Equine pastern dermatitis: a narrative review on clinical presentation, diagnosis, risk factors, prevention, and therapeutic approaches

Vinzenz Gerber Department of Clinical Veterinary Medicine, Vetsuisse Faculty, Swiss Institute of Equine Medicine (ISME), University of Bern, Bern, Switzerland

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Sarah Kaiser-Thom Department of Clinical Veterinary Medicine, Vetsuisse Faculty, Swiss Institute of Equine Medicine (ISME), University of Bern, Bern, Switzerland
Institute of Immunology, Heidelberg University Hospital, Heidelberg, Germany

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Solange Oesch Department of Clinical Veterinary Medicine, Vetsuisse Faculty, Swiss Institute of Equine Medicine (ISME), University of Bern, Bern, Switzerland

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Abstract

Equine pastern dermatitis (EPD) is a nonspecific cutaneous reaction pattern on the distal extremities, typically in the palmar/plantar area of the pastern. Although EPD is commonly seen in equine practice and can be a debilitating condition, peer-reviewed original studies on many aspects of this multifactorial syndrome are still scarce. This narrative review aims to give an overview of the clinical presentation (forms of EPD and clinical scores and differential diagnoses), risk factors, and therapeutic approaches. The emphasis is on intrinsic and extrinsic risk factors as most of the original work has been published on these aspects. The available data supports the effects of age, breed, and breed-related phenotypical traits (draft breeds with feathers and large cannon circumference) on the frequency and severity of EPD manifestations. Hind legs and unpigmented limbs are also more frequently affected. Genetic effects in draft breeds appear to be complex, and no commercial genetic tests currently exist. Evidence for meteorological effects like rainfall and humidity is inconclusive. Associations with Chorioptes infestation and bacterial microbiota imbalances but not with fungal infections have been consistently shown. Causality has not been demonstrated for specific infectious agents. Original studies have investigated the effects of antibacterial agents (Kunzea oil, phytosphingosines, and triclosan), fatty acids, aromatic oils, and humectants as well as therapeutic approaches to Chorioptes infestation in EPD-affected equids. While therapy remains largely empirical, knowledge of investigated risk factors for this multifactorial syndrome can inform diagnostic and therapeutic approaches. Raising owner awareness of EPD could be key to improving the welfare of affected horses.

Abstract

Equine pastern dermatitis (EPD) is a nonspecific cutaneous reaction pattern on the distal extremities, typically in the palmar/plantar area of the pastern. Although EPD is commonly seen in equine practice and can be a debilitating condition, peer-reviewed original studies on many aspects of this multifactorial syndrome are still scarce. This narrative review aims to give an overview of the clinical presentation (forms of EPD and clinical scores and differential diagnoses), risk factors, and therapeutic approaches. The emphasis is on intrinsic and extrinsic risk factors as most of the original work has been published on these aspects. The available data supports the effects of age, breed, and breed-related phenotypical traits (draft breeds with feathers and large cannon circumference) on the frequency and severity of EPD manifestations. Hind legs and unpigmented limbs are also more frequently affected. Genetic effects in draft breeds appear to be complex, and no commercial genetic tests currently exist. Evidence for meteorological effects like rainfall and humidity is inconclusive. Associations with Chorioptes infestation and bacterial microbiota imbalances but not with fungal infections have been consistently shown. Causality has not been demonstrated for specific infectious agents. Original studies have investigated the effects of antibacterial agents (Kunzea oil, phytosphingosines, and triclosan), fatty acids, aromatic oils, and humectants as well as therapeutic approaches to Chorioptes infestation in EPD-affected equids. While therapy remains largely empirical, knowledge of investigated risk factors for this multifactorial syndrome can inform diagnostic and therapeutic approaches. Raising owner awareness of EPD could be key to improving the welfare of affected horses.

