NAVLE Integumentary

Equine Photosensitization Study Guide

📅 March 28, 2026 ⏱ 25 min read

Overview and Clinical Importance

Photosensitization is a light-induced dermatitis caused by heightened sensitivity of the skin to ultraviolet (UV) radiation due to the presence of photodynamic agents (chromophores) in the circulation and skin. It is an important differential diagnosis for equine dermatological conditions and should be distinguished from simple sunburn, which occurs independently of a photodynamic agent.

Photosensitization primarily affects lightly pigmented (unpigmented) skin and areas with sparse hair coverage, including the muzzle, ears, eyelids, face, periocular regions, coronary bands, vulva, and areas with white markings. The clinical spectrum ranges from mild dermal discomfort to severe, life-threatening skin necrosis, particularly in cases of hepatogenous origin.

Type	Mechanism	Key Features
Type I: Primary (Direct)	Photodynamic agent ingested, injected, or absorbed through skin; reaches skin via circulation in preformed state	Normal liver function; good prognosis; examples: St. John's wort (hypericin), buckwheat (fagopyrin)
Type II: Aberrant Porphyrin Synthesis	Congenital defect in heme synthesis pathway; endogenous porphyrins act as photosensitizing agents	Very rare in horses; more common in cattle (bovine erythropoietic porphyria); may see pink teeth
Type III: Secondary (Hepatogenous)	Impaired hepatic excretion of phylloerythrin due to liver damage or cholestasis; accumulates in blood and skin	Most common type in horses; poor prognosis; elevated liver enzymes; may see icterus, weight loss, hepatic encephalopathy
Type IV: Idiopathic	Unknown pathogenesis; photodynamic agent not identified	Some forage-related cases; may be associated with clovers, alfalfa; normal liver function

Pathophysiology

Photosensitization occurs when photodynamic agents accumulate in the skin and absorb UV light energy (primarily UV-A at 320-400 nm wavelength). Upon absorption, these agents become energized and transfer energy to surrounding tissues, generating reactive oxygen species (ROS) that damage cell membranes. This leads to increased membrane permeability, cellular potassium leakage, lysosomal enzyme release, and ultimately inflammation, edema, vesiculation, and epidermal necrosis.

Key Pathophysiological Concepts

Melanin Protection: Dermal and hair pigments absorb UV energy before it reaches chromophores, explaining why lesions are confined to unpigmented skin
Phylloerythrin: A porphyrin degradation product of chlorophyll formed by enteric microorganisms. Normally conjugated by hepatocytes and excreted in bile. Clinical signs develop when serum concentrations exceed 8.0 micrograms/dL
Photochemical Reaction: UV light activates chromophores leading to free radical formation, lipid peroxidation, and oxidative tissue damage

Plant	Toxin	Key Features
St. John's Wort (Hypericum perforatum)	Hypericin (red fluorescent pigment)	Classic example; yellow flowers; perforated leaves; horses highly susceptible; toxin remains stable when dried
Buckwheat (Fagopyrum spp.)	Fagopyrin	Similar mechanism to hypericin; uncommon in horses
Wild Parsnip/Hogweed (Pastinaca sativa, Heracleum spp.)	Furocoumarins (bergapten, psoralen)	Can cause OCULAR changes (corneal edema, uveitis) in addition to dermatitis; contact or ingestion
Spring Parsley (Cymopterus watsonii)	Furocoumarins	More common in sheep; western United States
Bishop's Weed (Ammi majus)	Furocoumarins	More common in ruminants
Perennial Ryegrass, Clovers, Alfalfa	Unknown/variable	Contact photosensitization; mechanism unclear; sporadic outbreaks

Classification of Photosensitization

The Clare Classification System (1952) divides photosensitization into four types based on the source of the photodynamic agent:

High-YieldHepatogenous (Type III) photosensitization is the MOST COMMON type in horses. Always evaluate liver function in any horse presenting with photosensitization. Remember: PRIMARY photosensitization = normal liver enzymes; SECONDARY photosensitization = elevated liver enzymes (especially GGT).

