellular location of the parasite, competent cellmediated adaptive immune responses are considered es- Diagnosis sential for its elimination.

Ante mortem diagnosis of EPM remains challenging. Criteria for diagnosis include finding clinical signs consistent Epidemiology with EPM, ruling out other differential diagnoses, and finding Equine protozoal myeloencephalitis is a disease of horses S. neurona-specific antibodies through immunodiagnostic that have spent time in North or South America. There are testing. Proof of diagnosis post mortem is demonstration isolated reports of horses diagnosed with EPM elsewhere of protozoa in CNS lesions, often done with immunohistoWWW.FAEP.NET |

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chemical staining or polymerase chain reaction. Even when the organism is not seen, the diagnosis frequently is made presumptively if characteristic inflammatory changes are found.20,21 Two types of immunodiagnostic test are available for EPM: those that rely on threshold values of serum anti-S. neurona antibody (indirect fluorescent antibody test, ELISAs for antibody against various S. neurona surface antigens) and those that purport to detect specific antibody made within the CNS (western blot, serum:CSF antibody ratios, C-values). Blood samples for serum tests are easily obtained but the diagnostic assays are based on the yet-tobe validated principle that horses with EPM have distinctly higher serum antibody concentrations than do exposed/ subclinically infected horses.22 The rationale for tests of the second type, each of which requires a clean CSF sample, is that identification of CNS-origin antibody is the only way to discriminate EPM cases from exposed horses. The most popular test of each type – namely, serum IFAT and snSAG2,4/3 ratio, both have reported good (i.e., >80%) sensitivity and specificity for diagnosis of EPM among horses with solid post-mortem diagnoses.23,24 One drawback of the IFAT is that it is unable to differentiate between antibodies against S. neurona and S. fayeri (a nonpathogenic species)25 but an advantage is that submitted samples are tested for both S. neurona and N. hughesi antibodies. A recent study used samples from necropsy-confirmed EPM positive and negative cases to specifically compare results of serum IFAT and snSAG2,4/3 serum:CSF ratio tests. Sensitivity, specificity, and accuracy values were 59%, 71% and 68% for the serum IFAT and 88%, 100%, and 97% for the snSAG2,4/3 Figure 1

Figure 2

ratio test.21 Further large comparative clinical studies are needed to determine clearly the relative utilities of these 2 approaches, although the lack of a gold standard for diagnosis in horses that are not subjected to necropsy makes this challenging. What is clear, on the basis of both flawed concepts and unsupportive clinical data, is that neither CSF western blot nor serum SAG-1 ELISA is a robust diagnostic test for EPM.26-28 In contrast to the situation with western blots, results of snSAG ratio test results are relatively robust in the presence of a small amount of contaminating blood; however, false positives do occur in cases of moderate or severe blood- brain barrier (BBB) injury. For samples from horses with BBB injury (as detected by high CSF albumin concentrations or high albumin quotient values), additional total IgG testing is performed on the serum/CSF sample and a C-value calculated.29 CNS antibody production is indicated

by C-values greater than 1.0.

At the time it was last investigated more than a decade ago, PCR testing of CSF had high specificity but very low sensitivity for the diagnosis of EPM.30 False negatives are common because free parasitic DNA is destroyed by enzymes in the CSF and merozoites rarely enter the CSF. Testing by PCR of tissue samples is useful for post mortem diagnosis.

Ancillary procedures, including survey cervical radiographs, lameness examination and serology, may be required to rule out competing differential diagnoses. In horses with signs of brain involvement, suggestive lesions may be seen with advanced imaging techniques (Javsicas et al. 2008)31.

Consistent abnormalities are not found in complete and differential white blood cell counts and serum chemistry panels in horses with EPM. Abnormal CSF values occur in some Figure 3

24 The Practitioner Issue 4 • 2016

horses with EPM. It has been reported that as many as 35% of horses at a referral hospital have increased protein concentration (>65 mg/dL) or nucleated cell count (>6 cells/µL).32 In the author’s experience, in horses with mild clinical signs of EPM (i.e. those that typically are encountered in practice), a very low percentage have any abnormality on routine CSF analysis.

