Mitochondrial genome sequencing reveals potential origins of the scabies mite Sarcoptes scabiei infesting two iconic Australian marsupials
Tamieka A. Fraser1,2, Renfu Shao2, Nicholas M. Fountain-Jones3, Michael Charleston1,4, Alynn Martin1, Pam Whiteley5, Roz Holme6, Scott Carver1 and Adam Polkinghorne2*
1School of Biological Sciences, University of Tasmania, Sandy Bay, Hobart, TAS, Australia.
2Centre for Animal Health Innovation, School of Science and Engineering, University of the Sunshine Coast, Sippy Downs, QLD, Australia.
3University of Minnesota, Minneapolis, MN, USA.
4School of Information Technologies, University of Sydney, Camperdown, NSW, Australia.
5Faculty of Veterinary and Agricultural Sciences, The University of Melbourne, Werribee, VIC, Australia.
6Cedar Creek Wombat Rescue Inc. & Hospital, Cedar Creek, NSW, Australia.
Background Debilitating skin infestations caused by the mite, Sarcoptes scabiei, have a profound impact on human and animal health globally. In Australia, this impact is evident across different segments of Australian society, with a growing recognition that it can contribute to rapid declines of native Australian marsupials. Cross-host transmission has been suggested to play a significant role in the epidemiology and origin of mite infestations in different species but a chronic lack of genetic resources has made further inferences difficult. To investigate the origins and molecular epidemiology of S. scabiei in Australian wildlife, we sequenced the mitochondrial genomes of S. scabiei from diseased wombats (Vombatus ursinus) and koalas (Phascolarctos cinereus) spanning New South Wales, Victoria and Tasmania, and compared them with the recently sequenced mitochondrial genome sequences of S. scabiei from humans.
Results We found unique S. scabiei haplotypes among individual wombat and koala hosts with high sequence similarity (99.1% - 100%). Phylogenetic analysis of near full-length mitochondrial genomes revealed three clades of S. scabiei (one human and two marsupial), with no apparent geographic or host species pattern, suggestive of multiple introductions. The availability of additional mitochondrial gene sequences also enabled a re-evaluation of a range of putative molecular markers of S. scabiei, revealing that cox1 is the most informative gene for molecular epidemiological investigations. Utilising this gene target, we provide additional evidence to support cross-host transmission between different animal hosts.
Conclusions Our results suggest a history of parasite invasion through colonisation of Australia from hosts across the globe and the potential for cross-host transmission being a common feature of the epidemiology of this neglected pathogen. If this is the case, comparable patterns may exist elsewhere in the ‘New World’. This work provides a basis for expanded molecular studies into mange epidemiology in humans and animals in Australia and other geographic regions.