Integumentum commune
The equine skin (integument) is the largest organ of the horse. It consists of three layers: the epidermis (outermost, keratinized stratified squamous epithelium), dermis (collagen-rich connective tissue containing blood vessels, nerves, hair follicles, sebaceous and sweat glands), and hypodermis (subcutaneous fat and loose connective tissue). The horse has two types of sweat glands: apocrine (over most of the body, producing protein-rich sweat containing latherin; a natural surfactant unique to equids) and eccrine (limited to the frog of the hoof). The coat consists of guard hairs, a fine undercoat (varies by breed), tactile vibrissae around the muzzle and eyes, and the mane and tail. The skin provides thermoregulation, UV protection, sensory perception, and immune defense. Regional skin thickness varies from 1–5 mm, being thickest over the dorsum and thinnest on the inner thighs and axillae.
REGIONAL SKIN CONDITIONS: • HEAD/FACE: Melanomas are extremely common in gray horses over 15 years (up to 80% prevalence). Sarcoids frequently occur around the eyes, ears, and lips. Aural plaques (papillomavirus) cause white, crusty plaques inside the pinnae. • NECK: Cresty neck (regional adiposity) is a key indicator of Equine Metabolic Syndrome (EMS) and insulin dysregulation; a major laminitis risk factor. Score on the 0–5 Cresty Neck Scale; ≥3 warrants veterinary metabolic workup. Rain rot (Dermatophilus congolensis) commonly affects the dorsal neck and back. • WITHERS: Fistulous withers (supraspinous bursitis, often Brucella-associated) causes draining tracts. Saddle sores and pressure injuries from ill-fitting tack cause white hairs, alopecia, or open wounds. Fibrotic myopathy of the withers region may develop from chronic pressure. • BACK: Saddle fit issues manifest as white hairs (indicating prior pressure damage to melanocytes), dry spots after work (blocked sweat glands from pressure), muscle atrophy, or behavioral changes. Kissing spines may cause dorsal skin hypersensitivity. • BARREL/TRUNK: Urticaria (hives) presents as multiple raised wheals, often from allergic reactions (feed, insects, medications, contact allergens). Ringworm (dermatophytosis) commonly starts as circular patches on the girth area. Rain scald affects the dorsum and croup in wet conditions. • LEGS: Scratches (pastern dermatitis/mud fever) affects the caudal pastern, especially in horses with heavy feathering. Cannon keratosis presents as dry, scaly skin on the front of the cannon bones (common, usually cosmetic). Lymphangitis causes severe unilateral limb swelling with pain, heat, and lameness. Stocking up (dependent edema) causes bilateral distal limb swelling that resolves with exercise. Windpuffs (synovial effusion of the fetlock) are common but usually cosmetic. • PASTERN/FETLOCK: Pastern dermatitis (greasy heel/grease) involves inflammation, crusting, and exudation of the caudal pastern. The proliferative form (chronic progressive lymphedema in drafts) causes permanent fibrosis. Predisposing factors: wet/muddy conditions, heavy feathering, Chorioptes mites. • HOOVES: Thrush (Fusobacterium necrophorum) causes black, foul-smelling discharge in the frog sulci. White line disease (onychomycosis) shows separation and chalky material at the white line. Laminitis signs include bounding digital pulses, heat in the hooves, reluctance to walk, and the classic 'rocked back' stance. Hoof cracks may be cosmetic or pathologic depending on depth and location. Subsolar abscesses cause acute severe lameness. • TAIL/DOCK: Sweet itch (Culicoides hypersensitivity) is the most common allergic skin disease worldwide; causes intense pruritus of the mane base and tail head, leading to self-trauma, hair loss, and thickened skin. Tail rubbing may also indicate pinworms (Oxyuris equi), vaginal irritation, or food allergy. Melanomas cluster under the tail in gray horses. • PERINEAL AREA: Melanomas in grays commonly occur perianally and may obstruct defecation when large. Squamous cell carcinoma affects unpigmented perineal skin, especially in Appaloosas, Paints, and cremello horses. • UDDER/SHEATH: Sheath cleaning should be performed 1–2 times yearly; excessive smegma accumulation (including the 'bean' in the urethral fossa) can cause discomfort. Summer sores (habronemiasis) are granulomatous lesions caused by aberrant Habronema larvae deposited by flies on moist skin; common on the sheath, medial canthus, and lower legs.
Rain rot, also known as dermatophilosis, is a bacterial skin infection caused by *Dermatophilus congolensis*. Despite its common name, it is not a fungal infection. The organism thrives in warm, moist
Fungal infection caused by Trichophyton equinum (most common), T. mentagrophytes, or Microsporum species. Highly contagious between horses and to humans (zoonotic). Spread via direct contact or fomite
Sweet itch, also known as Culicoides hypersensitivity, is a Type I and IV hypersensitivity reaction to the saliva of biting midges (Culicoides species). It is the most common allergic skin disease of
Sarcoids are the most common skin tumors of horses, accounting for up to 40% of all equine neoplasia. They are caused by Bovine Papillomavirus types 1 and 2 and do not metastasize but can be locally a
Dermal melanomas are extremely common in gray horses, with up to 80% of gray horses over 15 years affected. They arise from melanocytes that accumulate excessive melanin during the graying process. In
Malignant tumor of keratinocytes, the second most common equine skin cancer. UV radiation is the primary risk factor. Most common on unpigmented skin; especially eyelids (most frequent ocular tumor),
Skin damage caused by photodynamic agents that accumulate in the skin and react with UV light to cause cell damage. Three types: primary (ingestion of photosensitizing plants like St. John's wort, buc
Type I hypersensitivity reaction causing localized dermal edema. Very common in horses. Triggers include insect bites, medications (especially NSAIDs, antibiotics), vaccines, feed allergens, contact a
Scratches, also known as mud fever or pastern dermatitis, is a multifactorial inflammatory condition of the skin on the back of the pastern and fetlock. It is often complicated by bacterial or fungal
## Overview Habronemiasis, or summer sores, is a seasonal parasitic skin disease caused by larvae of Habronema stomach worms deposited by flies into wounds or moist skin. The larvae cannot complete t
Caused by a skin reaction to the microfilariae of Onchocerca cervicalis. Adult worms live in the nuchal ligament; their microfilariae occur in the skin, where they can cause a hypersensitivity reactio
The most common autoimmune skin disease of horses. Autoantibodies target desmoglein-1 in the intercellular bridges (desmosomes) of the superficial epidermis, causing acantholysis (cell separation). Ca