Introduction

Equine pastern dermatitis (EPD) is an umbrella term for inflammatory cutaneous lesions on the lower legs of horses. This condition has been described for centuries1 and numerous lay terms exist, such as “scratches,” “mud fever,” “grease heel,” or “grapes.” Rather than a specific disease entity or diagnosis, EPD is considered a multifactorial syndrome manifesting as a nonspecific cutaneous reaction pattern on the distal extremities, typically in the palmar/plantar area of the pastern. In lighter horse breeds, mild to moderate manifestations of EPD predominate, while progression to severe debilitating forms, including chronic progressive lymphedema (CPL), is seen in cob- and draft-type horses.26

This narrative review aims to give an overview of the clinical presentation and diagnosis, intrinsic and extrinsic risk factors, and therapeutic approaches. Even though EPD is very common and its importance in equine practice is widely recognized, peer-reviewed studies on the etiology, pathogenesis, and treatment of EPD are still scarce. Accordingly, this review combines information based on textbooks and other educational articles with findings from original research. Detailed information from peer-reviewed publications is provided in Supplementary Table S1 (Clinical scoring of Equine Pastern Dermatitis lesions), Supplementary Table S2 (Intrinsic risk factors of Equine Pastern Dermatitis), and Supplementary Table S3 (Extrinsic risk factors of Equine Pastern Dermatitis), all including complete references.

Clinical Presentation

Although a universally accepted definition of EPD is lacking, the common denominator across the variable clinical manifestations is inflammatory skin lesions in the palmar/plantar area of the pastern. Three forms of increasing severity were already outlined in Percivall’s Hippopathology of 1875 (reviewed in Kugler)1 and are still described in modern educational articles.2 The initial signs of EPD include alopecia, dry scales, and crusts. Some degree of pain, pruritus, and thickening of the skin may also be present (mild form: “scratches,” “mud fever,” and “mud rash”; see Figure 1 for all 3 forms). With disease progression, lesions become exudative and crusting (exudative form: “grease heel,” and “dew poisoning”), often extending from the back of the heels further dorsally and proximally on the pastern and fetlock. In advanced chronic cases hyperkeratosis, lichenification, and fissured skin, sometimes with papillomatous hyperplasia, fibrosis, and exuberant granulation tissue can involve large areas of the distal limb (chronic proliferative form: verrucous dermatitis or “grapes”).7

Figure 1
Figure 1
Figure 1
Figure 1
Figure 1
Figure 1

Examples of 3 forms of equine pastern dermatitis (EPD): mild form (a); exudative form with crusts before clipping and treatment (b); exudative form after clipping and initial treatment (c); chronic proliferative form involving the dorsal pastern, lesions hidden under feathers before clipping and treatment (d); and chronic proliferative form with decreased signs of inflammation after clipping and local treatment (e).

Citation: Journal of the American Veterinary Medical Association 261, S1; 10.2460/javma.22.12.0569

Pain and sometimes pruritus can vary considerably. Lameness may be apparent in sensitive horses or more severe cases, especially when cellulitis develops. In advanced chronic cases, pain, inappetence, and secondary infestation of lesions (eg, myiasis; Supplementary Video S1) can affect the horses’ general condition and well-being.2,46,8

From a clinical perspective, these progressively more severe manifestations of EPD are not discrete forms in themselves but represent stages on a continuum.8 In EPD-affected horses of diverse breeds in Switzerland (n = 113), owners reported the condition to be constantly present in 40% of these animals.9 In other cases, episodes of EDP appeared acutely without previous episodes or they recurred after phases of remission. Crusts were observed in 90% of the study population, followed by scales, thickened skin, ulceration, and pruritus (approx 40 to 60%). Swelling, hair loss, and pain were less often reported by owners (approx 30%), and only a few horses (3%) were considered lame because of EPD (Supplementary Figure S1).

To better account for the transitions between the 3 forms and the various observed patterns and combinations of dermatological lesions, several clinical scoring systems have been described. These scoring systems have not been formally validated and differ between studies, but informative associations with risk factors and treatment effects have been reported (Supplementary Table S1, including complete references).

Diagnostic Approach

The minimal database in the examination of horses with EPD includes 3 elements: a complete history (including but not limited to signalment, onset and course of clinical signs, seasonality, EPD status of companion horses, previous treatments, and outcome); a thorough clinical examination; and an inspection of the living environment and management conditions of the affected animal to identify potential risk factors (Supplementary Tables S2 and S3).

