ORCID Profile
0000-0003-1526-225X
Current Organisation
University of Tasmania
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Research Topics
In Research Link Australia (RLA), "Research Topics" refer to ANZSRC FOR and SEO codes. These topics are either sourced from ANZSRC FOR and SEO codes listed in researchers' related grants or generated by a large language model (LLM) based on their publications.
Top 5 Research Topics
ANZSRC Field of Research (FoR)
Host-Parasite Interactions | Evolutionary biology | Wildlife and Habitat Management | Wildlife and habitat management | Environmental Science and Management | Conservation and Biodiversity | Evolutionary Biology | Host-parasite interactions | Biological adaptation | Population, Ecological and Evolutionary Genetics | Biological Adaptation
ANZSRC Socio-Economic Objective (SEO)
Control of Pests, Diseases and Exotic Species at Regional or Larger Scales | Expanding Knowledge in the Biological Sciences | Flora, Fauna and Biodiversity at Regional or Larger Scales |
Related Links
Publications
Tasman-PCR: a genetic diagnostic assay for Tasmanian devil facial tumour diseases
Publisher: The Royal Society
Date: 10-2018
DOI: 10.1098/RSOS.180870
Abstract: Tasmanian devils have spawned two transmissible cancer clones, known as devil facial tumour 1 (DFT1) and devil facial tumour 2 (DFT2). DFT1 and DFT2 are transmitted between animals by the transfer of allogeneic contagious cancer cells by biting, and both cause facial tumours. DFT1 and DFT2 tumours are grossly indistinguishable, but can be differentiated using histopathology, cytogenetics or genotyping of polymorphic markers. However, standard diagnostic methods require specialist skills and equipment and entail long processing times. Here, we describe Tasman-PCR: a simple polymerase chain reaction (PCR)-based diagnostic assay that identifies and distinguishes DFT1 and DFT2 by lification of DNA spanning tumour-specific interchromosomal translocations. We demonstrate the high sensitivity and specificity of this assay by testing DNA from 546 tumours and 804 normal devils. A temporal–spatial screen confirmed the reported geographic ranges of DFT1 and DFT2 and did not provide evidence of additional DFT clones. DFT2 affects disproportionately more males than females, and devils can be co-infected with DFT1 and DFT2. Overall, we present a PCR-based assay that delivers rapid, accurate and high-throughput diagnosis of DFT1 and DFT2. This tool provides an additional resource for devil disease management and may assist with ongoing conservation efforts.
Transcriptomics of Tasmanian Devil (Sarcophilus Harrisii) Ear Tissue Reveals Homogeneous Gene Expression Patterns across a Heterogeneous Landscape
Publisher: MDPI AG
Date: 12-10-2019
Abstract: In an era of unprecedented global change, exploring patterns of gene expression among wild populations across their geographic range is crucial for characterizing adaptive potential. RNA-sequencing studies have successfully characterized gene expression differences among populations experiencing ergent environmental conditions in a wide variety of taxa. However, few of these studies have identified transcriptomic signatures to multivariate, environmental stimuli among populations in their natural environments. Herein, we aim to identify environmental and sex-driven patterns of gene expression in the Tasmanian devil (Sarcophilus harrisii), a critically endangered species that occupies a heterogeneous environment. We performed RNA-sequencing on ear tissue biopsies from adult male and female devils from three populations at the extremes of their geographic range. There were no transcriptome-wide patterns of differential gene expression that would be suggestive of significant, environmentally-driven transcriptomic responses. The general lack of transcriptome-wide variation in gene expression levels across the devil’s geographic range is consistent with previous studies that documented low levels of genetic variation in the species. However, genes previously implicated in local adaptation to abiotic environment in devils were enriched for differentially expressed genes. Additionally, three modules of co-expressed genes were significantly associated with either population of origin or sex.
Untangling the model muddle: Empirical tumour growth in Tasmanian devil facial tumour disease
Publisher: Springer Science and Business Media LLC
Date: 24-07-2017
DOI: 10.1038/S41598-017-06166-3
Abstract: A pressing and unresolved topic in cancer research is how tumours grow in the absence of treatment. Despite advances in cancer biology, therapeutic and diagnostic technologies, there is limited knowledge regarding the fundamental growth and developmental patterns in solid tumours. In this ten year study, we estimated growth curves in Tasmanian devil facial tumours, a clonal transmissible cancer, in males and females with two different karyotypes (diploid, tetraploid) and facial locations (mucosal, dermal), using established differential equation models and model selection. Logistic growth was the most parsimonious model for diploid, tetraploid and mucosal tumours, with less model certainty for dermal tumours. Estimates of daily proportional tumour growth rate per day (95% Bayesian CIs) varied with ploidy and location [diploid 0.016 (0.014–0.020), tetraploid 0.026 (0.020–0.033), mucosal 0.013 (0.011–0.015), dermal 0.020 (0.016–0.024)]. Final tumour size (cm 3 ) also varied, particularly the upper credible interval owing to host mortality as tumours approached maximum volume [diploid 364 (136–2,475), tetraploid 172 (100–305), dermal 226 (134–471)]. To our knowledge, these are the first empirical estimates of tumour growth in the absence of treatment in a wild population. Through this animal-cancer system our findings may enhance understanding of how tumour properties interact with growth dynamics in other types of cancer.
Cancer Is Not (Only) a Senescence Problem
Publisher: Elsevier BV
Date: 03-2018
DOI: 10.1016/J.TRECAN.2018.01.002
Abstract: Age is one of the strongest predictors of cancer and risk of death from cancer. Cancer is therefore generally viewed as a senescence-related malady. However, cancer also exists at subclinical levels in humans and other animals, but its earlier effects on the body are poorly known by comparison. We argue here that cancer is a significant but ignored burden on the body and is likely to be a strong selective force from early during the lifetime of an organism. It is time to adopt this novel view of malignant pathologies to improve our understanding of the ways in which oncogenic phenomena influence the ecology and evolution of animals long before their negative impacts become evident and fatal.
Conservation management of Tasmanian devils in the context of an emerging, extinction-threatening disease: Devil Facial Tumor Disease
Publisher: Springer Science and Business Media LLC
Date: 06-09-2007
Disruption of metapopulation structure effectively reduces Tasmanian devil facial tumour disease spread at the expense of abundance and genetic diversity
Publisher: Cold Spring Harbor Laboratory
Date: 04-10-2021
DOI: 10.1101/2021.10.04.463046
Abstract: Metapopulation structure (i.e. the spatial arrangement of local populations and corridors between them) plays a fundamental role in the persistence of wildlife populations, but can also drive the spread of infectious diseases. While the disruption of metapopulation connectivity can reduce disease spread, it can also impair host resilience by disrupting gene flow and colonisation dynamics. Thus, a pressing challenge for many wildlife populations is to elucidate whether the benefits of disease management methods that reduce metapopulation connectivity outweigh the associated risks. Directly transmissible cancers are clonal malignant cell lines capable to spread through host populations without immune recognition, when susceptible and infected hosts become in close contact. Using an in idual-based metapopulation model we investigate the effects of the interplay between host dispersal, disease transmission rate and inter-in idual contact distance for transmission (determining within-population mixing) on the spread and persistence of a transmissible cancer, Tasmanian devil facial tumour disease (DFTD), from local to regional scales. Further, we explore population isolation scenarios to devise management strategies to mitigate disease spread. Disease spread, and the ensuing population declines, are synergistically determined by in iduals’ dispersal, disease transmission rate and within-population mixing. Low to intermediate transmission rates can be magnified by high dispersal and inter-in idual transmission distance. Once disease transmission rate is high, dispersal and inter-in idual contact distance do not impact the outcome of the disease transmission dynamics. Isolation of local populations effectively reduced metapopulation-level disease prevalence but caused severe declines in metapopulation size and genetic ersity. The relative position of managed (i.e. isolated) populations within the metapopulation had a significant effect on disease prevalence, highlighting the importance of considering metapopulation structure when implementing metapopulation-scale disease control measures. Our findings suggests that population isolation is not an ideal management method for preventing disease spread in species inhabiting already fragmented landscapes, where genetic ersity and extinction risk are already a concern, such as the Tasmanian devil.
