Equine Dermatitis Study Guide

Overview and Clinical Importance

Dermatitis in horses encompasses a broad spectrum of inflammatory skin conditions that represent some of the most frequently encountered dermatological problems in equine practice. These conditions range from mild, self-limiting reactions to severe, debilitating diseases that significantly impact equine welfare and performance. Understanding the etiology, clinical presentation, and management of equine dermatitis is essential for the NAVLE examination and clinical practice.

Equine dermatitis conditions can be broadly categorized into infectious (bacterial, fungal, parasitic), allergic/hypersensitivity (insect bite hypersensitivity, atopic dermatitis, contact dermatitis), and environmentally-induced (photosensitization, pastern dermatitis) causes. The skin serves as the body's largest organ and primary barrier against environmental insults, making accurate diagnosis and treatment of dermatological conditions critical for maintaining overall equine health.

Pastern Dermatitis (Scratches/Mud Fever)

Definition and Terminology

Equine pastern dermatitis (EPD) is a multifactorial syndrome rather than a single disease entity. It manifests as inflammatory cutaneous lesions on the distal extremities, typically affecting the palmar/plantar aspect of the pastern region. Common lay terms include scratches, mud fever, greasy heel, mud rash, dew poisoning, cracked heels, and grapes (for the chronic proliferative form).

Clinical Forms of Pastern Dermatitis

Etiology and Risk Factors

Primary Causes

Bacterial: Dermatophilus congolensis (most common), Staphylococcus aureus, Streptococcus spp., Pseudomonas spp.

Fungal: Zygomycota phylum, Malassezia spp., Pythium (oomycete)

Parasitic: Chorioptes equi (leg mites) - causes chorioptic mange

Other: Photosensitization, contact dermatitis, pastern leukocytoclastic vasculitis

Predisposing Factors

• Prolonged exposure to wet, muddy conditions (primary environmental factor)
• Draft breeds with feathered legs (trap moisture and debris)
• Unpigmented (white) skin on distal limbs
• Hind limbs more commonly affected than forelimbs
• Large cannon circumference
• Trauma from rough vegetation, sand, or abrasive bedding

Diagnosis

A thorough diagnostic workup is essential to identify underlying causes and guide appropriate treatment.

Treatment

Dermatophilosis (Rain Rot/Rain Scald)

Etiology and Pathogenesis

Dermatophilosis is caused by Dermatophilus congolensis, a gram-positive, branching, filamentous actinomycete bacterium. The organism produces zoospores that are released in wet conditions and penetrate damaged skin. The disease requires three factors: moisture, skin damage, and the presence of the organism.

Clinical Signs

Distribution: Dorsal trunk (rain scald), distal limbs (mud fever), face, and areas subject to wetting by rain or sweat

Primary lesions: Papules progress to characteristic 'paintbrush' lesions - matted tufts of hair with adherent crusts

Secondary changes: Alopecia, crusting, exudation; underside of crust shows yellowish-green pus

Symptoms: Lesions are typically painful (not pruritic); horse may resent grooming

Diagnosis

• Direct microscopy: Branching filaments with rows of cocci (railway-track appearance) on stained smear of crust/exudate
• Culture: Can be difficult; organism grows slowly; not always necessary if microscopy is diagnostic
• PCR: Available for definitive diagnosis; RT-qPCR offers rapid, sensitive detection
• Histopathology: Folliculitis, intraepidermal pustules, alternating layers of parakeratotic and orthokeratotic hyperkeratosis

Treatment and Prevention

Environmental: Keep horse dry; shelter from rain; ensure adequate drainage in paddocks

Topical: Chlorhexidine or iodophor shampoos; gently soak and remove crusts; dry thoroughly; topical antiseptics

Systemic: Procaine penicillin G (22,000 IU/kg IM BID for 5-7 days) for severe cases; organism is resistant to sulfonamides

Biosecurity: Do not share tack, grooming equipment, or blankets; contagious between horses; practice good hand hygiene

Insect Bite Hypersensitivity (Sweet Itch)

Definition and Pathophysiology

Insect bite hypersensitivity (IBH), also known as sweet itch, Queensland itch, summer eczema, or Culicoides hypersensitivity, is the most common allergic skin disease in horses worldwide. It is a Type I (IgE-mediated) and Type IV (cell-mediated) hypersensitivity reaction to salivary antigens from biting insects, primarily Culicoides midges (no-see-ums).

Epidemiology and Risk Factors

• Prevalence: Affects approximately 10% of horses worldwide; up to 60% in some populations
• Breed predisposition: Icelandic horses (exported from Culicoides-free environments), native ponies, some Warmblood lines
• Genetic component: Strong heritability; familial clustering observed
• Seasonality: Spring through fall (correlates with Culicoides activity); worse in warm, humid conditions
• Age of onset: Typically develops between 2-4 years of age after repeated exposure

Clinical Signs

Distribution: Dorsal pattern - mane, tail head, dorsal midline, face, ears; ventral midline in some cases

Primary signs: Intense pruritus, papules, wheals at bite sites

Secondary changes: Self-trauma leading to alopecia, excoriations, lichenification, secondary bacterial infection

Chronic changes: Hyperpigmentation, skin thickening, permanent hair loss, 'rat tail' appearance

Treatment and Management

Exam Focus: Remember the IBH mnemonic: SWEET = Seasonal, Wheals/pruritus, Ears-mane-tail distribution, Exclusion diagnosis, Treatment is avoidance first.

