Tasmanian Times

David Obendorf

Why the devils are dying?

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

Author Credits: [show_post_categories parent="no" parentcategory="writers" show = "category" hyperlink="yes"]


  1. pat synge

    February 16, 2005 at 4:54 pm

    Hypotheses are sometimes useful, sometimes not. It might be useful to know that Devil populations have crashed previously and, who knows, this might even be relevant to what is happening now. Especially if it could be shown that such crashes were caused by a similar disease rather than cyclical population fluctuations brought on by climatic or other factors. This would not necessarily prove that the cause was the same but might, for example, simply indicate that Devils have a susceptibility to this disease and when stressed (eg by overpopulation, hunger, poison or some other factor) have less resistance to it.

    Perhaps I am one of the “usual suspects” in suggesting that one of the contributing factors might be poison but I can assure Kevin Bonham that I suggest this in good faith. If I have a bias against forestry as most of it is practised here in Tasmania this is based on some specialist knowledge and sound reason, not prejudice. If I also believe that the widespread and indiscriminate use of poison is immoral, unjustifiable and likely to have widespread ramifications this does not indicate any lack of “good faith”.

    It’s certainly not unreasonable to suggest that research should be undertaken into whether the long term use of a wide range of toxic chemicals in both forestry and farming might be a factor in DFTD.

    I note that in the recently released DPIWE progress report there is mention that a pilot trial “is proposed” (page 27 of 29) in which Devil cell cultures would be exposed to a range of toxins and, if any changes are noted, that this would indicate that a much larger project is warranted.

    Not being a specialist I suppose it’s presumptious of me to suggest that this seems a rather simplistic approach. Perhaps a more holistic approach taking into account immune system response to toxin ingestion might also be appropriate? Has research already been undertaken in this area that may be relevant or would it be necessary to experiment on healthy Devils?

    This would, of course, be a devil of an ethical dilemma.

    Pat Synge

  2. Dr Kevin Bonham

    February 15, 2005 at 5:38 pm

    Generally a welcome contribution to the debate, as one would hope for from someone who actually knows what they are talking about on issues of this type.

    I must quibble with one thing Dr Obendorf says – his claim that the proposal of causes by “members of the general public” (read: “the usual suspects and a few sundry others”) has been “in good faith”. In cases it has been, while in other cases it has been clear that people already biased against certain industries (primarily forestry) have jumped to the conclusion that industry is to blame. Both in common ethical belief and in law, a public statement made with inadequate consideration and motivated by bias, malice or political intent is not “good faith” but its direct opposite!

    A few other comments:

    The Menna Jones theory that population crashes may be an artefact of the last 200 years of post-European-settlement impacts is only, as Jones makes clear in the quote above, a hypothesis, although it is clearly a very plausible one. The logical alternative is that such crashes may also have happened prior to European settlement and may indeed be a more or less normal event in the species’ long-term history. If such an alternative has been disproved I would be very interested in hearing of it.

    Also, if the (again plausible) “single rotten apple” hypothesis proposed by Dr Obendorf is correct, then the event triggering the disease would only have to have affected one devil to start with, and could have been more or less anything capable of having that impact. In this scenario, assuming that the initial spark must be something that is currently common or increasing in use (the line of attack some have pursued)would clearly be premature.

  3. pat synge

    February 13, 2005 at 2:51 am

    Thankyou, David Obendorf, for continuing to make the effort to help us in understanding the current situation re DFTD and for presenting your “desktop hypotheses” in this forum.

    David notes that Devils in captivity and in Wildlife Parks do not seem to be suffering from DFTD like those in the wild and suggests that the fact that they are isolated from diseased Devils may be the reason – which would seem entirely logical if the disease is contagious.

    If chemical ingestion plays a role in increasing susceptibility (by, perhaps, compromising the immune system response) the reasonable supposition that captive Devils do not eat poisoned carcasses might also contribute to their freedom from DFTD.

    It is my understanding that links between chemical ingestion and disease is extremely difficult to research but I would be interested to know what work (if any) is currently being undertaken in this area in relation to DFTD.

    Pat Synge

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