Discovery of Biomarkers for Tasmanian Devil Cancer (DFTD) by Metabolic Profiling of Serum
Publisher: American Chemical Society (ACS)
Date: 23-09-2016
DOI: 10.1021/ACS.JPROTEOME.6B00629
Abstract: Devil facial tumor disease (DFTD) is a transmissible cancer threatening Tasmanian devils (Sarcophilus harrisii) with extinction. There is no preclinical test available for DFTD, and thus our aim was to find biomarkers for DFTD by metabolic fingerprinting. Seventy serum s les from wild Tasmanian devils (35 controls, 35 with tumors) were analyzed by liquid chromatography-high-resolution mass spectrometry. Features were selected by multivariate models (PLS/DA, random forests) comparing age-matched training set (n = 20 × 2) and further complying with fold-change threshold (≥1.4) and Mann-Whitney U-tests with correction for multiple hypotheses (false discovery rate (FDR) q 0.45, p < 0.01). Additional potential markers included amino acid and lipid metabolites, while cortisol and urea were the most significant health predictors (AUC ≥ 0.90). PLS/DA resulted in AUC = 0.997 for the training set and overall sensitivity of 91% and specificity of 97%. A support vector machine model utilizing only the major peptide marker and seven other metabolites led to overall 94% sensitivity and specificity. The novel findings in this first DFTD metabolomics study shed light on metabolic changes in Tasmanian devils affected by DFTD and provide a valuable step toward the development of prognostic biomarkers.
Rapid evolutionary response to a transmissible cancer in Tasmanian devils
Publisher: Springer Science and Business Media LLC
Date: 30-08-2016
DOI: 10.1038/NCOMMS12684
Abstract: Although cancer rarely acts as an infectious disease, a recently emerged transmissible cancer in Tasmanian devils ( Sarcophilus harrisii ) is virtually 100% fatal. Devil facial tumour disease (DFTD) has swept across nearly the entire species’ range, resulting in localized declines exceeding 90% and an overall species decline of more than 80% in less than 20 years. Despite epidemiological models that predict extinction, populations in long-diseased sites persist. Here we report rare genomic evidence of a rapid, parallel evolutionary response to strong selection imposed by a wildlife disease. We identify two genomic regions that contain genes related to immune function or cancer risk in humans that exhibit concordant signatures of selection across three populations. DFTD spreads between hosts by suppressing and evading the immune system, and our results suggest that hosts are evolving immune-modulated resistance that could aid in species persistence in the face of this devastating disease.
Global meta‐analysis of over 50 years of multidisciplinary and international collaborations on transmissible cancers
Publisher: Wiley
Date: 13-03-2020
DOI: 10.1111/EVA.12938
Abstract: Although transmissible cancers have, so far, only been documented in three independent animal groups, they not only impact animals that have high economic, environmental and social significance, but they are also one of the most virulent parasitic life forms. Currently known transmissible cancers traverse terrestrial and marine environments, and are predicted to be more widely distributed across animal groups thus, the implementation of effective collaborative scientific networks is important for combating existing and emerging forms. Here, we quantify how collaborative effort on the three known transmissible cancers has advanced through the formation of collaborative networks among institutions and disciplines. These three cancers occur in bivalves (invertebrates—disseminated neoplasia DN), Tasmanian devils (vertebrate—marsupial devil facial tumour disease DFTD) and dogs (vertebrate—eutherian mammal canine transmissible venereal tumour CTVT). Research on CTVT and DN has been conducted since 1876 and 1969, respectively, whereas systematic research on DFTD only started in 2006. Yet, collaborative effort on all three diseases is global, encompassing six major Scopus subject areas. Collaborations steadily increased between 1963 and 2006 for CTVT and DN, with similar acceleration for all three cancers since 2006. Network analyses demonstrated that scientists are organizing themselves into efficient collaborative networks however, these networks appear to be far stronger for DFTD and DN, possibly due to the recent detection of new strains adding impetus to research and associated publications (enhancing citation trajectories). In particular, global and multidisciplinary collaborations formed almost immediately after DFTD research was initiated, leading to similar research effort and relatively greater research outputs compared to the other two diseases. Therefore, in the event of outbreaks of new lineages of existing transmissible cancers, or the discovery of new transmissible cancers in the future, the rapid formation of international collaborations spanning relevant disciplines is vital for the efficient management of these diseases.
Large‐effect loci affect survival in Tasmanian devils ( Sarcophilus harrisii ) infected with a transmissible cancer
Publisher: Wiley
Date: 05-10-2018
DOI: 10.1111/MEC.14853
A transmissible cancer shifts from emergence to endemism in Tasmanian devils
Publisher: American Association for the Advancement of Science (AAAS)
Date: 11-12-2020
Abstract: The emergence of a devastating transmissible facial cancer among Tasmanian devils over the past few decades has caused substantial concern for their future because these animals are already threatened by a regional distribution and other stressors. Little is known about the overall history and trajectory of this disease. Patton et al. used an epidemiological phylodynamic approach to reveal the pattern of disease emergence and spread. They found that low Tasmanian devil densities appear to be contributing to slower disease growth and spread, which is good news for Tasmanian devil persistence and suggests that care should be taken when considering options for increasing devil populations. Science , this issue p. eabb9772
Development of a SNP-based assay for measuring genetic diversity in the Tasmanian devil insurance population
Publisher: Springer Science and Business Media LLC
Date: 14-10-2015
Evolved Dependence in Response to Cancer
Publisher: Elsevier BV
Date: 04-2018
DOI: 10.1016/J.TREE.2018.01.012
Abstract: Evolved dependence is a process through which one species becomes 'dependent' on another following a long evolutionary history of interaction. This happens when adaptations selected in the first species for interacting lead to fitness costs when the second species is not encountered. Evolved dependence is frequent in host-parasite interactions, where hosts may achieve a higher fitness in the presence of the parasite than in its absence. Since oncogenic manifestations are (i) ubiquitous across multicellular life, (ii) involved in parasitic-like interactions with their hosts, and (iii) have effectively driven the selection of numerous adaptations, it is possible that multicellular organisms display evolved dependence in response to oncogenic processes. We provide a comprehensive overview of the topic, including the implications for cancer prevention and treatment.
Demonstration of immune responses against devil facial tumour disease in wild Tasmanian devils
Publisher: The Royal Society
Date: 10-2016
Abstract: Devil facial tumour disease (DFTD) is a recently emerged fatal transmissible cancer decimating the wild population of Tasmanian devils ( Sarcophilus harrisii ). Biting transmits the cancer cells and the tumour develops in the new host as an allograft. The literature reports that immune escape mechanisms employed by DFTD inevitably result in host death. Here we present the first evidence that DFTD regression can occur and that wild devils can mount an immune response against the disease. Of the 52 devils tested, six had serum antibodies against DFTD cells and, in one case, prominent T lymphocyte infiltration in its tumour. Notably, four of the six devils with serum antibody had histories of DFTD regression. The novel demonstration of an immune response against DFTD in wild Tasmanian devils suggests that a proportion of wild devils can produce a protective immune response against naturally acquired DFTD. This has implications for tumour–host coevolution and vaccine development.
