AETIOLOGY AND EPIDEMIOLOGY
DFT1 is a transmissible cancer that is transferred between Tasmanian devils by direct cell transfer through biting during social interactions (Hamede et al. 2013; Wells et al. 2017) and is the primary cause of DFTD within free- ranging populations.
It is of Schwann cell or Schwann cell precursor origin (Murchison et al. 2010; Murchison et al. 2012) and is believed to have arisen from a single female Tasmanian devil (Pearse and Swift 2006; Pearse et al. 2012). Since its emergence it has spread as a clone through free-ranging populations and has a 100% mortality rate in severely affected animals. The tumours are solid masses of variable size with an irregular surface usually contained within a pseudo-capsule and situated SC, progressing to erosion and ulceration of the overlying skin. They are generally found around the head and neck (a result of predominantly face-to-face interactions between individuals) and commonly within the oral and buccal cavities, where they appear plaque-like, particularly in the early stages before proliferating to more vegetative lesions. Primary tumours are found less frequently in other locations. Metastasis occurs haematogenously and is rapid, with regional lymph nodes associated with the primary tumours most commonly affected.Preclinical periods from infection to observable signs of disease (latency) are largely undetermined, but anecdotal evidence from capture-mark-recapture studies suggests a latent period of 2-13 mo (unpublished).
From 1996 to 2020 free-ranging Tasmanian devil populations are estimated to have declined from 53 000 to 16 900 with >90% of the species range presently containing DFTD (Cunningham et al. 2021). This equates to estimates of ~77% decline of Tasmanian devil numbers in areas where DFTD is present with ongoing small declines continuing in these areas. Interestingly though in one study site there was an increase in population density 8-10 yr post initial infection (Lazenby et al.
2018). Variation from predicted Tasmanian devil population responses, revealed by more than 20 yr of DFTD surveillance, has been investigated indicating a mix of host density, tumour genomic differences and other co-evolutionary drivers playing a role (Kozakiewicz et al. 2020; Hamede et al. 2023).Vertical transmission of DFT1 has not been demonstrated in long-term studies of managed populations. Even the weaned or orphaned young of severely affected mothers remained unaffected, as did subsequent generations from these animals.
Pye et al. (2016b) described a second transmissible tumour, devil facial tumour 2 (DFT2) from five animals found in the D'Entrecasteaux Channel Peninsula area of south-eastern Tas. from 2014-15. It is grossly indistinguishable from the far more common DFT1, but is histologically, immunohistochemically and cytogenetically distinct. It is believed to be transmissible based on genetic evidence of the presence of a Y chromosome (and so different from DFT1, which has no Y chromosome because it arose from a female) and different alleles to both host and DFT1 at microsatellite, structural variant and major histocompatibility complex (MHC) loci. No specific transmission evidence has been demonstrated for DFT2, but if so, it would appear that Tasmanian devils may be prone to developing cancers that can be somatically transferred as a clone. Given the paucity of cases of DFT2 and the widespread nature of DFT1, most of the research and understanding of DFTD relates to the original cancer and unless stated specifically within this chapter it should be assumed the information applies to DFT1.
2.