Equine Photosensitization
Photosensitization by Cause
Comparison
| Type | Cause | Key Sign | Treatment |
|---|---|---|---|
| Primary | Ingestion of photodynamic plants (St. John's Wort) | White skin lesions, no liver issues | Remove plant, shade, NSAIDs |
| Secondary | Liver damage from ragwort/toxins | Jaundice + skin lesions | Restore liver, shade, support |
| Drug-Induced | Tetracyclines, certain NSAIDs, phenothiazine | Lesions on white/non-pigmented skin | Stop drug, shade, symptomatic |
| Idiopathic | No identified cause | Anaphylaxis-like skin reaction | Systemic steroids, shade |
Photosensitization Management
Photosensitization Prevention
| Inspect pastures for ragwort, St. John's Wort, and alsike clover | |
| Provide sun shelter during peak UV hours (10am–4pm) | |
| Use fly sheets and masks on white-faced horses | |
| Monitor liver enzymes in horses on suspect pastures | |
| Avoid photosensitizing drugs in summer months | |
| Pigmented skin is resistant — white areas are vulnerable | |
| Rotate horses to clean pasture if toxins found | |
| Biopsy skin lesions to confirm and rule out other causes |
Photosensitization in horses causes severe sunburn-like skin damage to unpigmented (white or pink) areas -- despite normal sun exposure that causes no harm in unaffected animals. Most equine photosensitization is secondary (hepatogenous), caused by liver dysfunction that allows phylloerythrin, a porphyrin from chlorophyll metabolism, to accumulate in the skin. Primary photosensitization occurs from direct contact with photodynamic plants or chemicals. Both forms require removing the trigger, managing skin damage, and sun protection.
| Type | Primary Cause | First Response |
|---|---|---|
| Primary (direct photodynamic) | St. John's Wort, buckwheat, phenothiazine | Remove plant exposure; apply sun protection immediately |
| Secondary / hepatogenous | Pyrrolizidine alkaloids, alsike clover, mycotoxins, algae | Full liver workup; stall during daylight; remove trigger |
| Diagnostic pattern | Lesions restricted to white / pink skin only | Bloodwork: GGT, SDH, AST, bilirubin, bile acids to rule in/out liver disease |
Why Liver Disease Causes Sunburn
When horses eat green plants, gut bacteria break down chlorophyll, producing phylloerythrin. In a healthy horse, the liver conjugates and excretes phylloerythrin in bile. When liver function is impaired (from liver disease, hepatotoxic plants, or mycotoxins), phylloerythrin accumulates in the bloodstream and deposits in skin. Phylloerythrin absorbs sunlight and undergoes photochemical reactions that produce free radicals and reactive oxygen species directly in skin tissue -- causing cell death, inflammation, and what looks externally like a chemical burn or extreme sunburn.
Causes: Plants Are the Most Common Trigger
Hepatogenous causes (liver-mediated): pyrrolizidine alkaloid-containing plants are the most significant -- ragwort (Senecio), groundsel (Senecio), and others cause progressive hepatic fibrosis. Alsike clover causes 'trifoliosis' or 'dew poisoning' -- photosensitization combined with stomatitis. Mycotoxin-contaminated hay or grain causes mycotoxic lupinosis. Blue-green algae (cyanobacteria) in ponds is a less common but serious hepatotoxin. Primary photosensitization causes (no liver disease): St. John's Wort (Hypericum perforatum) is the most common; buckwheat; phenothiazine compounds historically used as anthelmintics.
Clinical Signs
Skin changes are restricted to areas with white (unpigmented) skin -- facial blazes and stars, white legs, pink muzzle and eyelids. Pigmented skin is protected because melanin absorbs the photoreactive wavelengths. Affected skin develops: erythema (redness), edema (swelling), oozing serum, scab formation, and eventual sloughing of damaged skin. The horse shows discomfort -- rubbing, head-shaking, reluctance to go into sunlight. In severe cases, eyelid swelling may impair vision; muzzle swelling affects eating. Systemic signs of liver disease may accompany hepatogenous cases: weight loss, jaundice (yellow tinge to sclera and mucous membranes), depression, colic.
Diagnosis
Diagnosis is primarily clinical (distribution of lesions to unpigmented areas is highly characteristic). Rule in/out primary vs. secondary: bloodwork including liver enzymes (GGT, SDH, AST are equine-specific liver markers), bilirubin, albumin, and bile acids. Elevated liver enzymes with consistent clinical signs confirm hepatogenous photosensitization. Investigate pasture for photodynamic plants. Liver biopsy may be necessary to determine the extent and cause of liver pathology and guide prognosis.
Treatment and Management
Immediate: remove the horse from sunlight -- stall during daylight, turn out only after dark. Remove suspected photodynamic plants from pasture access; review hay and grain sources for potential mycotoxin contamination. Skin management: gentle cleaning of affected areas, zinc oxide or petroleum jelly-based barrier creams, UV-protective fly masks and fly sheets for white-faced horses, topical antibiotics if secondary bacterial infection is present. Systemic anti-inflammatory: NSAIDs (phenylbutazone or flunixin) for pain and inflammation. Liver-supportive therapy: SAMe (S-adenosylmethionine) and silymarin (milk thistle extract) are commonly used; high-quality hay-only diet removing all supplements and green pasture while evaluating extent of hepatic involvement. Prognosis depends entirely on the underlying liver disease -- early pyrrolizidine alkaloid hepatotoxicity may progress to irreversible cirrhosis regardless of management.
Sources: Phylloerythrin pathway from Fowler (1968) American Journal of Veterinary Research; pyrrolizidine alkaloid hepatotoxicity from Cheeke (1988) Toxicants of Plant Origin Vol. 1; photosensitization clinical review from Geyer et al. (2004) Veterinary Dermatology; trifoliosis from Nation (1989) Australian Veterinary Journal.