Equine pastern dermatitis is not a single disease but rather a cutaneous reaction pattern in horses. This dermatitis should be considered a syndrome rather than a diagnosis. Uncovering the underlying causes before treatment is key to minimizing treatment failure and frustration. To achieve a positive therapeutic outcome, treating the predisposing and perpetuating factors is just as important as addressing the primary cause of equine pastern dermatitis.
Equine pastern dermatitis can affect any equine breed but is most common in draft horses. Feathering over the pasterns is a predisposing factor.
Equine pastern dermatitis occurs without a sex predilection and mostly in adult horses. The dermatitis typically involves the caudal aspect of the pasterns, with the hindlimbs most commonly affected. If not addressed, the lesions can spread cranially to the front of the pastern and fetlock.
The lesions are usually bilaterally symmetric; however, they can affect just one limb. The lesions are most often detected on, but are not limited to, the nonpigmented areas of the pasterns. The clinical signs vary, depending on the cause, duration, and previous therapy. Initially, there is edema, erythema, and scaling, which rapidly progress to exudation, matting of the hair, and crusting. If the underlying cause is vasculitis, ulcers may be noted. Secondary bacterial infection is a common complication and a perpetuating factor. With chronicity, the skin may become thickened and fissured due to constant movement and flexion. The lesions are often painful and can result in lameness.
There are three different presentations of equine pastern dermatitis:
- The mild form (scratches, mud fever, mud rash is the mildest and most prevalent form of equine pastern dermatitis. This form is characterized by alopecia, dry scales, and crusts with potential epidermal hyperplasia. Pruritus and pain are variable.
- The exudative form (grease heel, dew poisoning) is characterized by erythema, erosion, alopecia, and serous to purulent crusting dermatitis. Epidermolysis and vasculitis are often involved.
- The chronic proliferative form (grapes, verrucous pododermatitis is characterized by excessive granulation tissue (fibroblastic proliferation) that becomes cornified. Nodular proliferations of hyperkeratosis and lichenification occur. Fissures and papillomatous areas may develop and are common sequelae in draft breeds.
Photosensitization, both systemic and contact forms, may affect the pasterns of horses with white extremities. The most common cause of equine contact photosensitization is exposure to clover pastures; this form primarily involves the muzzle and distal extremities. Systemic photosensitization is subdivided into primary and hepatogenous causes. Primary systemic photosensitization occurs when a preformed or metabolically derived photosensitizing agent reaches the skin by ingestion, contact, or injection. Causes of primary photosensitization are St. John's wort (Hypericum perforatum), buckwheat (Polygonum fagopyrum), and perennial rye grass (Lolium perenne). Hepatogenous systemic photosensitization occurs when an increased concentration of phylloerythrin is in the blood as a result of liver disease. This type of photosensitization is most commonly due to pyrrolizidine alkaloid toxicosis. All types cause dermatitis in the presence of ultraviolet light.
Chronic progressive lymphedema
Chronic progressive lymphedema of draft horses, which is characterized by progressive swelling, hyperkeratosis, and fibrosis of the distal limbs in shires, Clydesdales, and Belgian draft horses, has been under investigation at the University of California, Davis.
The clinical signs and pathologic changes are similar to those of chronic lymphedema (elephantiasis nostras verrucosa) in humans. Factors that have been proposed to contribute to this disease are abnormal functioning of the dermal lymphatic system, resulting in severe swelling and fibrosis; a compromised immune system; and secondary skin infections. Researchers suspect that a deficiency or abnormality in elastin, a connective tissue component, is the underlying element and may cause lymphatic degeneration in these horses. The lesions do not respond well to therapy. As the disease progresses and becomes more chronic, enlargement of the lower extremity becomes permanent, and the swelling is firm during palpation. Progressive skinfolds and nodule formation are first noted on the caudal aspect of the pastern, affecting both pigmented and nonpigmented skin; with chronicity, skinfolds and nodules encompass the entire lower extremity. Over time, the lesions cause a lack of mobility and often become traumatized during normal exercise. The prognosis is poor because of the lack of a specific treatment for the structural defect; development of secondary infections, which in turn cause further degradation of elastin; poor delivery and response to supportive symptomatic therapy; and development of systemic illness and debilitation as the disease progresses.