## Overview Anhidrosis is the partial or complete inability to sweat in response to increased body temperature or exercise. Because horses dissipate 65 to 70 percent of heat through evaporation of sw
## Overview Hyperhidrosis is sweating out of proportion to temperature or exercise. It may be generalized or patchy. Causes include pain, equine grass sickness, Horner's syndrome (unilateral facial s
## Overview Alopecia areata is an uncommon, non-inflammatory, non-pruritic autoimmune disorder in which the immune system targets hair-follicle antigens, resulting in focal to widespread hair loss. T
Overgrowth of granulation tissue beyond the wound margin, preventing epithelialization and wound closure. Extremely common in equine limb wounds due to poor blood supply, high motion, limited soft tis
Caused by the oomycete Pythium insidiosum (NOT a true fungus; it's a water mold). Found in tropical and subtropical regions with standing water. Zoospores in stagnant water enter through skin wounds o
Inflammation and failure of the laminar bond between the hoof wall and the distal phalanx (coffin bone). One of the most devastating equine conditions. Primary causes: endocrinopathic (EMS/insulin dys
Thrush is a degenerative bacterial infection of the frog, most commonly caused by *Fusobacterium necrophorum* and other anaerobic bacteria. It thrives in moist, anaerobic environments such as dirty st
White line disease is a condition in which the inner [hoof wall](/anatomy/horse-hoof-anatomy) separates from the sole at the white line, allowing opportunistic fungi and bacteria to invade the non-pig
## Overview Cannon keratosis, commonly called stud crud or cannon crud, is a non-contagious skin condition characterized by thickened, greasy, hyperkeratotic patches on the cranial aspect of the hind
Inflammation of the lymphatic vessels, usually secondary to bacterial infection (Staphylococcus, Streptococcus, Corynebacterium pseudotuberculosis) entering through a skin wound. Ulcerative lymphangit
## Overview A hoof abscess is a localized pocket of infection between the sensitive and insensitive layers of the hoof. It is the most common cause of sudden non-weight-bearing lameness. Bacteria ent
DAILY SKIN CARE: Run your hands over your horse's entire body daily during grooming; you'll catch lumps, bumps, heat, swelling, and sensitivity early. Know what's normal for YOUR horse. WHEN TO CALL THE VET IMMEDIATELY: Any rapidly growing mass; non-healing wound after 2 weeks; sudden severe lameness (abscess or laminitis); hot, swollen limb with fever (lymphangitis); signs of allergic reaction with respiratory distress; any eye involvement. SEASONAL CONSIDERATIONS: • SPRING: Sweet itch begins; sarcoid activity increases; rain rot season starts; laminitis risk peaks with pasture sugar surges • SUMMER: Fly-borne diseases peak (habronemiasis, onchocerciasis); photosensitization risk; anhidrosis becomes apparent; UV-related tumors progress • FALL: Ringworm season (shared blankets/tack); rain rot continues; prepare for winter coat • WINTER: Reduced UV risk; rain rot under blankets (check regularly!); thrush in wet conditions; mud fever from winter turnout PREVENTION: • Maintain dry, clean footing in paddocks and stalls • Regular farrier care every 6–8 weeks • Fly management program (masks, sheets, sprays, environmental control) • Don't share tack/grooming tools between horses (ringworm/rain rot prevention) • Provide shade and shelter from rain • Monitor body condition score and cresty neck score for EMS/laminitis risk • Apply sunscreen to unpigmented skin areas (zinc oxide-based) • Pick hooves daily; treat thrush promptly • Maintain good ventilation under blankets; check for rain rot weekly • Know your horse's normal digital pulse strength • Keep a photo log of any lumps/masses to track changes over time
Rain rot, also known as dermatophilosis, is a bacterial skin infection caused by *Dermatophilus congolensis*. Despite its common name, it is not a fungal infection. The organism thrives in warm, moist conditions and causes characteristic crusty, paintbrush-like scabs along the horse's back, neck, and rump. ## What it is *Dermatophilus congolensis* is an actinomycete bacterium that exists on the skin of many horses without causing disease. When the skin barrier is compromised by prolonged moisture, insect bites, or trauma, the organism invades the epidermis and causes superficial pustules that rupture and form thick crusts. The crusts contain embedded hairs and have a classic "paintbrush" appearance when lifted. ## Signs and symptoms - Tufted, paintbrush-like scabs along the dorsal surface (back, croup, neck, withers) - Hair epilates easily in clumps with pus or crust on the underside - Exposed skin underneath is pink, moist, and sometimes raw - Lesions may spread to the face and legs in severe cases - Usually not pruritic (not itchy), which helps distinguish it from other skin conditions - Worsens significantly during wet weather ## Causes and risk factors Rain rot develops when the skin remains wet for prolonged periods, especially in combination with skin trauma from insects or grooming. Risk factors include poor stable hygiene, horses kept outdoors in wet conditions without shelter, heavy feathering, and compromised immune function. The disease is more common in young horses and during periods of high rainfall. ## How it is diagnosed Diagnosis is usually straightforward based on the characteristic appearance and distribution of lesions. Microscopic examination of crusts can confirm the presence of *Dermatophilus* organisms (railroad track appearance of bacterial filaments). Bacterial culture is occasionally used in complicated cases. ## Treatment and management Treatment involves removing the crusts (after softening with oil or antimicrobial shampoo) and applying topical antibacterial agents. Keeping the horse dry is essential. In severe or widespread cases, systemic antibiotics may be required. Improving stable hygiene and providing shelter from prolonged rain help prevent recurrence. Most cases resolve within 1 to 3 weeks with appropriate treatment. ## When to call the vet Contact your veterinarian if the lesions are widespread, the horse is systemically ill, or the condition does not improve with basic topical treatment within a week or two. Severe cases can lead to secondary infections or significant discomfort. ## Prevention Prevention centers on keeping the horse as dry as possible and maintaining good skin hygiene. Providing adequate shelter during wet weather, avoiding sharing grooming equipment during outbreaks, and promptly treating any skin trauma reduce risk. ## Frequently asked questions **Is rain rot contagious?** Yes, it can spread between horses through direct contact or shared equipment, especially in wet conditions. **Is rain rot the same as rain scald?** Yes, the terms are often used interchangeably, though "rain scald" sometimes refers specifically to lesions on the back and rump. **Can rain rot affect the legs?** Yes, lesions can appear on the lower legs, though the classic presentation is along the dorsal midline. This information is for educational purposes only. Always consult with a licensed veterinarian for diagnosis and treatment of your horse. Signs include: Tufted, paintbrush-like scabs along the dorsal surface (back, croup, neck, withers); hair epilates easily in clumps with pus or crust on the underside; exposed skin underneath is pink, moist, and sometimes raw; lesions may spread to the face and legs in severe cases; usually not pruritic; worsens significantly during wet weather
