Iga Stasiak1,2, DVM; Brandon Lillie1, DVM, PhD, DACVP; Graham Crawshaw2, BVet Med, DACZM; Tomas Ganz3, PhD, MD; Dorothee Bienzle1, DVM, PhD, DACVP; Dale Smith1, DVM, DVSc
1Department of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada; 2Toronto Zoo, Scarborough, ON, Canada; 3David Geffen School of Medicine at UCLA, Department of Medicine, Los Angeles, CA, USA
Hemochromatosis has been associated with liver disease and mortality in captive Egyptian fruit bats (Rousettus aegyptiacus). Although evolutionary adaptation to low levels of iron in the natural diet has been implied, the physiologic basis for susceptibility has not been established. In humans, the iron regulatory protein hepcidin appears to play a crucial role in iron balance and the development of hereditary hemochromatosis. A deficiency or resistance to hepcidin has been implicated in human hereditary hemochromatosis and may play a role in Egyptian fruit bat hemochromatosis. A preliminary investigation was carried into the role of hepcidin in iron metabolism in bats. The coding gene sequence of the hepcidin gene was determined for three species with variable susceptibility to hemochromatosis; Egyptian fruit bat, straw-coloured fruit bat (Eidolon helvum), and common vampire bat (Desmodus rotundus). Baseline blood parameters were compared to those obtained 14 days after intramuscular administration of 100 mg/kg iron dextran (Dextafer®) in the Egyptian fruit bat and straw-colored fruit bat. Hematologic parameters assessed included plasma ferritin, transferrin saturation, plasma iron, and a complete blood cell count (CBC). Liver biopsy samples were obtained at baseline and 14 days after iron administration from all three species and assessed for morphology (histopathology), liver iron content (atomic absorption spectrophotometry), and relative gene expression of hepcidin (RTqPCR). Results were compared between all three species, including two distinct populations of Egyptian fruit bat, with and without underlying hemochromatosis.