Pastern leukocytoclastic vasculitis
Pastern leukocytoclastic vasculitis (photoaggravated vasculitis) is an additional clinical cause of equine pastern dermatitis. This disease is poorly understood and affects mature horses. It is unique to horses and often, but not exclusively, targets unpigmented distal extremities. Pastern leukocytoclastic vasculitis is believed to be due to immunocomplex deposition on the blood vessel walls of the distal limbs, triggering vasculopathy and resulting in clinically well-demarcated circular, erythematous, exudative lesions with tightly adherent crusts. The prevalence of clinical signs in the summer suggests that it is photoaggravated. The medial and lateral aspects of the pasterns are most commonly affected. The lesions appear painful rather than pruritic. Edema of the affected limb(s) and lameness are common sequelae. Chronic cases may develop a rough or warty surface.
A detailed history is very important in the dermatologic workup of equine pastern dermatitis. Important information includes the age of the patient at onset, the month the problem was first noted, and whether the condition has been seasonal and/or pruritic. Before the examination, additional questioning should investigate the use of topical medications or home remedies and whether the lesions improved or worsened with each treatment. Environmental conditions can be predisposing or primary factors in equine pastern dermatitis; therefore, when possible, a detailed description of the environment (bedding, pasture, sand, insect burden, moisture) should be provided or a personal inspection conducted. Long-term exposure to moisture, such as wet bedding or muddy pastures, is retained by the long hairs of the fetlock and pastern in draft horses and contributes to skin maceration. In cases of contact irritant or allergic dermatitis, all four pasterns are usually affected.
To rule out potential infectious or zoonotic conditions, such as dermatophytosis (Trichophyton equinum, Microsporum canis, or Microsporum gypseum infection) and Cheyletiella sp infection, the clinician should consider whether other in-contact animals or humans are affected.
Pastern folliculitis or pyoderma is mainly caused by infection with Staphylococcus aureus or Dermatophilus congolensis. Initially, papules and/or pustules (rare) are noted with a Staphylococcus infection; however, with chronicity, they may not be seen. The lesions of D. congolensis infection typically include crusting and exudation; when the crusts are removed, they have a "paintbrush" appearance and the underlying skin surface is ulcerative.
Chronic moisture and trauma to the epidermal barrier are required for this organism to cause infection. Because culture samples obtained by swabbing can produce misleading results due to surface contamination, biopsy for culture is needed for a definitive diagnosis. Ideally, an area of intact, nonulcerated skin (plaque or nodules) of the affected pastern is surgically scrubbed and deep biopsies are performed with sterile precautions. The specimens are then placed into culture medium and submitted to a microbiology laboratory for tissue maceration and culture and sensitivity testing.
Dermatophytosis rarely causes pastern folliculitis; however, it is important to rule out. A definitive diagnosis requires positive dermatophyte test medium (DTM) culture results in conjunction with positive microscopic identification of macrocondia. It is essential to add vitamin B complex to DTM in the office or at a commercial laboratory because T. equinum requires niacin to grow. M. canis and M. gypseum grow readily on a standard fungal culture medium and DTM.
Chorioptic mange is a significant cause of pastern dermatitis in draft horses because of their long pastern feathers, which provide an ideal microenvironment for the mites. This condition is intensely pruritic. Affected horses may constantly rub the area and are often observed stamping their feet.5 Chorioptes infection should be highly suspected if other in-contact horses are affected and have clinical signs of pruritus. The mites typically are easily harvested from the skin.