Fungal infection caused by Trichophyton equinum (most common), T. mentagrophytes, or Microsporum species. Highly contagious between horses and to humans (zoonotic). Spread via direct contact or fomites (shared tack, grooming tools, blankets). Spores survive in the environment for months to years. Signs include: Circular patches of alopecia with gray, crusty, scaly borders (1–5 cm diameter); commonly starts in the girth/saddle area; may coalesce into large irregular patches; usually NOT pruritic initially; hairs at margins are brittle and break easily; heals from center outward
Sweet itch, also known as Culicoides hypersensitivity, is a Type I and IV hypersensitivity reaction to the saliva of biting midges (Culicoides species). It is the most common allergic skin disease of horses worldwide and causes intense pruritus, particularly along the mane and tail base. ## What it is Horses with sweet itch develop an exaggerated immune response to proteins in Culicoides saliva. This leads to intense itching, self-trauma, and characteristic skin changes. The condition has a strong genetic component and is more common in certain breeds (Icelandic horses, Welsh ponies, Shires). It is strictly seasonal in most regions, appearing in spring and worsening through summer and early fall when midge populations are highest. ## Signs and symptoms - Intense pruritus (itching) focused on the mane base, tail head, and ventral midline - Self-excoriation leading to hair loss, thickened skin, and open sores - "Rat tail" appearance from hair loss and scaling at the tail head - Thickened, rugose (wrinkled) skin in chronic cases - May extend to ears, face, and withers in severe cases - Seasonal recurrence that often worsens with each passing year ## Causes and risk factors Sweet itch is caused by an allergic reaction to Culicoides midge saliva. Genetic predisposition plays a major role. Environmental factors such as proximity to standing water (midge breeding sites) and warm, humid weather increase exposure. Horses with a family history of sweet itch are at significantly higher risk. ## How it is diagnosed Diagnosis is usually based on the characteristic seasonal pattern, distribution of lesions, and intense pruritus. Intradermal skin testing or blood tests for allergen-specific IgE can support the diagnosis but are not always definitive. Ruling out other causes of pruritus (mites, infections, other allergies) is important. ## Treatment and management There is no cure, so management focuses on reducing exposure and controlling symptoms. Key strategies include stabling during peak midge activity (dusk and dawn), using fly sheets and masks designed for sweet itch, applying topical repellents, and using systemic antihistamines or corticosteroids during flare-ups. In severe cases, allergen-specific immunotherapy (desensitization) or other immunomodulatory drugs may be considered. Consistent management from year to year helps reduce the severity of clinical signs. ## When to call the vet Contact your veterinarian if your horse develops intense itching, hair loss along the mane or tail, or skin thickening, especially if it follows a seasonal pattern. Early and consistent management can significantly improve quality of life. ## Prevention Prevention centers on reducing midge exposure through environmental management (eliminating standing water) and physical barriers (sweet itch rugs and hoods). Starting preventive measures early in the season before clinical signs appear is more effective than treating established disease. ## Frequently asked questions **Can sweet itch be cured?** No. It is a lifelong allergic condition, but symptoms can be well controlled with consistent management. **Does sweet itch affect all horses the same way?** No. Severity varies greatly between individuals. Some horses have mild seasonal itching while others suffer severe self-trauma and skin changes. **Are there any long-term treatments?** Allergen-specific immunotherapy can help some horses, but results are variable. Most horses require ongoing seasonal management. This information is for educational purposes only. Always consult with a licensed veterinarian for diagnosis and treatment of your horse. Signs include: Intense pruritus (itching) focused on the mane base, tail head, and ventral midline; self-excoriation leading to hair loss, thickened skin, and open sores; rat tail appearance from hair loss and scaling at the tail head; thickened, rugose skin in chronic cases; may extend to ears, face, and withers in severe cases; seasonal recurrence that often worsens with each passing year
Sarcoids are the most common skin tumors of horses, accounting for up to 40% of all equine neoplasia. They are caused by Bovine Papillomavirus types 1 and 2 and do not metastasize but can be locally aggressive with a high recurrence rate after incomplete treatment. There are six clinical types: occult, verrucous, nodular, fibroblastic, mixed, and malevolent. ## What it is Sarcoids are locally invasive fibroblastic tumors associated with Bovine Papillomavirus infection. They can occur anywhere on the body but are most common around the eyes, ears, lips, axillae, groin, and sheath. The tumors do not spread to distant sites but can grow aggressively locally, especially after trauma or incomplete surgical removal. They are one of the most frustrating conditions in equine practice due to their high recurrence rate. ## Signs and symptoms - Variable appearance depending on type: - Occult: flat, circular, alopecic (hairless) patches - Verrucous: wart-like, roughened surface - Nodular: firm, subcutaneous nodules - Fibroblastic: fleshy, often ulcerated and bleeding masses - Mixed: combination of types - Malevolent: highly invasive, spreading along lymphatics - May be single or multiple - Can transform from indolent to aggressive forms, especially after trauma or biopsy - Tend to recur after surgical removal if margins are incomplete ## Causes and risk factors Sarcoids are caused by Bovine Papillomavirus (BPV) types 1 and 2. The virus is thought to be transmitted by flies or direct contact. Genetic predisposition plays a role, with some horses and breeds being more susceptible. Trauma to the skin appears to facilitate tumor development or transformation to more aggressive types. ## How it is diagnosed Diagnosis is usually based on clinical appearance. Biopsy can confirm the diagnosis but carries a risk of stimulating more aggressive growth, so it is often avoided when the clinical presentation is classic. In ambiguous cases, histopathology is required. ## Treatment and management Treatment options include surgical excision (with wide margins when possible), cryotherapy, laser ablation, topical chemotherapy (e.g., AW4-Ludes or 5-fluorouracil), intralesional chemotherapy, and immunotherapy (e.g., BCG or autogenous vaccines). No single treatment is universally effective, and recurrence rates are high. The choice of treatment depends on the type, location, size, and number of sarcoids. Many horses require a combination of therapies and long-term monitoring. ## When to call the vet Contact your veterinarian if you notice any new skin masses, especially around the eyes, ears, or sheath, or if an existing lesion begins to grow or change in appearance. Early intervention generally offers better treatment outcomes. ## Prevention There is no proven prevention strategy. Minimizing skin trauma and fly control may help reduce risk. Horses with existing sarcoids should be monitored closely for new lesions or changes in existing ones. ## Frequently asked questions **Are sarcoids cancerous?