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Authors: David Owen

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Persecution of devils continues, despite the threat to them from DFTD. The remains of
these persecuted devils were found in a bag by the side of a road in 2004. (Courtesy
Nick Mooney)

This may only point to the Tasmanian devil not caring for urban environments and being more common in the bush. The ease of capture supports the contention of probably high human-induced mortality rates of devils during that era of intense thylacine trapping.

Tasmanian devils may well have undergone a decline early in the 1900s, but there is no hard evidence disease was the cause. What is certain is that persecution of the animal by a variety of means, together with land clearing, affected the population through unnatural reduction in numbers and population displacement and fragmentation. Any high-density population today that suffered mortalities of eight animals a night, as reported by Stevenson, would be wiped out in a few years.

In 1999 Menna Jones, researching devils along Tasmania's east coast, observed some with tumours near Little Swanport, more than 250 kilometres south of where Baars had taken his photographs in 1996. Two years later she trapped three tumorous devils on the Freycinet Peninsula. Her subsequent monitoring there indicated that the peninsula's population was in serious decline.

Nick Mooney's trapping made him painfully aware of how the disease was spreading. In March 2003 he wrote an internal Parks and Wildlife departmental memo calling for more assistance to combat the problem. That meant funding. The memo's advice and recommendations were not acted on, despite government knowledge of the seriousness of the issue: in answer to a question in Parliament on 20 August 2003, Environment Minister Bryan Green stated that in some areas devil populations had crashed by 85 per cent. Instead of funding, for baseline studies in particular, an essentially cost-free working group was formed, comprising veterinarians, wildlife specialists and veterinary pathologists.

Mooney went public. On 1 September 2003, the front-page headline in
The Mercury
read, ‘Tassie Devil Under Threat'. The report, and a detailed feature on the problem, meant that for the first time the public became aware of the bizarre DFTD and its potentially disastrous consequence of extinction. Among the disturbing revelations: that virtually nothing was known about the disease, its origins, or whether or how it was transferred from animal to animal; that it spread through the body, and dissolved skull bone; that Tasmania's government animal health laboratory, at Mount Pleasant in Launceston, had neither the expertise nor staff to investigate it; that quarantining devils on islands (or repopulating the mainland) carried risks because even healthy-looking devils might be carriers; that devils might now be fatally susceptible to an emerging fox population; that research could take three years or more to establish the genetic sequence of a virus, should the disease be caused by a virus; that environmental pollutants might be involved; and that the disease might be capable of crossing to other species such as quolls.

One positive, if it could be called that, lay in the slow travelling speed of DFTD through areas of dispersed devil populations. In those areas the natural breeding patterns might be sufficient to match the disease.

Wildlife park owner Androo Kelly noted that low devil numbers left them more vulnerable than ever to persecution through poisoning, trapping and shooting, and he also took issue with political insensitivity to wildlife:

There's a new culture in the top level of government. Wildlife is just tucked in with primary industries and the agenda is primary-industry driven. We don't do enough about wildlife disease. People outside this State can't believe that we don't have a response to something affecting such an icon animal in our environment . . . We don't give them enough respect.
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How best, then, to tackle the mystery disease? The scientific starting point for DFTD assumed that it could be a retrovirus, that is, a virus occurring naturally in devil DNA but lying dormant until triggered, at which point it attacks cell DNA. Small lumps or lesions first appear in and around the mouth, which grow rapidly into tumours. Death through breakdown of body functions and starvation usually occurs within five months.
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The analysis is essentially a two-step process. Identifying the type of cancer cells involved is the first step, but is a complex one, since it involves analysing cancerous cells which have changed dramatically from when they were healthy. Equally important is identifying from what part of the body they originated, such as from muscles, lymph or skin. Once the type of cancer has been determined, the second step is to identify the possible causes of the disease, namely the trigger or triggers. Speculation as to those would ensure that Tasmania's newest environmental problem would not be confined to laboratory microscopes.

