The Pathology of Devil Facial Tumor Disease (DFTD) in Tasmanian Devils (<i>Sarcophilus harrisii</i>)

Loh, Richmond; Bergfeld, Jemma; Hayes, Dane; O’Hara, A.J.; Pyecroft, Stephen; Raidal, Shane R.; Sharpe, Robert W.

doi:10.1354/vp.43-6-890

Cited by 158 publications

(214 citation statements)

References 3 publications

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“…DFTD tumors associated with the DFT1 clone are generally composed of pleomorphic round cells arranged in distinct bundles, cords or packets (5). In contrast, the tumors from RV and SN were characterized by sheets of pleomorphic (amorphic to stellate and fusiform) cells arranged in a solid pattern (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…DFTD is spread between Tasmanian devils by biting and causes tumors usually on the face or inside the mouth ( Fig. 1) (4,5). DFTD readily metastasises, and the disease usually causes death of affected animals within months of the appearance of symptoms (4,5).…”

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confidence: 99%

“…1) (4,5). DFTD readily metastasises, and the disease usually causes death of affected animals within months of the appearance of symptoms (4,5). Since it was first observed in 1996 in northeast Tasmania, DFTD has spread through most of Tasmania and has triggered widespread devil population declines (Fig.…”

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confidence: 99%

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A second transmissible cancer in Tasmanian devils

Pye

Pemberton²,

Tovar

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

207

328

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Clonally transmissible cancers are somatic cell lineages that are spread between individuals via the transfer of living cancer cells. There are only three known naturally occurring transmissible cancers, and these affect dogs, soft-shell clams, and Tasmanian devils, respectively. The Tasmanian devil transmissible facial cancer was first observed in 1996, and is threatening its host species with extinction. Until now, this disease has been consistently associated with a single aneuploid cancer cell lineage that we refer to as DFT1. Here we describe a second transmissible cancer, DFT2, in five devils located in southern Tasmania in 2014 and 2015. DFT2 causes facial tumors that are grossly indistinguishable but histologically distinct from those caused by DFT1. DFT2 bears no detectable cytogenetic similarity to DFT1 and carries a Y chromosome, which contrasts with the female origin of DFT1. DFT2 shows different alleles to both its hosts and DFT1 at microsatellite, structural variant, and major histocompatibility complex (MHC) loci, confirming that it is a second cancer that can be transmitted between devils as an allogeneic, MHC-discordant graft. These findings indicate that Tasmanian devils have spawned at least two distinct transmissible cancer lineages and suggest that transmissible cancers may arise more frequently in nature than previously considered. The discovery of DFT2 presents important challenges for the conservation of Tasmanian devils and raises the possibility that this species is particularly prone to the emergence of transmissible cancers. More generally, our findings highlight the potential for cancer cells to depart from their hosts and become dangerous transmissible pathogens.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

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A second transmissible cancer in Tasmanian devils

Pye

Pemberton²,

Tovar

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

207

328

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“…Since its first appearance in northeastern Tasmania in 1996, the infection has spread across most of the range of Tasmanian devils, causing population declines of up to 90 per cent in affected populations [69]. The disease manifests as large tumours, particularly around the head of the affected animal, and is inevitably fatal once clinical signs are apparent [75,76]. In populations with MHC types similar to the tumour [73], prevalence increases rapidly after the initial arrival of the disease, affecting the majority of the adult population within 3-4 years ( figure 3).…”

Section: Current Extinctionsmentioning

confidence: 99%

Disease and the dynamics of extinction

McCallum

2012

Phil. Trans. R. Soc. B

131

122

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Invading infectious diseases can, in theory, lead to the extinction of host populations, particularly if reservoir species are present or if disease transmission is frequency-dependent. The number of historic or prehistoric extinctions that can unequivocally be attributed to infectious disease is relatively small, but gathering firm evidence in retrospect is extremely difficult. Amphibian chytridiomycosis and Tasmanian devil facial tumour disease (DFTD) are two very different infectious diseases that are currently threatening to cause extinctions in Australia. These provide an unusual opportunity to investigate the processes of disease-induced extinction and possible management strategies. Both diseases are apparently recent in origin. Tasmanian DFTD is entirely host-specific but potentially able to cause extinction because transmission depends weakly, if at all, on host density. Amphibian chytridiomycosis has a broad host range but is highly pathogenic only to some populations of some species. At present, both diseases can only be managed by attempting to isolate individuals or populations from disease. Management options to accelerate the process of evolution of host resistance or tolerance are being investigated in both cases. Anthropogenic changes including movement of diseases and hosts, habitat destruction and fragmentation and climate change are likely to increase emerging disease threats to biodiversity and it is critical to further develop strategies to manage these threats.

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“…In devils with advanced disease, the tumor may metastasize to a range of internal organs, such as regional lymph nodes, lung, spleen, liver, and kidney. After showing signs of the disease, animals die within 5-6 months and, to date, it is believed that no affected devil has recovered (Hawkins et al, 2006;Loh et al, 2006a).…”

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A Histological and Immunohistochemical Analysis of Lymphoid Tissues of the Tasmanian Devil

Kreiss

Obendorf

Hemsley

et al. 2009

The Anatomical Record

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Tasmanian devil lymphoid tissues (thymus, spleen, and lymph node) from seven animals, including pouch young, juvenile, and adult devils, were investigated using histological and immunohistochemical techniques. Antibodies against the conserved intracytoplasmic portion of CD3 and CD79b (T-and B-cell markers, respectively) and MHC II were used to label immune cells. The thymus from the juvenile devils and the pouch young had CD3þ cells that were primarily located in the medulla of the organ. The spleen consisted of red and white pulp areas with characteristic lymphoid follicles with CD79bþ and MHC IIþ cells and nonfollicular T-cell-dominated periarteriolar lymphoid sheaths. Peripheral lymph nodes presented three distinct regions, outer cortex and medulla (both with primarily CD79bþ and MHC IIþ cells) and paracortex (mainly CD3þ cells). Tissue architecture and distribution of the immune cells were similar to that seen in eutherian mammals and other marsupials, indicating that the Tasmanian devil has all the structural elements necessary for effective adaptive immunity. Anat Rec, 292:611-620, 2009. V V C 2009 Wiley-Liss, Inc.

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The Pathology of Devil Facial Tumor Disease (DFTD) in Tasmanian Devils (Sarcophilus harrisii)

Cited by 158 publications

References 3 publications

A second transmissible cancer in Tasmanian devils

A second transmissible cancer in Tasmanian devils

Disease and the dynamics of extinction

A Histological and Immunohistochemical Analysis of Lymphoid Tissues of the Tasmanian Devil

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