The extent, distribution, and macroscopic character of lesions as well as the degree of discomfort and pruritus can be systematically assessed using criteria described in several scoring systems (Supplementary Table S1). In feathered horses, proper examination of the skin lesions is often impossible without clipping the affected region (Figure 1, compare to Supplementary Figure S4 after clipping). When clipping is too painful for the horse, sedation and initial cleaning and softening of crusts might be necessary before clipping. If possible, superficial swab, crust, hair, or tissue samples for bacteriology or mycology and impression smears for cytology should be collected before cleaning is attempted.5 The clinician should bear in mind that EPD is an unspecific reaction pattern that can appear clinically indistinguishable irrespective of specific inciting factors. The clinical presentation can be dynamic with phases of remission followed by acute exacerbations that can recur or persist resulting in chronic disease. This might depend on seasonal and other risk factors, the duration and chronicity of disease, and the effects of previous treatments.

In uncomplicated, mild to moderate cases, thorough history taking, clinical examination, and assessment of environmental risk factors can be sufficient to formulate a treatment plan. Depending on the presentation, the initial work-up will also include skin scraping, cytology, bacterial culture, or a combination of these. If secondary hepatogenous photosensitivity is suspected, a serum chemistry panel can be performed to detect underlying hepatic disease.

To identify underlying triggering factors and in cases with atypical presentations, further diagnostic steps should be directed at confirming or ruling out specific etiological and accompanying factors (eg, chorioptic mange; see also Supplementary Table S3) or differential diagnoses. In severe chronic cases, potential triggering or contributing factors can be obscured and reassessment may be more rewarding after the initial treatment has improved the presentation and decreased secondary lesions and infections. Diagnostic methods are described in detail in educational articles4,10,11 on equine dermatology.

The list of differential diagnoses is extensive, as a variety of inflammatory and crusting skin conditions can affect the pastern and lower extremities. This includes common diseases with atypical localizations in the pastern area (eg, equine sarcoid); toxic/metabolic, immunological, and infectious disorders, which may not be restricted to the distal extremities (eg, primary or secondary photosensitization, pemphigus foliaceus, sarcoidosis, and habronematosis); and also rare conditions occurring in (sub-)tropical regions (eg, phytosis and epizootic lymphangitis). Depending on the clinical presentation, 2 disorders that should chiefly be considered are pastern leukocytoclastic vasculitis (PLV) and CPL.

Idiopathic PLV is a clinical and histological entity. This possibly photoaggravated immune complex disorder affects predominantly but not exclusively distal limbs with white markings manifesting as mostly well-demarcated, circular, painful, erythematous, exudative lesions with tightly adherent crusts. PLV can be difficult to differentiate from exudative and crusting forms of EPD and might contribute to its development or exacerbation. The typical clinical appearance (particularly the well-defined demarcation, sometimes with raised borders, and the predominantly lateral/medial rather than palmar/plantar localization of the lesions, Supplementary Figure S2) should raise suspicion for PLV and lead to histological confirmation by biopsy for differentiation from uncomplicated mild to moderate EPD. PLV occurs in diverse, predominantly lighter breeds including Warmblood, Quarter Horses, Thoroughbreds, and Arabians and carries a guarded prognosis.1214

Previously, the terms “chronic proliferative pastern dermatitis,” verrucous dermatitis (“dermatitis verrucose”), and CPL have variably been used for the severe chronic proliferative form of EPD in heavy draft breeds (Supplementary Figure S3). CPL has also been characterized as a distinct disorder with underlying lymphatic dysfunction,1517 and we have included reported intrinsic risk factors and therapeutic aspects of CPL in this review.

Risk Factors for EPD

A considerable number and various combinations of intrinsic (internal and individual; Supplementary Table S2, including complete references) and extrinsic (environmental, infectious, and iatrogenic; Supplementary Table S3, including complete references) factors can predispose to the development of EPD, precipitate its onset, aggravate it, or perpetuate its course. Knowledge of these influences is key to guiding diagnosis (ie, selection of tests), prophylaxis, and therapy (ie, avoidance of specific risk factors).