Superficial Skin Scrape
Multiple skin scrapings are key to ruling out superficial mites, especially Chorioptes spp. Superficial scrapings of crusts and debris can be collected using a dulled #10 blade and put into mineral oil on several glass slides. Other collection methods include the use of a stiff scrubbing brush or denture-type toothbrush to sweep the dander, crusts, and debris into a petri dish and the use of acetate tape preparations. The mites are often easier to detect during cool weather because of favorable environmental factors, and they tend to localize at the coronet during the summer. Because the mites are quite mobile, the slides should immediately be examined with a microscope using a 10x objective lens. Some authors suggest applying a small amount of insecticide to the slide to immobilize the mites.
Cytology and Diff-Quik Stain
Cytology is for immediate evaluation of secondary bacterial and Malassezia infections, which are considered perpetuating factors of equine pastern dermatitis. Scotch 3M Gloss Finish Multitask Tape stained directly with methylene blue or direct impressions using a glass slide, heat fixation, and Diff-Quik stain are simple, economical methods of collecting and processing diagnostic samples. Observation with a 100x microscope objective lens for bacteria engulfed within degenerative neutrophils and variably stained budding yeast organisms is often rewarding.
Cytology may also provide insight into autoimmune, nodular, and neoplastic conditions. Acantholytic cells within a group of nonvacuolated neutrophils, in the presence of minimal to no bacterial infection, support further dermatohistopathologic investigation to obtain a definitive diagnosis of a pemphigus complex. Eosinophils should indicate a differential list composed of allergic, ectoparasitic, intermediate fungal, or foreign body causes. A homogenous population of cells with an increased mitotic index and atypical nuclear:cytoplasmic ratio predicates the need for a biopsy to rule out neoplasia.
Direct Examination of Hairs
A trichogram provides information on the stage of hair growth (anagen versus telogen) and can identify dermatophytic spores. These spores can be evaluated by adding one or two drops of a clearing agent (e.g., 10% potassium hydroxide solution) to affected plucked hairs, applying a coverslip, and then gently heating the slide for 15 to 20 minutes using the microscope lamp. Under a 4x objective lens, infected hairs appear pale and swollen and have identifiable small circular arthrospores within or on the surface of affected hair shafts. The potassium hydroxide preparation is time-consuming and can take several attempts to master; thus it is not often used in general practice.
Dermatophyte Test Medium Culture
When hair and crust samples are embedded in an in-house dermatophyte culture, a few drops of niacin (vitamin B complex) must be added to the DTM to satisfy the growth requirements of T. equinum.
If samples are submitted to a commercial laboratory, contact the microbiologist to ascertain whether niacin is contained within or added to the culture medium. When preparing the site to take samples, use isopropyl alcohol to cleanse the hairs of saprophytic (clinically irrelevant) fungi. The alcohol must be allowed to dry before collection to avoid a false-negative result. DTM helps suppress growth of saprophytes and contaminant bacteria because it contains chlortetracycline, gentamicin, and cycloheximide.
Dermatophytes metabolize the protein first, creating alkaline metabolites that interact with the phenol red pH indicator, resulting in a color change to red, along with colony growth. False-positive color changes occur when saprophytes have exhausted the carbohydrate source on the plate and then use protein, causing a late color change to red. Seven to 14 days of growth on the medium are typically required to visualize macroconidia. Once the color change to red has been identified with concurrent colony growth, microscopic examination is important to confirm the diagnosis. Use clear cellophane tape and press lightly onto the colony within the culture medium to collect the macroconidia. Then apply one or two drops of lactophenol cotton blue, or methylene blue (last dip in Diff-Quik stain) if the former is not readily available, and examine the tape with a microscope under a 40x objective lens. If no macroconidia are visible, wait a few days for the colony to mature; then repeat the procedure.
