NAVLE Integumentary

Equine Photosensitization Study Guide

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.

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.

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