Infectious disease and sickness behaviour: tumour progression affects interaction patterns and social network structure in wild Tasmanian devils
Publisher: The Royal Society
Date: 09-12-2020
Abstract: Infectious diseases, including transmissible cancers, can have a broad range of impacts on host behaviour, particularly in the latter stages of disease progression. However, the difficulty of early diagnoses makes the study of behavioural influences of disease in wild animals a challenging task. Tasmanian devils ( Sarcophilus harrisii ) are affected by a transmissible cancer, devil facial tumour disease (DFTD), in which tumours are externally visible as they progress. Using telemetry and mark–recapture datasets, we quantify the impacts of cancer progression on the behaviour of wild devils by assessing how interaction patterns within the social network of a population change with increasing tumour load. The progression of DFTD negatively influences devils' likelihood of interaction within their network. Infected devils were more active within their network late in the mating season, a pattern with repercussions for DFTD transmission. Our study provides a rare opportunity to quantify and understand the behavioural feedbacks of disease in wildlife and how they may affect transmission and population dynamics in general.
The genomic basis of tumor regression in Tasmanian devils (Sarcophilus harrisii)
Publisher: Oxford University Press (OUP)
Date: 13-10-2018
DOI: 10.1093/GBE/EVY229
Reduced effect of Tasmanian devil facial tumor disease at the disease front
Publisher: Wiley
Date: 06-10-2012
DOI: 10.1111/J.1523-1739.2011.01747.X
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 ersity 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.
Extreme Competence: Keystone Hosts of Infections
Publisher: Elsevier BV
Date: 04-2019
Immunoglubolin dynamics and cancer prevalence in Tasmanian devils (Sarcophilus harrisii)
Publisher: Springer Science and Business Media LLC
Date: 29-04-2016
DOI: 10.1038/SREP25093
Abstract: Immunoglobulins such as IgG and IgM have been shown to induce anti-tumour cytotoxic activity. In the present study we therefore explore total serum IgG and IgM expression dynamics in 23 known-aged Tasmanian devils ( Sarcophilus harrisii ) of which 9 where affected by Devil Facial Tumour Disease (DFTD). DFTD is clonally transmissible cancer that has caused massive declines in devil numbers. Our analyses revealed that IgM and IgG expression levels as well as IgM/IgG ratios decreased with increasing devil age. Neither age, sex, IgM nor IgG expression levels affected devil DFTD status in our analyses. However, devils with increased IgM relative to IgG expression levels had significantly lower DFTD prevalence. Our results therefore suggest that IgM/IgG ratios may play an important role in determining devil susceptibility to DFTD. We consequently propose that our findings warrant further studies to elucidate the underpinning(s) of devil IgM/IgG ratios and DFTD status.
Rare and unique adaptations to cancer in domesticated species: An untapped resource?
Publisher: Wiley
Date: 29-01-2020
DOI: 10.1111/EVA.12920
Abstract: Strong and ongoing artificial selection in domestic animals has resulted in amazing phenotypic responses that benefit humans, but often at a cost to an animal's health, and problems related to inbreeding depression, including a higher incidence of cancer. Despite high rates of cancer in domesticated species, little attention has been devoted to exploring the hypothesis that persistent artificial selection may also favour the evolution of compensatory anticancer defences. Indeed, there is evidence for effective anti‐cancer defences found in several domesticated species associated with different cancer types. We also suggest that artificial selection can favour the “domestication” of inherited oncogenic mutations in rare instances, retaining those associated to late and/or less aggressive cancers, and that by studying these seemingly rare anticancer adaptations, novel cancer treatments may be found.
Seasonal, demographic and density-related patterns of contact between Tasmanian devils (Sarcophilus harrisii): Implications for transmission of devil facial tumour disease
Publisher: Wiley
Date: 08-2008
Conserving adaptive potential: lessons from Tasmanian devils and their transmissible cancer
Publisher: Springer Science and Business Media LLC
Date: 02-2019
Variants in the host genome may inhibit tumour growth in devil facial tumours: Evidence from genome-wide association
Publisher: Springer Science and Business Media LLC
Date: 24-03-2017
DOI: 10.1038/S41598-017-00439-7
Abstract: Devil facial tumour disease (DFTD) has decimated wild populations of Tasmanian devils ( Sarcophilus harrisii ) due to its ability to avoid immune detection and pass from host to host by biting. A small number of devils have been observed to spontaneously recover from the disease which is otherwise fatal. We have sequenced the genomes of these rare cases and compared them to the genomes of devils who succumbed to the disease. Genome-wide association, based on this limited s ling, highlighted two key genomic regions potentially associated with ability to survive DFTD. Following targeted genotyping in additional s les, both of these loci remain significantly different between cases and controls, with the PAX3 locus retaining significance at the 0.001 level, though genome-wide significance was not achieved. We propose that PAX3 may be involved in a regulatory pathway that influences the slowing of tumour growth and may allow more time for an immune response to be mounted in animals with regressed tumours. This provides an intriguing hypothesis for further research and could provide a novel route of treatment for this devastating disease.
Reversible epigenetic down-regulation of MHC molecules by devil facial tumour disease illustrates immune escape by a contagious cancer
Publisher: Proceedings of the National Academy of Sciences
Date: 11-03-2013
Abstract: Contagious cancers that pass between in iduals as an infectious cell line are highly unusual pathogens. Devil facial tumor disease (DFTD) is one such contagious cancer that emerged 16 y ago and is driving the Tasmanian devil to extinction. As both a pathogen and an allograft, DFTD cells should be rejected by the host–immune response, yet DFTD causes 100% mortality among infected devils with no apparent rejection of tumor cells. Why DFTD cells are not rejected has been a question of considerable confusion. Here, we show that DFTD cells do not express cell surface MHC molecules in vitro or in vivo, due to down-regulation of genes essential to the antigen-processing pathway, such as β 2 -microglobulin and transporters associated with antigen processing. Loss of gene expression is not due to structural mutations, but to regulatory changes including epigenetic deacetylation of histones. Consequently, MHC class I molecules can be restored to the surface of DFTD cells in vitro by using recombinant devil IFN-γ, which is associated with up-regulation of the MHC class II transactivator, a key transcription factor with deacetylase activity. Further, expression of MHC class I molecules by DFTD cells can occur in vivo during lymphocyte infiltration. These results explain why T cells do not target DFTD cells. We propose that MHC-positive or epigenetically modified DFTD cells may provide a vaccine to DFTD. In addition, we suggest that down-regulation of MHC molecules using regulatory mechanisms allows evolvability of transmissible cancers and could affect the evolutionary trajectory of DFTD.
Cathelicidin-3 associated with serum extracellular vesicles enables early diagnosis of a transmissible cancer
Publisher: Cold Spring Harbor Laboratory
Date: 07-12-2021
DOI: 10.1101/2021.12.06.471373
Abstract: The identification of practical early diagnosis biomarkers is a cornerstone of improved prevention and treatment of cancers. Such a case is devil facial tumour disease (DFTD), a highly lethal transmissible cancer afflicting virtually an entire species, the Tasmanian devil ( Sarcophilus harrisii ). Despite a latent period that can exceed one year, to date DFTD diagnosis requires visual identification of tumour lesions. To enable earlier diagnosis, which is essential for the implementation of effective conservation strategies, we analysed the extracellular vesicle (EV) proteome of 87 Tasmanian devil serum s les. The antimicrobial peptide cathelicidin-3 (CATH3) was enriched in serum EVs of both devils with clinical DFTD (87.9% sensitivity and 94.1% specificity) and devils with latent infection (i.e., collected while overtly healthy, but 3-6 months before subsequent DFTD diagnosis 93.8% sensitivity and 94.1% specificity). As antimicrobial peptides can play a variety of roles in the cancer process, our results suggest that the specific elevation of serum EV-associated CATH3 may be mechanistically involved in DFTD pathogenesis. This EV-based approach to biomarker discovery is directly applicable to improving understanding and diagnosis of a broad range of diseases in other species, and these findings directly enhance the capacity of conservation strategies to ensure the viability of the imperilled Tasmanian devil population.
