Practitioner Issue 3, 2017

Page 1

Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 3 • 2017 PRURITUS: CAUSES AND CONTROL STRATEGIES SUSAN L. WHITE DVM, MS, DACVIM




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The President's Line Ruth-Anne Richter, BSc (Hon), DVM, MS - FAEP President Dear Fellow Equine Practitioners, I am excited to report, as we’ve just concluded the 13th Annual Promoting Excellence Symposium, that this year’s symposium was a complete success, and was well supported by our loyal attendees. Despite particular challenges during an active hurricane season, this year’s event surpassed previous attendance records altogether. This was truly nothing short of a miracle, given that damage to our beachside venue from Hurricane Irma made the facility incapable of hosting the 2017 PES, and rather than cancel the meeting entirely, the FAEP council opted to seek alternative sites. Tremendous effort on the part of the FVMA staff made it possible to move the entire conference to Orlando within four weeks of the meeting date, and once again PES proved to be of terrific value to all who attended. A very special “thank you” again to the FVMA staff, without whom these outstanding continuing education programs would not be possible. With this successful conference behind us, we have turned our complete attention to our annual CE offering in Ocala, the “Horse Capital of the World.” We invite you to attend the 55th Annual Ocala Equine Conference January 19-22, 2018. Our event, “For Practitioners by Practitioners,” will take place at the newly-renovated Hilton Ocala, and features a program of cutting-edge lectures from world-class speakers, and also provides 25 hours of high-quality continuing education. We are excited to once again host the ever-popular, extensive ultrasound wet lab, featuring instruction in small groups from experts in the field. The Ocala Equine Conference provides an exciting opportunity for the exchange of ideas and partnership in the equine veterinary medical team, in an intimate environment. We invite you to join us for outstanding CE, and to connect with more than 50 industry representatives who will showcase their products and services in the vibrant exhibit hall. We hope you will join us in Ocala next January as we launch an exciting 2018 season, and please feel free to contact us if you have any questions about the FAEP and the services we provide, and about our conferences. We always welcome your comments and suggestions, and encourage you to contact our council members or the FVMA and FAEP staff by email at, or by phone at (407) 851-3862. We also can be reached toll-free at (800) 992-3862.


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Opinions and statements expressed in The Practitioner reflect the views of the contributors and do not represent the official policy of the Florida Association of Equine Practitioners or the Florida Veterinary Medical Association, unless so stated. Placement of an advertisement does not represent the FAEP’s or FVMA’s endorsement of the product or service. FAEP | 7207 MONETARY DRIVE, ORLANDO, FL 32809 | PH: (800) 992-3862 | FAX: (407) 240-3710 | EMAIL: INFO@FVMA.ORG | WEBSITE: WWW.FAEP.NET

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PRURITUS: Causes and Control Strategies SUSAN L. WHITE | DVM, MS, DACVIM Pruritus often leads to self-inflicted trauma, alopecia, and moderate to severe secondary skin lesions, resulting in horses which are visually disfigured and/or unsound for work. Because of the many possible diagnoses of a pruritic skin disease, the history, especially the environment, seasonality, age of onset and progress of the disease, as well as previous treatment modalities and response, are very important in making a diagnosis. Time spent obtaining a detailed, complete history is rewarding, and often equally as important as the examination and diagnostic tests.

Insect Bite Hypersensitivity (IBH)

A large percentage of horses affected with seasonal pruritic dermatitis are hypersensitive to the bites of insects. Any biting insect, including Culicoides spp. (No-see-ums, midges, punkies), stable flies (Stomoxys calcitrans), horn flies (Hematobia sp), black flies or "buffalo gnats" (Simulian spp.), horse and deer flies (Tabanidae and Chrysops spp.), and mosquitoes (primarily Culex and Aedes spp.), can cause insect hypersensitivity dermatitis. "Chiggers" (Trombiculids) and ticks can also lead to hypersensitivity reactions. Insect bite-induced hypersensitivities are characterized by intense pruritus which often leads to excoriation, extensive hair loss, secondary infections, and chronically to hyperkeratosis and lichenification. Several different clinical syndromes have been associated with hypersensitivities to different insects. Queensland

Culicoides lesions are dorsally distributed, with severe involvement of the mane and tail area.

or Sweet Itch, initiated by the bites of the hematophagous Culicoides species, is classically characterized by a diffuse dorsal distribution with severe involvement of the mane and tail area. However, there are several species of Culicoides in different geographic areas, and different species have different preferred areas of feeding, with some species having a predilection for biting the ventral aspect of the body. The only region generally not affected by Culicoides is the flank.1 A hereditary predisposition to develop hypersensitivity to Culicoides spp. has been shown in some breeds of horses and clinical evidence supports a familial tendency for hypersensitivity in many, if not all, breeds.2,3 Although Culdicoides spp gnats are the most common and consequently the most studied, there are a wide variety of gnats in certain regions of the country (such as the Southeast) that occur in great numbers, can be found almost any time of the day, and cause annoyance, irritation, and serve as atopenes, contributing to hypersensitivity reactions. Simulian flies are blood suckers, and bites are covered with small accumulations of dried blood. In mass attacks, urticaria and angioedema may occur and can be associated with systemic signs of weakness with an increased pulse and respiratory rate, particularly in small, young animals. Bites of Simulian spp. are most commonly associated with lesions on the head and within the inner pinnae, but in "swarm attacks" may bite any region of the horse. A generalized ventral distribution of lesions may also be caused by black flies.1 Bites of horn flies (Haematobia irritatins) have been implicated in Ventral Midline Dermatitis, characterized by sharply demarcated focal lesions which often ooze serum. Horn flies prefer shade, and thus a few flies on a horse in the sunshine will be found on the ventral midline. In areas of heavy horn fly populations, these flies may be found everywhere on the body surface, including the body, legs and face. Horn flies breed only in cattle manure, and therefore most severe infestations are within a quarter of a mile of cattle farms. However, these flies may travel farther on wind currents, as they have been found on horses without nearby cattle. Stable flies (Stomoxys calcitrans) are vicious biters, as opposed to house flies (Musca spp), which feed on body secretions. Initial lesions may consist of erythema, wheals, and raised nodules with a central crust. Exudative dermatitis of the legs, due to reactions to extensive

6  The Practitioner  Issue 3 • 2017

Bites from horn flies have been implicated in Ventral Midline Dermatitis.

Multiple tick bites may induce edema, nodules, or ulcerated, crusted areas.



stable fly bites and/or urticaria and large nodules that are pruritic, characterize hypersensitivities to stable flies. Mosquito bites produce wheals and papules that are variably pruritic, and are often painful. The lesions do not have a central crust like the bites of other insects. Most individual lesions resolve in one to two days, however larger persistent nodules may develop in certain individuals. Chiggers and harvest mites (trombiculids) are free-living, and are found in undeveloped or overgrown fields and wooded areas. Adults are plant parasites, but the six-legged larval form requires blood or tissue fluids for further development. Mites are non-host specific and normally feed on small rodents. Infestations of horses may occur if horses are pastured or ridden in contaminated areas, and are most prevalent in the summer and fall. Feeding larvae cause papules with 1-2 mm crusts and can be intensely pruritic. Larvae remain on the host for two to seven days before dropping off to molt and are often absent by the time the horse is presented for examination. The larvae are 0.2-0.4 mm long and yelloworange to red in color and, if found, confirm the diagnosis. Horses may develop hypersensitivities to ticks, either larvae ("seed ticks") or adults. Bites may induce individual large nodules with a central crust and/or ulcer. Multiple bites may induce generalized edema, multiple nodules or ulcerated crusted areas. Very small larvae are easily overlooked even in massive infestations. Pruritus may be extreme, resulting in severe secondary lesions. Ticks are most commonly found on the legs, tail, head, and ears. Allergic diseases involve the interaction of three major factors: genetic constitution, exposure to allergens, and a dysregulation of the immune response determined by genetic predisposition and degree of exposure to allergens. However, other environmental factors such as infectious disease, contact with endotoxins and degree of infestation of endoparasites may also influence the prevalence of allergic diseases. Insect hypersensitivities are characterized by a Type I reaction. Type I hypersensitivity reactions develop in genetically-programmed susceptible individuals and is mediated by IgE antibodies and some subtypes of IgG, which are produced by plasma cells near epithelial surfaces and specific to individual antigens. A specific antibody binds to the surface receptors of tissue mast cells and blood basophils, and, when cross-linked by specific antigen, causes degranulation of and release of inflammatory and vasoactive mediators from mast cells. Horses with IBH have been shown to have a strong Th2-type immune response with the relative “overproduction� of IL-4, IL-5, IL-6, IL-13, and IL-31. Lack of suppression of the TH2 response by T- regulatory cells further enhances the immune response. A compromise in skin barrier function has been demonstrated in atopic humans and dogs and is thought to occur in horses. Irregular


or patchy components that form the tight junctions between epithelial cells allow for allergen entry, which is exacerbated by secondary skin infections. Furthermore, IL-31 binds directly to receptors on nerve fibers and promotes the sensation (along with other inflammatory mediators) of itch.4,5


