COS 96-5 - Reduced impact of Tasmanian devil facial tumor disease at the current disease front

Thursday, August 11, 2011: 9:20 AM
10B, Austin Convention Center
Menna E. Jones1, Rodrigo K. Hamede1, Alexandre Kreiss2, Katherine Belov3, Anne-Maree Pearse4 and Hamish I. McCallum5, (1)School of Biological Sciences, University of Tasmania, Hobart, Australia, (2)Menzies Research Institute Tasmania, Hobart, Tasmania, Australia, (3)Faculty of Veterinary science, The University of Sydney, Sydney, Australia, (4)Department of Primary Industry, Parks, Water and Environment, Tasmanian State Government, Launceston, Australia, (5)School of Environment, Griffith University, Brisbane, Australia

A novel infectious cancer, devil facial tumor disease (DFTD), is threatening the Tasmanian devil (Sarcophilus harrisii), the world’s largest marsupial carnivore, with extinction. Transmission is by direct transfer of live tumor cells during biting, with tumor growth in the new host enabled by very low genetic diversity, particularly at the Major Histocompatibility Complex (MHC) genes associated with tumor recognition. Mortality is 100% by the end of first year of adult life (2-3 years) in eastern Tasmania, where the cancer originated and where the tumor is genetically highly similar to the host. Tasmanian devil populations have some genetic substructuring across their island range, with populations in the more isolated northwest differing from the east and from the tumour at neutral and functional (MHC) loci. Four years ago, we established a study site on the northwest disease front, where the tumor is encountering these different northwest genotypes for the first time. Here we report on very different patterns in the progress of the disease epidemic and its demographic impacts in this population compared with three populations in eastern Tasmania.


Over four years, DFTD prevalence has remained low in all age classes (<10%), and there has been no indication of changes in population size or age structure or significant declines in population growth rate. This is in striking contrast to DFTD-affected devil populations in eastern Tasmania, which exhibited sudden increases in DFTD prevalence and rapid declines in population size, average age and population growth rates following DFTD arrival.

Different MHC expression is a plausible explanation for the variant patterns of epidemic progression and population impacts in the northwest population. It is conceivable that individuals with different numbers of MHC antigens to the tumor could recognise foreign MHC antigens on the tumor and mount an immune response, thus becoming less likely to acquire DFTD. Two wild-caught individuals in the northwest population have antibodies to DFTD, suggesting exposure to DFTD and production of a protective immune response.

Another plausible explanation is that the tumour could be evolving into a less aggressive form, as occurred in the canine transmissible venereal tumor. Seven different strains of DFTD have been detected to date. The northwest tumors are tetraploid cells, which usually grow more slowly than diploid cells. This explanation is supported by preliminary results which indicate that most DFTD devils at the northwest site do not succumb to infection as quickly as in the east.

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