Transmission dynamics of Tasmanian devil facial tumor disease may lead to disease-induced extinction
Publisher: Wiley
Date: 12-2009
DOI: 10.1890/08-1763.1
Abstract: Most pathogens threatening to cause extinction of a host species are maintained on one or more reservoir hosts, in addition to the species that is threatened by disease. Further, most conventional host-pathogen theory assumes that transmission is related to host density, and therefore a pathogen should become extinct before its sole host. Tasmanian devil facial tumor disease is a recently emerged infectious cancer that has led to massive population declines and grave concerns for the future persistence of this largest surviving marsupial carnivore. Here we report the results of mark-recapture studies at six sites and use these data to estimate epidemiological parameters critical to both accurately assessing the risk of extinction from this disease and effectively managing this disease threat. Three sites were monitored from before or close to the time of disease arrival, and at three others disease was well established when trapping began, in one site for at least 10 years. We found no evidence for sex-specific differences in disease prevalence and little evidence of consistent seasonal variation in the force of infection. At all sites, the disease was maintained at high levels of prevalence (>50% in 2-3-year-old animals), despite causing major population declines. We also provide the first estimates of the basic reproductive rate R0 for this disease. Using a simple age-structured deterministic model, we show that our results are not consistent with transmission being proportional to the density of infected hosts but are consistent with frequency-dependent transmission. This conclusion is further supported by the observation that local disease prevalence in 2-3-year-olds still exceeds 50% at a site where population density has been reduced by up to 90% in the past 12 years. These findings lend considerable weight to concerns that this host-specific pathogen will cause the extinction of the Tasmanian devil. Our study highlights the importance of rapidly implementing monitoring programs to determine how transmission depends on host density and emphasizes the need for ongoing management strategies involving a disease-free "insurance population," along with ongoing field monitoring programs to confirm whether local population extinction occurs.
New insights into the role of MHC diversity in devil facial tumour disease
Publisher: Public Library of Science (PLoS)
Date: 06-06-2012
Disease swamps molecular signatures of genetic-environmental associations to abiotic factors in Tasmanian devil (Sarcophilus harrisii) populations
Publisher: Cold Spring Harbor Laboratory
Date: 24-09-2019
DOI: 10.1101/780122
Abstract: Landscape genomics studies focus on identifying candidate genes under selection via spatial variation in abiotic environmental variables, but rarely by biotic factors such as disease. The Tasmanian devil ( Sarcophilus harrisii ) is found only on the environmentally heterogeneous island of Tasmania and is threatened with extinction by a nearly 100% fatal, transmissible cancer, devil facial tumor disease (DFTD). Devils persist in regions of long-term infection despite epidemiological model predictions of species’ extinction, suggesting possible adaptation to DFTD. Here, we test the extent to which spatial variation and genetic ersity are associated with the abiotic environment and/or by DFTD. We employ genetic-environment association (GEAs) analyses using a RAD-capture panel consisting of 6,886 SNPs from 3,286 in iduals s led pre- and post-disease arrival. Pre-disease, we find significant correlations of allele frequencies with environmental variables, including 349 unique loci linked to 64 genes, suggesting local adaptation to abiotic environment. Following DFTD arrival, however, we detected few of the pre-disease candidate loci, but instead frequencies of candidate loci linked to 14 genes correlated with disease prevalence. Loss of apparent signal of abiotic local adaptation following disease arrival suggests sw ing by the strong selection imposed by DFTD. Further support for this result comes from the fact that post-disease candidate loci are in linkage disequilibrium with genes putatively involved in immune response, tumor suppression and apoptosis. This suggests the strength GEA associations of loci with the abiotic environment are sw ed resulting from the rapid onset of a biotic selective pressure.
Wildlife nidoviruses: biology, epidemiology, and disease associations of selected nidoviruses of mammals and reptiles
Publisher: American Society for Microbiology
Date: 13-07-2023
Abstract: Wildlife is the source of many emerging infectious diseases. Several viruses from the order Nidovirales have recently emerged in wildlife, sometimes with severe consequences for endangered species. The order Nidovirales is currently classified into eight suborders, three of which contain viruses of vertebrates. Vertebrate coronaviruses (suborder Cornidovirineae ) have been extensively studied, yet the other major suborders have received less attention. The aim of this minireview was to summarize the key findings from the published literature on nidoviruses of vertebrate wildlife from two suborders: Arnidovirineae and Tornidovirineae . These viruses were identified either during investigations of disease outbreaks or through molecular surveys of wildlife viromes, and include pathogens of reptiles and mammals. The available data on key biological features, disease associations, and pathology are presented, in addition to data on the frequency of infections among various host populations, and putative routes of transmission. While nidoviruses discussed here appear to have a restricted in vivo host range, little is known about their natural life cycle. Observational field-based studies outside of the mortality events are needed to facilitate an understanding of the virus-host-environment interactions that lead to the outbreaks. Laboratory-based studies are needed to understand the pathogenesis of diseases caused by novel nidoviruses and their evolutionary histories. Barriers preventing research progress include limited funding and the unavailability of virus- and host-specific reagents. To reduce mortalities in wildlife and further population declines, proactive development of expertise, technologies, and networks should be developed. These steps would enable effective management of future outbreaks and support wildlife conservation.
Hematologic and serum biochemical changes associated with Devil Facial Tumor Disease in Tasmanian Devils
Publisher: Wiley
Date: 09-2016
DOI: 10.1111/VCP.12391
Abstract: Devil Facial Tumor Disease (DFTD) is an infectious tumor causing significant population declines in wild Tasmanian Devils. While clinical assessment and pathology have been well reported for DFTD, there is a lack of information on hematologic and biochemical alterations associated with DFTD. The purpose of the study was to determine hematologic and serum biochemical variation in healthy, wounded, and DFTD-affected Tasmanian Devils. Blood s les were collected from wild Tasmanian Devils at 5 sites in Tasmania. Hematology and clinical biochemistry variables were compared between clinically healthy, wounded, and DFTD-affected devils. Differences were also analyzed among stages of DFTD, including in iduals pre- and postclinical signs developing, and between ulcerated and nonulcerated DFTD tumors. Statistically significantly increased counts in WBC, neutrophils, and platelets, and concentration of fibrinogen, as well as decreased counts in lymphocytes, erythrocytes, and HGB concentration were observed in DFTD-affected devils compared to healthy devils. Activities of ALP, ALT, and GLDH, concentrations of sodium, potassium and albumin, and sodium-to-potassium ratio and albumin-to-globulin ratio were significantly lower, and AST activity was significantly higher in animals with DFTD when compared to clinically healthy animals. No significant differences were found among stages of DFTD or ulcerated and nonulcerated tumors. The differences in hematology and clinical chemistry variables in devils with DFTD compared to healthy devils are nonspecific and reflective of acute phase response and inflammation, and anemia of chronic disease. Similar changes are observed with wounds but to a lesser extent.
Secret Lives of Carnivorous Marsupials. By Andrew Baker and Chris Dickman. Clayton South (Australia): CSIRO Publishing. AU $140.00. viii + 320 p.; ill.; index. ISBN: 978-1-4863-0514-8. 2018.
Publisher: University of Chicago Press
Date: 09-2019
DOI: 10.1086/705064
Oncogenesis as a Selective Force: Adaptive Evolution in the Face of a Transmissible Cancer
Publisher: Wiley
Date: 15-02-2018
Abstract: Similar to parasites, malignant cells exploit the host for energy, resources and protection, thereby impairing host health and fitness. Although cancer is widespread in the animal kingdom, its impact on life history traits and strategies have rarely been documented. Devil facial tumour disease (DFTD), a transmissible cancer, afflicting Tasmanian devils (Sarcophilus harrisii), provides an ideal model system to monitor the impact of cancer on host life-history, and to elucidate the evolutionary arms-race between malignant cells and their hosts. Here we provide an overview of parasite-induced host life history (LH) adaptations, then both phenotypic plasticity of LH responses and changes in allele frequencies that affect LH traits of Tasmanian devils in response to DFTD are discussed. We conclude that akin to parasites, cancer can directly and indirectly affect devil LH traits and trigger host evolutionary responses. Consequently, it is important to consider oncogenic processes as a selective force in wildlife.