Other allergies of the horse are atopic dermatitis, food allergies, or contact allergies. Atopy is defined as a geneticallyprogrammed disease in which the patient becomes sensitized to environmental antigens that in a nonatopic animal creates no disease. Human and canine atopy has been proven to be genetically-programmed, and there is reasonable evidence that atopy of horses is also determined genetically. Atopic reactions are a Type I hypersensitivity to allergens (termed atopenes), that are absorbed percutaneously, inhaled, or ingested. The hypersensitivity is not solely IgE- and IgGddependent and is a complex disorder of the immunologic system that results in a perturbation of many aspects of the immune response. Environmental factors such as horses stabled most of the time early in life may be sensitized at an early age to molds found in barns. Early high challenge with insect bites, parasitism, viral infections, and vaccination with modified live virus vaccines, may all influence the onset and occurrence of clinical disease in atopic individuals. Atopic animals often exhibit clinical signs of disease much earlier than horses with acquired insect hypersensitivities. Atopic horses may present between one to four years of age, although clinical signs may first appear as old as seven years old. Clinical signs may be seasonal or persistent year-round, dependent on the atopene. Many atopic horses' clinical signs will progress from seasonal to year-round over time. The primary clinical signs are pruritus and urticaria that are generally symmetric. Regions of the body such as the face, ears, neck, and legs may be affected, or a more dorsal distribution of lesions on the mane, back, and tail may occur. Atopic horses may also present with sterile eosinophilic folliculitis or tufted papules that become crusted and alopecic. It is important to remember that allergic reactions develop to common environmental antigens and that no new substances need be introduced to initiate the clinical disease. Secondary lesions caused by self-inflicted trauma due to pruritus often result in more extensive lesions and secondary superficial infections. It is not unusual for atopic horses (particularly in the Southeast) to have concurrent insect hypersensitivities, or, more rarely, a food allergy. Food allergies are relatively rare and are poorly documented in the literature. Food allergies may be presented as persistent or recurrent urticaria or pruritus with accompanying secondary lesions. Food allergies are best diagnosed by limiting the diet to one forage for four weeks and then adding back one foodstuff per week. Most authors prefer

grass hay as high protein hays such as alfalfa or peanut hay may contain the inciting agent.6 Soy, a common ingredient in any commercial concentrate feed, is also a relatively common allergen. In the author's experience, the most common offending feed is sweet feed or any other feed with molasses. An alternative to limiting the diet to just one forage is to eliminate molasses-based feeds, commercial grain mixes, or pellets and supplements containing alfalfa for three-four weeks, and then challenge the horse with the eliminated feed to determine the response to the feed. Contact dermatitis is characterized clinically by hyperemia, papules, and vesicles, and may appear like urticaria. It is generated by the percutaneous absorption of a substance which acts as a hapten and combines with a cutaneous protein. A T-cell response occurs against both hapten and protein. Once sensitized, lesions may be seen as early as five-six hours, or as late as 24-72 hours after contact with the offending substance. Pruritus may be a component of the clinical response. Secondary skin changes associated with prolonged and/or repeated exposure include: hyperpigmentation, lichenification, ulceration, and secondary pyoderma and mimic lesions associated with chronic insect allergies. Ingredients of many topical medications and insect repellents can produce contact

Contact dermatitis is characterized by hyperemia, papules, and vesicles, and may appear like urticaria.

8  The Practitioner†Issue 3 • 2017

allergies. Consequently, care must be used in the selection contaminated by bacteria or fungi. Occasionally horses may and use of topical medications in other allergic dermatosis. have "irritable skin," where large positive reactions are seen Skin lesions due to agents producing irritation alone may also at all injection sites, including the saline control. Despite the resemble contact allergies. Removal of the offending material number of difficulties and inexact science of IDT, it remains allergens for avoidance and as both diagnostic and curative, although time consuming, the preferred test for identifying ASIT, particularly for atopy.5,6 offers the best solution. A positive ID skin test means a horse has skin sensitizing antibody; it does not mean clinical disease is present. Size Diagnosis of the reaction site does not necessarily correlate with the Diagnosis is made from the signalment, history, clinical clinical importance of the allergen. Positive reactions can signs, and ruling out of other possible diagnoses. IBH typi- occur in clinically normal horses. The frequency of positive cally improves and exacerbates seasonally, whereas atopy may reactions to molds and insects in clinically normal horses occur at any time of the year. Urticaria, commonly found in tends to increase with the age of the horse. Thus the results atopy, is not a diagnosis but a cutaneous reaction pattern that of ID test must be evaluated in concert with the historical may be induced by a wide variety of causes, both immuno- and clinical findings. logic and nonimmunologic. Rule outs for urticaria include drug and vaccine reactions, stinging and biting insects (such Serologic Tests for Circulating IgE In the RAST, or radioallergosorbent test, and ELISA, or as wasps), and arachnids, infections, contacts, vasculitis, and cold, stress or exercise-induced lesions. The distribution of enzyme linked immunosorbent assay, the antigen to be lesions on an affected horse with IBH is dependent on the tested is attached to a solid substrate and is exposed to the patient's serum. A specific antibody binds to the antigen on biting characteristics of the insect responsible. Since there is the solid surface, which is subsequently washed. The amount still much to be learned about the identification and feeding of bound IgE is determined by the addition of a labeled habits of many of the insects implicated in allergic dermatoses, antiglobin with an indicator attached. There is, however, it may not be possible to identify the exact etiological agent. poor correlation between the results obtained by serology and intradermal skin testing.8 Increased concentration of Intradermal Allergy Testing IgE in heavily parasitized animals may give false positive Intradermal skin testing (IDT) is not used to make a defini- reactions. IgGd may also contribute to allergic dermatoses, tive diagnosis, but to identify allergens that can be avoided and is not detected by any of the serologic tests for IgE. Curor used in allergen specific immunotherapy (ASIT). Fifty rent methodology to overcome some of the limitations of percent or more of clinically normal horses in past reports serologic testing include prior absorbance of test serum for have been found to respond positively to intradermal skin helminth-associated and nonspecific IgE. Investigation of testing, although clinically normal horses generally respond the correlation between ID testing, RAST, and two ELISAs to fewer antigens.5-7 Nevertheless, intradermal skin test- for circulating IgE concentrations in horses with atopic dering with currently available antigens on selected cases may matitis, recurrent urticaria, and normal horses showed none provide identification of reactive antigens and guide part of of the three serum allergy tests detected allergen hypersentherapeutic management. sitivity with any reliability.9 Furthermore, IDT determines Antigens should be chosen from the environment of the tissue-fixed IgE and the entire inflammatory cascade. Since horse, including insects, plants (grasses, weeds, and trees), augmentation of the B cell response occurs in tissues, IDT grains, and forages. Both regional and seasonal variations in remains the test of choice. As with IDT, a positive serologic allergens exist, thus knowledge of the prevalence of plants test means a horse has a circulating antibody; it does not and pollens helps determine antigen selection. The optimal mean clinical disease is present. concentration of antigens in test solutions is variable and is still an active area of investigation. Control of Atopy and Insect-Mediated False negative reactions may occur if the horse has received Hypersensitivities glucocorticoids, antihistamines, or progestagens. There is Control of insect-mediated hypersensitivities by avoidno reliable information on withdrawal times of these medi- ance is the primary therapy. However, complete avoidance cations prior to skin testing. Anecdotal withdrawal times, can be difficult to impossible since several different insects developed by individual clinicians, are: three weeks for oral with different feeding patterns may be involved (Table 1). or topically administered corticosteroides, eight weeks for However, stabling of horses during peak feeding times of injectable corticosteroides, and 10 days for antihistamines and products and diets containing omega-3/omega-6 fatty biting insects identified in clinical disease can substantially acids. Phenothiazine tranquilizers and excessive excitement reduce the antigenic load. Stabling horses in barns with may also result in false negative reactions. Detomidine seda- clock-operated mist sprayers of nonresidual pyrethrins may offer the best overall protection. Because some horses may tion is useful for testing excitable horses. False positive reactions may occur if the allergen is in- develop a contactant or hypersensitivity response to repelnately irritant to the horse, or if the allergen vial has become lants, strategic use of fans to prevent insects from landing on