Creatine kinase (CK) activity may be high in CSF, reflecting diffusion of the BB isoenzyme from damaged CNS grey matter (Furr and Tyler 1990).33 Unfortunately, inadvertent inclusion of a small plug of epidural fat or dura during CSF collection can dramatically elevate CK activity, thus reducing the specificity of the test.

Figure 4

Clinical signs (Figures 1-7)

Protozoa may infect any part of the CNS, making almost any neurological sign possible. The disease usually begins insidiously but also may present acutely and be severe at onset. Signs of spinal cord involvement are seen much more commonly than signs of brain disease. Horses with EPM involving the spinal cord have asymmetric (usual) or symmetric truncal and limb weakness and ataxia. If all lesions are behind the second thoracic spinal cord segment (T2), only the pelvic limbs are affected. If a lesion (or lesions) is located in front of T3, all 4 limbs may be affected. In the rare instance when the spinal cord behind the second sacral spinal cord segment (S2) is involved, there are signs of cauda equina syndrome, which may include degrees of rectal, anal, bladder and penile paralysis, and reduced sensation of the skin of the tail and perineum. When grey matter of the ventral horn of the spinal cord is damaged for more than 1 to 2 weeks, there may be obvious focal muscle atrophy and electromyographic changes in denervated muscle. Common locations for atrophy in horses with EPM are the gluteal, biceps femoris, infraspinatus/supraspinatus and serratus ventralis muscles. Lesions in the spinal cord also may result in demarcated areas of spontaneous sweating or loss of reflexes and cutaneous sensation.

Neurological signs noticed at the walk or during neurological examination include any to all of the following: asymmetric stride length, toe dragging, circumduction of pelvic limbs and hypometria (also described as floating or marching) of thoracic limbs. Other signs are noted only when the horse is ridden. There may be difficulty maintaining a specific lead or performing gait transitions, cross cantering or cross galloping, and difficulty negotiating turns. Some signs that usually are attributed to primary musculoskeletal disease, such as back soreness or upward fixation of the patella(s), can be caused by weak or asymmetric use of muscle groups in horses with EPM that are in training.

The most common manifestation of brain disease in horses with EPM is a brain stem syndrome with signs of obtundation and asymmetric vestibular (VIII) nerve dysfunction. There may also be facial paralysis (VII), dysphagia (X), tongue paralysis (XII), laryngeal paralysis (X), strabismus (III, IV, IV), failure of

Figure 5

Figure 6

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Figure 7

globe retraction (VI) and deviation of the mandible (Vm).

With involvement of the rostral brain stem or cerebrum, EPM may manifest as seizures, visual deficit/abnormal menace response, reduced perception of touch on the opposite side of the face, or behavioral abnormality.

Without treatment, EPM usually progresses. Progression to recumbency occurs over hours to years and may occur steadily or in a stop-start manner.

Treatment

Since 2000, the folate inhibitor combination sulfadiazine/pyrimethamine (SDZ/PYR), the triazine coccidiostats ponazuril (PNZ) and diclazuril (DCZ), and the nitrothiazole nitazoxanide (NTZ) have all been licensed by the Federal Drug Administration for the treatment of EPM and commercial products have been launched.34 NTZ was withdrawn in 2009. Multi-center studies of SDZ/PYR, PNZ, NTZ, and DCZ reported improvement rates of 57.1 to 61.5%.34 Many dosage permutations and combinations of these products and the use of pharmacologically similar products occur in clinical practice although efficacies have not been investigated. A loading dose of 15 mg/kg PNZ (3 times the normal dose) achieves steady state concentrations of PNZ several days earlier than is the case with conventional dosing.35 A sodium salt formulation of diclazuril has been shown to have good oral bioavailability and may have potential as a feed additive.36 Some veterinarians use a compounded

form of diclazuril IV, although there are no published data for its safety or efficacy and its use is not recommended.