There is no documented predilection for sex, except for males of heavy draft breeds that are more susceptible to severe EPD/CPL.18 Age at onset of clinical signs ranged from 1 to 21 years across different breeds.9 In a study7 on EPD in draft horses, lesion severity increased with age. Overall, EDP is more frequent and manifestations are more severe in heavier cob-type and draft breeds.2,4,1922 Characteristics like large dimensions of extremities and presence of feathers increase the risk for severe EPD.7 In CPL, thick extremities may be predisposed to decreased lymphatic drainage.15 Fetlock feathers can retain heat and moisture, and they might harbor ectoparasites (see also extrinsic risk factors, Supplementary Table S3). They can also hide EPD lesions delaying identification and treatment (compare Figure 1 and Supplementary Figure S4).

Lesions are usually bilaterally symmetric, even though just 1 limb can be affected. Limb position and pigmentation are among the most commonly noted intrinsic risk factors.2,4,5 Original epidemiological studies confirmed higher frequencies of involvement in hind limbs across different breeds and EPD forms. In contrast, unpigmented legs (white markings up to pastern level) were more frequently affected in lighter breeds (Warmblood, Swiss Franches-Montagnes horses) but not in heavy German draft horses (Supplementary Table S2, including complete references).

Several investigations have focused on heritability estimates, genomic associations, and candidate genes for severe EPD and CPL (Supplementary Table S1, including complete references). The genetic background appears to be complex. It is likely that a number of loci influence the development of these severe manifestations and that the effect of these respective loci differs between draft breeds.21 No candidate genes or specific markers could be confirmed, and no commercial genetic tests currently exist for EPD or CPL.16,17,23 However, based on the reported heritabilities, studbook programs using estimation of breeding values in heavy draft horses could potentially reduce the genetic predisposition for EPD and CPL in affected breeding lines.17,24 In the individual patient, however, except for clipping of feathers, intrinsic risk factors for EPD are largely nonmodifiable.

In contrast, extrinsic risk factors are typically amenable to prophylactic and therapeutic modification. They can be broadly grouped into environmental conditions and specific infectious agents; original studies are summarized accordingly in Supplementary Table S3 (including complete references).

Educational articles24,6,8 agree that chronic wetting of the skin of the distal limbs and unhygienic management conditions promote EPD. Accordingly, EPD is thought to be more common during wet and colder seasons.8 However, the results of original studies are conflicting and meteorological effects might depend on the presence of other factors (Supplementary Table S2). Some authors proposed an interaction of increased moisture and opportunistic pathogens such as Staphylococcus aureus.25 Interestingly, this is supported by the observation that effects of meteorological factors (rainfall) on the bacterial composition of the skin were more marked in EPD-affected compared to unaffected pasterns.26 Intrinsic factors like feathering, which can retain moisture, soil, and debris, and extrinsic factors, such as pasture occupation density, pasture and stable hygiene, and capacity of the ground to absorb water before becoming wet and muddy, might also modulate meteorological effects (Supplementary Figure S5).

The increased risk of pasterns with white markings developing EPD suggests that exposure to sunlight could play a role, due to the decreased capacity of unpigmented skin to absorb UV light and scavenge free radicals.11 Further reported environmental risk factors are sandy ground (especially in Arabian horses) and alkaline soils.2,4 Sources of physical or chemical irritants that may also trigger or perpetuate EPD include treated bedding, tack and training devices (eg, bell boots), shampoos, lotions, and not least inappropriate topical medications.2,5,8 The effects of environmental allergens causing contact hypersensitivity (eg, to bedding materials) or atopic disease have also been mentioned.2,6 However, to the authors’ knowledge, no published epidemiological data or controlled studies have confirmed these potential physical, chemical, or allergic triggers.