Dermatophytosis (Ringworm)

Etiology

Dermatophytosis is a superficial fungal infection of the skin and hair caused by dermatophyte fungi. The primary causative agents in horses are Trichophyton equinum (most common) and Trichophyton mentagrophytes. Other species include Microsporum gypseum, M. canis, and T. verrucosum.

Clinical Signs

Distribution: Most common in girth and saddle areas ('girth itch'); can spread to face, neck, and body

Primary lesions: Papular eruption followed by circular areas of alopecia with crusts and scaling

Characteristics: Lesions expand centrifugally; hairs at margins are broken and easily epilated

Symptoms: Variable pruritus; usually not painful; may be subclinical in some horses

Diagnosis

• Fungal culture: Gold standard; pluck hairs from lesion margins; may take 2-4 weeks
• Direct microscopy (KOH prep): Fungal hyphae and arthrospores on/in hair shafts
• Wood's lamp: Limited utility; only M. canis and M. equinum fluoresce (not T. equinum)
• PCR: Rapid species identification; increasingly available

Treatment

Self-limiting: Most cases resolve spontaneously in 1-3 months; treatment accelerates resolution and reduces contagion

Topical (first-line): Lime sulfur 1:16 or enilconazole 1:100 - whole body, leave-on rinses twice weekly; chlorhexidine/miconazole combinations

Systemic (severe cases): Griseofulvin (10 mg/kg PO daily) - CONTRAINDICATED in pregnant mares (teratogenic); Terbinafine

Environmental: Disinfect all tack, blankets, grooming tools; antifungal bathroom cleaners effective for Trichophyton

Photosensitization

Definition and Classification

Photosensitization is a light-induced inflammatory skin reaction that occurs when photodynamic compounds accumulate in the skin and become activated by ultraviolet light. It is distinct from sunburn and more severe. Lesions are restricted to non-pigmented (white) and lightly-haired skin areas.

Clinical Signs

Distribution: Non-pigmented skin only - muzzle, eyelids, ears, white leg markings, coronary bands

Progression: Erythema, edema, pain; progresses to vesicles, bullae, exudation, crusting, skin sloughing, necrosis

Behavior: Photophobia (squinting, seeking shade); restlessness

Systemic signs (Type II): Icterus, weight loss, hepatoencephalopathy signs (head pressing, wandering)

Treatment

Remove cause: Identify and remove access to toxic plants; discontinue offending medications

Sun protection: House horse indoors; turnout only at night; fly masks/sheets with UV protection; zinc oxide sunscreen

Supportive care: NSAIDs for pain/inflammation; corticosteroids in early stages; wound care for ulcerated areas

Treat underlying cause: For Type II - supportive liver care; remove hepatotoxic plants; prognosis guarded if significant liver damage

Contact and Atopic Dermatitis

Contact Dermatitis

Contact dermatitis is an inflammatory skin reaction resulting from direct contact between the skin and an irritating or allergenic substance. It may be irritant (occurs in all exposed animals on first exposure) or allergic (Type IV hypersensitivity - requires prior sensitization).

Common causes: Fly sprays, shampoos, liniments, topical medications (especially neomycin), blanket/tack materials, plants (buttercups, nettles)

Clinical signs: Erythema, papules, vesicles, pruritus, scaling, alopecia; distribution corresponds to contact area

Diagnosis: History of exposure; distribution pattern; resolution with avoidance; patch testing (rarely performed)

Treatment: Identify and avoid offending substance; anti-inflammatory therapy (topical or systemic steroids); supportive skin care

Atopic Dermatitis

Equine atopic dermatitis is an IgE-mediated hypersensitivity to environmental allergens such as pollens, molds, and dust mites. It is the second most common allergic skin disease after IBH.

Clinical signs: Recurrent urticaria, pruritus (variable distribution), coat changes; may or may not be seasonal

Diagnosis: Clinical signs plus exclusion of other causes; supported by intradermal testing or serum IgE testing; positive response to allergen-specific immunotherapy (ASIT)

Treatment: Allergen avoidance when possible; corticosteroids for acute flares; antihistamines; ASIT (approximately 70% improvement rate)

Summary: Quick Differential Diagnosis Guide

Memory Aids and Board Tips

EPD Forms Mnemonic: 'MEC'

Mild (scratches) → Exudative (grease heel) → Chronic proliferative (grapes)

Dermatophilus Diagnosis: 'RAILWAY TRACKS'

When you see branching filaments with parallel rows of cocci (tram-line/railway-track appearance) on direct microscopy, think Dermatophilus congolensis.

IBH: 'SWEET'

Seasonal (spring-fall)

Wheals and intense pruritus

Ears, mane, tail distribution

Exclusion diagnosis (rule out others)

Treatment is avoidance FIRST

Photosensitization: 'WHITE = WATCH'

If lesions are ONLY on white/unpigmented skin → Think photosensitization → Check liver function (Type II is more common)