There is experimental support for the enhanced antiprotozoal effect of combinations of PYR with either DCZ or PNZ in treatment of other coccidian infections in non-equid species37 so the author routinely combines PNZ and SDZ/PYR when treating horses for clients with the necessary financial resources. Such treatments constitute unapproved and/or extra-label use, albeit of FDA-approved products.

Another drug used commonly as an anticoccidial in calves, decoquinate, was evaluated in horses with presumptive EPM, at dosage of 0.5 mg/kg daily for 10 days, in combination with the immunomodulator levamisole, 1 mg/ kg daily.38 Success rates of 93.6% and 89.3% were reported on the basis of improved neurologic gait score at the end of treatment and reversion of serum snSAG1,5,6 titers, respectively. Decoquinate has been shown to have potent inhibitory and cidal activity in vitro against 2 different isolates of S. neurona.39 If this drug combination continues to perform well in wider use it will obviously become an important treatment option.

Horses may relapse soon after the initial course of treatment is discontinued, or up to several years after improvement or apparent resolution of signs. Although there is no consensus on how to treat relapses, the author prefers to change or add antiprotozoal drugs. If a horse relapses twice, the author usually recommends indefinite intermittent therapy with SDZ/PYR, 2 days/week at double the standard dose. Alternatively, daily diclazuril or ponazuril may safely prevent relapses. Daily dosing of foals with diclazuril at 0.5 mg/kg (half the treatment dose rate) was found to prevent seroconversion against S. neurona suggesting that protozoal replication is prevented by this regimen.40 A similar rationale can be used to treat horses only around stressful events that may predispose to relapses.

Of the available drugs, only PYR has significant adverse side effects. Toxicity reflects inhibition of mammalian dihydrofolate reductase by PYR, inducing folate deficiency.

Signs include reproductive and neonatal disorders, glossitis, and bone marrow suppression, including anemia, leukopenia, neutropenia, and thrombocytopenia, in decreasing frequency.41,42 Horses treated with SDZ/PYR should be kept on good quality green forage (e.g. alfalfa hay or pasture), which is likely to be rich in folate. There is no advantage

26â&#x20AC;&#x201A; The Practitionerâ&#x20AC; Issue 4 â&#x20AC;˘ 2016

to supplementation with folic acid during treatment, and some evidence from other species indicate that this practice could increase the possibility of toxicity.42 Most cases of bone marrow suppression resolve if treatment is suspended for 1–2 weeks. Folic acid (100 mg daily) is appropriate for treatment of folate deficiency once PYR is discontinued. If signs are severe, treatment with folinic acid (100 mg IV or per os daily for one month, then every other day for one month) is indicated.

In mild acute cases of EPM (grade 1), additional therapy is unnecessary. In horses with moderate or severe disease, anti-inflammatory and antioxidant treatment is usually provided for the first 1 to 2 weeks. If the horse is grade 3 or worse, a corticosteroid may be added. Vitamin E is often given empirically throughout the period of antiprotozoal treatment for additional anti-oxidant effect. Oral administration of vitamin E has been shown to result in increased concentrations of alpha-tocopherol in serum and CSF. As a relatively crude way to address putative immunodeficiency and ‘boost’ cellular immunity, immune stimulants (Table 4) are sometimes given to horses with EPM.

Prognosis

On the basis of drug efficacy studies and clinical experience, it is reasonable to expect that about 60% of moderately or severely affected horses will improve at least one grade after treatment. Only 10–20% of such horses will completely recover and 10–20% of successfully treated horses will suffer at least one relapse. The outlook for mildly affected horses (grade 1) is considerably better, particularly if treatment is begun promptly. Although there are no published data for the latter, more common class of treated horse, at least 80% of such cases can be expected to improve and at least 50% should recover completely, with low possibility of recurrence.

