Photosensitization (PS) occurred in Shorthorn calves from 3 herds in Boone County, Missouri, in late August and early September 1989. In herd 1, 3 calves, 3-4 weeks old, from a herd of 35 cows with calves were mildly photosensitized. The cattle were confined to 37 acres of permanent pasture of mixed grass and red clover undersown in the previous year’s wheat crop. Skin lesions were most conspicuous on sparsely haired areas around the face and ears. According to the owner, these calves had avoided exposure to full sun for the previous 2 weeks. Two of the calves had slightly elevated gamma glutamyl transferase (GGT) activity. Other evidence of mild liver damage was indicated by a slight elevation in bilirubin (Table 1). These calves recovered during the next week. In herd 2, the 8 affected calves were 2-3 weeks old. The calves and dams were kept in a 4-acre pasture of fescue and red clover. On September 1, the owner noticed flaking skin and hair loss on the backs of the ears of several calves. More calves were affected the next day, and hair loss along the dorsal midline was evident. All calves were photophobic, and 6 of the 8 had diarrhea. At clinical examination on September 6, all 8 calves had lesions evident at various locations (8/8 ears, 6/8 head, 5/8 withers, 4/8 back, and 2/8 dewlap). Other signs of moderate PS included lacrimation, erythema, cutaneous edema, fissuring of the epithelium, and scattered crusting of serum on nonpigmented exposed skin. Serum values for aspartate aminotransferase (AST) were within the normal range. Elevated GGT activity was compatible with damage to the biliary tree. Recovery occurred during the next 3 weeks. Photosensitization is the development of hyperreactivity of the skin to sunlight. The photoreactive molecule, synonymous with photosensitizer, functions as an energy transducer to convert light energy into molecular electronic energy in the form of activated chemical species. Specific biochemical and functional effects of PS reactions include formation of photoadducts with DNA and proteins, peroxidation of lipids, photo-oxidation of membrane proteins, inhibition of transport of essential metabolites, and leakage of lysosomal enzymes. Irrespective of the cause, clinical PS resembles a severe sunburn. The progressive clinical manifestation of PS consists of lacrimation, photophobia, erythema, cutaneous edema, fissuring of the epithelium, exudation and crusting of serum, and necrosis and sloughing of nonpigmented exposed skin Corneal edema is also evident in many cases. Additional clinical signs consistent with liver damage commonly seen in secondary PS include icterus, anorexia, and depression.