Southdown and Corriedale sheep may inherit a hepatobiliary incompetence that results in photosensitization.
In Southdown sheep with congenital photosensitization, the inherited hepatobiliary defect leads to hepatic uptake of unconjugated bilirubin and organic anions. Plasma concentrations of unconjugated bilirubin are consistently increased, and because bilirubin is partially excreted, icterus is not a clinical sign. Phylloerythrin is less effectively excreted, and affected lambs become photosensitized when they first begin grazing on green plant material.
Unless chlorophyll is excluded from the diet or exposure to sunlight is prevented, the lesions and stress of photosensitization in Southdown sheep result in death within weeks. Affected sheep 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 in Southdown sheep with congenital photosensitization is small and has pericanalicular deposits of lipofuscin; this semilethal trait appears to be inherited as a simple recessive trait. Elimination of carriers is the only feasible method of control.
In affected Corriedale sheep, hepatic pigmentation is grossly apparent, and brown-black, melanin-like pigment is confined to centrilobular parenchymal cells. There is no obvious icterus; however, phylloerythrin excretion is sufficiently impaired to produce photosensitization. Hepatic pigmentation is obvious grossly, and brown-black, melanin-like pigment is confined to centrilobular parenchymal cells.
Hepatocellular incompetence in Corriedale sheep is transmitted as an autosomal recessive trait. Control is by the detection and removal of carriers.