Prevention

An inactivated vaccine was marketed under conditional approval by the USDA. The conditional license lapsed in March 2008 and the vaccine is no longer available. There was no published evidence for or against preventative efficacy for this product.

Prevention of EPM by anti-protozoal agents is probably effective but probably cost- prohibitive. Prevention of infection by S. neurona may be possible by daily administration of a drug such as DCZ or PNZ.40,43 The disadvantage of this approach is that normal immune responses to the organism may be prevented. An alternative approach is metaphylaxis, wherein intermittent doses of drug are given which allow an initial round of protozoal proliferation and normal immune responses to take place, but prevent invasion of the CNS. Ponazuril given at 20 mg/kg every 7 days but not every 14 days significantly reduced S. neurona antibody in the CSFof

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S. neurona-challenged horses, suggesting the potential utility of such an approach.44 Common-sense measures can be instituted to prevent contamination of feed with S. neurona sporocysts. Opossums can be trapped and removed or kept away by free-ranging dogs.

Spilled grain, fallen fruit and animal or bird feed should be removed, and horse food sources should be monitored and secured. The utility of controlling intermediate hosts in an effort to reduce environmental sporocyst load is doubtful; however, if there are heavy populations of host animals on a problem premise, then such animals should be trapped and removed. Products useful for cleaning of areas potentially contaminated with sporocysts have been described.45 Selected References: 1. Dubey JP, Davis SW, Speer CA, et al. Sarcocystis neurona n. sp. (Protozoa: Apicomplexa), the etiologic agent of equine protozoal myeloencephalitis. J Parasitol 1991;77:212-218.

2. Marsh AE, Barr BC, Packham AE, et al. Description of a new Neospora species (Protozoa: Apicomplexa: Sarcocystidae).

J Parasitol 1998;84:983-991.

3. Dubey JP, Lindsay DS, Saville WJA, et al. A review of Sarcocystis neurona and equine protozoal myeloencephalitis (EPM). Veterinary Parasitology 2001;95:89-131.

4. Stanek JF, Stich RW, Dubey JP, et al. Epidemiology of Sarcocystis neurona infections in domestic cats (Felis domesticus) and its association with equine protozoal myeloencephalitis (EPM) case farms and feral cats from a mobile spay and neuter clinic. Veterinary Parasitology 2003;117:239-249.

5. Dubey JP, Saville WJA, Stanek JF, et al. Sarcocystis neurona infections in raccoons (Procyon lotor): evidence for natural infection with sarcocysts, transmission of infection to opossums (Didelphis virginiana), and experimental induction of neurologic disease in raccoons. Veterinary Parasitology 2001;100:117-129.

6. Cheadle MA, Yowell CA, Sellon DC, et al. The striped skunk (Mephitis mephitis) is an intermediate host for Sarcocystis neurona. International Journal for Parasitology 2001;31:843-849.

7. Cheadle MA, Tanhauser SM, Dame JB, et al. The ninebanded armadillo (Dasypus novemcinctus) is an intermediate host for Sarcocystis neurona. International Journal for Parasitology 2001;31:330-335.

8. Mullaney T, Murphy AJ, Kiupel M, et al. Evidence to support horses as natural intermediate hosts for Sarcocystis neurona.

Vet Parasitol 2005;133:27-36.

9. Pitel PH, Pronost S, Gargala G, et al. Detection of Sarcocystis neurona antibodies in French horses with neurological signs. International Journal for Parasitology 2002;32:481-485.

10. Goehring LS, van Oldruitenborgh-Oosterbaan MMS. Equine protozoal myeloencephalitis in the Netherlands? An overview. Tijdschrift Voor Diergeneeskunde

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

2001;126:346-351.

11. WJA S, SM R, PS M, et al. Analysis of risk factors for the development of equine protozoal myeloencephalitis in horses.