Table 1




Stable flies

Manure, rotting vegetation


Horn flies

Cattle manure


Horse & Deer flies

Vegetation & water



Standing water & manure

Twilight to dawn

Simulian (Black) flies

Running water

Morning & evening



Dusk to two hours past sunset

the horse are advisable in stalls and loafing sheds. Screens administration of prednisone or prednisolone often will used to exclude insects must have 60 squares per square inch provide adequate control. of screen to exclude Culicoides spp. Permethrin products, Antihistamines, particularly hydroxyzine hydrochloride, which can be applied at less frequent intervals, may aid in can be used at a dose of 0.5-1.5 mg/kg every eight-12 hours protecting horses at pasture. Several spot-on permethrin orally. Hydroxyzine is more effective in controlling urticaria products with 44-64 percent permethrin are marketed spe- than pruritus, but is a useful part of the management stratcifically for horses. These products are applied to the poll, egy. Other antihistamines that may offer some benefit are: withers, tail, head, and upper legs every one to four weeks cetirizine (0.2-0.4 mg/kg BID); chlorpheniramine (0.25 mg/ (read labels). Topical permethrin sprays (look for a greater kg BID); diphenhydramine (0.75-1 mg/kg BID); pyrilamine than two percent concentration of permethrin or cyper- maleate (1 mg/kg BID). Some authors also recommend methrin) can be used for other areas of the body on a daily tricyclic antidepressants doxepin hydrochloride (0.5 - 0.75 basis. The use of petroleum jellies and oils as a mechanical mg/kg BI, or amitriptyline (1-2 mg/kg BID).6 barrier may decrease the occurrence of bites, especially when Allergen-specific immune therapy consists of a series of inisolated areas of the body, such as the inside of the ears, are jections with increasing concentrations of antigens identified affected. Pyrethrin-impregnated, plastic mesh stable sheets by IDT given over several weeks, followed by maintenance are available and have been found useful by some owners, injections given every 20-40 days. Improvement is gradual as have "body suits" of light weight fly sheets and fine mesh. and generally recognized after six-12 months of treatment. The use of corticosteroids in topically-applied creams or If used as part of the therapy for IBH, the injection series leave-on rinses is helpful. Systemic corticosteroids remain the should be timed such that the maintenance dose is achieved best overall palliative therapy for generalized intense pruritus. prior to the onset of the insect exposure. Experience with Treatment should be initiated with 1-2 mg/kg prednisolone ASIT in horses has shown 30-70 percent of cases improve orally/day in the morning until the pruritus and secondary with therapy. Many horses with chronic insect hypersensiskin trauma are under control. The dose is then tapered to tivities have a Type IV (delayed) allergic response to insect the least amount that will control the clinical signs. Every bites, as well as an immediate Type I response. Since delayed other day administration (0.5 mg/kg PO) is desirable for hypersensitivity is not immunoglobulin-mediated, response long-term use. Prednisone may be used in some cases, but, to a hyposensitization regimen is less likely. It is important to because of its limited and variable oral bioavailability, not all remember that hyposensitization begun during the middle horses will respond to its use.9 In severe non-responsive cases, of the insect season and height of the horse’s cutaneous dexamethasone at 0.05 -0.1 mg/kg parenterally or orally may response is very unlikely to improve the horse during the interrupt the inflammatory response. Once the pruritus and current season. skin lesion development is under control, prednisolone or Atopic horses are the most likely to respond favorably to prednisone may be substituted. A combination of the best hyposensitization. Atopic horses improve at least 50 to 100 managerial practices possible, and oral every-other-day percent with partial improvement in 80 percent of atopic

10  The Practitioner  Issue 3 • 2017

horses with concurrent insect allergies. A recent retrospective study reported that 84 percent of owners reported a good response in horses treated with immunotherapy. Of these, 93 percent of owners of horses that improved reported that their horses needed treatment with parenteral steroids prior to immunotherapy, and after one year of immunotherapy 59 percent were managed with immunotherapy alone.10 Systemic corticosteroids may be used as in insect hypersensitivities and, in cases of recurrent or persistent urticaria, hydroxyzine orally every 12 hours may control reoccurrence of hives. Hydroxyzine will not resolve existing urticaria. Doxipen, a tricyclic antidepressant that also has antihistaminic effects, has been used for atopy (0.6-1.2 mg/ kg orally every 12 hours)6, however this author has no experience with it. Urticarial reactions may be associated with antigen exposure by systemic administration, inhalation, or ingestion. Definitive diagnosis of the etiologic agent is accomplished by removal and challenge. All possible antigens in the environment must be tested as hypersensitivity may develop to an antigen that has been present for a prolonged period of time. Recurrent urticaria can occur to common environmental antigens such as straw, blankets, and tack as well as hay and grains.

Differential Diagnoses

Other dermatoses that may also exhibit pruritus are onchocerciasis, oxyuriasis, dermatophytois, pemphigus foliaceus, pediculosis, and chorioptic mange. Onchocerciasis, a hypersensitivity to the microfilaria of Onchocerca cervicalis, has a lesion distribution that can mimic Culicoides allergic dermatitis. Since Culicoides spp. are the major vector of Onchocerca, differentiation between the two can be difficult. Finding large numbers of microfilaria in the skin of clinically affected horses is helpful but not diagnostic, and an inflammatory reaction to the larvae on histopathological examination is necessary. Ivermectin and moxidectin kill microfilaria in the skin within 14 days, but do not eliminate adult Onchocerca in the ligamentum nuchae. Clinically, the incidence of onchocerciasis has decreased with the common and frequent use of ivermectin or moxidectin for internal parasite control. However, strategic use of anthelmintics for gastrointestinal parasite control may result in more frequent occurrence of onchocerciasis. Infestations with Oxyuris equi are characterized by tail rubbing with loss of tail hairs and excoriations of the underlying skin. Diagnosis is made by examining an acetate tape that has been applied to the anal region for Oxyuris ova. Early infestations of dermatophytes may appear as localized wheals. Some infestations may be accompanied by a marked response to fungal products and have a more generalized edema, particularly on the legs, which may be painful and/or pruritic. Pemphigus



Chorioptic mites are most frequently found on horses with large amounts of lower limb hair.

foliaceus may also be pruritic, particularly when horses are exposed to sunlight, as solar radiation exacerbates pruritus. In cool weather, lice and chorioptes mange are common conditions exhibiting pruritus. Chorioptes mites affect the lower limbs and are most frequently found on horses with large amounts of lower limb hair (draft breeds, Andalusians). Skin scrapings for diagnosis of chorioptes should be mixed with rotenone or other insecticide as the mites move very fast and may crawl off the slide before examination. Although sucking lice (Haematopinus asini) are controlled with avermectins, biting lice (Bovicoli (Damalinia) equi, Wenedkiella equi equi) and chorioptic mites feed on epithelial tissue debris and are poorly controlled by parenterally administered avermectins. These parasites are most effectively treated with topical agents such as lyme sulfur or permethrin. Persistence of parasite populations occur in low numbers often on asymptomatic animals, thus all in-contact animals and common tack or grooming equipment should be treated. Secondary skin infections with Staphylococcus sp or