Conservation management of Tasmanian devils in the context of an emerging, extinction-threatening disease: Devil Facial Tumor Disease
Publisher: Springer Science and Business Media LLC
Date: 06-09-2007
Faecal glucocorticoid metabolite levels of intensive captive, free‐range captive and wild Tasmanian devils
Publisher: Wiley
Date: 05-06-2023
DOI: 10.1111/JZO.13072
Abstract: Captivity can alter the stress physiology and behaviour of an animal in both the short‐ and long‐term through repetitive exposure to novel stressors and, subsequently, may reduce the success of conservation efforts such as translocation and reintroduction. The Tasmanian devil ( Sarcophilus harrisii ) is threatened with extinction from a fatal facial tumour disease which has led to the establishment of an insurance meta‐population designed for future reintroductions of disease‐free devils. The meta‐population is comprised of intensive captive and free‐range captive environments however, no study has yet examined the long‐term physiological implications of captivity on devils. We used non‐invasive faecal glucocorticoid metabolite (FGM) monitoring to determine if there were any differences in adrenal activity among intensive captive, free‐range captive and wild devils. FGM levels were not age or sex dependent, and we found that all population types had similar intra‐population variability and mean FGMs. In conclusion, both types of captive environment appear to maintain stress profiles similar to wild devils.
The evolution of two transmissible cancers in Tasmanian devils
Publisher: Cold Spring Harbor Laboratory
Date: 27-05-2022
DOI: 10.1101/2022.05.27.493404
Abstract: Tasmanian devils have spawned two transmissible cancer lineages, named devil facial tumour 1 (DFT1) and devil facial tumour 2 (DFT2). We investigated the genetic ersity and evolution of these clones by analysing 78 DFT1 and 41 DFT2 genomes relative to a newly assembled chromosome-level reference. Time-resolved phylogenetic trees reveal that DFT1 first emerged in 1986 (1982-1989), and DFT2 in 2011 (2009-2012). Subclone analysis documents transmission of heterogeneous cell populations. DFT2 has faster mutation rates than DFT1 across all variant classes, including substitutions, indels, rearrangements, transposable element insertions and copy number alterations, and we identify a hypermutated DFT1 lineage with defective DNA mismatch repair. Several loci show plausible evidence of positive selection in DFT1 or DFT2, including loss of chromosome Y and inactivation of MGA , but none are common to both cancers. This study illuminates the parallel long-term evolution of two transmissible cancers inhabiting a common niche in Tasmanian devils.
Individual and temporal variation in pathogen load predicts long-term impacts of an emerging infectious disease
Publisher: Wiley
Date: 15-02-2019
DOI: 10.1002/ECY.2613
The Devil is in the detail: Conservation biology, animal philosophies and the role of animal ethics committees
Publisher: Royal Zoological Society of New South Wales
Date: 2012
DOI: 10.7882/FS.2012.040
Transmission dynamics of Tasmanian devil facial tumor disease may lead to disease-induced extinction
Publisher: Wiley
Date: 12-2009
DOI: 10.1890/08-1763.1
Abstract: Most pathogens threatening to cause extinction of a host species are maintained on one or more reservoir hosts, in addition to the species that is threatened by disease. Further, most conventional host-pathogen theory assumes that transmission is related to host density, and therefore a pathogen should become extinct before its sole host. Tasmanian devil facial tumor disease is a recently emerged infectious cancer that has led to massive population declines and grave concerns for the future persistence of this largest surviving marsupial carnivore. Here we report the results of mark-recapture studies at six sites and use these data to estimate epidemiological parameters critical to both accurately assessing the risk of extinction from this disease and effectively managing this disease threat. Three sites were monitored from before or close to the time of disease arrival, and at three others disease was well established when trapping began, in one site for at least 10 years. We found no evidence for sex-specific differences in disease prevalence and little evidence of consistent seasonal variation in the force of infection. At all sites, the disease was maintained at high levels of prevalence (>50% in 2-3-year-old animals), despite causing major population declines. We also provide the first estimates of the basic reproductive rate R0 for this disease. Using a simple age-structured deterministic model, we show that our results are not consistent with transmission being proportional to the density of infected hosts but are consistent with frequency-dependent transmission. This conclusion is further supported by the observation that local disease prevalence in 2-3-year-olds still exceeds 50% at a site where population density has been reduced by up to 90% in the past 12 years. These findings lend considerable weight to concerns that this host-specific pathogen will cause the extinction of the Tasmanian devil. Our study highlights the importance of rapidly implementing monitoring programs to determine how transmission depends on host density and emphasizes the need for ongoing management strategies involving a disease-free "insurance population," along with ongoing field monitoring programs to confirm whether local population extinction occurs.
Anthropogenic selection enhances cancer evolution in Tasmanian devil tumours
Publisher: Wiley
Date: 06-11-2014
DOI: 10.1111/EVA.12117
The tumour is in the detail: Local phylogenetic, population and epidemiological dynamics of a transmissible cancer in Tasmanian devils
Publisher: Wiley
Date: 20-06-2023
DOI: 10.1111/EVA.13569
Abstract: Infectious diseases are a major threat for bio ersity conservation and can exert strong influence on wildlife population dynamics. Understanding the mechanisms driving infection rates and epidemic outcomes requires empirical data on the evolutionary trajectory of pathogens and host selective processes. Phylodynamics is a robust framework to understand the interaction of pathogen evolutionary processes with epidemiological dynamics, providing a powerful tool to evaluate disease control strategies. Tasmanian devils have been threatened by a fatal transmissible cancer, devil facial tumour disease (DFTD), for more than two decades. Here we employ a phylodynamic approach using tumour mitochondrial genomes to assess the role of tumour genetic ersity in epidemiological and population dynamics in a devil population subject to 12 years of intensive monitoring, since the beginning of the epidemic outbreak. DFTD molecular clock estimates of disease introduction mirrored observed estimates in the field, and DFTD genetic ersity was positively correlated with estimates of devil population size. However, prevalence and force of infection were the lowest when devil population size and tumour genetic ersity was the highest. This could be due to either differential virulence or transmissibility in tumour lineages or the development of host defence strategies against infection. Our results support the view that evolutionary processes and epidemiological trade‐offs can drive host‐pathogen coexistence, even when disease‐induced mortality is extremely high. We highlight the importance of integrating pathogen and population evolutionary interactions to better understand long‐term epidemic dynamics and evaluating disease control strategies.
Is adaptive therapy natural?
Publisher: Public Library of Science (PLoS)
Date: 02-10-2018
Hematologic and serum biochemical reference intervals for wild Tasmanian devils (Sarcophilus harrisii)
Publisher: Wiley
Date: 27-11-2015
DOI: 10.1111/VCP.12304
Abstract: The Tasmanian devil (Sarcophilus harrisii) is a carnivorous marsupial threatened with extinction by a fatally infectious cancer known as devil facial tumor disease (DFTD). Conservation efforts including captive breeding and island translocations are underway to address this threat. The objectives of this study were to determine hematologic and serum biochemical reference intervals (RI) to aid in health assessment of Tasmanian devils, and to examine seasonal, sex, reproductive status and age variations. We collected jugular blood s les from in idual wild Tasmanian devils at 2 different locations over a 2-year period to determine hematologic and serum biochemical RI by nonparametric methods using the central 0.95 fraction. A total of 307 blood s les were collected from 187 devils. Significant age differences were found for ALP, CK, cholesterol, calcium, phosphate, albumin, globulins, albumin: globulin ratio, and glucose. Significant differences between sexes were observed for AST, creatinine, and potassium. Significant seasonal or reproductive status variation in adult males or breeding females were observed for PCV, HGB, RBC, MCHC, MCH, MCV, neutrophils and lymphocytes, fibrinogen, total plasma protein, AST, ALP, ALT, GLDH, bilirubin, urea, calcium, chloride, total protein, albumin, A:G, and glucose. Many of the differences observed between subgroups can be explained by growth requirements, reproductive demands, and seasonal effects on activity. This study has determined comprehensive RI for the Tasmanian devil, which will be used to assess animals targeted for captive breeding and translocations, or affected by DFTD.
