The epidemiology of ulcerative mycosis of the platypus (Ornithorhynchus anatinus)

Platypuses ( Ornithorhynchus anatinus) in the north of the island state of Tasmania suffer from a serious disease called ulcerative mycosis, which is responsible for high morbidity and, presumably, mortality rates in areas where the disease occurs. The disease is caused by the fungus Mucor amphibiorum, which is also found in Queensland and New South. However, it does not cause disease in platypuses in those states. This thesis reports on the results of an integrated study of the epidemiology of the disease aimed at determining why only northern Tasmanian platypuses are affected. Pathogenicity trials involving various cane toads (Bufo marinus) as the experimental model indicated that Tasmanian, platypus-derived isolates of M. amphibiorum were more likely to cause a serious, long-term infection than Queensland or West Australian toad-derived isolates. Also, analysis of DNA sequences from four Tasmanian, platypusderived isolates of M. amphibiorum, two Queensland toad-derived isolates and one West Australian slender tree frog (Litoria adelensis)-derived isolate suggest that the area sequenced is not highly variable between isolates from different areas. Based on the DNA analysis and pathogenicity trials, the isolates could be split into three groups; firstly, Tasmanian, platypus-derived isolates, secondly, West Australian slender tree frog-derived isolates and Queensland cane-toad (+) mating type isolates, and thirdly the Queensland cane toad-derived (-) mating type. A closely related fungus, Mucor circinelloides, was also sequenced and tested in pathogenicity trials to determine if it was implicated in the disease. The results suggest that its isolation from diseased animals represents accidental environmental contamination. Sampling of platypus tail fat for the immunomodulating xenobiotics PCB, DDT and Lindane from animals within and outside the endemic area for ulcerative mycosis showed equal levels in all areas. Ulcerated animals did not have elevated levels in comparison to healthy animals. However, some animals from both enedemic and nonendemic areas had greatly elevated levels of PCBs, which may impact on other areas of platypus health. Lymphocyte proliferation assays developed for the platypus showed a low response to mitogens in comparison to most other mammals, but there was no difference between responses for animals from endemic and non-endemic areas. A lowered response to some mitogens was noted in ulcerated animals. A Western blot was developed that could detect antibodies to M. amphibiorum in animals with both active and healed ulcers, but not in healthy platypuses. The possibility that Tasmania possesses a sub-population of atopic platypuses was investigated with an ELISA for the detection of M. amphibiorum specific lgE. There are a number of hypotheses why ulcerative mycosis occurs in Tasmanian, but not mainland, platypuses. The fungus M. amphibiorum may have been introduced into the state, exposing a previously naive population. Tasmanian platypuses, having been isolated from mainland Australia for at least 12,000 years, may be genetically distinct and inherently susceptible to the disease. It is possible that the Tasmanian platypuses' immune system is suppressed, either genetically or by some environmental contaminant. Alternatively, the fungus M. amphibiorum in Tasmania represents a more pathogenic strain than that found in mainland Australia. This thesis will argue that the fungus M. amphibiorum has been introduced into the state on numerous occasions, but in most instances these introductions did not result in infections of platypuses. However, prior to 1982, an isolate of M. amphibiorum successfully infected a platypus, probably because of its ability to produce infective bodies at a much faster rate than other isolates, and the inherent susceptibility of Tasmanian platypuses. Also, some Tasmanian platypuses have suppressed T cell function, which ultimately results in the death of such ulcerated animals.