J Am Vet Med Assoc 2000;217:xxx-xxx.

12. CK F, DE G, JL L, et al. Epizootic of equine protozoal myeloencephalitis on a farm. J Am Vet Med Assoc 1997;210:923927.

13. Bentz BG, Ealey KA, Morrow J, et al. Seroprevalence of antibodies to Sarcocystis neurona in equids residing in Oklahoma. Journal of Veterinary Diagnostic Investigation 2003;15:597-600.

14. Vardeleon D, Marsh AE, Thorne JG, et al. Prevalence of Neospora hughesi and Sarcocystis neurona antibodies in horses from various geographical locations. Veterinary Parasitology 2001;95:273-282.

15. Morley P, Traub-Dargatz J, Saville W, et al. Equine protozoal myeloencephalitis.

Journal of Equine Veterinary Science 2001;21:262-270.

16. Wendte JM, Miller MA, Nandra AK, et al. Limited genetic diversity among Sarcocystis neurona strains infecting southern sea otters precludes distinction between marine and terrestrial isolates. Vet Parasitol 2009.

17. Cohen ND, MacKay RJ, Toby E, et al. A multicenter case-control study of risk factors for equine protozoal myeloencephalitis. Javma-Journal of the American Veterinary Medical Association 2007;231:1857-1863.

18. Morley PS, Traub-Dargatz JL, Benedict KM, et al. Risk factors for owner-reported occurrence of equine protozoal myeloencephalitis in the US equine population. Journal of Veterinary Internal Medicine 2008;22:616-629.

19. Rossano MG, Kaneene JB, Marteniuk JV, et al. A herdlevel analysis of risk factors for antibodies to Sarcocystis neurona in Michigan equids. Prev Vet Med 2003;57:7-13.

20. Fayer R, Mayhew IG, Baird JD, et al. Epidemiology of equine protozoal myeloencephalitis in North America based on histologically confirmed cases. A report. J Vet Intern Med 1990;4:54-57.

21. Johnson AL, Morrow JK, Sweeney RW. Indirect Fluorescent Antibody Test and Surface Antigen ELISAs for Antemortem Diagnosis of Equine Protozoal Myeloencephalitis. J Vet Intern Med 2013.

22. Furr MO. Equine protozoal myeloencephalitis In: Furr MO,Reed SM, eds. Equine Neurology. Ames: Blackwell Publishing, 2008;197-212.

23. Duarte PC, Ebel ED, Traub-Dargatz J, et al. Indirect fluorescent antibody testing of cerebrospinal fluid for diagnosis of equine protozoal myeloencephalitis. Am J Vet Res 2006;67:869-876.

24. Reed SM, Howe DK, Morrow JK, et al. Accurate Antemortem Diagnosis of Equine Protozoal Myeloencephalitis (EPM) Based on Detecting Intrathecal Antibodies against Sarcocystis neurona Using the SnSAG2 and SnSAG4/3 ELISAs. Journal of Veterinary Internal Medicine 2013;27:1193-1200.

25. Saville WJA, Dubey JP, Oglesbee MJ, et al. Experimental infection of ponies with Sarcocystis fayeri and differentiation

from Sarcocystis neurona infections in horses. Journal of Parasitology 2004;90:1487-1491.

26. Johnson AL, Burton AJ, Sweeney RW. Utility of 2 Immunological Tests for Antemortem Diagnosis of Equine Protozoal Myeloencephalitis (Sarcocystis neurona Infection) in Naturally Occurring Cases. Journal of Veterinary Internal Medicine 2010;24:1184-1189.

27. Daft BM, Barr BC, Gardner IA, et al. Sensitivity and specificity of western blot testing of cerebrospinal fluid and serum for diagnosis of equine protozoal myeloencephalitis in horses with and without neurologic abnormalities. J Am Vet Med Assoc 2002;221:1007-1013.