** Sarcoids are locally invasive tumors but do not metastasize (spread to distant organs). They are considered a form of neoplasia but are not malignant in the traditional sense. **Can sarcoids be cured?** Some sarcoids can be successfully treated and not recur, but many horses experience recurrence or develop new lesions. Long-term management is often required. **Should sarcoids be biopsied?** Biopsy can stimulate more aggressive growth in some cases, so it is often avoided when the clinical appearance is typical. Histopathology is recommended when the diagnosis is uncertain. This information is for educational purposes only. Always consult with a licensed veterinarian for diagnosis and treatment of your horse. Signs include: Variable appearance depending on type; commonly found around eyes, ears, lips, axillae, groin, and sheath; range from flat hairless patches to fleshy protruding masses; may be single or multiple; can transform from indolent to aggressive types, especially after trauma or biopsy; tend to recur after removal
Dermal melanomas are extremely common in gray horses, with up to 80% of gray horses over 15 years affected. They arise from melanocytes that accumulate excessive melanin during the graying process. Initially benign but approximately 66% will eventually become malignant with metastasis to internal organs (lymph nodes, lungs, liver, spleen, guttural pouches). Non-gray horses can also develop melanomas, which tend to be more aggressive. Signs include: Firm, dark (black/brown) nodules most commonly under the tail, perianal region, parotid salivary gland area, eyelids, and commissure of lips; usually slow-growing; may ulcerate; large perineal masses can obstruct defecation; internal metastasis may cause weight loss, colic, or organ dysfunction
Malignant tumor of keratinocytes, the second most common equine skin cancer. UV radiation is the primary risk factor. Most common on unpigmented skin; especially eyelids (most frequent ocular tumor), penis/prepuce, vulva, and perineum. Breeds at higher risk include Appaloosas, Paints, Cremellos, and draft crosses with pink skin. Signs include: Non-healing ulcerated or proliferative lesion on unpigmented skin; crusty, bleeding mass; commonly affects third eyelid, eyelid margin, penis, prepuce, or vulva; locally invasive; may metastasize to regional lymph nodes (10–20%); penile SCC may cause dysuria or hemorrhagic discharge
Skin damage caused by photodynamic agents that accumulate in the skin and react with UV light to cause cell damage. Three types: primary (ingestion of photosensitizing plants like St. John's wort, buckwheat, or alsike clover), hepatogenous (impaired hepatic excretion of phylloerythrin due to liver disease; most clinically significant), and idiopathic. Affects unpigmented/white skin only. Signs include: Erythema, edema, and pain of unpigmented skin areas (white markings on face, legs); progresses to oozing, crusting, and sloughing of necrotic skin; horse is painful and may be photophobic; hepatogenous type also shows jaundice, weight loss, elevated liver enzymes; severely affected skin may slough in sheets
Type I hypersensitivity reaction causing localized dermal edema. Very common in horses. Triggers include insect bites, medications (especially NSAIDs, antibiotics), vaccines, feed allergens, contact allergens (bedding, topical products), inhaled allergens, and stress. Usually self-limiting (12–24 hours) but may recur if the allergen is not identified. Signs include: Multiple raised, round to irregular wheals (2–20 cm) appearing rapidly over the neck, trunk, and hindquarters; may pit on pressure; usually non-pruritic; skin between wheals is normal; angioedema (deeper swelling) may affect muzzle, eyelids, or distal limbs; rarely may accompany anaphylaxis with respiratory distress
Scratches, also known as mud fever or pastern dermatitis, is a multifactorial inflammatory condition of the skin on the back of the pastern and fetlock. It is often complicated by bacterial or fungal infection and, in some cases, Chorioptes mites. Chronic cases can lead to thickened, proliferative skin ("grapes") and significant lameness. ## What it is Scratches develops when the skin barrier of the pastern is compromised by chronic moisture, trauma, or heavy feathering. This allows secondary bacterial (commonly *Staphylococcus* or *Dermatophilus*) and sometimes fungal infection to take hold. In draft breeds and horses with heavy feathering, *Chorioptes* mites are a frequent complicating factor. The condition can range from mild crusting to severe, painful, proliferative dermatitis. ## Signs and symptoms - Erythema (redness), crusting, and exudation of the caudal pastern - Thick, adherent scabs that are painful to remove - Swelling of the pastern and fetlock region - Lameness in moderate to severe cases - Cracking and bleeding of the skin in advanced cases - In chronic cases, thickened, lichenified skin or proliferative "grape-like" masses (especially in drafts) - Secondary cellulitis possible in severe infections ## Causes and risk factors Scratches is multifactorial. Major contributing factors include prolonged exposure to mud and moisture, heavy feathering that traps moisture, skin trauma, photosensitization, vasculitis, and immune-mediated disease. Secondary bacterial and fungal infections are common. Draft breeds and horses kept in muddy paddocks are at highest risk. ## How it is diagnosed Diagnosis is based on clinical appearance, history, and response to treatment. Skin scrapings may be performed to check for mites. Bacterial and fungal cultures can help guide therapy in resistant cases. Biopsy is occasionally needed for chronic or unusual presentations. ## Treatment and management Treatment involves keeping the area clean and dry, carefully removing crusts (after softening), and applying appropriate topical antimicrobial and anti-inflammatory agents. Systemic antibiotics may be needed in severe or complicated cases. Addressing underlying factors (improving drainage, clipping heavy feathers, treating mites if present) is essential. In chronic proliferative cases, surgical removal of "grapes" may be required. ## When to call the vet Contact your veterinarian if your horse develops painful swelling, lameness, or spreading lesions on the pasterns. Severe cases can lead to cellulitis or deep infection if not treated promptly. ## Prevention Prevention focuses on keeping the pasterns as clean and dry as possible. Improving paddock drainage, avoiding prolonged standing in mud, regular grooming and feather clipping (when appropriate), and prompt treatment of any skin trauma help reduce risk. ## Frequently asked questions **Is scratches contagious?** It is not directly contagious, but the bacteria and mites involved can spread between horses in the same environment. **Can scratches be cured?** Mild cases usually resolve with treatment and management changes. Chronic or severe cases in heavily feathered horses can be recurrent and require ongoing management. **Should I clip the feathers on my horse's legs?** In many cases, carefully clipping the feathers helps keep the area drier and makes treatment more effective, though some owners prefer to keep feathers for protection. This information is for educational purposes only. Always consult with a licensed veterinarian for diagnosis and treatment of your horse. Signs include: Erythema (redness), crusting, and exudation of the caudal pastern; thick, adherent scabs that are painful to remove; swelling of the pastern and fetlock region; lameness in moderate to severe cases; cracking and bleeding of the skin in advanced cases; in chronic cases, thickened, lichenified skin or proliferative grape-like masses; secondary cellulitis possible in severe infections