In fact, the next day a revelation about the Mooney Parks and Wildlife memo intensified focus on the political response to the crisis, as two versions of Mooney's document came to light. In the original, written as a brief to inform Environment Minister Green of the situation, Mooney had written that funding for baseline monitoring of devils had been ‘recommended on many occasions but never resourced',
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and that new funds were needed to investigate the disease. The Tasmanian Greens party made this document public. The second, altered version—the ‘official' memo which landed on Green's desk— omitted this critical phrase (critical in both senses of the word), and also said that the situation would be dealt with within the current budget.

Ironically, back in 1987 monitoring studies had been recommended for the Mount William area—precisely where, nine years later, Baars was to provide graphic evidence of the disease.

At this point, with a few thousand dollars shifted from other projects, Mooney and a visiting US colleague, Marco Restani, embarked on a statewide snapshot survey, which was to prove of critical importance. Forty sites were chosen across the state, excepting the southwest, and

. . . each of these 40 sites was sampled for one night with 30 traps spread strategically (set in the sorts of places devils were likely to be caught) along 10 km of road . . . Devils were caught at 23 of 40 sites, five sites of which showed DFTD-affected individuals. At six other sites, an apparent ‘footprint' of DFTD was detected (multiple juveniles only or no devils in areas where they were recently very common and multiple captures could be expected). DFTD appeared to be spread over much of the eastern half of Tasmania.
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A
Mercury
editorial, meanwhile, took to task the political sanitising of Mooney's memo:

Tasmania has two types of feisty devils. One wears a green Guernsey and is thriving in the VFL [Victorian Football League]. The other is facing a threat that could drive it to the edge of extinction. This hideous possibility, given the infamy that the thylacine's death has earned Tasmania, should be thoroughly exercising the minds of Premier Jim Bacon and Environment Minister Bryan Green. They should contemplate that, despite what the history books might record about their achievements, presiding over the demise of the animal that has come to symbolise Tasmania around the world would earn them a special place . . . The Government should be responding on several levels to the disease, and keeping Tasmanians fully informed along the way. It needs a strategy, as Mr Mooney suggests, to ensure the survival of the species. The thylacine's extinction, so most believe, is an inglorious event in our history. It is a reminder of our environmental insensitivity and inability to act to conserve a threatened species. It must not happen again.
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Bacon soon afterwards announced, in his first statement on the disease, that research into the virus would be ‘fast-tracked'. On the same day David Parer entered the debate. In 30 years of making wildlife documentaries around the world he had seen enough evidence of species decline and extinction to fear that a pattern of sustained habitat destruction may have triggered the disease.

Veterinary pathologist Dr David Obendorf sounded another warning, commenting that lack of knowledge of and control over endemic diseases in wild animals could have adverse implications for Tasmania's status as a disease-free island, should the devil disease ever be transmitted to livestock. Understanding livestock diseases meant little without equal understanding of their equivalents in wildlife, and he cited as an example the role of wallabies in the spread of the sheep-wasting disease OJD.

Obendorf, Parer and Mooney weren't alone with their frustrations and fears. Restani speculated that:

carnivores, such as the devil, often reflect ecosystem health . . .

In my opinion, the disease epizootic signals us to take note of the current condition of Tasmanian ecosystems, particularly the interactions among devils, feral cats, quolls and foxes . . .

As a scientist with 20 years' experience studying wildlife throughout the US, Canada and Greenland, I have seen only sylvatic plague rival the population destruction wrought by the devil disease. We know nothing . . . and are helpless to develop an effective conservation strategy.
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Numerous potential triggers were suggested: the rabbit-killing calicivirus; the widespread use of 1080 poison; farm chemicals, especially organophosphates; and land clearance. In an island with as much bush and large tracts of remote wilderness as Tasmania, land clearance seems an unlikely cause of a virulent disease, but resulting population fragmentation might be a cause: when populations become physically cut off from one another they inbreed, and the resulting lack of genetic diversity, already low in an island population, might trigger the action of a dormant retrovirus. Isolated populations can also become stressed if overcrowding occurs. Stressed animals are invariably more susceptible to disease.