Eco‐evolutionary perspectives of the dynamic relationships linking senescence and cancer
Publisher: Wiley
Date: 13-05-2015
Isotopic niche variation in Tasmanian devils Sarcophilus harrisii with progression of devil facial tumor disease
Publisher: Wiley
Date: 06-2021
DOI: 10.1002/ECE3.7636
Abstract: Devil facial tumor disease (DFTD) is a transmissible cancer affecting Tasmanian devils Sarcophilus harrisii . The disease has caused severe population declines and is associated with demographic and behavioral changes, including earlier breeding, younger age structures, and reduced dispersal and social interactions. Devils are generally solitary, but social encounters are commonplace when feeding upon large carcasses. DFTD tumors can disfigure the jaw and mouth and so diseased in iduals might alter their diets to enable ingestion of alternative foods, to avoid conspecific interactions, or to reduce competition. Using stable isotope analysis (δ 13 C and δ 15 N) of whiskers, we tested whether DFTD progression, measured as tumor volume, affected the isotope ratios and isotopic niches of 94 infected Tasmanian devils from six sites in Tasmania, comprising four eucalypt plantations, an area of smallholdings and a national park. Then, using tissue from 10 devils s led before and after detection of tumors and 8 devils where no tumors were detected, we examined whether mean and standard deviation of δ 13 C and δ 15 N of the same in iduals changed between healthy and diseased states. δ 13 C and δ 15 N values were generally not related to tumor volume in infected devils, though at one site, Freycinet National Park, δ 15 N values increased significantly as tumor volume increased. Infection with DFTD was not associated with significant changes in the mean or standard deviation of δ 13 C and δ 15 N values in in idual devils s led before and after detection of tumors. Our analysis suggests that devils tend to maintain their isotopic niche in the face of DFTD infection and progression, except where ecological conditions facilitate a shift in diets and feeding behaviors, demonstrating that ecological context, alongside disease severity, can modulate the behavioral responses of Tasmanian devils to DFTD.
The evolution of two transmissible cancers in Tasmanian devils
Publisher: American Association for the Advancement of Science (AAAS)
Date: 21-04-2023
Abstract: Tasmanian devils have spawned two transmissible cancer lineages, named devil facial tumor 1 (DFT1) and devil facial tumor 2 (DFT2). We investigated the genetic ersity and evolution of these clones by analyzing 78 DFT1 and 41 DFT2 genomes relative to a newly assembled, chromosome-level reference. Time-resolved phylogenetic trees reveal that DFT1 first emerged in 1986 (1982 to 1989) and DFT2 in 2011 (2009 to 2012). Subclone analysis documents transmission of heterogeneous cell populations. DFT2 has faster mutation rates than DFT1 across all variant classes, including substitutions, indels, rearrangements, transposable element insertions, and copy number alterations, and we identify a hypermutated DFT1 lineage with defective DNA mismatch repair. Several loci show plausible evidence of positive selection in DFT1 or DFT2, including loss of chromosome Y and inactivation of MGA , but none are common to both cancers. This study reveals the parallel long-term evolution of two transmissible cancers inhabiting a common niche in Tasmanian devils.
Genetic diversity, inbreeding and cancer
Publisher: The Royal Society
Date: 21-03-2018
Abstract: Genetic ersity is essential for adaptive capacities, providing organisms with the potential of successfully responding to intrinsic and extrinsic challenges. Although a clear reciprocal link between genetic ersity and resistance to parasites and pathogens has been established across taxa, the impact of loss of genetic ersity by inbreeding on the emergence and progression of non-communicable diseases, such as cancer, has been overlooked. Here we provide an overview of such associations and show that low genetic ersity and inbreeding associate with an increased risk of cancer in both humans and animals. Cancer being a multifaceted disease, loss of genetic ersity can directly (via accumulation of oncogenic homozygous mutations) and indirectly (via increased susceptibility to oncogenic pathogens) impact abnormal cell emergence and escape of immune surveillance. The observed link between reduced genetic ersity and cancer in wildlife may further imperil the long-term survival of numerous endangered species, highlighting the need to consider the impact of cancer in conservation biology. Finally, the somewhat incongruent data originating from human studies suggest that the association between genetic ersity and cancer development is multifactorial and may be tumour specific. Further studies are therefore crucial in order to elucidate the underpinnings of the interactions between genetic ersity, inbreeding and cancer.
Biting injuries and transmission of Tasmanian devil facial tumour disease
Publisher: Wiley
Date: 03-09-2013
DOI: 10.1111/J.1365-2656.2012.02025.X
Abstract: The Tasmanian devil is threatened with extinction by devil facial tumour disease (DFTD), a unique infectious cancer in which the tumour cells themselves, which derive from a single long-dead host devil, are the infective agent and the tumour is an infectious parasitic cell line. Transmission is thought to occur via direct inoculation of tumour cells when susceptible and infected in iduals bite each other or by fomitic transfer of tumour cells. The nature of transmission and the extent to which biting behaviour and devil ecology is associated with infection risk remains unclear. Until our recent study in north-west Tasmania showed reduced population and in idual impacts, DFTD had caused massive population declines in all populations monitored. In this paper, we investigate seasonal patterns of injuries resulting from bites between in iduals, DFTD infection status and tumour location in two populations to determine whether the number of bites predicts the acquisition of DFTD and to explore the possibility that the reduced impacts of DFTD in north-west Tasmania are attributed to reduced bite rates. Devils with fewer bites were more likely to develop DFTD and primary tumours occurred predominantly inside the oral cavity. These results are not consistent with transmission occurring from the biter to the bitten animal but suggest that dominant in iduals delivering bites, possibly by biting the tumours of other devils, are at higher risk of acquiring infection than submissive in iduals receiving bites. Bite rates, which were higher during autumn and winter, did not differ between sites, suggesting that the reduced population impacts in north-west Tasmania cannot be explained by lower bite rates. Our study emphasizes the importance of longitudinal studies of in idually marked animals for understanding the ecology and transmission dynamics of infectious diseases and parasites in wild populations.
Tracing the rise of malignant cell lines: Distribution, epidemiology and evolutionary interactions of two transmissible cancers in Tasmanian devils
Publisher: Wiley
Date: 28-06-2019
DOI: 10.1111/EVA.12831
Emergence, transmission and evolution of an uncommon enemy: Tasmanian devil facial tumour disease
Publisher: Cambridge University Press
Date: 14-11-2019
Identifying key questions in the ecology and evolution of cancer
Publisher: Wiley
Date: 28-02-1970
DOI: 10.1111/EVA.13190
Abstract: The application of evolutionary and ecological principles to cancer prevention and treatment, as well as recognizing cancer as a selection force in nature, has gained impetus over the last 50 years. Following the initial theoretical approaches that combined knowledge from interdisciplinary fields, it became clear that using the eco‐evolutionary framework is of key importance to understand cancer. We are now at a pivotal point where accumulating evidence starts to steer the future directions of the discipline and allows us to underpin the key challenges that remain to be addressed. Here, we aim to assess current advancements in the field and to suggest future directions for research. First, we summarize cancer research areas that, so far, have assimilated ecological and evolutionary principles into their approaches and illustrate their key importance. Then, we assembled 33 experts and identified 84 key questions, organized around nine major themes, to pave the foundations for research to come. We highlight the urgent need for broadening the portfolio of research directions to stimulate novel approaches at the interface of oncology and ecological and evolutionary sciences. We conclude that progressive and efficient cross‐disciplinary collaborations that draw on the expertise of the fields of ecology, evolution and cancer are essential in order to efficiently address current and future questions about cancer.