Malassezia sp may occur concurrently in atopic horses.1,11 It is well documented that atopic dogs are prone to both bacterial pyoderma and Malassezia infections. Staphylococcal infections may be an impetigo characterized by an accumulation of neutrophils on the skin surface, or may act as superantigens, which enhance the activation of large numbers of T cells and contribute to the inflammatory reaction in the skin. In this case, small groups of stapholococci may be seen adherent to keratinocytes without the presence of neutrophils. Malassezia sp are considered to be commensal surface organisms in dogs, but in one study were not demonstrated on normal horses. Clinical infections of Malassezia infections are characterized by greasy to waxy, foul-smelling, variably pruritic dermatitis in the axillae, groin, udder and prepuce. Superficial overgrowth of staphylococcal organisms and Malassezia infections may be treated topically with shampoos and antibiotics, and antifungal agents respectively. Staphylococcal impetigo responds best to systemic antimicrobial treatment. In all cases of pruritic dermatitis, managerial procedures to decrease exposure to exciting agents, as well as symptomatic therapy to reduce pruritus, is warranted. All avenues available to decrease exposure to insects should be fully implemented. Heat, humidity, and solar radiation exacerbate pruritus, thus the provision of shade and wind currents by fans can provide relief. Simple feeds and whole grains are better than mixed, multiple grain, sweet feeds. Cold water rinses and shampoos can rehydrate dry skin and reduce the amount of topical allergens on the skin. Colloidal oatmeal, pramoxine (a topical anesthetic), and 1 percent hydrocortisone shampoos or leave-on rinses (hydrocortisone is not absorbed) may reduce pruritus and minimize or reduce the amount of systemic antipruritics needed. A complete and detailed investigation into the etiology of the disease should occur simultaneously with general symptomatic care. The client must understand that hypersensitivities and atopy are lifelong, and the horse will need continuous management, and or therapy. Often a patient may be symptom free with low exposure to inciting antigens and symptomatic as the antigen "load" increases. Antigen exposure is additive, thus comprehensive management is needed to best control clinical disease.


Fadok VA. Update on equine allergies. Vet Clin North Am Equine Prac. 2013, 29:541-550

6. Yu AA. Treatment of equine allergies. Proceedings Am Assoc Equine Pract Resort Symposium, 2015 7.

Marcella R. equine allergy therapy. Vet Clin North Am Equine Prac. 2013, 29: 551-557


Lorch G, Hillier A, et al. Comparion of immediate intradermal test reactivity with serum IgE quantification by use of a radioallergosorbent test and two ELISA in horses with and without atopy. J Am Vet Med Ass 2001, 218:1314-1322 9. Peroni DL, Stanley S, et al. Prednisone per os is likely to have limited efficacy in horses. Equine Vet J 2002, 34:283-287 10. White SD, Vandenabeele SIJ, et al. Malassezia species isolated from the intermammary and preputial fossa areas of horses. J Vet Int med 2006, 20: 395-398 11. Stepnik CT, Outerbridge CA, et al. Equine atopic skin disease and response to allergen-specific immunotherapy: a retrospective study at the University of California-Davis (1991-2008). Vet Dermatol 2012, 23:29-36

Susan L. White DVM, MS, DACVIM Dr. White is the Josiah Meigs Distinguished Professor Emeritus in large animal medicine at the University of Georgia’s College of Veterinary Medicine. She is board- certified in Large Animal Internal Medicine, and has a master’s degree in veterinary pathology. Dr. White is a recipient of the ACVIM Kirk Award for professional excellence and is currently president of the American College of Veterinary Internal Medicine. She has published over 75 articles and book chapters and is a frequent speaker at CE meetings. Dr. White has had a long-standing interest in equine dermatology. She has lectured both nationally and internationally in large animal dermatology for over 25 years. She maintains a consulting service in equine dermatology nationally.

References 1.

White SD. A diagnostic approach to the pruritic horse. Equine Vet Education 2015, 27: 156-166


Schurinkl van Grevenhof, AE, et al. Heritability and repeatability of insect bite hypersensitivity in Dutch Shetland breeding mares. J Ani Science 2015, 87: 484-490 Schurink A, Ducro BJ. Genetic parameters of insect bite hypersensitivity in Dutch Friesian broodmares. J Ani Science 2014, 89: 1286-1293 Marcelaa R, Sousa CA. Current understanding of the pathophysiologic mechanisms of canine atopic dermatitis. JAVMA 2012, 241:194-207

3. 4.

12  The Practitioner  Issue 3 • 2017


















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Anhidrosis: Review and Updates MARTHA MALLICOTE | DVM, DACVIM Anhidrosis continues to be a very frustrating condition in the performance equine. Horses with anhidrosis display signs of poor thermoregulation, caused by inadequate sweating for the ambient weather conditions. The condition affects horses of all age groups, breeds, coat colors, genders, and activities, and is common among horses in hot, humid environments. Despite the enormous financial and emotional costs of anhidrosis, the causes and pathogenesis of the condition are largely unknown and no consistently effective treatment has been found. Clinical presentation, proposed treatments, and experimental data regarding macrolide-induced hyperthermia are reviewed with a focus on available evidence. Introduction Anhidrosis is defined as a decreased ability to sweat in response to hyperthermia. Failure to sweat has been described in both horses and man, and it manifests primarily in hot and humid climates – the addition of humidity appears important in eliciting signs. It is an important problem particularly in performance horses because thermoregulation is mainly accomplished by sweating. In the horse, between 65-70 percent of body heat is lost via the evaporation of sweat. A humid environment further decreases efficiency of sweat evaporation and cooling of the horse. Various suggestions have been proposed to explain the pathophysiology of anhidrosis, including hypothyroidism, hypochloremia and other electrolyte depletion, adrenal hypofunction, and abnormally increased epinephrine levels. None of these associations have been satisfactory except that decreased fractional excretion of chloride is a consistent finding. Hypothyroidism specifically has been disproven as an etiology for the syndrome. In chronic anhidrosis cases, ultrastructural examination reveals atrophied sweat glands, and there is a poor response to exogenous epinephrine injected into these glands. In acutely affected horses, these abnormalities are not yet present. Thus, a transition between acute and reversible disease into irreversible anhidrosis appears to occur, but the timing of this change is nonspecific. The discrete defects in sweat gland function or signaling that cause anhidrosis have not yet been determined, but there are several steps that could be the source of dysfunction. These include: prior to the binding of epinephrine to its sweat gland receptor, between receptor binding and opening of anion channels in the apical membrane of the sweat gland cell, or during the formation/expulsion of sweat. Some evidence is developing to support the hypothesis that anhidrosis results from a defect or defects early in the sequence of events that transduces agonist-receptor binding into chloride channel formation. The switch that flips persistent but

Horse with common forehead/face alopecia seen with chronic anhidrosis.

reversible desensitization into permanent anhidrosis is completely unknown. Prevalence Anhidrosis has been recognized for quite some time; the first published reports are from 1957, and describe signs in horses imported to tropical countries. Since then, researchers have not identified any age, sex, breed, or color predisposition for developing anhidrosis other than an interesting lack of reports in Arabian horses. Raising foals in a hot, humid climate is not protective, as both locally-bred and imported horses may be affected. An epidemiological analysis conducted in Florida revealed a strong association between family history of anhidrosis and risk of the condition, suggesting a genetic connection that warrants further investigation. Epidemiologic studies primarily conducted in Florida have suggested a prevalence of between 2- 6 percent of horses, though the prevalence may vary depending on the severity of climate with as much as 13 percent of horses affected in a report from veterinary hospitals in Pakistan. In a study of non-racetrack Florida farms, 1.8 percent of horses were anhidrotic and 11.2 percent of farms reported at least one case of anhidrosis. Clinical Signs Onset can be gradual or acute, with tachypnea and failure to cool after exercise the most common initial clinical finding. Affected horses experience episodes of tachypnea, hyperthermia, and limited sweating or failure to sweat in response during exertion. In situations that should elicit