## Overview Habronemiasis, or summer sores, is a seasonal parasitic skin disease caused by larvae of Habronema stomach worms deposited by flies into wounds or moist skin. The larvae cannot complete their life cycle and provoke intense granulomatous inflammation. Lesions are pruritic, non-healing, and contain yellow calcified granules. They commonly appear on the sheath, medial canthus, lower legs, and wounds, and typically regress in winter. ## Causes Habronema larvae deposited by house or stable flies into damaged skin. ## Diagnosis Clinical appearance and seasonal pattern. Biopsy shows eosinophilic granulomas with larvae or mineralized debris. Differential includes sarcoid, squamous cell carcinoma, and proud flesh. ## Treatment Ivermectin or moxidectin systemically, topical ivermectin or corticosteroids, and surgical debulking of large lesions. Fly control is essential. Lesions often recur annually. ## Recovery and Prognosis Good with treatment, but recurrence each summer is common without rigorous fly control. ## Prevention Effective fly control, prompt wound care, and regular deworming. Signs include: non-healing reddish-brown granulomatous lesions; yellow sulfur granules; intense itching; common on sheath, medial canthus, legs, and wounds; seasonal
Caused by a skin reaction to the microfilariae of Onchocerca cervicalis. Adult worms live in the nuchal ligament; their microfilariae occur in the skin, where they can cause a hypersensitivity reaction. Culicoides midges are the intermediate host. Die-off of microfilariae after ivermectin treatment can cause a transient worsening of signs. Signs include: Ventral midline dermatitis (most characteristic); patchy alopecia and scaling on face, chest, withers, and legs; depigmentation (vitiligo-like) of face and ventral midline; 'bull's eye' lesion on the forehead; pruritus variable; may contribute to uveitis (rare); usually improves with regular ivermectin deworming
The most common autoimmune skin disease of horses. Autoantibodies target desmoglein-1 in the intercellular bridges (desmosomes) of the superficial epidermis, causing acantholysis (cell separation). Can be triggered by medications, infections, or UV exposure. Requires immunosuppressive therapy and carries a guarded prognosis for complete remission. Signs include: Generalized crusting, scaling, and alopecia; starts on the face and limbs, then generalizes; characteristic annular crusts with peripheral collarettes; footpad coronary band crusting and pain; ventral edema; may have fever, depression, and weight loss; acantholytic cells on cytology are diagnostic; may wax and wane
## Overview Anhidrosis is the partial or complete inability to sweat in response to increased body temperature or exercise. Because horses dissipate 65 to 70 percent of heat through evaporation of sweat, affected animals are at high risk of hyperthermia, especially in hot, humid climates. The condition is most prevalent in the southeastern United States and Gulf Coast states but can occur elsewhere during heat waves. Onset may be gradual or acute. ## Causes The precise mechanism is incompletely understood. Over-stimulation and subsequent down-regulation of sweat-gland beta-adrenergic receptors is a leading hypothesis. A genetic component is suspected. Temporary anhidrosis can also be induced by macrolide antibiotics. Chronic idiopathic anhidrosis persists across seasons. ## Diagnosis Diagnosis is usually presumptive based on history and clinical signs (elevated respiratory rate, failure to cool after exercise, minimal or absent sweat when other horses are sweating heavily). An intradermal terbutaline or epinephrine sweat test can confirm reduced sweat production. Bloodwork rules out other causes of hyperthermia. ## Treatment The only consistently effective intervention is relocation to a cooler climate, after which many horses resume sweating. Management in hot climates focuses on preventing heat stress: early-morning or late-evening work, fans, misting, and electrolyte supplementation. No pharmacologic or supplement therapy has met evidence-based standards for long-term efficacy. ## Recovery and Prognosis Horses moved to cooler environments often regain the ability to sweat and can return to athletic use. Those that remain in hot, humid climates require lifelong management to avoid dangerous hyperthermia. The condition itself is not fatal if heat stress is prevented. ## Prevention No specific prevention exists. Careful acclimatization and avoidance of peak heat may reduce clinical expression in susceptible horses. Signs include: reduced or absent sweating; elevated respiratory rate after exercise; prolonged recovery time; dry, flaky skin in chronic cases; exercise intolerance in heat
## Overview Hyperhidrosis is sweating out of proportion to temperature or exercise. It may be generalized or patchy. Causes include pain, equine grass sickness, Horner's syndrome (unilateral facial sweating), pheochromocytoma, and other systemic diseases. Persistent sweating at rest warrants investigation. ## Causes Pain, autonomic dysfunction, grass sickness, endocrine tumors, or environmental factors. ## Diagnosis History and physical examination looking for associated signs (colic, dysphagia, Horner's syndrome). Further testing as indicated. ## Treatment Directed at the underlying cause. Supportive cooling and fluid replacement as needed. ## Recovery and Prognosis Depends entirely on the primary condition. ## Prevention Depends on etiology. Signs include: excessive sweating disproportionate to temperature or work; may be patchy or generalized; associated signs depend on cause (grass sickness, Horner's syndrome, pain)
## Overview Alopecia areata is an uncommon, non-inflammatory, non-pruritic autoimmune disorder in which the immune system targets hair-follicle antigens, resulting in focal to widespread hair loss. The skin itself remains normal. Lesions most often involve the face, mane, tail, and neck. The condition is primarily cosmetic; secondary skin infections are uncommon unless the horse traumatizes the area. ## Causes The disease is immune-mediated. Auto-antibodies against trichohyalin and hair keratins have been demonstrated in horses. Genetic predisposition is suspected; Appaloosas and Quarter Horses appear over-represented in some series. Stress or concurrent illness may trigger or exacerbate lesions