Transmissible cancer in Tasmanian devils: localized lineage replacement and host population response
Publisher: The Royal Society
Date: 07-09-2015
Abstract: Tasmanian devil facial tumour disease (DFTD) is a clonally transmissible cancer threatening the Tasmanian devil ( Sarcophilus harrisii ) with extinction. Live cancer cells are the infectious agent, transmitted to new hosts when in iduals bite each other. Over the 18 years since DFTD was first observed, distinct genetic and karyotypic sublineages have evolved. In this longitudinal study, we investigate the associations between tumour karyotype, epidemic patterns and host demographic response to the disease. Reduced host population effects and low DFTD infection rates were associated with high prevalence of tetraploid tumours. Subsequent replacement by a diploid variant of DFTD coincided with a rapid increase in disease prevalence, population decline and reduced mean age of the population. Our results suggest a role for tumour genetics in DFTD transmission dynamics and epidemic outcome. Future research, for this and other highly pathogenic emerging infectious diseases, should focus on understanding the evolution of host and pathogen genotypes, their effects on susceptibility and tolerance to infection, and their implications for designing novel genetic management strategies. This study provides evidence for a rapid localized lineage replacement occurring within a transmissible cancer epidemic and highlights the possibility that distinct DFTD genetic lineages may harbour traits that influence pathogen fitness.
The evolution of resistance and tolerance as cancer defences
Publisher: Cambridge University Press (CUP)
Date: 11-12-2019
DOI: 10.1017/S0031182019001501
Abstract: Although there is a plethora of cancer associated-factors that can ultimately culminate in death (cachexia, organ impairment, metastases, opportunistic infections, etc.), the focal element of every terminal malignancy is the failure of our natural defences to control unlimited cell proliferation. The reasons why our defences apparently lack efficiency is a complex question, potentially indicating that, under Darwinian terms, solutions other than preventing cancer progression are also important contributors. In analogy with host-parasite systems, we propose to call this latter option ‘tolerance’ to cancer. Here, we argue that the ubiquity of oncogenic processes among metazoans is at least partially attributable to both the limitations of resistance mechanisms and to the evolution of tolerance to cancer. Deciphering the ecological contexts of alternative responses to the cancer burden is not a semantic question, but rather a focal point in understanding the evolutionary ecology of host-tumour relationships, the evolution of our defences, as well as why and when certain cancers are likely to be detrimental for survival.
Simulating devil facial tumour disease outbreaks across empirically derived contact networks
Publisher: Wiley
Date: 23-01-2012
Sex bias in ability to cope with cancer: Tasmanian devils and facial tumour disease
Publisher: The Royal Society
Date: 21-11-2018
Abstract: Knowledge of the ecological dynamics between hosts and pathogens during the initial stages of disease emergence is crucial to understanding the potential for evolution of new interspecific interactions. Tasmanian devil ( Sarcophilus harrisii ) populations have declined precipitously owing to infection by a transmissible cancer (devil facial tumour disease, DFTD) that emerged approximately 20 years ago. Since the emergence of DFTD, and as the disease spreads across Tasmania, the number of devils has dropped up to 90% across 80% of the species's distributional range. As a result, the disease is expected to act as a strong selective force on hosts to develop mechanisms of tolerance and/or resistance to the infection. We assessed the ability of infected devils to cope with infection, which translates into host tolerance to the cancer, by using the reaction norm of the in idual body condition by tumour burden. We found that body condition of infected hosts is negatively affected by cancer progression. Males and females presented significant differences in their tolerance levels to infection, with males suffering declines of up to 25% of their body condition, in contrast to less than 5% in females. Sex-related differences in tolerance to cancer progression may select for changes in life-history strategies of the host and could also alter the selective environment for the tumours.
Life-history change in disease-ravaged Tasmanian devil populations
Publisher: Proceedings of the National Academy of Sciences
Date: 22-07-2008
Abstract: Changes in life history are expected when new sources of extrinsic mortality impact on natural populations. We report a new disease, devil facial tumor disease, causing an abrupt transition from iteroparity toward single breeding in the largest extant carnivorous marsupial, the Tasmanian devil ( Sarcophilus harrisii ), in which males can weigh as much as 14 kg and females 9 kg. This change in life history is associated with almost complete mortality of in iduals from this infectious cancer past their first year of adult life. Devils have shown their capacity to respond to this disease-induced increased adult mortality with a 16-fold increase in the proportion of in iduals exhibiting precocious sexual maturity. These patterns are documented in five populations where there are data from before and after disease arrival and subsequent population impacts. To our knowledge, this is the first known case of infectious disease leading to increased early reproduction in a mammal. The persistence of both this disease and the associated life-history changes pose questions about longer-term evolutionary responses and conservation prospects for this iconic species.
Transmissible cancer and longitudinal telomere dynamics in Tasmanian devils (Sarcophilus harrisii)
Publisher: Wiley
Date: 18-10-2022
DOI: 10.1111/MEC.16721
Abstract: A plethora of intrinsic and environmental factors have been shown to influence the length of telomeres, the protector of chromosome ends. Despite the growing interest in infection–telomere interactions, there is very limited knowledge on how transmissible cancers influence telomere maintenance. An emblematic ex le of transmissible cancer occurs in the Tasmanian devil ( Sarcophilus harrisii ), whose populations have been dramatically reduced by infectious cancer cells. To investigate associations between telomere dynamics and the transmissible cancer, we used longitudinal data from a Tasmanian devil population that has been exposed to the disease for over 15 years. We detected substantial temporal variation in in idual telomere length (TL), and a positive significant association between TL and age, as well as a marginally significant trend for devils with devil facial tumour disease (DFTD) having longer telomeres. A proportional hazard analysis yielded no significant effect of TL on the development of DFTD. Like previous studies, we show the complexity that TL dynamics may exhibit across the lifetime of organisms. Our work highlights the importance of long‐term longitudinal s ling for understanding the effects of wildlife diseases on TL.
Darwin, the devil, and the management of transmissible cancers
Publisher: Wiley
Date: 08-10-2020
DOI: 10.1111/COBI.13644
Two decades of the impact of Tasmanian Devil Facial Tumour Disease (DFTD)
Publisher: Oxford University Press (OUP)
Date: 26-10-2018
DOI: 10.1093/ICB/ICY118
Abstract: The Tasmanian devil, a marsupial carnivore, has been restricted to the island state of Tasmania since its extinction on the Australian mainland about 3000 years ago. In the past two decades, this species has experienced severe population decline due to the emergence of devil facial tumor disease (DFTD), a transmissible cancer. During these 20 years, scientists have puzzled over the immunological and evolutionary responses by the Tasmanian devil to this transmissible cancer. Targeted strategies in population management and disease control have been developed as well as comparative processes to identify variation in tumor and host genetics. A multi-disciplinary approach with multi-institutional teams has produced considerable advances over the last decade. This has led to a greater understanding of the molecular pathogenesis and genomic classification of this cancer. New and promising developments in the Tasmanian devil’s story include evidence that most immunized, and some wild devils, can produce an immune response to DFTD. Furthermore, epidemiology combined with genomic studies suggest a rapid evolution to the disease and that DFTD will become an endemic disease. Since 1998 there have been more than 350 publications, distributed over 37 Web of Science categories. A unique endemic island species has become an international curiosity that is in the spotlight of integrative and comparative biology research.
