The primary cause of the malignant cancer, colloquially called Devil Facial Tumour Disease, still remains a mystery.

Readers would be aware of the various cause-effect associations that have been proposed in good faith, by members of the general public.

These include:

(1) The potential for environmental triggers such as bio-accumulated chemicals.

(2) The switching on of one or more oncogenes*1 that may exist in the devils genome, and

(3) The possible transfer of a tumour-causing virus from another animal to the devil.

The Devil is in the detail

Since European settlement there have been documented reports of Tasmanian devils experiencing population crashes. At least three major declines in devils where identified by the well-known Tasmanian zoologist, Dr Eric Guiler.

His observations were supported by another eminent zoologist, Mr Bob Green of the Victoria Museum in Launceston. They discovered that devils had reached very low densities on at least three occasions in the last 150 years (in the decades of 1850s, 1900s and 1940s).

Depending on the intensity of these population crashes, there is a strong likelihood that these crashes caused genetic selection and lessened the overall genetic diversity within the devil population. In fact Dr Menna Jones published work on Tasmanian devil populations across its range has shown just that.

Menna wrote:

“It is possible that the repeated reductions and expansions of devil populations are a phenomenon only of the last 200 years since the European settlement of Tasmania. Conversion of a large proportion of the dry forests within devil core range to a patchy mosaic of grazing land and forest remnants (excluding extensively cleared areas which have a detrimental effect on devil populations) is likely to have resulted in increased numbers of prey species (wombats, macropods and brush-tail possums) with a concomitant long term increase in devil populations. Since pastoral development in the early 1800s, devil populations may have reached unnaturally high densities at times, conditions conducive to epidemic spread of diseases……”

The genetic and allelic diversity [in devils] is uniformly low in all sub-populations [sampled].

One explanation for the low levels of genetic variability in Tasmanian devils is that the genetic diversity has been compromised by the repeated, extended periods of low population density in Tasmanian devils [i.e. population crashes].*2

Her meticulous field work and tenacity

At the October 2003 workshop Menna and I proposed that these populations crashes could be causing genetic diversity to be significantly reduced and that this characteristic could be a genetic ‘trigger’ priming the devil population to increased disease susceptibility.

Prior to joining the DPIWE DFTD team, Dr Jones worked as a university-based research zoologist specialising on the biology of Tasmanian large dasyurids (the two quoll species and devils). Indeed Menna was the person who in 2001 alerted the State fauna authority that devils were dying from this cancer. Menna had eye-witnessed the demise of devils at her field study sites on the East Coast of Tasmania. But for her meticulous field work and tenacity, this disease may well have gone unnoticed. Menna also worked with Androo Kelly at Trowunna Wildlife Park and together with film producer, David Parer in capturing on camera the up close and personal life of Tasmanian Devils*3.

If we take these understandings about the biology of the devil and combine it with the basic knowledge we have on the way this cancer expresses itself in devil populations, a plausible hypothesis for this transmission of this disease can be proposed.

In May 2004, I presented this theory to the DFTD Taskforce scientists. Click for diagram [80Kb]. It is a theory that can be tested.

One rotten apple in the barrel

To date no cases of DFTD have been diagnosed from captive devils from Tasmania Wildlife Parks. I did a review of the tumour cases in devils from zoos in 1993 and although devils are quite prone to a range of sarcomatous cancers there have been no unusual clusters of facial cancers that mimic DFTD in the literature.

As mentioned earlier on Tasmanian Times, Tasmania’s shame: The Devil Disease, it is universally acknowledged that this is a highly unusual cancer in both its apparent infectious nature of spread and its very high attack rate within populations.

One important and perhaps obvious difference between captive populations of devils and wild populations of devils would be the opportunity for direct contact with cancerous devils and therefore access to living tumour material. Other things equal between devils in captivity and in the wild, the wild populations with cancerous individuals do have direct contact and access to obviously cancerous devils whilst the captive devils do not.

Fighting and facial biting are a recognised behavioural trait of devils, as David Parer’s film on Devils exquisitely shows, and that behaviour occurs in both in captivity and the wild.

Thousands of 1080-poisoned marsupial carcases

Tasmanian Devils scientific name is Sarcophilus, it means ‘lover of meat’. And the meat they eat comes in a variety of forms – sick, injured & dead wildlife, roadkills, dead farm animals and of course thousands of 1080-poisoned marsupial carcases.

Cannibalism is also a recognised feature of Tasmanian devil behaviour; in fact it is the recognised way the muscle parasite, Trichinella pseudospiralis survives amongst devils. This parasite was only discovered in the early 1990s when devil numbers were considered to be at record high levels.

In wildlife parks any captive devils with obvious facial or skin cancers would be taken off exhibit, assessed by vets and usually euthanased before they died of the cancer. Consequently cannibalisation of cancerous devils in captivity would not be the norm and wouldn’t be permitted. The physical absence of contact with diseased devils might simply explain why the DFTD cancer doesn’t occur in captive devil populations and could also provide the explanation for why this cancer has spread between devils in high density wild populations. This theory is very unique but it does plausibly explain what has been observed.

Menna’s initial work and the further field studies by the Taskforce demonstrated that this cancer spreads rapidly within a population, very much like an animal-to-animal infectious contagion would behave.

This is where the one rotten apple in the barrel concept is a good simile.

Here’s the set up:

• A particularly unique type of cancer develops in an index devil (the rotten apple). (Ann Maree Pearce’s work confirms that chromosome rearrangements of all the DFTD tumours so far tested from affected devils are identical regardless of the gender of the devil.)
• An ‘inbred’ devil population that is so highly related to one another that the normal rejection of transplanted cells from another devil breaks down (a barrel of identical apples).
• Devil-devil behaviours (social contact) and opportunities for transmission (fighting-biting & cannibalism).
• In nature the cancer is fatal, however, diseased devils, particularly adults, may continue to express normal fighting-biting behaviours right up until seriously weakened by the cancer. These cancerous devils are available for consumption by other devils in the population.

I believe the hypothesis can be tested experimentally with the minimum of difficulty.

If the DFTD diagnostic team has been successful at culturing the tumour cell lines in vitro (i.e. in the laboratory test tube) then they can begin to test parts of this theory. Even without this capability they could be implanting tumour cells as inoculated ‘grafts’ from cancerous devils to healthy devils and then looking at whether there is any establishment and tumour growth in those new host devils.

In the absence of any other plausible alternative (1) to find an external cause or trigger and (2) to explain the high attack rate and almost contagion like spread, I offer this desktop hypothesis.

The thoughts and opinions of readers are welcomed.

*1. Oncogene – a gene with the potential to initiate cancerous proliferation of cells.
*2. Jones M.E. et al 2004 Genetic diversity and population structure of Tasmanian devils, the largest marsupial carnivore.
*3. ‘Terrors in Tasmania’ – A Film by David Parer and Elizabeth Parer-Cook, ABC Natural History Unit

A bio of Dr David Obendorf is on the earlier article:
Tasmania’s shame: The Devil Disease,

For the major debate, go to COMMENTS on:
Chemical fears. The Devil Disease