Dermatophilus congolensis Preparation
To identify Dermatophilus spp, peel off a crust, clip the excess hair from the sample, and place it into one or two drops of saline on a clean slide. Allow the sample to macerate (soften) for 15 minutes, and remove the larger pieces. Crush the remaining material on the slide and allow it to air-dry; then heat-fix the slide, stain it with Diff-Quik or methylene blue, allow it to dry, and examine it under a microscope with a 100x objective lens. Oil immersion should allow visualization of filamentous, branching, parallel rows of cocci-shaped bacteria in a "railroad track" orientation.
Biopsy should be considered if immune-mediated disorders, nodular or draining tract lesions, or neoplastic conditions are suspected. Biopsies are also recommended when treatment has been pursued and failures or relapses have occurred. In most cases, especially when pastern leukocytoclastic vasculitis is suspected, skin biopsies should be interpreted by a dermatohistopathologist with an interest in equine skin diseases. Acute changes, including leukocytoclastic vasculitis, thrombosis, and vessel wall necrosis, are often scarce and can easily be overlooked. If severe secondary bacterial dermatitis is present, administration of antibiotics for a minimum of 21 days is recommended before performing a biopsy to provide a clearer picture of the underlying cause.
Biopsy for Culture
If a bacterial or fungal infection is suspected or is not responding to appropriate therapy, a biopsy is warranted. When a biopsy specimen is obtained for culture, surface contaminants need to be eliminated by clipping the hair and performing a surgical scrub. The biopsy specimen should be obtained in as sterile a manner as possible and submitted in a sterile container or medium. The specimen should be sent to the laboratory as soon as possible to minimize the growth of superficial contaminants.
Complete Blood Count and Chemistry Panel
Evaluation of hematologic and biochemical parameters is useful to rule out hepatogenous photosensitization disorders and metabolic illnesses and to obtain a baseline before treatment of an immune-mediated disorder.
Choosing the appropriate therapy involves recognition and identification of predisposing, perpetuating, and primary factors.
Environmental modifications to minimize exacerbation of a primary underlying problem include:
- Avoiding pastures and paddocks with mud, water, or sand (e.g., Arabian horses and sand)
- Keeping horses in clean, dry stalls during wet weather
- Avoiding turnout before the morning dew has dried
- Using an alternative source of bedding (treated or aromatic types of wood shavings contain chemicals that can cause contact hypersensitivity) if contact allergy (affecting all pasterns) is suspected
- Clipping excessive hair over the pasterns, if present, to decrease moisture retention
- Avoiding ultraviolet light exposure by stabling or using leg wraps if pastern leukocytoclastic vasculitis is suspected
In equine pastern dermatitis, secondary bacterial infections with Staphylococcus spp are common sequelae that complicate the diagnosis. Antibacterial shampoos can help control overcolonization of bacteria when used daily for 7 to 10 days, then two to three times weekly. Available active ingredients include benzoyl peroxide (2%), ethyl lactate, and chlorhexidine (2%). A topical ointment containing 2% mupirocin has excellent penetration into the epidermis and can be used for both Dermatophilus or staphylococcal bacterial infections. Close clipping and cleansing are paramount to the success of any ointment.
Providing a dry, stable environment is often the most effective treatment. Some dermatologists recommend using a padded, water-repellent bandage (changed every 1 to 2 days). Facilitator (Blue Ridge Pharmaceuticals) is a hydroxyethylated amylopectin liquid bandage applied every 1 to 3 days after cleansing. If lesions are exudative, astringent solutions, such as lime sulfur (4 to 6 oz/gal) or aluminum acetate solution, can be used.
Lime sulfur dips and sprays can be used for localized treatment of the pastern for dermatophytes and mites. Enilconazole is a topically labeled treatment for dermatophytosis in horses in many countries other than the United States and has shown good success. Shampoos containing a combination of miconazole or ketoconazole and chlorhexidine demonstrate synergistic activity and improved resolution of dermatophyte infections.
Topical steroids can be used for immune-mediated conditions such as pastern leukocytoclastic vasculitis or pemphigus. Triamcinolone spray (0.015%; Genesis, Virbac) and/or hydrocortisone (1%) leave-on conditioner (Resicort, Virbac) can be used in conjunction with systemic immunomodulators to treat these conditions. In addition, good success has been noted with topical betamethasone (1%) or alclometasone (0.05%) applied to the lesions.
