In the areas already surveyed, the disease has the most dramatic effect in those with high-density populations with up to 100% mortality of resident devils in 12-18 months. In lower density areas, population decline has been less marked. The disease appears to kill most devils once they reach adulthood, with a few juveniles affected. In the medium term, there is some population recovery but populations are made up mostly of young animals.
DFTD begins as lesions and lumps around the mouth. The lesions and lumps develop into cancerous tumours that spread from the face to the entire body. The tumours interfere with feeding, and the affected animal may starve to death.
Using cultures of the cancerous tissue to study the condition, researchers have identified the cancer as neuroendocrine in nature, and all cancer cells have identical chromosomal rearrangements. A virus was initially thought to be the cause of DFTD, but no evidence of such a virus could be detected in the cancer cells. The cancer cells themselves are an infective agent, with transmission of the disease occurring by biting, feeding on the same material, and aggressive mating. Final confirmation of this came when researcher Anne-Maree Pearse and colleagues found an infected animal that had a chromosomal abnormality in its nontumorous cells that did not appear in its tumour cells, proving that the tumour cells could not be descended from the animal's own cells.
No definitive conclusion can be drawn at this stage from the results of the histology. However the use of immunohistochemistry has shown that the most consistent tumour type isolated appears to be of a neuroendocrine origin.
Cytogenetics work has established the Normal Tasmanian Devil karyotype and the chromosome rearrangements of the tumour. This has led to the hypothesis that DFTD may be directly passed from animal to animal by implantation of the cell line during fighting and biting.