Transmissible cancer influences immune gene expression in an endangered marsupial, the Tasmanian devil (Sarcophilus harrisii)
Publisher: Wiley
Date: 15-03-2022
DOI: 10.1111/MEC.16408
Abstract: Understanding the effects of wildlife diseases on populations requires insight into local environmental conditions, host defence mechanisms, host life‐history trade‐offs, pathogen population dynamics, and their interactions. The survival of Tasmanian devils ( Sarcophilus harrisii ) is challenged by a novel, fitness limiting pathogen, Tasmanian devil facial tumour disease (DFTD), a clonally transmissible, contagious cancer. In order to understand the devils’ capacity to respond to DFTD, it is crucial to gain information on factors influencing the devils’ immune system. By using RT‐qPCR, we investigated how DFTD infection in association with intrinsic (sex and age) and environmental (season) factors influences the expression of 10 immune genes in Tasmanian devil blood. Our study showed that the expression of immune genes (both innate and adaptive) differed across seasons, a pattern that was altered when infected with DFTD. The expression of immunogbulins IgE and IgM:IgG showed downregulation in colder months in DFTD infected animals. We also observed strong positive association between the expression of an innate immune gene, CD16, and DFTD infection. Our results demonstrate that s ling across seasons, age groups and environmental conditions are beneficial when deciphering the complex ecoevolutionary interactions of not only conventional host‐parasite systems, but also of host and diseases with high mortality rates, such as transmissible cancers.
Infection of the fittest: devil facial tumour disease has greatest effect on individuals with highest reproductive output
Publisher: Wiley
Date: 10-05-2017
DOI: 10.1111/ELE.12776
Conservation implications of limited genetic diversity and population structure in Tasmanian devils (Sarcophilus harrisii)
Publisher: Springer Science and Business Media LLC
Date: 07-02-2017
The ecology and evolution of wildlife cancers: Applications for management and conservation
Publisher: Wiley
Date: 23-03-2020
DOI: 10.1111/EVA.12948
Abstract: Ecological and evolutionary concepts have been widely adopted to understand host–pathogen dynamics, and more recently, integrated into wildlife disease management. Cancer is a ubiquitous disease that affects most metazoan species however, the role of oncogenic phenomena in eco‐evolutionary processes and its implications for wildlife management and conservation remains undeveloped. Despite the pervasive nature of cancer across taxa, our ability to detect its occurrence, progression and prevalence in wildlife populations is constrained due to logistic and diagnostic limitations, which suggests that most cancers in the wild are unreported and understudied. Nevertheless, an increasing number of virus‐associated and directly transmissible cancers in terrestrial and aquatic environments have been detected. Furthermore, anthropogenic activities and sudden environmental changes are increasingly associated with cancer incidence in wildlife. This highlights the need to upscale surveillance efforts, collection of critical data and developing novel approaches for studying the emergence and evolution of cancers in the wild. Here, we discuss the relevance of malignant cells as important agents of selection and offer a holistic framework to understand the interplay of ecological, epidemiological and evolutionary dynamics of cancer in wildlife. We use a directly transmissible cancer (devil facial tumour disease) as a model system to reveal the potential evolutionary dynamics and broader ecological effects of cancer epidemics in wildlife. We provide further ex les of tumour–host interactions and trade‐offs that may lead to changes in life histories, and epidemiological and population dynamics. Within this framework, we explore immunological strategies at the in idual level as well as transgenerational adaptations at the population level. Then, we highlight the need to integrate multiple disciplines to undertake comparative cancer research at the human–domestic–wildlife interface and their environments. Finally, we suggest strategies for screening cancer incidence in wildlife and discuss how to integrate ecological and evolutionary concepts in the management of current and future cancer epizootics.
Rate of intersexual interactions affects injury likelihood in Tasmanian devil contact networks
Publisher: Oxford University Press (OUP)
Date: 25-04-2019
Abstract: Identifying the types of contacts that result in disease transmission is important for accurately modeling and predicting transmission dynamics and disease spread in wild populations. We investigated contacts within a population of adult Tasmanian devils (Sarcophilus harrisii) over a 6-month period and tested whether in idual-level contact patterns were correlated with accumulation of bite wounds. Bite wounds are important in the spread of devil facial tumor disease, a clonal cancer cell line transmitted through direct inoculation of tumor cells when susceptible and infected in iduals bite each other. We used multimodel inference and network autocorrelation models to investigate the effects of in idual-level contact patterns, identities of interacting partners, and position within the social network on the propensity to be involved in bite-inducing contacts. We found that males were more likely to receive potentially disease-transmitting bite wounds than females, particularly during the mating season when males spend extended periods mate-guarding females. The number of bite wounds in iduals received during the mating season was unrelated to any of the network metrics examined. Our approach illustrates the necessity for understanding which contact types spread disease in different systems to assist the management of this and other infectious wildlife diseases.
Age‐related variation in the trophic characteristics of a marsupial carnivore, the Tasmanian devil Sarcophilus harrisii
Publisher: Wiley
Date: 07-2020
DOI: 10.1002/ECE3.6513
Contact networks in a wild Tasmanian devil (Sarcophilus harrisii) population: Using social network analysis to reveal seasonal variability in social behaviour and its implications for transmission of devil facial tumour disease
Publisher: Wiley
Date: 11-2009
DOI: 10.1111/J.1461-0248.2009.01370.X
Abstract: The structure of the contact network between in iduals has a profound effect on the transmission of infectious disease. Using a novel technology--proximity sensing radio collars--we described the contact network in a population of Tasmanian devils. This largest surviving marsupial carnivore is threatened by a novel infectious cancer. All devils were connected in a single giant component, which would permit disease to spread throughout the network from any single infected in idual. Unlike the contact networks for many human diseases, the degree distribution was not highly aggregated. Nevertheless, the empirically derived networks differed from random networks. Contact networks differed between the mating and non-mating seasons, with more extended male-female associations in the mating season and a greater frequency of female-female associations outside the mating season. Our results suggest that there is limited potential to control the disease by targeting highly connected age or sex classes.
Fifth International Biannual Evolution and Ecology of Cancer Conference (Cooperation, Conflict and Parasitism) meeting report—Wellcome Genome Campus, Hinxton, UK
Publisher: Wiley
Date: 11-2019
DOI: 10.1111/EVA.12862
Faecal glucocorticoid metabolite levels of intensive captive, free-range captive, and wild Tasmanian devils
Publisher: Cold Spring Harbor Laboratory
Date: 11-01-2023
DOI: 10.1101/2023.01.11.523346
Abstract: Captivity can alter the stress physiology and behaviour of an animal in both the short- and long-term through repetitive exposure to novel stressors and, subsequently, may reduce the success of conservation efforts such as translocation and reintroduction. The Tasmanian devil ( Sarcophilus harrisii ) is threatened with extinction from a fatal facial tumour disease which has led to the establishment of an insurance meta-population designed for future reintroductions of disease-free devils. The meta-population is comprised of intensive captive and free-range captive environments however, no study has yet examined the long-term physiological implications of captivity on devils. We used non-invasive faecal glucocorticoid metabolite (FGM) monitoring to determine if there were any differences in adrenal activity between intensive captive, free-range captive, and wild devils. FGMs were not age- or sexdependent, and we found that all population-types had similar intra-population variability and mean FGMs. In conclusion, both types of captive environment maintain stress profiles similar to wild devils.
Transmissible cancer and the evolution of sex
Publisher: Public Library of Science (PLoS)
Date: 06-06-2019
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Discovery Early Career Researcher Award - Grant ID: DE170101116
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Funder: Australian Research Council
View Funded ActivityDiscovery Projects - Grant ID: DP230100162
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View Funded ActivityLinkage Projects - Grant ID: LP170101105
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