Southdown and Corriedale sheep may inherit a hepatobiliary incompetence that results in photosensitization.
In mutant Southdown sheep, the inherited defect involves hepatic uptake of unconjugated bilirubin and organic anions. Plasma levels of unconjugated bilirubin are consistently increased and, because bilirubin is partially excreted, icterus is not a clinical feature. Phylloerythrin is less effectively excreted, and affected lambs become photosensitized when they first begin grazing green plant material. Unless chlorophyll is excluded from the diet, or exposure to sunlight is prevented, lesions and stress of photosensitization result in death within weeks. Mutant sheep so protected develop progressive renal lesions in which radial, fibrous bands form in the medulla, along with increasing numbers of cystic tubules. The changes ultimately result in renal insufficiency and death. The liver is small, with pericanalicular deposits of lipofuscin. This semilethal trait appears to be inherited as a simple recessive trait. Elimination of carriers is the only feasible control.
In mutant Corriedale sheep, the hepatocellular incompetence involves excretion of conjugated bilirubin and other conjugated metabolites. There is no obvious icterus, but phylloerythrin excretion is sufficiently impaired to produce photosensitization. Hepatic pigmentation is obvious grossly. Brown-black, melanin-like pigment is confined to centrilobular parenchymal cells. This condition is transmitted as an autosomal recessive trait. Control is by detection and removal of carriers.