14  The Practitioner  Issue 3 • 2017

copious sweating, these animals will have minimal or no sweat production. If forced to exercise in hot weather, respiratory rate may exceed 100 breaths/minute and temperatures may exceed 105 degrees Fahrenheit. In chronic cases, horses develop dry flaky skin (especially on the forehead), hair loss, fatigue, anorexia, and decreased water consumption. Some areas still sweat, which is confusing to owners. In temperate and subtropical climates, there is partial recovery of the ability to sweat during winter; however, the degree of recovery becomes progressively less with each ensuing year. Before settling into a permanently anhidrotic state, some horses go through one or more short cycles of sudden onset anhidrosis followed by spontaneous recovery. Diagnosis Anhidrosis can often be diagnosed presumptively, based on appropriate clinical signs and examination by a veterinarian. Patients will present with increased respirations and failure to cool after exercise. In situations that should elicit copious sweating, anhidrotic horses will have minimal or no sweat production. Confirmatory testing utilizing intradermal injections of epinephrine or terbutaline can be performed if the diagnosis is unclear or to evaluate treatments. A quantitative test using terbutaline is described (MacKay, 2008). The terbutaline is diluted to 0.01, 0.1, 1, 10, 100, and 1000 mg/L and administered intradermally in the neck. Either the sweat can be collected (as described for quantitative test) or a normal horse can be injected at the same time and qualitatively compared to the suspect anhidrotic horse. Treatment There is no proven therapy for anhidrosis that passes even the lowest standard of evidence-based medicine. Moving the horse to a cooler climate allows recovery from clinical signs and often also resets the sweating ability of that animal - horses are often noted to start sweating once in a cooler environment. It is essential that non-sweaters living in Florida are carefully managed to prevent high body temperatures from occurring. Common methods include providing shaded areas or stalls during the daytime with water available for misting and cooling the animal. For pastured animals, a pond will allow cooling during the day. Misting fans and sprinklers are also useful means of providing water. Many horse owners feel that various feed supplements offer relief to their horses, but this is an anecdotal observation with minimal research support. Other treatments are attempted with minimal evidence, including oral supplementation with dark beer, salts, vitamins/electrolytes, or thyroxine. Most of these are not dangerous, but also do not appear to reliably improve the animal’s ability to sweat. Medical treatment has also been attempted with ACTH, alpha-2 agonists, prostaglandins (Lutalyse), antihistamines, and Methyldopa (Aldo-Met), but is not logical based on our understanding of the disease, generally WWW.FAEP.NET |


unsuccessful and may be risky to the horse. A recent clinical trial evaluating treatment with acupuncture and herbal medication yielded a very minimal and short-lived effect. Treated horses were given four acupuncture treatments at weekly intervals and four weeks of herbal medication, while control horses received sham acupuncture and hay powder. The herbal formula used was Modified Xiang Ru San (Jing Tang Herbal Pharmacy, Reddick, FL), which contains dolichoris (bian dou), magnolia (hou po), lonicera (jin yin hua), forsythia (lian qiao), and elsholtzia (xiang ru). Acupuncture consisted of dry needling, hemoacupuncture, and electro-acupuncture of a set of designated acupoints to treat the TCVM diagnosis of summer heat (the usual pattern diagnosis made in cases of equine anhidrosis). The tendency for spontaneous reversion to sweating in some horses, and for improvement during the cool months in virtually all anhidrotic horses has sometimes been misinterpreted as evidence of the efficacy of a putative treatment. For most situations, it is important to at least differentiate for owners between harmless and potentially dangerous treatments. Current Research Over the last several years, we have found that foals given macrolide antimicrobials develop profound anhidrosis that resolves 30 to 45 days following cessation of treatment. We have demonstrated this effect with a variety of macrolides, and shown it does not occur in response to chloramphenicol, a related antimicrobial. This form of anhidrosis may prove useful in determining the cause of naturally-occurring anhidrosis. The next step is to investigate the effect of macrolides on Arabian foals, and we are seeking some foals to enroll in this trial.

Affected horses are commonly noted to utilize (and often empty) available troughs or ponds in an attempt to cool off.

- Continued on page 23






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Examination of the Horse Eye Brooks

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Ulcerative Keratopathies of the Horse



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Immune Mediated and Non-Immune Mediated Iridocyclitis in the Horse


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Selecting Diagnostics in Equine Reproduction, a Clinical Approach

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Current Understanding of Biofilm and Latent Endometritis Ferris

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- Continued from page 15

A. Performing the QITST. B. Expected responses for normal and anhidrotic horses.

Additional work is also underway to investigate a genetic component to anhidrosis. Epidemiologic study and clinical experience suggests there is a genetic impact on disease, so this area warrants further specific investigation to clarify and more thoroughly describe the impact of genetics on the clinical disease. Ultimately, the use of clinically proven treatments for anhidrosis will require identification of the specific etiology of disease and clinical trials of proposed treatments. We look forward to better understanding how to manage this important syndrome in performance horses. References/Suggested Reading

Johnson, E. B., MacKay, R. J. & Hernandez, J. A. 2010: An epidemiologic study of anhidrosis in horses in Florida. J Am Vet Med Assoc 236, 1091-1097. MacKay, R. J. 2008: Quantitative intradermal terbutaline sweat test in horses. Equine Vet J 40, 518-520. Marlin, D. J., Schroter, R. C., Scott, C. M., White, S., Nyrop, K. A., Maykuth, P. L. & Harris, P. A. 1999: Sweating and skin temperature responses of normal and anhidrotic horses to intravenous adrenaline. Equine Vet J Suppl 30, 362-369. Mayhew, I. G. & Ferguson, H. O., II. 1987: Clinical, clinicopathologic, and epidemiologic features of anhidrosis in central Florida thoroughbred horses. J Vet Intern Med 1, 136-141. McCutcheon, L. J. & Geor, R. J. 1998: Sweating. Fluid and ion losses and replacement. Vet Clin North Am Equine Pract 14, 75-95.

Beadle, R. E., Norwood, G. L. & Brencick, V. A. 1982: Summertime plasma-catecholamine concentrations in healthy and anhidrotic horses in Louisiana. Am J Vet Res 43, 1446-1448.

Rakhit, S., Murdoch, R. & Wilson, S. M. 1998: Persistent desensitisation of the beta-2 adrenoceptors expressed by cultured equine sweat gland epithelial cells. J Exp Biol 201, 259-266.

Bovell, D. L., Lindsay, S. L., Corbett, A. D. & C., S. 2006: Immunolocalization of aquaporin-5 expression in sweat gland cells from normal and anhidrotic horses. Vet Dermatol 17, 17-23.

Scott, C. M., Marlin, D. J. & Schroter, R. C. 2001: Quantification of the response of equine apocrine sweat glands to beta2-adrenergic stimulation. Equine Vet J 33, 605-612.

Bovell, D. L., Riggs, C. M., Sidlow, G., Troester, S., MacLaren, W., Yip, W. & Ko, W. H. 2013: Evidence of purinergic neurotransmission in isolated, intact horse sweat glands. Veterinary Dermatology 24, 398-E386. Bowker, K. D. 1995: Response of anhidrotic horses to nutrient supplementation.Animal Sciences, University of Florida, Gainesville, FL.

Warner, A. E. & Mayhew, I. G. 1982: Equine anhidrosis - A survey of affected horses in Florida. J Am Vet Med Assoc 180, 627-629.

Breuhaus, B. A. 2009: Thyroid Function in Anhidrotic Horses. J Vet Intern Med 23, 168-173. Guthrie, A. J., VandenBerg, J. S., Killeen, V. M. & Nichase, E. 1992: Use of a semiquantitative sweat test in Thoroughbred horses. J. S. Afr. Vet. Assoc. 63, 162-165. Hubert, J. D. & Beadle, R. E. 1998: Equine anhidrosis. Comp. Cont. Educ. Pract. 20, 846-852. Hubert, J. D. & Beadle, R. E. 2002: Equine anhidrosis. Vet. Clin. North Am. Equine Pract. 18, 355-369. Jenkinson, D., Loney, C., Elder, H. Y., Montgomery, I. & Mason, D. K. 1989: Effects of season and lower ambient temperature on the structure of the sweat glands in anhidrotic horses. Equine Vet J 21, 59-65. Jenkinson, D. M., Elder, H. Y. & Bovell, D. L. 2006: Equine sweating and anhidrosis - Part 1- equine sweating. Vet Dermatol 17, 361-392. Jenkinson, D. M., Elder, H. Y. & Bovell, D. L. 2007: Equine sweating and anhidrosis Part 2: Anhidrosis. Vet. Dermatol. 18, 2-11. Jenkinson, D. M., Montgomery, I., Elder, H. Y., Mason, D. K., Collins, E. A. & Snow, D. H. 1985: Ultrastructural variations in the sweat glands of anhidrotic horses. Equine Vet J 17, 287-291.



Martha Mallicote, DVM, DACVIM Martha Mallicote completed her undergraduate work at College of Charleston, and is a 2006 graduate of the University of Tennessee College of Veterinary Medicine. Since then, she has worked in both ambulatory and referral hospital settings, including an internal medicine fellowship at Rood and Riddle Equine Hospital. In 2012, Dr. Mallicote completed her residency in large animal internal medicine at the University of Florida, and has now joined the large animal medicine faculty at UF. Her professional interests include endocrinology, neonatology, and veterinary business management.