The antibiotics most commonly used in horses are trimethoprim-potentiated sulfonamides (15 to 35 mg/kg PO q12-24h for 2 to 3 weeks), often in conjunction with topical antibacterial shampoos2. Adverse reactions include drug-induced urticaria, pruritus, exfoliative dermatitis, erythema multiforme, anemia, and leukopenia. In horses that are intolerant to sulfonamide-based medications, enrofloxacin (the injectable form; 7.5 mg/kg PO q24h) has been used with success. This drug should be avoided in foals and growing horses because of its potential for chondrotoxicity and, therefore, reserved for severe staphylococcal infections.
Systemic antifungal therapy is often unnecessary in horses. Griseofulvin powder is available for horses; however, no pharmacokinetic data have been published for griseofulvin, and its efficacy is questionable. Ketoconazole, itraconazole, and fluconazole are effective for the systemic treatment of dermatophytosis in humans, cats, and dogs. These agents are not currently approved in the United States for use in horses.
Ketoconazole (30 mg/kg/day) has very low absorption (23%) from the gastrointestinal tract in horses and can be very expensive.22 Itraconazole (5 to 10 mg/kg/day) has been used in horses with variable success. One published pharmacokinetic report of fluconazole use in horses recommended a single loading dose of 14 mg/kg followed by 5 mg/kg/day. The cost of these medications limits their use; however, recent patent expirations have allowed more affordable generic products.
Conditions such as pastern leukocytoclastic vasculitis and pemphigus foliaceus often require administration of immunosuppressive doses of steroids to control the immune-mediated reaction and decreased exposure to ultraviolet light to minimize photoaggravation of the disorder.
Typically, dexamethasone (0.1 to 0.2 mg/kg) or prednisolone (2 mg/kg) is administered daily for 7 to 14 days, then gradually tapered to the lowest dose required to maintain remission of the lesions. Pentoxifylline (8 to 10 mg/kg PO q8-12h), a phosphodiesterase inhibitor, has immunomodulatory properties, including inhibition of tumor necrosis factor-a, interleukin-1, and interleukin-6; thus it is useful as a steroid-sparing agent. In addition, pentoxifylline increases erythrocyte deformability and platelet aggregation, thereby inhibiting thrombosis and improving wound healing. Long-term control of immune-mediated equine pastern dermatitis can often be achieved using topical steroids and/or pentoxifylline once the lesions have been controlled.
Topical organophosphates (malathion [0.5%], coumaphos [0.06%]) have been historically used as effective ectoparasiticides; however, because of concerns regarding toxicities and the environment, other treatment options should be considered. Permethrins at concentrations greater than 2% have both insecticidal and significant repellent activity. Therefore, these products are most useful in preventing Culicoides- and tick-related equine pastern dermatitis. Selenium sulfide shampoo followed by lime sulfur (6 oz/gal) sponged on every 5 days for 1 month has been successfully used to treat parasites embedded within equine pastern dermatitis lesions with significant amounts of crust or debris.
Although a recent European study demonstrated that one treatment with fipronil spray (0.25%) was effective against Chorioptes bovis infestation, this use is considered to be off-label. Because these mites can live off the host for up to 70 days, environmental decontamination of the barn, stalls, bedding, tack, and grooming equipment is essential.
Ivermectin (1%) solution (300 µg/kg PO weekly for four doses, based on feeding habits) is most often the miticidal treatment of choice because topical treatments are labor intensive. To minimize treatment failures and relapses with contagious conditions, all in-contact animals must also be treated.