Plant	Hepatotoxin	Clinical Notes
Senecio spp. (Ragwort, Groundsel)	Pyrrolizidine alkaloids (PAs)	MOST IMPORTANT cause; irreversible liver damage; cumulative toxicity; horses extremely susceptible; toxic dose: 15 mg/kg dried plant over 2 weeks
Amsinckia spp. (Fiddleneck)	Pyrrolizidine alkaloids	Western US; often contaminates grain
Crotalaria spp. (Rattlebox)	Pyrrolizidine alkaloids (monocrotaline)	Seeds most toxic; can also cause acute fibrosing alveolitis
Cynoglossum officinale (Hound's Tongue)	Pyrrolizidine alkaloids	Europe and North America
Heliotropium spp. (Heliotrope)	Pyrrolizidine alkaloids	Arid regions
Alsike Clover (Trifolium hybridum)	Unknown (? mycotoxin)	Northeast US; more common in hay; pink/white flowers; causes "big liver syndrome"
Blue-Green Algae (Cyanobacteria)	Microcystins	Farm ponds; especially in warm weather; acute hepatotoxicity

Etiology: Causative Agents

Plants Causing Primary Photosensitization

Plants Causing Hepatogenous (Secondary) Photosensitization

These plants cause liver damage, leading to impaired phylloerythrin excretion:

Board Tip - Memory Aid for PA Plants: "SCHAFE" - Senecio, Crotalaria, Heliotropium, Amsinckia, Fiddleneck (Amsinckia), Echium. All contain pyrrolizidine alkaloids causing hepatogenous photosensitization. Remember: PA toxicity is CUMULATIVE and IRREVERSIBLE in horses.

Drugs Causing Primary Photosensitization

Phenothiazine (anthelmintic - classic example)
Tetracyclines (especially doxycycline)
Sulfonamides (trimethoprim-sulfamethoxazole)
Thiazide diuretics
Methylene blue, Rose bengal, Acriflavines

Parameter	Reference Range	Primary PS	Hepatogenous PS
GGT	5-24 IU/L	Normal	ELEVATED (most sensitive and specific)
SDH	0-8 IU/L	Normal	Elevated (acute hepatocellular injury)
AST	150-270 IU/L	Normal	Elevated (not liver-specific)
GLDH	0-14 IU/L	Normal	Elevated (hepatocellular)
Total Bilirubin	1-3 mg/dL	Normal	Elevated (especially conjugated)
Bile Acids	less than 20 micromol/L	Normal	Elevated (liver function test)

Clinical Signs

Clinical signs typically develop within hours after exposure to strong sunlight in sensitized horses. Progression follows a predictable pattern:

Early Signs

Photophobia and discomfort in bright sunlight
Restlessness, scratching and rubbing of ears, eyelids, and muzzle
Erythema (redness) of unpigmented skin
Edema of affected areas

Progressive Signs

Serous exudation (oozing)
Vesicle and blister formation
Scab and crust formation
Pain and pruritus

Severe/Advanced Signs

Skin necrosis and sloughing ("leathery" appearance)
Secondary bacterial infection
Myiasis (fly strike) - skin attracts flies
Severe stress and debilitation

Anatomic Distribution

Lesions are confined to unpigmented, sparsely haired areas with maximum sun exposure: muzzle (especially dorsum), periocular regions, ears (tips and inner pinnae), eyelids, face, vulva, coronary bands, and areas with white hair/pink skin (pasterns, legs). The distribution pattern is diagnostic and distinguishes photosensitization from other dermatoses.

Additional Signs in Hepatogenous Photosensitization

Icterus (jaundice) - yellowish mucous membranes
Weight loss and poor body condition
Anorexia and depression
Hepatic encephalopathy signs (head pressing, circling, aimless wandering, behavioral changes, yawning)
Bilateral laryngeal paralysis (inspiratory stridor) - less common
Diarrhea or constipation

High-YieldPhotosensitization vs. Sunburn - KEY DISTINCTION: Sunburn affects only truly hairless pink skin (muzzle, around eyes). Photosensitization affects ALL unpigmented skin, INCLUDING areas covered by white hair. If a horse has lesions on white-haired areas of the body (legs, blaze), think PHOTOSENSITIZATION, not sunburn.