Professor of Veterinary Anatomy and Equine Lameness at the École Nationale Vétérinaire ďAlfort, France.


In the demonstration section of the wet lab, both groups will observe Dr. Jean-Marie Denoix while he performs both physical and biomechanical examinations, plus ultrasound on live horses.

For More Information, Visit Us at W W W .FA EP.N ET

Gumshoe Sleuthing to Determine the Cause of Injury SARAH LE JEUNE | DVM, DACVS, DACVSMR, CERT VET ACU/CHIRO

Complementary medicine, including acupuncture, can be useful both in detecting and treating lameness.

Recent advances in sport horse medicine and rehabilitation very safe, has minimal detrimental side effects, and is well have made it possible for equine athletes to reach new levels tolerated by most horses. Horses experiencing performance of excellence. Client demand for superior diagnostics and issues associated with musculoskeletal pain, who must innovative treatment strategies require equine practitioners comply with prohibited substance policies mandated by to be more informed than ever before. In addition to show associations, can benefit show-side from acupuncture western advances in sport horse medicine, complementary and/or chiropractic treatments. This occurs at most elite modalities such as acupuncture and chiropractic have competitions in compliance with the FEI. become increasingly recognized as being effective and valuable for the equine athlete to treat musculoskeletal These treatments are often sought directly by horse owners, conditions associated with the demands of intensive sometimes without the involvement of their primary vetphysical conditioning and performance. Blending the best erinarian, leading to a disconnection between traditional of traditional and complementary medicine provides an veterinary medicine and these complementary therapies. integrative approach of treating the whole horse rather This has caused the creation of a rift between conventional than focusing on a specific region or structure. medicine and complementary medicine, which is at the detriment to the horse because both practices can be mutually A 2008 survey conducted by the American Association of beneficial and rich in information to optimize treatment. Equine Practitioners identified that 20% of equine practitioner respondents perform some form of complementary Lameness is a very common problem in horses and acumedicine treatment modality themselves (most commonly puncture can be used not only in the treatment, but also in acupuncture and chiropractic), and of those that do not, the detection of lameness in horses. It is interesting to note 80% refer cases specifically for complementary medicine to that most horse owners cannot adequately detect lameness veterinarians who have this expertise. Multiple veterinary until it is severe, i.e. present at the walk or trot. The author institutions including the University of California, Colorado recently conducted a prospective study to answer the quesState University, the University of Florida, Oregon State tion of whether the acupuncture scan could be useful in University, and Virginia Tech, to name a few, are including screening for lameness in performance horses.1 The study acupuncture and chiropractic in their clinical services and population consisted of 102 performance horses (jumpers, veterinary curriculum. dressage horses and Western performance horses) evenly distributed into lame and sound groups. These horses Horse owners are attracted to acupuncture because it is first underwent an acupuncture scan and then a routine WWW.FAEP.NET |



lameness exam. The results of this study show that 78% (40/51) of sound horses were negative during the acupuncture scan (did not have a painful response at any of the acupuncture points palpated), whereas, only 18% (9/51) of lame horses were negative during the acupuncture scan, (P < 0.001), indicating that acupuncture scanning has a sensitivity of 82.4% in detecting lameness and a specificity of 78.4%. This suggests that horses that have a positive acupuncture scan should undergo a lameness exam to identify if they are lame, and if so, the cause of their lameness.

often multifactorial. Back pain is commonly associated with lameness and it is critical to identify whether the horse is indeed suffering from primary back pain or if the back pain is secondary to distal limb lameness. Horses with back pain should therefore undergo a full lameness exam, potentially with limb blocks to rule out lower limb lameness. In addition, such factors as saddle fit, tack fit, shoeing, conditioning program, and rider ability should be assessed when dealing with such a case. Several studies report that acupuncture is effective in treating back pain in horses.2, 3 In the author’s experience, it takes at least three consecutive (weekly) treatments to obtain a long-lasting clinical resolution of back pain and these horses benefit from regular (monthly) acupuncture treatments. The duration and quality of the therapeutic effect may be improved by incorporating chiropractic treatments in addition to acupuncture, but clinical studies are needed to confirm this clinical impression.

Acupuncture can certainly be used to help relieve pain in many lameness conditions, particularly muscular pain, but it is critical that the primary cause of lameness is also addressed with traditional methods. In the author’s experience, performance horses undergoing regular acupuncture treatments have a decreased necessity for joint injections, particularly of the distal hock joints. The author speculates that acupuncture helps the horse travel in a biomechanically sound manner which may stress distal joints less than Lameness is the most common cause of poor perforwhen they are compensating for muscle pain. mance in sport horses. Lameness typically results from Back pain is very common in riding horses and can be very difficult to diagnose and treat with conventional methods. Back pain is a good example of a term that encompasses a wide variety of conditions, with just as many etiologies. The clinical signs are non-specific and the most consistent feature of a back problem is a loss of performance. Acute soreness is often associated with falling or some other traumatic incident, but this is rarely the case. Horses experiencing back pain may have difficulty posturing to urinate, may be reluctant to lie down or roll, there may be reluctance to saddling or grooming, may be reluctant to picking up their feet, may appear to collapse behind while ridden, may have difficulty moving, particularly backwards, or may appear unilaterally or bilaterally lame when working, with stiffness in the hind end. Behaviorally, the horse may refuse to work on the bit or jump, or may exhibit any other form of evasion. Horses experiencing chronic pain can also exhibit withdrawn social behavior and possibly experience a decreased appetite and decreased nutritional intake. This is due to the effect of chronic pain on the emotional centers of the limbic system which motivates the individual to withdraw from damaging situations, to protect a damaged body part while it heals, and to avoid similar experiences in the future.4-7 The human model of spinal rehabilitation includes a multidisciplinary approach in the management of back problems. Advances in the treatment of equine back pain incorporate some of the same philosophies. The difficulty lies in identifying the exact cause of back pain, as this is A chiropractic exam is an important component of an integrative sports medicine examination.

26  The Practitioner  Issue 3 • 2017

Advances in the treatment of equine back pain incorporate some of the same philosophies as the human model of spinal rehabilitation.

pain associated with the musculoskeletal system, including joints, bones, tendons, ligaments, muscle and nerves. The majority of cases of lameness are localized to areas within the distal limb; however, the sources of lameness are diverse and the causes are numerous, including but not limited to wear-and-tear, overuse, and trauma.

approach focuses on the entire horse and can potentially detect and address preclinical problems before actual structural damage has occurred. Due to the increased strain placed on equine athletes, it is important to examine sport horses on a regular basis every six to 12 weeks depending on the intensity of work and the presence of clinical problems, to detect and address subtle biomechanical and physiological changes.

There are four major biomechanical mechanisms in the horse that function to conserve energy and to reduce stress on the skeletal structures of the horse: the stomatognathic An integrative sports medicine examination should include: system, the bow and string, the stay apparatus, and the use of the body in ambulation, called engagement. The anat- 1. Detailed history: emphasis on duration of clinical probomy of the horse has evolved to allow the horse to move as lem, previous treatments, diet, dental care, shoeing, efficiently as possible, with as little stress as possible. Any type/intensity/change of work, warm-up/cool-down, imbalance in the system will cause asymmetrical loading of access to turnout, social behavior. limbs, and over time, this asymmetrical and unbalanced use 2. Static exam: emphasis on stance, foot balance, muscle will cause the overloaded structures to become inflamed, symmetry, careful palpation of topline and all limbs, creating lameness. passive range of motion of all limbs, passive range of motion of TMJ, cervical flexions, hoof testers on Today, traditional methods of diagnosis and treatment proall four feet tocols rely on pain and inflammation to locate a problem. 3. DAPE: diagnostic acupuncture palpation exam Gait analysis, blocking, palpation, hoof testers, flexion tests, 4. Dynamic exam: careful evaluation of walk, trot, canter etc. all rely on pain and inflammation. Conventional treatin straight line and circle, on soft and hard ground (no ments, therefore, most often center on anti-inflammatory canter on hard ground), followed by horse evaluated medication, either locally and/or systemically, shoeing ridden by regular rider/trainer if performance problem changes, and rest, and pay little attention to the biomeis subtle and/or by clinician. chanics and efficiency of movement. Positive results are 5. Stress tests: lower and upper limb flexions of limbs seen when the patient appears to be moving without pain 6. Chiropractic exam or apparent lameness and they are then released from 7. Evaluation of saddle. SADDLE FIT:8 care. This is in contrast to the integrative (incorporating acupuncture and chiropractic) approach to treatment that Saddle fit is a very important component of equine perforfocuses on the functionality and biomechanics of the whole mance and should be checked regularly by an experienced horse and how this can change over time. The integrative clinician. The points listed below should be evaluated. WWW.FAEP.NET |



Balance: The center of the seat should be parallel to the ground. Withers clearance: Two or three fingers should fit between normal withers and the saddle. (Low “mutton” withers may allow a little more; very high withers, a little less.) Clearance should be all around, not just at the top. It is important to check that there is sufficient wither clearance even with the weight of the rider. Gullet width: The gullet should be three or four fingers wide, so that it will not interfere with the spinal processes or the spinal musculature. Panel contact: Panels should rest on the horse’s back evenly from front to back, not overstuffed in the middle (the saddle will rock) or bridging (with a gap in the middle). Billet alignment: Billets should hang perpendicular to ground so that the girth is not angled. Shoulder fit: Panels viewed from the front should be parallel to the scapula. Tree points should be behind both scapulae. Straightness: The saddle should not tilt to one side when viewed from the back.