in individual horses. ## Diagnosis Diagnosis is based on clinical appearance (well-demarcated patches of hair loss with normal skin) and histopathology showing lymphocytic bulbitis of anagen follicles. Trichography and skin scrapings help exclude other causes of alopecia such as dermatophytosis or follicular dysplasia. Seasonal worsening is reported by some owners. ## Treatment No consistently effective treatment exists. Spontaneous regrowth occurs in some horses. Anecdotal responses to systemic or topical corticosteroids, minoxidil, or tacrolimus have been described, but evidence is limited. Most cases are managed by benign neglect. ## Recovery and Prognosis Prognosis for the horse’s health is excellent. Hair regrowth is variable and may be incomplete or cyclical. The condition does not affect athletic performance or longevity. ## Prevention No preventive measures are known. Signs include: focal or multifocal patches of hair loss; normal underlying skin; most common on face, mane, and tail; no pruritus or pain
Overgrowth of granulation tissue beyond the wound margin, preventing epithelialization and wound closure. Extremely common in equine limb wounds due to poor blood supply, high motion, limited soft tissue, and the horse's inherent exuberant healing response. Wounds on the body rarely develop proud flesh due to better wound contraction and epithelialization. Signs include: Raised, pink to red, cauliflower-like tissue protruding above wound edges; bleeds easily; non-painful; prevents wound closure; most common on the distal limbs; more common in wounds left to heal by second intention; may become very large if left untreated; requires sharp debridement, pressure bandaging, or corticosteroid application
Caused by the oomycete Pythium insidiosum (NOT a true fungus; it's a water mold). Found in tropical and subtropical regions with standing water. Zoospores in stagnant water enter through skin wounds or the GI tract. Causes rapidly progressive, invasive granulomatous lesions. Without treatment, prognosis is poor. Immunotherapy vaccine (PitiumVac) may be effective if caught early. Signs include: Large, rapidly growing, ulcerated granulomatous mass, usually on the distal limbs, ventral abdomen, or chest; contains draining tracts with yellowish-gray necrotic tissue ('kunkers' or coral-like concretions); intensely pruritic; horse may self-mutilate; tissue is firm and woody; may invade bone; unresponsive to antibiotics and antifungals; fatal if untreated
Inflammation and failure of the laminar bond between the hoof wall and the distal phalanx (coffin bone). One of the most devastating equine conditions. Primary causes: endocrinopathic (EMS/insulin dysregulation; most common), sepsis-related (grain overload, colitis, retained placenta), supporting limb (excessive weight-bearing on one limb), and corticosteroid-induced. The laminae can fail within hours, leading to rotation or sinking of the coffin bone. Signs include: Acute: bounding digital pulses; heat in the hooves; reluctance to walk; 'walking on eggshells' gait; characteristic rocked-back stance shifting weight to hindlimbs; pain response to hoof testers. Chronic: divergent hoof rings wider at the heel; dropped/flat sole; widened white line; 'Aladdin slipper' hoof shape; radiographic coffin bone rotation or distal displacement; Consult veterinarian for specific symptoms.
Thrush is a degenerative bacterial infection of the frog, most commonly caused by *Fusobacterium necrophorum* and other anaerobic bacteria. It thrives in moist, anaerobic environments such as dirty stalls or packed mud and produces a characteristic black, foul-smelling discharge in the frog sulci. While mild cases are often cosmetic, severe infections can invade sensitive tissue and cause significant lameness. ## What it is Thrush primarily affects the central and collateral sulci of the frog. The bacteria break down the horn tissue, creating necrotic, tar-like material and deepening the clefts. In advanced cases the infection can reach the sensitive corium beneath the frog, leading to pain, hemorrhage, and lameness. The condition is more common in the hind feet because they are often exposed to more moisture and manure. Poor hoof conformation, lack of regular cleaning and trimming, and prolonged exposure to wet or unsanitary conditions are major predisposing factors. Thrush is not usually a primary disease but a secondary problem that develops when the natural defenses of the frog are compromised. ## Signs and symptoms - Black, tar-like, foul-smelling discharge in the frog sulci - Soft, necrotic, or crumbling frog tissue - Deepened central sulcus or collateral sulci - Sensitivity or pain when the frog is pressed or picked - Lameness in severe cases when infection reaches sensitive tissue - Occasional hemorrhage if the area is aggressively cleaned - Worse in wet weather or when the horse stands in manure and mud ## Causes and risk factors Thrush is caused by anaerobic bacteria that flourish when the frog is kept in a constantly moist, dirty environment. Key risk factors include infrequent hoof picking and cleaning, poor stable hygiene, horses that stand in wet or muddy conditions for long periods, and conformational issues that cause the frog to stay compressed or underdeveloped. Horses with contracted heels or deep sulci are more susceptible. ## How it is diagnosed Diagnosis is usually straightforward based on the classic appearance and smell during routine hoof cleaning. In mild cases the infection is superficial. In more advanced cases the veterinarian or farrier may probe the sulci to determine the depth of involvement and check whether sensitive tissue has been reached. Radiographs are rarely needed unless there is suspicion of deeper involvement or concurrent problems. ## Treatment and management Treatment involves thorough cleaning of the affected areas, removal of necrotic tissue, and application of antibacterial agents. Common approaches include daily cleaning with dilute bleach solution or commercial thrush treatments, keeping the feet dry, and improving stable hygiene. In deeper cases, a farrier may pare out infected tissue or apply a protective bandage or boot. Addressing any underlying conformational or management issues is essential to prevent recurrence. ## When to call the vet Call your veterinarian or farrier if the horse becomes lame, if there is significant bleeding, or if the infection appears very deep or is not responding to routine cleaning and treatment within a few days. Severe or neglected thrush can lead to deeper infection and permanent damage to the frog and digital cushion. ## Prevention Prevention is mainly about good management. Pick feet daily, maintain clean and dry stabling, and ensure regular professional trimming so the frog stays healthy and well-formed. Horses that are prone to thrush benefit from more frequent hoof care and, in some cases, the use of drying agents or improved drainage in their environment. ## Frequently asked questions **Is thrush painful for the horse?** Mild thrush is often not painful, but once it invades sensitive tissue it can cause significant discomfort and lameness. **Can thrush spread to other parts of the hoof?** Yes. In severe cases it can undermine the bars or reach the digital cushion and sensitive structures, leading to more serious problems. **How long does it take to clear up thrush?** Mild cases often improve within a week or two with consistent cleaning and better management. Deeper infections can take several weeks of diligent treatment. This information is for educational purposes only. Always consult with a licensed veterinarian for diagnosis and treatment of your horse. Signs include: Black, tar-like, foul-smelling discharge in the frog sulci; soft, necrotic, or crumbling frog tissue; deepened central sulcus or collateral sulci; sensitivity or pain when the frog is pressed or picked; lameness in severe cases when infection reaches sensitive tissue; occasional hemorrhage if the area is aggressively cleaned; worse in wet weather or when the horse stands in manure and mud