- ↑ Scott DW, Miller WH (2003) Miscellaneous skin diseases, in Scott DW, Miller WH (eds): Equine Dermatology. London, Saunders, pp:687-690
- ↑ Yu AA (2003) Pastern dermatitis, in Current Therapy in Equine Medicine, ed 4. Philadelphia, WB Saunders, pp:201-203
- ↑ English M, Pollen S (1995) Pastern dermatitis and unguilysis in 2 draft horses. Equine Pract 17(8):25
- ↑ Logas DB, Barbet JL (1999) Diseases of the skin, in Colahan PT, Merritt AM, Moore JN, Mayhew IG (eds): Equine Medicine and Surgery V. Goleta, CA, American Veterinary Publications, pp:1910-1934
- ↑ Standard AA (2000) Miscellaneous. Vet Dermatol 11(3):217-223
- ↑ Yu AA (2004) Equine pastern dermatitis. Proc 19th AAVD/ACVD Meet pp:117-122
- ↑ Rosenkrantz WS (2004) Photo-induced dermatitis-vasculitis in the horse. Proc 19th AAVD/ACVD Annu Meet pp:123-127
- ↑ Boord M (2003) Photosensitivity, in Current Therapy in Equine Medicine, ed 4. Philadelphia, WB Saunders, pp:174-176
- ↑ De Cock HE, Affolter VK, Wisner ER, et al (2003) Progressive swelling, hyperkeratosis and fibrosis of distal limbs in Clydesdales, shires and Belgian draft horses suggestive of primary lymphedema. Lymphat Res Biol 1(3):191-199
- ↑ De Cock HE, Affolter VK, Farver TB, et al (2006) Measurement of skin desmosine as an indicator of altered cutaneous elastin in draft horses with chronic progressive lymphedema. Lymphat Res Biol 4(2):67-72
- ↑ Pascoe RR, Knottenbelt DC (1999) Immune-mediated diseases, in Pascoe RR (ed): Manual of Equine Dermatology. London, WB Saunders, pp:165-166
- ↑ Pascoe RR, Knottenbelt DC (1999) Iatrogenic or idiopathic disorders, in Pascoe RR (ed): Manual of Equine Dermatology. London, WB Saunders, pp:201-202
- ↑ Scott DW, Miller WH (2003) Bacterial skin diseases, in Scott DW, Miller WH (eds): Equine Dermatology. London, WB Saunders, pp:234-242
- ↑ Pascoe RR, Knottenbelt DC (1999) Infectious diseases, in Pascoe RR (ed): Manual of Equine Dermatology. London, WB Saunders, pp:102-106
- ↑ Littlewood JD (2000) Dermatosis of the equine distal limb. Proc 4th World Congress Vet Dermatol pp:129-133
- ↑ Scott DW, Miller WH (2003) Parasitic diseases, in Scott DW, Miller WH (eds): Equine Dermatology. London, WB Saunders, pp:331-333
- ↑ Scott DW, Miller WH (2003) Fungal skin diseases, in Scott DW, Miller WH (eds): Equine Dermatology. London, WB Saunders, pp:261-276
- ↑ Scott DW, Miller WH (2003) Diagnostic methods, in Scott DW, Miller WH (eds): Equine Dermatology. London, WB Saunders, pp:91-98
- ↑ Haines GR, Brown MP, Gronwall RR, Merritt KA (2000) Serum concentrations and pharmacokinetics of enrofloxacin after intravenous and intragastric administration to mares. Can J Vet Res 64(3):171-177
- ↑ Korenek NL, Legendre AM, Andrews FM, et al (1994) Treatment of mycotic rhinitis with itraconazole in three horses. J Vet Intern Med 8(3):224-227, 1994
- ↑ Latimer FG, Colitz CM, Campbell NB, Papich MG (2001) Pharmacokinetics of fluconazole following intravenous and oral administration and body fluid concentrations of fluconazole following repeated oral doses in horses. Am J Vet Res 62(10):1606-1611
- ↑ Scott DW, Miller WH (2003) Dermatologic therapy, in Scott DW, Miller WH (eds): Equine Dermatology. London, WB Saunders, p:189