Sarah le Jeune, DVM, DACVS, DACVSMR, Cert Vet Acu/Chiro Dr. le Jeune is a member of the American College of Veterinary Sports Medicine and Rehabilitation, and focuses on the diagnosis and treatment of lameness and various performancerelated musculoskeletal injuries by an integrative approach including acupuncture and chiropractic. She is the chief of the Equine Integrative Sports Medicine Service at UC Davis. Dr. Sarah le Jeune is also a board-certified equine surgeon and has been a member of the UC Davis Equine Surgery faculty since 2003. She is a certified veterinary acupuncturist with extensive acupuncture training from the Colorado State University and the Chi Institute in Florida. She also obtained certification in veterinary chiropractic by the International Veterinary Chiropractic Association.

Saddle length: The saddle should not extend beyond the scapulae and last rib. References/Suggested Reading

1) le Jeune SS, Jones JH : Prospective Study on the Correlation of Positive Acupuncture Scans and Lameness in 102 Performance Horses, American Journal of Traditional Chinese Veterinary Medicine 2014 2) Evaluation of electroacupuncture treatment of horses with signs of chronic thoracolumbar pain. Xie H, Colahan P, Ott EA.J Am Vet Med Assoc. 2005 Jul 15; 227(2):281-6. 3) Effect of EA on chronic back pain in Sport horses P. Kulchaiwat , H. Xie; AJTCVM, Vol 4(1) 2009 4) Lynn B. Cutaneous nociceptors. In: Winlow W, Holden AV. The neurobiology of pain: Symposium of the Northern Neurobiology Group, held at Leeds on 18 April 1983. Manchester: Manchester University Press; 1984. ISBN 0-7190-0996-0. p. 106. 5) Raj PP. Taxonomy and classification of pain. In: Niv D, Kreitler S, Diego B, Lamberto

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A. The Handbook of Chronic Pain. Nova Biomedical Books; 2007. ISBN 1-60021-044-9. 6) Vernon H, Aker P, et al. Pressure pain threshold evaluation of the effect of spinal manipulation in the treatment of chronic neck pain: A pilot study. J Manip Physiol Ther 1990; 13:13-16. 7) Kandel, Eric R., et al. Principles of Neuroscience, McGraw-Hill, 1991. 8)

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28  The Practitioner  Issue 3 • 2017

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Diagnosing Lameness in the Tarsus and Proximal Suspensory: Treating Them as a Region KURT SELBERG | MS, DVM, MS, DACVR

Figure 1: The left image is the left tarsus, the middle image is the right tarsus, and the right image is a fused radiograph and nuclear scintigraphy. The blue arrow is highlighting mild linear abnormal radiotracer at the distal extent of the talocalcaneal joint. This corresponds to focal areas of articular lysis bordered by sclerosis on the lateral radiograph (yellow arrow). The left talocalcaneal joint is normal.

Hind limb lameness due to pathologic changes in the distal tarsus and proximal metatarsus is common, and affects many breeds and disciplines. The complexity of diagnosis of distal tarsal pain and proximal metatarsal pain lies in the reliability in localization of lameness via local and intra-articular analgesia in this region1,2. Additional challenges are met imaging the complex region of the tarsus and proximal metatarsus. Osteoarthritis is the most common cause of lameness associated with the tarsus in horses. It has been linked with repeated trauma to the bones and ligaments that comprise the distal aspect of the tarsus, most commonly the structures of the distal intertarsal and tarsometatarsal joints. Radiography is generally the first-line diagnostic imaging modality for joint disease, including the tarsus. Radiographic findings consistent with osteoarthrosis include periarticular osteophyte production, periarticular and subchondral lysis, narrowing of the affected joints, and development of enthesophytes at the attachment of the ligaments surrounding the tarsometatarsal and distal intertarsal joints. The most common areas to identify these changes are the dorsal, dorsomedial, and dorsolateral

aspects of the distal intertarsal and tarsometatarsal joints. The location necessitates using dorsoplantar, lateromedial, dorsolateral – plantaromedial oblique and dorsomedial – plantarolateral oblique images to fully evaluate the tarsus3-5. However, some lesions of the distal tarsus may be undetected or underestimated by radiographic evaluation alone. There tends to be poor correlation of the degree of lameness and alteration in performance with radiographic changes of the tarsus and metatarsus6. It is likely that this poor correlation stems in part from the under-diagnosis of pathologic changes. There is evidence to suggest that location of the pathologic change may have some bearing on clinical significance. Those horses with osteoarthritis along the medial aspect of the tarsometatarsal joint tended to be lame in that limb. Talocalcaneal joint osteoarthrosis is typically lame because of the disease process7. Nuclear medicine has widespread availability, and may help diagnose radiographically occult lesions. The use of MR and its correlations back with nuclear medicine has helped the understanding of the disease process and location8. Additionally, locations thought to be uncommonly affected by osteoarthritis, such as the plantar aspect of the distal tarsal joints, may be overlooked on radiographs alone (Figure 1).

30  The Practitioner  Issue 3 • 2017

of anatomy and which soft tissue may be affected or causing the fragmentation to discern potentially significant from insignificant. The muscle interosseous medius, also known as the suspensory ligament due to its transformation to mainly fibrous tissue, is a well-documented source of hind limb lameness in the horse.10-12 The bulk of the suspensory ligament originates on the plantaroproximal aspect of the 3rd metatarsal bone. At its proximal extent, the origin is bilobed and valentine or trapezoid in shape. However, there is a small bundle of fibers that continues proximally to the fourth tarsal bone and plantar aspect calcaneus12. Hind limb suspensory ligament injury is a common problem in the sport horse. Despite the frequency of this injury, diagnosis can be challenging, as horses can vary in their presenting signs, and the often bilateral nature of the disease confounds the diagnosis. Palpation of the proximal suspensory ligament, despite moderate injury, may have minimal response during the physical exam. Response to hind limb flexion is generally moderate to marked, which may overlap with clinical signs associated with lameness originating primarily from the tarsus. Imaging/pathologic findings associated with the hind suspensory ligament vary. Pathologic changes may include Figure 2: Dorso 25 medial - plantarolateral oblique of a westone or more of the following: diffuse enlargement, dorsal ern performance horse with an acute lameness localizing the or plantar margin tearing, diffuse fiber damage, fibrosis/ tarsus. The arrows highlight a biarticular fracture of the central scarring, and osseous changes. Persistent hypoechoic areas, tarsal bone. regardless the angle of beam incidence, are typically indicative of areas of fiber damage. Variations of anatomy do occur and are important to realize. For example, there is a Bone contusions, better defined as bone marrow lesions, hypoechoic region on both on and off angle approximately are typically occult radiographically and may present with just distal to the origin of the suspensory ligament. This site normal radiographs despite having a consistent modermay be confused for core lesions, which are less common ate to severe lameness. Advanced imaging progresses this in the hind suspensory ligament. knowledge and helps target treatment. Focal or diffuse areas of increased echogenicity indepenFractures involving the distal tarsus are not common. Howdent of angle of incidence are consistent with fibrosis/scar ever, when horses present with an acute lameness suspicious of a fracture, diagnosis may be a challenge as the fractures may be radiographically occult with conventional views. The central tarsal bone tends to be more affected. Often the fracture configuration is biarticular, extending in a dorsomedial to plantarolateral fashion. These may be most apparent on a Dorso 15-25 lateral-plantar lateral oblique image (Figure 2). Fragmentation may be seen with traumatic injury, collateral ligament injuries, or Figure 3: Lateral is to the left. Non-weight bearing images perpendicular (left) and off angle can be benign. Fragmentation in the (right) to the fiber of the suspensory ligament. There is a focal area of hyperechogenicity along proximal tubercle of the talus is typithe dorsolateral aspect of the suspensory ligament (red arrow), consistent with (chronic) focal cally benign9, but may be met with fiber disruption/desmopathy. The proximomedial bone margin is mildly irregular in the right uncertainty due to the low frequency image (yellow arrow). Note that the ultrasound transducer is place plantar to slightly medial in which they are encountered. It is to make the bone margin parallel with the bottom of the ultrasound screen. This increases important in cases of fragmentation to conspicuity of the bone and ultimately lesions. have a comprehensive understanding WWW.FAEP.NET |