28. Andrews FM, Geiser DR, Sommardahl CS, et al. Albumin quotient, IgG concentration, and IgG index determinations in cerebrospinal fluid of neonatal foals. Am J Vet Res 1994;55:741-745.

29. Furr M, Howe D, Reed S, et al. Antibody Coefficients for the Diagnosis of Equine Protozoal Myeloencephalitis. Journal of Veterinary Internal Medicine 2011;25:138-142.

30. AE M, BC B, J M, et al. Sequence analysis and polymerase chain reaction amplification of small subunit ribosomal DNA from Sarcocystis neurona. Am J Vet Res 1996;57:975-981.

31. Javsicas LH, Watson E, MacKay RJ. What is your neurologic diagnosis? Equine protozoal myeloencephalitis. J Am Vet Med Assoc 2008;232:201-204.

32. Reed SM, Granstrom DE, Rivas LJ, et al. Results of cerebrospinal fluid analysis in 119 horses testing positive to the Western blot test on serum and CSF to equine protozoal encephalomyelitis. In Proceedings AAEP 1994;41:199.

33. Furr MO, Tyler RD. Cerebrospinal fluid creatine kinase activity in horses with central nervous system disease: 69 cases (1984-1989). J Am Vet Med Assoc 1990;197:245-248.

34. MacKay RJ. Equine protozoal myeloencephalitis: treatment, prognosis, and prevention. Clin Tech Equine Pract 2006;5:9-16.

35. Mitchell SM, Zajac AM, Davis WL, et al. The effects of ponazuril on development of apicomplexans in vitro. J Eukaryot Microbiol 2005;52:231-235.

36. Dirikolu L, Karpiesiuk W, Lehner AE, et al. New therapeutic approaches for equine protozoal myeloencephalitis: Pharmacokinetics of diclazuril sodium salts in horses.

Veterinary Therapeutics 2006;7:52-+.

37. DS L, NS R, BL B. Treatment of acute Toxoplasma gondii infections in mice with diclazuril or a combination of diclazuril and pyrimethamine. J Parasitol 1995;81:315-318.

38. Ellison SP, Lindsay DS. Decoquinate Combined with Levamisole Reduce the Clinical Signs and Serum SAG 1, 5, 6 Antibodies in Horses with Suspected Equine Protozoal Myeloencephalitis. International Journal of Applied Research in Veterinary Medicine 2012;10:1-7.

39. Lindsay DS, Nazir MM, Maqbool A, et al. Efficacy of decoquinate against Sarcocystis neurona in cell cultures. Vet Parasitol 2013.

28 The Practitioner Issue 4 • 2016

OSPHOS® (clodronate injection)

40. Pusterla N, Packham A, Mackie S, et al. Daily feeding of diclazuril top dress pellets in foals reduces seroconversion to Sarcocystis neurona. Veterinary Journal 2015;206:236-238.

41. Piercy RJ, Hinchcliff KW, Reed SM. Folate deficiency during treatment with orally administered folic acid, sulphadiazine and pyrimethamine in a horse with suspected equine protozoal myeloencephalitis (EPM). Equine Vet J 2002;34:311-316.

42. RE T, FT B, DR M, et al. Congenital defects in newborn foals of mares treated for equine protozoal myeloencephalitis during pregnancy. J Am Vet Med Assoc 1998;212:697-701.

43. Furr M, McKenzie H, Saville WJA, et al. Prophylactic administration of ponazuril reduces clinical signs and delays seroconversion in horses challenged with Sarcocystis neurona.

Journal of Parasitology 2006;92:637-643.

44. MacKay RJ, Tanhauser ST, Gillis KD, et al. Effect of intermittent oral administration of ponazuril on experimental Sarcocystis neurona infection of horses. American Journal of Veterinary Research 2008;69:396-402.

45. Dubey JP, Saville WJ, Sreekumar C, et al. Effects of high temperature and disinfectants on the viability of Sarcocystis neurona sporocysts. Journal of Parasitology 2002;88:1252-1254.