Drug Class	Examples and Dosing	Indication
NSAIDs	Flunixin meglumine 1.1 mg/kg IV/PO q12-24h	Anti-inflammatory, analgesic; first-line for acute inflammation
Corticosteroids (Systemic)	Prednisolone 1 mg/kg PO q24h; Dexamethasone 0.05-0.1 mg/kg IV/IM	Early stages; reduces inflammatory response; taper gradually; caution with liver disease
Topical Corticosteroids	Dexamethasone ophthalmic ointment; Hydrocortisone cream	Local inflammation; soothing affected skin
Antibiotics (Systemic)	Procaine penicillin G 22,000 IU/kg IM q12h; Gentamicin (if needed)	Secondary bacterial infection of skin wounds
Topical Wound Care	Almond oil, dexpanthenol, silver sulfadiazine cream, polyhexanide solution	Skin moisturization; wound healing; prevent desiccation
Ocular (if affected)	Gentamicin ophthalmic; Atropine 1% (mydriatic); NaCl 5% (corneal edema)	For furocoumarin-induced photosensitization (parsnip, hogweed) with corneal edema/uveitis
Hepatic Support	Milk thistle (silymarin), B vitamins, IV fluids with dextrose, lactulose	Hepatogenous cases; hepatic encephalopathy management

Diagnosis

Clinical Assessment

Diagnosis is primarily based on signalment, clinical signs, history, and distribution of lesions. Key historical factors include recent pasture changes, new hay source, access to toxic plants, recent drug administration, and exposure to sunlight.

Diagnostic Criteria

Photophobia and dermatitis affecting unpigmented/sparsely haired skin
Evidence of exposure to photosensitizing agents OR hepatotoxins
Lesions confined to sun-exposed, unpigmented areas
Temporal relationship between sun exposure and clinical signs

Laboratory Evaluation

NAVLE TipGGT is the BEST screening test for hepatic disease in horses. It is highly specific for liver disease and rarely normal in moderate-to-severe hepatopathy. GGT greater than 400 IU/L is associated with poor prognosis. If multiple horses on a property have elevated GGT, suspect TOXIC cause.

Additional Diagnostics

Skin biopsy: Shows necrotizing dermatitis with superficial vasculitis, dermal edema, and eosinophilic/lymphocytic infiltration
Liver biopsy: Gold standard for hepatogenous cases; can confirm PA toxicity (megalocytosis, bile duct hyperplasia, fibrosis)
Pasture/hay evaluation: Botanical analysis to identify toxic plants
Porphyrin levels: Elevated in blood, urine, and feces in Type II (aberrant porphyrin synthesis)
Abdominal ultrasound: May show hepatomegaly (acute) or hepatic atrophy (chronic)

Type	Prognosis
Primary Photosensitization	GOOD - Skin lesions heal remarkably well once causative agent removed and UV exposure prevented; complete recovery expected
Hepatogenous Photosensitization	POOR to GUARDED - Dependent on extent of liver damage; PA toxicity is irreversible; chronic management often required; may be fatal
Porphyria (Type II)	POOR - Congenital defect; lifelong management required; affected animals should not be bred

Treatment and Management

Immediate Management

Remove from sunlight: House indoors or provide complete shade; allow turnout ONLY at night
Eliminate causative agent: Remove access to toxic plants; change hay/pasture source; discontinue suspect medications
Prevent further UV exposure: Use fly sheets, fly masks with UV protection, leg wraps for white legs; apply zinc oxide or SPF 30-55 sunscreen to affected areas

Medical Treatment

Supportive Care

Fly control: Essential to prevent myiasis; use fly sheets, fly repellents, wound dressings
Wound care: Keep lesions clean; gentle debridement of necrotic tissue if needed; allow scabs to remain in place
Nutritional support: Low-protein diet for hepatic cases; avoid alfalfa and clover; provide good-quality grass hay
Fluid therapy: IV fluids for dehydration; add dextrose if hepatic encephalopathy present

Prognosis

High-YieldEven with extensive skin necrosis, skin lesions from photosensitization heal remarkably well if the horse survives. The prognosis is determined by the underlying CAUSE, not the severity of skin lesions. In hepatogenous cases, the prognosis is related to the degree of hepatic damage.

Prevention

Regular pasture inspection for toxic plants; remove Senecio, St. John's wort, ragwort
Inspect hay for contamination with photosensitizing plants
Avoid overgrazed pastures where toxic weeds proliferate
Provide shade in paddocks for horses with white markings
Apply sunscreen to vulnerable areas during peak sun hours
Use UV-protective fly masks and sheets for high-risk horses
Turn out at night during summer months for susceptible horses
Screen GGT in multiple horses if outbreak suspected

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