Environmental and iatrogenic effects may compromise the skin barrier and leave it more vulnerable to infections that might induce, perpetuate, or aggravate EPD. A viral pathogen “horsepox” has been mentioned as a potentially infectious agent in EPD,13 but its significance is questionable. Conversely, parasitic, fungal, and bacterial infections are consistently listed as pathophysiological factors in educational articles.2,4,6,8 Their associations with EPD, but not their causative roles, have been investigated in several original studies (Supplementary Table S2).

Infestation with Chorioptes bovis is the most frequently cited parasitic condition in educational articles2,27 and a causal relationship has been assumed. C bovis has been reported in EDP-affected draft breeds, cob/pony-type horses, and a donkey but not in EPD-affected horses of lighter breeds.25,2729 This ectoparasite can induce pruritus with manifest behavioral signs (stamping, biting, chewing, rubbing, or scratching with the risk of self-trauma) in many, but not all, infested horses. However, the extent of infestation was not related to lesion severity.27,28 C bovis appears to mainly cause discomfort to the horse, rather than significantly alter the course of EPD.

Other parasites found in EPD lesions include trombiculid mites, Pelodera strongyloides, a saprophytic nematode, and a percutaneous infection by the larval stages of Strongyloides westeri, the equine threadworm.30,31 Furthermore, myiasis from fly larvae (Supplementary Video S1) is sometimes observed in severely affected (and neglected) animals.2,4,6,8

Dermatophytes and Malassezia species have also been proposed as possible contributors to EPD development,2,4,6 but except for the identification of Microsporum equinum in 1 investigation,32 their presence in EPD lesional samples was not confirmed in original studies25,29,33 using specific diagnostic methods (Supplementary Table S3).

Bacterial involvement is mentioned as a primary or secondary extrinsic factor in most educational articles2,4,6,8 on EPD. Original studies25,3234 using bacterial culture repeatedly showed mixed flora or pure culture of various bacteria with staphylococcal species and β-hemolytic streptococci most consistently identified in EPD-affected horses. In a study35 specifically investigating S aureus, it was more frequently isolated from affected horses’ pasterns and nostrils and showed increased virulence, but multi-resistant isolates were not increased in EPD.

Dermatophilus congolesis, which is associated with wet and humid conditions in other equine dermatological presentations (“rain scald”) and is specifically mentioned as a potential primary or secondary factor in most educational articles,25,29,33 was either infrequently identified in EPD cases or not at all when investigating this infectious agent by cytology, specific culture media, PCR, or a combination of these. In PLV lesions (Supplementary Figure S2), colonization with coagulase-positive Staphylococcus intermedius13 and multidrug-resistant Pseudomonas aeruginosa36 has been reported in single cases.

However, these bacteriological results are based on swabs or crust material from affected pasterns, not on biopsied tissue, which is the sample of choice for the identification of infectious agents colonizing deeper skin layers. Histology including silver stains on biopsied tissue revealed intradermal spirochetes in a single severely EPD-affected case in the southern United States,30 leading the authors to a comparison with papillomatous digital dermatitis in cattle, a condition in which spirochetes are thought to play an important role. The presence of spirochetes was not confirmed in a larger study7 in Europe.

Bacterial culture is the current standard method to examine bacterial flora associated with EPD in clinical practice and most original studies (Supplementary Table S2). However, it is inherently selective and restricts the spectrum of investigated species. Recent investigations have used next-generation sequencing of the bacterial 16S rRNA gene to provide a more comprehensive picture of the microbiota in EPD.26,34,37 Affected pasterns showed more pronounced changes and reduced diversity of the microbiota. The recent use of antimicrobials and rainfall influenced the composition of the microbiota with changes more pronounced in EPD-affected compared to control pasterns. Similar disturbances and reduced diversity of microbiota are reported in other inflammatory skin conditions like bovine digital dermatitis and ovine foot rot, as well as diabetic ulcers, chronic pressure sores, and impaired wound healing in humans. In EPD-affected pasterns, Staphylococcaceae were the most distinct of the differentially abundant bacterial families. Culture-independent assays have allowed for a more inclusive view of bacterial flora in EPD, but whether the observed reduced bacterial diversity and profound disordering of the pastern skin microbiota occur primarily or secondarily in EPD remains to be shown.