Robert J. MacKay, DACVIM, PhD, BVSc (Dist) Professor of Large Animal Medicine Dr. Rob MacKay has been a faculty clinician-researcher at the University of Florida Large Animal Hospital since 1987. His clinical responsibilities include internal medicine in all species, with a large predominance of equine cases.

Since working with his residency mentor, Dr. Joe Mayhew, at the University of Florida in the early 1980s, Dr. MacKay has maintained a strong interest in neurologic diseases of horses with special emphasis in infectious etiologies including equine protozoal, myeloencephalitis, toxic neuropathies including pastureassociated stringhalt and creeping indigo toxicity, and developmental abnormalities including CVSM (wobblers).

Dr. MacKay’s research has covered several aspects of EMP life cycle and diagnostics relevant to clinical practice as well as aspects of equine endotoxemia and anhidrosis.

The new FDA approved intramuscular bisphosphonate injection for navicular syndrome from Dechra Veterinary Products

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, chloro-containing bisphosphonate. Chemically, clodronate disodium is (dichloromethylene) diphosphonic acid disodium salt and is manufactured from the tetrahydrate form.

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

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

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. 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.

He is author of numerous chapters and conference proceedings on these topics and has spoken at multiple national meetings including the AAEP, ACVIM, and FAEP. Distributed by: Dechra Veterinary Products 7015 College Boulevard, Suite 525 Overland Park, KS 66211 866-933-2472

Learn more at www.OSPHOS.com

© 2016 Dechra Ltd. OSPHOS is a registered trademark of Dechra Ltd. All rights reserved. NADA 141-427, Approved by FDA

The ’90s make for a fun party theme, not an effective equine vaccine.

You can party like it’s 1999 all you want, but when it comes to effective horse health solutions, it’s time to get serious. Other manufacturers rely on vaccines from the past century. Vetera® is designed with every horse’s long-term health in mind. Through our recently updated portfolio of vaccines, we are committed to providing horses with the best defense against the viruses that threaten them today.

Ask your veterinarian or visit vetera-vaccines.com to learn about our updated portfolio of vaccinations.

www.bi-vetmedica.com Vetera is a registered trademark of Boehringer Ingelheim Vetmedica GmbH. ©2016 Boehringer Ingelheim Vetmedica, Inc. BIVI/VETE/161022

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30 The Practitioner

Issue 4 • 2016

THIS IS

My Horse

™

When we started giving American Pharoah the Healthy Weight, we just noticed an immediate difference. It kept him looking healthy and sharp during the intense Triple Crown campaign. At the end of the season, he ran against older horses in the Breeders' Cup Classic and won by 6 1/2 lengths, breaking the track record!

So, all of our horses now get at least one of the Platinum formulas. Some get Osteon for their bones, especially the growing colts. Pharoah and some others get the Healthy Weight, and all of them get Platinum Equine as an overall health supplement.

Bob Baffert, Trainer

American Pharoah

Winner of 4 Kentucky Derbies, 6 Preakness Stakes, 2 Belmont Stakes, and 12 Breeders’ Cup races.

Platinum Performance® Client since 2012

The first horse to win the American “Grand Slam”: 2015 Kentucky Derby, Preakness Stakes, Belmont Stakes & the Breeders’ Cup Classic

Bob Baffert is a sponsored endorsee and actual client.

this is My Platinum Platinum Performance® Equine supports: • Joint Health • Hoof Health • Skin & Coat Health

• Performance & Recovery • Digestive Health • Bone & Tendon Health

Osteon®

866-553-2400

www.PlatinumPerformance.com

• Supports Bone & Connective Tissue Health

Healthy Weight • Provides Calories for Horses That Need to Gain Weight • Provides a Natural Source of Antioxidant, Vitamin E

To find the right Platinum Performance® solution, and to learn about the science behind the supplements, please call us or visit our website today. © 2016 PLATINUM PERFORMANCE, INC.