Figure 4: This is a medial approach to ultrasound examination of the suspensory ligament. The image is at the level of the body of the suspensory ligament. There is a central hypoechogenic area (yellow arrow) in the suspensory ligament and the periphery is hyperechogenic. In this case, the hypoechogenic area is off angle imaging of the fiber and the hyperechogenic periphery is the fat/muscle, which is not angle dependent. This is a normal suspensory ligament and is showing a pit fall in examination and interpretation.

tissue (Figure3). Dystrophic mineralization can also occur, and if subtle, can be difficult to distinguish from scarring. Measuring the cross-sectional area (CSA) can be helpful for comparing the size to the opposite limb. Assessing mild enlargement can be difficult, particularly as there is no guarantee that the contralateral limb is normal. Measurements on cross-sectional areas of the hind suspensory ligament are not standardized for each breed. Normal CSA for a warmblood may not be the same as a reining quarter horse. For the warmblood, this may be up to 2 cm, and for the quarter horse it may be 1.8. It is helpful to get a sense of normal variations in measurements in non-lame horses that are similar in size, breed, and discipline. It is more helpful to use imaging characteristics to assess size and margin. These include loss of the normal space between the dorsal margin of the suspensory ligament and plantar bone margin, displacement of the medial plantar vessels, and extension of the ligament beyond the plantar confines of the splint bone. Pathologic changes in the suspensory ligament often do not result in marked enlargement, but focal marginal change (dorsal most frequent). Using CSA only may result in underdiagnoses or potentially over-diagnosis. Pitfalls exist as in all interpretation. It is important to realize the suspensory ligament is comprised of multiple tissue types and has different echogenicity as it is imaged with ultrasound (Figure 4). Pathologic changes to the bone can occur in addition to ligamentous, pathologic change, or it can be the primary abnormality. Both long axis and transverse imaging are important for evaluating the plantar cortex of MT3. Abnormalities can include bone proliferation, resorption and avulsion fragmentation. MR imaging is very good for assessing changes to surface, cortical, and medullary portions, and ultrasound can actually be superior for identifying small avulsions and enthesopathies. This is in part due

to acoustic shadowing from fragmentation, good contrast between bone and ligament structures, and thin tissue sampling. The axial margins of MT2 and MT4 also should be evaluated for proliferative changes that could impinge on the suspensory ligament. In conclusion, a combination of history, lameness evaluation, response to diagnostic analgesia, and multiple imaging modalities is needed to make a diagnosis. Imaging modalities should be viewed as complementary modalities and used as such. To get the most out of imaging findings, it is important to take into consideration clinical history, physical and moving examinations, and diagnostic anesthesia findings. References/Suggested Reading 1.

2. 3.

4. 5. 6.

Claunch KM, Eggleston RB, Baxter GM. Effects of approach and injection volume on diffusion of mepivacaine hydrochloride during local analgesia of the deep branch of the lateral plantar nerve in horses. http://dxdoiorgproxy-remotegalibugaedu/102460/javma245101153. October 2014. doi:10.2460/ javma.245.10.1153. Dyson SJ, ROMERO JM. An Investigation of Injection Techniques for Local Analgesia of the Equine Distal Tarsus and Proximal Metatarsus. equine vet j. 1993; 25(1):30-35. Eksell P, Uhlhorn H, Carlsten J. Evaluation of different projections for radiographic detection of tarsal degenerative joint disease in Icelandic horses. Vet Radiol Ultrasound. 1999; 40(3):228-232. ttir SBORO, Ekman S, Eksell P, Lord P. High detail radiography and histology of the centrodistal tarsal joint of Icelandic horses age 6 months to 6 years. August 2005:1-7. ttir SBORO, Axelsson M, Eksell P, Sigurdsson H, Carlsten J. Radiographic and clinical survey of degenerative joint disease in the distal tarsal joints in Icelandic horses. April 2006:1-5. Fairburn A, Dyson S, Murray R. Clinical significance of osseous spurs on the dorsoproximal aspect of the third metatarsal bone. equine vet j.

32  The Practitioner†Issue 3 • 2017

OSPHOS® (clodronate injection) 7.

Shelley J, Dyson S. Interpreting radiographs 5: Radiology of the equine hock. equine vet j. 1984.


Daniel AJ, Judy CE, Rick MC, Saveraid TC, Herthel DJ. Comparison of radiography, nuclear scintigraphy, and magnetic resonance imaging for detection of specific conditions of the distal tarsal bones of horses: 20 cases (2006-2010). Journal of the American Veterinary Medical Association. 2012; 240(9):1109-1114. doi:10.2460/ javma.240.9.1109. Espinosa P, Lacourt M, Alexander K, David F, Laverty S. Fragmentation of the proximal tubercle of the talus in horses: 9 cases (2004-2010). Journal of the American Veterinary Medical Association. 2013; 242(7):984-991. doi:10.2460/javma.242.7.984.


10. Tóth F, Schumacher J, Schramme M, Kelly G. Proximal suspensory desmitis of the hind limbs. Compendium Equine. 2009. 11. Dyson SJ, Weekes JS, Murray RC. Scintigraphic Evaluation of the Proximal Metacarpal and Metatarsal Regions of Horses with Proximal Suspensory Desmitis. Vet Radiol Ultrasound. 2007; 48(1):78-85. doi:10.1111/j.1740-8261.2007.00208.x. 12. Dyson S. Hind limb lameness associated with proximal suspensory desmopathy and injury of the accessory ligament of the suspensory ligament in five horses. Equine Veterinary Education. 2014; 26(10):538-542. doi:10.1111/ eve.12217.

Kurt Selberg MS, DVM, MS, DACVR Kurt Selberg is a North Idaho native, where his family owned a quarter horse ranch. After completing his doctorate in veterinary medicine from Washington State University, he completed an equine sports medicine internship at Virginia Equine Imaging in Middleburg, VA. He received his training in diagnostic imaging from Colorado State University, and is a Diplomate of the American College of Veterinary Radiologists. Following his residency, he completed fellowships in advanced imaging with training from Colorado State University, and from Musculoskeletal Radiologists in Fort Collins, Colorado. He was an Assistant Professor of equine diagnostic imaging at the University of Georgia for four years.

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

He recently returned to Colorado, for an equine diagnostic imaging position at Colorado State University in September of 2016. His area of interest is the equine athlete and musculoskeletal diagnostic imaging. Dr. Selberg is a certified member and lecturer at many of the International Society of Equine Locomotor Pathology continuing education events. He is also an FEI treating veterinarian. Aside from radiology, he also enjoys skiing, fishing, spending time with good friends and family, his lovely wife Katie, his little girl Beckett, a yellow dog, and soon the next addition to his family, a little boy.

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.

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Proven effective Easy to administer Easy on the budget For more information, call us toll free at 888-524-6332 or visit *Federal law restricts this drug to use by or on the order of a licensed veterinarian. FOR ORAL USE IN HORSES ONLY. Pregnant women or women who suspect they are pregnant should not handle OvaMed®. Protective gloves must be worn by all persons handling this product. Refer to the product sheet for comprehensive product information. OvaMed® is a registered trademark of Bimeda, Inc. Regu-Mate® is a registered trademark of Intervet BV. Copyright Bimeda 2017