Reduced Effect of Tasmanian Devil Facial Tumor Disease at the Disease Front

Abstract

Pathogen-driven declines in animal populations are increasingly regarded as a major conservation issue. The Tasmanian devil (Sarcophilus harrisii) is threatened with extinction by devil facial tumor disease, a unique transmissible cancer. The disease is transmitted through direct transfer of tumor cells, which is possible because the genetic diversity of Tasmanian devils is low, particularly in the major histocompatibility complex genes of the immune system. The far northwest of Tasmania now holds the last remaining disease-free wild devil populations. The recent discovery of unique major histocompatibility complex genotypes in the northwestern region of Tasmania has raised the possibility that some animals may be resilient to the disease. We examined the differences in the epidemiology and population effects of devil facial tumor disease at 3 well-studied affected sites in eastern Tasmania and 1 in western Tasmania (West Pencil Pine). In contrast to the 3 eastern sites, there has been no rapid increase in disease prevalence or evidence of population decline at West Pencil Pine. Moreover, this is the only onsite at which the population age structure has remained unaltered 4 years after the first detection of disease. The most plausible explanations for the substantial differences in population effects and epidemiology of the disease between eastern and western sites are geographic differences in genotypes or phenotypes of devils and functional differences between tumor strains in the 2 regions. We suggest that conservation efforts focus on identifying whether either or both these explanations are correct and then, if resistance alleles exist, to attempt to spread the resistant alleles into affected populations. Such assisted selection has rarely been attempted for the management of wildlife diseases, but it may be widely applicable.

Transmissible cancer in Tasmanian devils: localized lineage replacement and host population response

“…There were insufficient data to include any interactions with sex; however, no study has previously reported an effect of sex in the epidemiology of DFTD or in the likelihood of infection [16,20,22]. Tumours of unknown karyotypes and those with evidence of both diploid and tetraploid karyotypes were pooled as there were insufficient data to model them separately, and animals were only included in the analysis on the first occasion that they were captured with a tumour-given that all tumours sampled more than once (11 tetraploid and 18 diploid) kept their original karyotype, subsequent recaptures were omitted.…”

“…This is accompanied by severe declines in individual survival rates and population growth rates, leading to regional-scale decline in population size of more than 90% [22], as well as collapse of age structure [23,24]. At WPP, disease prevalence remained low (less than 20% in adults; less than 10% in juveniles), there was no population decline, and age structure remained unaltered for up to 4 years following the outbreak [20]. Inexplicably, DFTDinfected individuals at WPP had higher survival rates than those in eastern populations [20].…”

“…At WPP, disease prevalence remained low (less than 20% in adults; less than 10% in juveniles), there was no population decline, and age structure remained unaltered for up to 4 years following the outbreak [20]. Inexplicably, DFTDinfected individuals at WPP had higher survival rates than those in eastern populations [20].…”

“…We have reported reduced impacts of the disease at one study site, West Pencil Pine (hereafter WPP) in the northwest of Tasmania, compared with the impact of the disease observed at other sites [20]. The epidemiological pattern of DFTD at sites across eastern Tasmania, as the disease spread from its northeastern origin where it was first detected in 1996, is of a rapid increase in force of infection reaching a prevalence of more than 50% within 2-4 years after local epidemic outbreak [16].…”

“…11 000 years) and evolutionarily stable canine transmissible venereal tumour (CTVT) [18]. The devil transmissible tumour is spread by biting [19], resulting in tumours inside and around the mouth, and is almost always fatal 6-12 months from the appearance of clinical signs [20]. Both DFTD and CTVT have evolved mechanisms of immune escape in allogeneic hosts, in part via epigenetic downregulation of major histocompatibility complex (MHC) gene expression in tumour cells [14,21].…”