White line disease is a condition in which the inner [hoof wall](/anatomy/horse-hoof-anatomy) separates from the sole at the white line, allowing opportunistic fungi and bacteria to invade the non-pigmented horn. It can undermine large sections of the hoof wall and, in advanced cases, compromise the stability of the hoof capsule. The condition is often secondary to poor hoof quality, chronic [laminitis](/conditions/laminitis), or irregular farriery. ## What it is The white line is the junction where the insensitive laminae of the hoof wall meet the sole. When this area separates, it creates a space that traps moisture and debris, allowing fungal and bacterial organisms to proliferate. The organisms digest the horn, causing it to become powdery, cheesy, or hollow. Over time the separation can extend up the wall and around the foot, weakening the attachment between the wall and the [coffin bone](/anatomy/coffin-bone-distal-phalanx-p3). While the name suggests a fungal infection, bacteria are often involved as well. The condition is frequently seen in horses with previous laminitis, thin or brittle hoof walls, or inconsistent trimming schedules that allow the white line to stretch. ## Signs and symptoms - Visible separation at the white line on the solar surface - Chalky, powdery, or cheesy material in the separated area - Hollow sound when the hoof wall is tapped with a hammer - Undermining of the hoof wall that may extend from the toe into the quarters - Hoof wall that feels unstable or flexible when pressure is applied - Lameness if the separation becomes extensive or reaches sensitive tissue - In severe cases, abscess formation or further wall detachment ## Causes and risk factors White line disease is usually secondary to another problem that weakens the white line attachment. Common predisposing factors include chronic or repeated [laminitis](/conditions/laminitis), poor hoof quality and nutrition, irregular or infrequent trimming, excessive moisture, and mechanical stress from long toes or flared walls. Horses with thin soles or previous white line defects are more susceptible to recurrence. ## How it is diagnosed Diagnosis is made by visual inspection of the solar surface and careful probing of the white line. A farrier or veterinarian will often use hoof testers and may take radiographs to assess how far the separation extends and whether it has affected the coffin bone attachment. In some cases, resection of the undermined wall is needed both for treatment and to fully evaluate the extent of the damage. ## Treatment and management Treatment focuses on removing all undermined and infected horn, stabilizing the remaining hoof wall, and addressing any underlying causes. This usually involves careful hoof wall resection by a skilled farrier, followed by regular cleaning and application of antifungal or antibacterial agents. Supportive shoeing or glue-on shoes are often used to protect the foot while new horn grows down. Managing any concurrent [laminitis](/conditions/laminitis) or metabolic issues is critical for long-term success. ## When to call the vet Contact your veterinarian or farrier if you notice significant separation, lameness, or signs of abscess formation. Extensive white line disease can lead to instability of the hoof capsule and secondary laminitis if not addressed promptly. Deep or rapidly progressing cases should be evaluated professionally. ## Prevention Prevention centers on maintaining strong, well-balanced hooves through regular professional trimming, good nutrition, and prompt treatment of any underlying issues such as laminitis. Avoiding prolonged exposure to excessive moisture and keeping the feet clean also helps reduce risk. Horses with a history of white line disease benefit from more frequent farrier visits and careful monitoring. ## Frequently asked questions **Is white line disease contagious?** No. It is not contagious between horses. It is an opportunistic infection that occurs when the white line is already compromised. **Can white line disease cause laminitis?** Severe cases that undermine large areas of wall can increase stress on the laminae and potentially contribute to laminitis, especially in horses already at risk. **How long does it take for white line disease to heal?** Healing depends on how much wall has been lost. New healthy horn must grow down from the coronary band, which can take 6 to 12 months for the toe area. This information is for educational purposes only. Always consult with a licensed veterinarian for diagnosis and treatment of your horse. Signs include: Visible separation at the white line on the solar surface; chalky, powdery, or cheesy material in the separated area; hollow sound when the hoof wall is tapped with a hammer; undermining of the hoof wall that may extend from the toe into the quarters; hoof wall that feels unstable or flexible when pressure is applied; lameness if the separation becomes extensive or reaches sensitive tissue; in severe cases, abscess formation or further wall detachment
## Overview Cannon keratosis, commonly called stud crud or cannon crud, is a non-contagious skin condition characterized by thickened, greasy, hyperkeratotic patches on the cranial aspect of the hind cannons. It is a form of seborrheic dermatosis and is usually bilateral. The condition is cosmetic in most horses and does not cause lameness. ## Causes Excessive keratin production and sebum accumulation from local skin glands are responsible. A primary idiopathic form exists; secondary forms may follow irritation or allergic skin disease. Genetic predisposition is suspected in some lines. ## Diagnosis The appearance of well-demarcated, greasy, crusty patches on the front of the hind cannons is characteristic. Skin scrapings and cytology rule out infection or parasites if the lesion is atypical. ## Treatment Gentle cleansing with keratolytic or antiseborrheic shampoos improves appearance. Topical moisturizers or mild corticosteroid preparations may help chronic cases. Aggressive scrubbing worsens the condition. Most horses require only periodic management. ## Recovery and Prognosis The condition is chronic and often lifelong but does not affect health or performance. Cosmetic improvement is achievable with regular care. ## Prevention No specific prevention exists. Avoiding harsh grooming of the area reduces secondary irritation. Signs include: greasy, thickened, crusty patches on the front of the hind cannons; sparse hair in affected areas; bilateral distribution; no pruritus in uncomplicated cases
Inflammation of the lymphatic vessels, usually secondary to bacterial infection (Staphylococcus, Streptococcus, Corynebacterium pseudotuberculosis) entering through a skin wound. Ulcerative lymphangitis (caused by C. pseudotuberculosis) is reportable in some jurisdictions. Sporadic lymphangitis causes severe, painful unilateral limb swelling. Chronic recurrence leads to permanent fibrosis (elephantiasis). Signs include: Acute: severe, painful, hot, unilateral limb swelling (2–3x normal); fever (103–106°F); depression; anorexia; marked lameness; serum oozing from skin; lymph node enlargement; may see nodular lymphatic cording. Chronic: permanent thickened limb ('stovepipe leg'); recurring episodes; fibrosis of subcutaneous tissue
