Long‐term pathogen control or eradication in wildlife is rare and represents a major challenge in conservation. Control is particularly difficult for environmentally transmitted pathogens, including some of the most conservation‐critical wildlife diseases. We undertook a treatment programme aimed at population‐scale eradication of the environmentally transmitted Sarcoptes scabiei mite (causative agent of sarcoptic mange) during an epizootic in bare‐nosed wombats (Vombatus ursinus). Field trial results were used to parameterize a mechanistic host‐disease model that explicitly described indirect transmission, host behaviour and viable disease intervention methods. Model analysis shows that elimination of S. scabiei in the wild is most sensitive to the success of treatment delivery, and duration of the programme. In addition, we found the frequency that wombats switch burrows was an important positive driver of mite persistence. Synthesis and applications. This research emphasizes the utility of applying model‐guided management techniques in order to achieve practical solutions for controlling disease in the field. We find that control efforts of Sarcoptes scabiei are most successful when simultaneous improvements are made to the current best‐practice protocol, specifically the implementation of better treatment application methods in combination with a longer lasting treatment. These suggested management changes may also reduce the resources and field effort required to implement a successful regime. Furthermore, our approach and findings have applicability to other species affected by S. scabiei (e.g. wolves, red foxes, Spanish ibex and American black bear), as well as other conservation‐critical systems involving environmental transmission (e.g. bat white‐nose syndrome and amphibian chytridiomycosis).

Emerging and invasive pathogens can have long‐lasting impacts on susceptible wildlife populations, including localized collapse and extirpation. Management of threatening disease is of widespread interest and requires knowledge of spatiotemporal patterns of pathogen spread. Theory suggests disease spread often occurs via two patterns: homogenous mixing and travelling waves. However, high‐resolution empirical data demonstrating localized (within population) disease spread patterns are rare. This study examined the spread of sarcoptic mange (aetiological agent Sarcoptes scabiei) in a population of bare‐nosed wombats (Vombatus ursinus), and investigated whether pathogen spread occurred by homogenous mixing or a travelling wave. Using 7 years of population surveys and 4 years of disease severity surveys, we show that mange was first detected in the east of a wombat population in northern Tasmania, and progressed westward as a travelling wave. Wombat mortality rates reached 100% behind the wave, with a 94% decline in overall wombat abundance within the park. Synthesis and applications. Globally distributed pathogens may have severe impacts on susceptible host species. This is the first study to quantify population‐level impacts of sarcoptic mange upon bare‐nosed wombats, showing a wave of mange disease which resulted in a dramatic population decline. Successful management of the spread of this and similar pathogens may hinge on the capacity to establish transmission barriers at local or between‐population scales.

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Due to its suspected increase in host range and subsequent global diversification, Sarcoptes scabiei has important implications at a global scale for wildlife conservation and animal and human health. The introduction of this pathogen into new locations and hosts has been shown to produce high morbidity and mortality, a situation observed recently in Australian and North American wildlife.Of the seven native animal species in Australia known to be infested by S. scabiei, the bare-nosed wombat (Vombatus ursinus) suffers the greatest with significant population declines having been observed in New South Wales and Tasmania. The origins of sarcoptic mange in Australian native animals are poorly understood, with the most consistent conclusion being that mange was introduced by settlers and their dogs and subsequently becoming a major burden to native wildlife. Four studies exist addressing the origins of mange in Australia, but all Australian S. scabiei samples derive from only two of these studies. This review highlights this paucity of phylogenetic knowledge of S. scabiei within Australia, and suggests further research is needed to confidently determine the origin, or multiple origins, of this parasite.At the global scale, numerous genetic studies have attempted to reveal how the host species and host geographic location influence S. scabiei phylogenetics. This review includes an analysis of the global literature, revealing that inconsistent use of gene loci across studies significantly influences phylogenetic inference. Furthermore, by performing a contemporary analytical approach on existing data, it is apparent that (i) new S. scabiei samples, (ii) appropriate gene loci targets, and (iii) advanced phylogenetic approaches are necessary to more confidently comprehend the origins of mange in Australia. Advancing this field of research will aid in understanding the mechanisms of spillover for mange and other parasites globally.Electronic supplementary materialThe online version of this article (doi:10.1186/s13071-016-1578-2) contains supplementary material, which is available to authorized users.

Sarcoptic mange, caused by the parasitic mite Sarcoptes scabiei, causes a substantive burden of disease to humans, domestic animals and wildlife, globally. There are many effects of S. scabiei infection, culminating in the disease which hosts suffer. However, major knowledge gaps remain on the pathogenic impacts of this infection. Here, we focus on the bare-nosed wombat host (Vombatus ursinus) to investigate the effects of mange on: (i) host heat loss and thermoregulation, (ii) field metabolic rates, (iii) foraging and resting behaviour across full circadian cycles, and (iv) fatty acid composition in host adipose, bone marrow, brain and muscle tissues. Our findings indicate that mange-infected V. ursinus lose more heat to the environment from alopecia-affected body regions than healthy individuals. Additionally, mange-infected individuals have higher metabolic rates in the wild. However, these metabolic demands are difficult to meet, because infected individuals spend less time foraging and more time inactive relative to their healthy counterparts, despite being outside of the burrow for longer. Lastly, mange infection results in altered fatty acid composition in adipose tissue, with increased amounts of omega-6 acids, and decreased amounts of omega-3 acids, a consequence of chronic cutaneous inflammation and inhibition of anti-inflammatory responses. These findings highlight the interactions of mange-induced physiological and behavioural changes, and have implications for the treatment and rehabilitation of infected individuals.