Therapeutic and Preventative Approaches

Management and treatment plans should be based on a thorough clinical assessment and identification of risk factors relevant to the individual case. This is not trivial given the multifactorial nature of this syndrome and the wide variety of products used to treat EPD. Moreover, the availability (and registration for use in horses) of these products often differs between countries. In Switzerland, owners of EPD-affected horses reported using medications with over 50 different ingredients in the form of mostly topical (often combination products) and systemic applications (Supplementary Figure S6). Expected actions ranged from the promotion of wound healing to astringent, antimicrobial, antiparasitic, fungicidal, anti-inflammatory, and unknown mechanisms.9

Educational articles26,8 largely agree on the general principles for EDP prevention and treatment. These include avoiding wetness and humidity in the pastern area and maintaining good environmental hygiene and care of the horse, mainly by adjusting turnout, improving pasture and stable hygiene, or cleaning and drying of the legs after exposure. These points appear rational and self-explanatory, but the limited evidence regarding the role of meteorological risk factors in EPD is inconclusive (Supplementary Table S3). Depending on the clinical presentation and individual situation, further environmental factors to consider are UV light exposure and contact with specific soils and beddings. Prevention in susceptible horses may employ barrier creams before exposure, combined cleansing and drying after exposure (eg, turnout in strong sunlight or endurance racing on sand).

Feathers are an important intrinsic factor predisposing to severe EPD, and they should be clipped to decrease moisture retention and allow access for regular inspection, maintenance of hygiene, and application of topical treatments (compare Figure 1 and Supplementary Figure S4). Clipping and debridement may need to be performed under sedation or even general anesthesia in severe cases.

Topical preparations are applied after gentle clipping and initial cleansing to further remove crust material, debridement, and disinfection of the lesions. These typically contain ingredients promoting wound healing (eg, zinc-oxide, dexpanthenol, colloidal silver, or honey) with astringent (eg, benzoyl peroxide or aluminum acetate), hypertonic, and drawing (eg, magnesium sulfate) properties or antiseptic/antimicrobial agents (eg, chlorhexidine, benzoyl peroxide, or silver sulfadiazine). Although frequently used, some authors advise against povidone-iodine because it may be irritating to the skin.6

Furthermore, many creams and lotions contain antimicrobials (eg, neomycin, thiostrepton, gramacidine, polymixine, or gentamicin), antifungal agents (eg, nystatin or clotrimazole) or corticosteroids (eg, triamcinolone, bethamethasone, prednisolone, or hydrocortisone), or a combination of these. In dermatophyte infections, lime sulfur dips and miconazole shampoos are also recommended. For the treatment of secondary infections, especially by staphylococci, some authors2,6 advocate the antimicrobial agent mupirocin. Generally, topical treatments should be pursued until a clear improvement is observed, but as they can also irritate the skin, close monitoring is essential. Also, prolonged application of corticosteroids may delay epithelialization and wound healing.

Three original studies have investigated topical treatments of EPD. A blinded, placebo-controlled study in Tasmania (Australia) investigated kunzea oil, an essential etheric oil from the shrub Kunzea ambigua, which is supposed to have antifungal and antimicrobial properties, specifically against S aureus. Eleven treated horses and 10 controls, all of lighter breeds and with mild to moderate EPD, completed the study. Total lesion scores and lesion areas significantly decreased after treatment. Seven of the treated horses showed complete resolution compared to 2 resolved cases in the control group.32

An observational, noncontrolled study in 12 horses reported a good response of EPD lesions to a topical preparation containing antibacterial agents and humectants. In 10 horses, mainly of lighter breeds, complete resolution was reported by the owners. Two cob-type cases were not or only partially treated, indicating that therapeutic success was not complete in all cases.33

A randomized, single-blinded, placebo-controlled trial investigated a novel preparation in young German Warmblood horses. Thirty-three affected horses were divided into 3 groups, either treated with a spot-on containing essential fatty acids and aromatic oils, a preparation containing additional antimicrobial phytosphingosines, or the placebo preparation. There was no difference in EPD occurrence between the 3 groups, but lesion scores were lower in both of the treated groups. The authors25 concluded that these topical preparations did not prevent EDP but that the essential fatty acids might have some therapeutic benefit in alleviating clinical signs.

