Pathogenesis of hemosiderosis in lemurs: Role of dietary iron,tannin, and ascorbic acid

Clinical disease associated with excess iron deposition (hemosiderosis) in the duodenum, liver, and spleen occurs in captive lemurs. In this report we review the occurrence of hemosiderosis and related disease in the Zoological Society of San Diego lemur collection; we then define and describe potential pathogenic factors with the goal of establishing rational husbandry methods to limit or prevent the disease. At the San Diego Zoo, all 49 lemurs necropsied since 1968 were hemosiderotic, the severity increasing with increasing age; liver and kidney disease were common. Our review of iron metabolism, current knowledge on the pathogenesis of hemosiderosis in humans, and the diets of captive and wild lemurs reveals several key dietary substances that may contribute to lemur hemosiderosis: iron, tannins, and ascorbic acid. In captivity, excess dietary iron (commercial monkey chow) and high levels of ascorbic acid (citrus fruits) lead to enhanced iron uptake and increased toxicity of stored iron due to free radical formation. In the wild, lemurs have an unusual preference for leaves, fruits, and bark high in tannin, a polyphenolic secondary plant compound that rapidly chelates iron, protein, and minerals in the gastrointestinal (GI) tract, preventing their absorption. These findings suggest that hemosiderosis in captive lemurs results from a diet high in iron, high in ascorbic acid, and lacking in tannin. Immediate correction of captive diets may limit hemosiderosis in lemurs in the future.