## Overview A hoof abscess is a localized pocket of infection between the sensitive and insensitive layers of the hoof. It is the most common cause of sudden non-weight-bearing lameness. Bacteria enter through cracks, nail holes, or sole bruises. Once the abscess drains, comfort improves dramatically. ## Causes Bacterial invasion through defects in the hoof capsule. ## Diagnosis Severe lameness, bounding digital pulse, heat, and focal pain with hoof testers. Radiographs rule out fracture or deeper infection. ## Treatment Establish ventral drainage by paring a small hole, poultice, and bandage. Anti-inflammatories for pain. Antibiotics are not routinely required once drainage is achieved. Tetanus status should be current. ## Recovery and Prognosis Excellent once drained. Most horses are markedly more comfortable within 24 hours. ## Prevention Regular hoof care, clean environment, and prompt attention to sole bruises. Signs include: sudden severe often non-weight-bearing lameness; bounding digital pulse; heat in the hoof; focal hoof-tester pain; dramatic improvement once drained
REGIONAL SKIN CONDITIONS: • HEAD/FACE: Melanomas are extremely common in gray horses over 15 years (up to 80% prevalence). Sarcoids frequently occur around the eyes, ears, and lips. Aural plaques (papillomavirus) cause white, crusty plaques inside the pinnae. • NECK: Cresty neck (regional adiposity) is a key indicator of Equine Metabolic Syndrome (EMS) and insulin dysregulation; a major laminitis risk factor. Score on the 0–5 Cresty Neck Scale; ≥3 warrants veterinary metabolic workup. Rain rot (Dermatophilus congolensis) commonly affects the dorsal neck and back. • WITHERS: Fistulous withers (supraspinous bursitis, often Brucella-associated) causes draining tracts. Saddle sores and pressure injuries from ill-fitting tack cause white hairs, alopecia, or open wounds. Fibrotic myopathy of the withers region may develop from chronic pressure. • BACK: Saddle fit issues manifest as white hairs (indicating prior pressure damage to melanocytes), dry spots after work (blocked sweat glands from pressure), muscle atrophy, or behavioral changes. Kissing spines may cause dorsal skin hypersensitivity. • BARREL/TRUNK: Urticaria (hives) presents as multiple raised wheals, often from allergic reactions (feed, insects, medications, contact allergens). Ringworm (dermatophytosis) commonly starts as circular patches on the girth area. Rain scald affects the dorsum and croup in wet conditions. • LEGS: Scratches (pastern dermatitis/mud fever) affects the caudal pastern, especially in horses with heavy feathering. Cannon keratosis presents as dry, scaly skin on the front of the cannon bones (common, usually cosmetic). Lymphangitis causes severe unilateral limb swelling with pain, heat, and lameness. Stocking up (dependent edema) causes bilateral distal limb swelling that resolves with exercise. Windpuffs (synovial effusion of the fetlock) are common but usually cosmetic. • PASTERN/FETLOCK: Pastern dermatitis (greasy heel/grease) involves inflammation, crusting, and exudation of the caudal pastern. The proliferative form (chronic progressive lymphedema in drafts) causes permanent fibrosis. Predisposing factors: wet/muddy conditions, heavy feathering, Chorioptes mites. • HOOVES: Thrush (Fusobacterium necrophorum) causes black, foul-smelling discharge in the frog sulci. White line disease (onychomycosis) shows separation and chalky material at the white line. Laminitis signs include bounding digital pulses, heat in the hooves, reluctance to walk, and the classic 'rocked back' stance. Hoof cracks may be cosmetic or pathologic depending on depth and location. Subsolar abscesses cause acute severe lameness. • TAIL/DOCK: Sweet itch (Culicoides hypersensitivity) is the most common allergic skin disease worldwide; causes intense pruritus of the mane base and tail head, leading to self-trauma, hair loss, and thickened skin. Tail rubbing may also indicate pinworms (Oxyuris equi), vaginal irritation, or food allergy. Melanomas cluster under the tail in gray horses. • PERINEAL AREA: Melanomas in grays commonly occur perianally and may obstruct defecation when large. Squamous cell carcinoma affects unpigmented perineal skin, especially in Appaloosas, Paints, and cremello horses. • UDDER/SHEATH: Sheath cleaning should be performed 1–2 times yearly; excessive smegma accumulation (including the 'bean' in the urethral fossa) can cause discomfort. Summer sores (habronemiasis) are granulomatous lesions caused by aberrant Habronema larvae deposited by flies on moist skin; common on the sheath, medial canthus, and lower legs.
DAILY SKIN CARE: Run your hands over your horse's entire body daily during grooming; you'll catch lumps, bumps, heat, swelling, and sensitivity early. Know what's normal for YOUR horse. WHEN TO CALL THE VET IMMEDIATELY: Any rapidly growing mass; non-healing wound after 2 weeks; sudden severe lameness (abscess or laminitis); hot, swollen limb with fever (lymphangitis); signs of allergic reaction with respiratory distress; any eye involvement. SEASONAL CONSIDERATIONS: • SPRING: Sweet itch begins; sarcoid activity increases; rain rot season starts; laminitis risk peaks with pasture sugar surges • SUMMER: Fly-borne diseases peak (habronemiasis, onchocerciasis); photosensitization risk; anhidrosis becomes apparent; UV-related tumors progress • FALL: Ringworm season (shared blankets/tack); rain rot continues; prepare for winter coat • WINTER: Reduced UV risk; rain rot under blankets (check regularly!); thrush in wet conditions; mud fever from winter turnout PREVENTION: • Maintain dry, clean footing in paddocks and stalls • Regular farrier care every 6–8 weeks • Fly management program (masks, sheets, sprays, environmental control) • Don't share tack/grooming tools between horses (ringworm/rain rot prevention) • Provide shade and shelter from rain • Monitor body condition score and cresty neck score for EMS/laminitis risk • Apply sunscreen to unpigmented skin areas (zinc oxide-based) • Pick hooves daily; treat thrush promptly • Maintain good ventilation under blankets; check for rain rot weekly • Know your horse's normal digital pulse strength • Keep a photo log of any lumps/masses to track changes over time
See the Body (Skin / Integument) on our interactive 3D horse model. Open 3D Model