While it may be plausible to contemplate a natural virus keeping control over population explosions, it's equally the case that with each successive crash the genetic diversity of the species changes and probably diminishes. The implication of this, if it is correct, is that the devil is on a self-inflicted trajectory to extinction. (Dingoes and humans are assumed to have wiped out mainland devils. But could devils there have experienced natural population crashes from which they eventually couldn't recover, through population fragmentation across the vast continent into pools of very low genetic diversification?)

At the other end of the spectrum, the devil may have become the victim of the virus ‘crossing over' from another species. Mount Pleasant pathologist Roy Mason, familiar with viral tumours affecting cats, speculated that feral cats may have transferred the virus to devils through fighting. Adult male cats are most susceptible to tumours, from fighting one another, and adult male devils, which accumulate many bite scars, have the highest rate of DFTD.

A number of retroviral sequences have jumped species barriers, including HIV/AIDS and SARS. And occasionally a cocktail of factors come into play. In South-East Asia land clearing destroyed the natural habitat of a bat species, and the bats began to roost in trees above pig pens. Their faeces, urine and dead bodies dropped into the pens and were ingested by the pigs. The pigs' owners and their families contracted the bat virus. Efforts to rid Melbourne's botanic gardens of fruit bats have resulted in some migrating to King Island in Bass Strait. Seals there could ingest dead bats. Those seals that are attracted to fish farms in the region are relocated to other Tasmanian waters (about 700 a year), potentially, therefore, transmitting a virus from another species to a distant location. It's an unlikely way of an exotic disease infiltrating a seemingly secure island— but only as unlikely as the possibility ten years ago that devils were about to face an extinction crisis.

Control of wild animals for economic reasons is hardly unique to Tasmania but it is the manner in which it is done that can prove contentious, especially if it threatens Tasmania's remaining carnivorous marsupial icon. Rabbit calicivirus has been cited as a potential cause of or contributor to the disease. Calicivirus was introduced in 1996 in the latest effort to control rabbits. Devils, of course, eat dead rabbits . . .

Devils also eat dead wallabies, kangaroos, pademelons and possums, which are targeted by the forestry industry because they eat tree seedlings. Once an area has been selected for plantation forestry, whether through clear-felling or conversion of farmland, and seeds sewn aerially or manually, the area is then scattered with carrots laced with the chemical toxin sodium monofluoroacetate (1080 poison). The result is good for seedlings but devastating to the browsers. The kill estimate of Forestry Tasmania and private plantation owners for the year 2003 was just under 100 000 macropods. As well as devils, endangered quolls and wedge-tailed eagles eat these poisoned carcasses, and domestic dogs are known to have died this way. The continued use of 1080 has caused much public anger in Tasmania. At the least, mass kills of browsers impacts locally upon devil populations, where suddenly their main prey base disappears.

Nick Mooney, while not discounting 1080, considers agricultural pesticides and forestry plantation sprays to have more obviously lethal potential to trigger the disease, given that some have carcinogenic properties—as does diesel fuel, which is used in vast quantities in rural Tasmania, and there is no doubt devils come into contact with it.

If any of these primary industry products, or a combination of them, were found to be the trigger, the management consequences would be profound.

There is always more. Over decades in the twentieth century, Australia, the United States and other countries solved a rural problem of dusty roads by regularly spraying them with an oil- based, liquid industrial waste. This liquid was laced with manmade toxic chemicals, PCBs (polychlorinated biphenyls), used in the manufacture of products including coolants, hydraulic fluids, paints, newsprint and varnishes. Some of the toxins have a life of hundreds of years, and many roads in the United States have been dug up in detoxification programs. PCBs were used in Tasmania until 1987, a decade after being banned in the United States and Europe, because they ‘cause cancer and many other problems in animals', and in humans they ‘may damage the immune system, hinder sexual development and impair intellectual ability'.
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