Treatment of C bovis infestation did not decrease the severity of EPD in feathered horses but alleviated signs of discomfort. Treatment of chorioptic mange appears more promising with topical (eg, lime sulfur, permethrin; phoxim, fipronil, or doramectin) than with systemic interventions (eg, ivermectin, moxidectin) alone. As the parasite is not host specific and can survive in the environment for several weeks, these aspects should also be considered by treating in-contact animals of other species, removing bedding material, and performing thorough environmental decontamination including stall and barn surfaces, tack, and grooming material. Even then, in feathered horses expectations for complete elimination should be tempered to the significant reduction of Chorioptes numbers and lessening of discomfort.16,28,3840

Systemic antimicrobial (eg, trimethoprim-sulfonamides) and anti-inflammatory (eg, dexamethasone, prednisolone, or pentoxifylline) treatment can be indicated when signs of discomfort, pain, lameness, or elevated body temperature are apparent, which is often when owners seek veterinary advice.9 Cellulitis should be addressed quickly and aggressively and may need intravenous broad-spectrum antibiosis and complementary physical therapy (“hydrotherapy”). Systemic oxytetracycline was used in a case of severe EPD following the identification of spirochetes in biopsy samples.30

Management of EPD cases can be challenging, not least because owners often start treatment without seeking veterinary advice. Overzealous use of topical medications and home remedies has been mentioned as a risk factor by some authors.2,5,8

In Switzerland, a majority of owners reported that they consulted a veterinarian to confirm the diagnosis, but overall almost 70% of treatment decisions were made by the owners.9 While all systemic medications containing antibacterial, antiparasitic, or anti-inflammatory agents were prescribed by veterinarians, this was only the case in 9% of topical creams promoting wound healing and 55% of creams containing antibacterial, antimycotic, and/or anti-inflammatory agents.

With adequate and consequent treatment, and if PLV and other differential diagnoses and complicating factors are excluded,12 the prognosis is usually good in mild to moderate cases of EPD. It is much more guarded in severe chronic proliferative cases where complete resolution of the clinical signs cannot be achieved (Figure 1; Supplementary Figures S3 and S4). Severe EPD/CPL is incurable, but lifelong intensive management may slow down disease progression. Besides providing regular skin care and treatment of secondary infections as outlined above, mitigating tissue edema by controlled exercise, compression bandages, and manual lymph drainage is advised.16,17 Furthermore, surgical treatment including “epidermal shaving” and a combination of sharp dissection and electrocautery have been described.17,41

Conclusions and Outlook

We have learned much about EPD since Percivall’s Hippopathology of 1875 (reviewed by Kugler),1 but most original studies have focused on intrinsic and extrinsic risk factors, which provide only indirect evidence informing management to prevent and improve clinical EPD. The value of practical management recommendations regarding humidity, meteorological, and hygienic environmental conditions has not been investigated, and recommendations on medical treatment are still largely empirical. Adequately powered, controlled trials assessing management and treatment protocols for the different forms of this syndrome are required. Consistent use of validated scoring systems would facilitate comparisons between studies and could also assist owners in deciding when to seek professional advice. Raising owner awareness would be key to improving the welfare of susceptible and affected horses.

Supplementary Materials

Supplementary materials are posted online at the journal website: avmajournals.avma.org.

Please note that references 42–44 appear only in Supplementary Table S2.

Acknowledgments

A special thank you goes to all horse owners that participated in studies helping us to better understand this complex syndrome and improve affected horses’ well-being. We also thank Drs. Alessandra Ramseyer, Rebekka Käser, Lina Galliker, and Daphne Sangiorgio for documentation of clinical cases and Dr. Lisa Thomann for assistance with this manuscript.

The authors declare no competing interests.

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