ACVPM Toxicology Practice Exam

Secondary photosensitization happens when the liver is damaged by plant toxins, so the body can’t properly excrete a chlorophyll breakdown product (phylloerythrin). That compound then circulates and, after sunlight exposure, causes phototoxic skin reactions. Plants that commonly produce hepatotoxic compounds in grazing animals set up this sequence, so ingestion can be followed by GI signs from stomach or liver irritation and, later, sun-sensitive skin lesions.

The plants listed are classic culprits because they’re known to cause hepatic injury that leads to secondary photosensitization. Agave and lantana are well-documented hepatotoxins; Kochia (burning bush) is linked to photosensitization after liver injury; Nolina (brunchgrass) and Panic grass are grasses/shrubs associated with this condition; Tetradymia species (horsebrush and related) are classic desert-era photosensitizers; Tribulus (puncture vine) also features in toxicosis that can produce this pattern. Together, they reflect the hepatic pathway that leads to secondary photosensitization with GI signs accompanying or preceding the photosensitive skin responses.

Nettle, rhubarb, and mustards are not typical causes of secondary photosensitization; they don’t primarily produce the liver-damaging hepatotoxins that drive phylloerythrin accumulation and photodermatitis.