Sympathy for the devil

By Kate McDonald
Thursday, 29 November, 2007

Up to 100 Tasmanian devils will be captured and quarantined as part of an ongoing insurance population strategy designed to ensure the survival of the species.

Save the Tasmanian Devil program manager Dr Steven Smith said the first stage will begin in late January, following months of surveys in the state's west and north-west to identify animals with no evidence of Tasmanian Devil Facial Tumour disease.

The uninfected devils will be put in quarantine and then sent to zoos on the mainland.

At present, 48 Tasmanian devils have been sent to wildlife parks to establish an 'insurance' population, to ensure the species' survival should the disease continue to decimate the wild population.

The Tasmanian strategy is also aimed at ensuring a genetically diverse population for breeding programs.

Apart from the 48 devils sent to the mainland, it is thought that only two individual devils are being kept in zoos outside their native land.

These are the two given as a wedding present for Princess Mary of Denmark. The two are housed at Copenhagen Zoo.

Smith said the new intake is part of the Insurance Population Strategy, developed with the Australasian Regional Association of Zoological Parks and Aquaria (ARAZPA), which identified the need to build on the number of devils already in the insurance population.

"The Insurance Strategy identifies a range of options that can be considered to build this insurance population up," he said.

"These options include both intensively managed populations as well as extensively managed. However the immediate priority is to build up the intensively managed population."

Australian researchers have confirmed that Devil Facial Tumour Disease (DFTD) is a contagious clonal cell line transmitted by biting and that one of the problems the devils face in fighting the disease is a lack of genetic diversity.

In early 2006, Anne-Maree Pearse and Kate Swift from the Tasmanian Department of Primary Industries published a stimulating yet shocking theory, known as the allograft hypothesis.

By studying the tumour chromosomes, the duo discovered that in all animals studied, an identical yet complex rearrangement had occurred.

Taking into consideration the aggressive nature of Tasmanian devils and their known penchant for fighting, Pearse and Swift proposed that the disease was transmitted by allograft, in which an infectious cell line is passed between the animals through bites.

Only one other type of contagious cancer is known, called canine transmissible venereal sarcoma, but this is not usually fatal in healthy dogs. DFTD is most definitely fatal.

Recently, a team led by the University of Sydney's Dr Kathy Belov has provided further evidence that the tumour is a contagious clonal cell line. Not only that, but the devils are unable to mount an immune response due to a lack of genetic diversity.

In a paper published online in the Proceedings of the National Academy of Sciences, Belov and colleagues from the University of Tasmania, the Department of Primary Industries and the Australian Museum found that a depleted major histocompatibility complex (MHC) is responsible for the devils' inability to fight back.

"This is a really unusual cancer because it is a transmissible cancer or contagious," Belov said.

"The cell itself is the infectious agent rather than it being a bacteria or a virus. We confirmed by microsatellite typing that all the tumours were identical and that they were different from the host."

What is even more unusual about DFTD is that not only is it a tumour but a tissue graft. Even so, the host immune system should recognise the graft as foreign from its cell surface antigens, but in this case that does not occur.

"Basically, there is so little diversity in the MHC genes that the host that is affected by the tumour, and the tumour cell itself, have identical MHC types," Belov said.

"So the host doesn't see the cancer cells as foreign and doesn't mount an immune response."

It does not augur well for the devil. Belov and her team have recommended that, with no natural barriers to the spread of the disease, affected individuals be removed from population and that efforts to establish captive disease-free colonies be boosted.

"What we are putting a lot of effort into now is looking for as many different MHC types as possible, because we believe it is important to get as much MHC diversity as possible in the captive colonies and to try to maintain as much diversity as we can find."

Belov has been inspired by a fellow scientist and by this work on the devil's MHC to start looking for someone to sequence its genome.

She has worked in marsupial immunogenetics for almost all of her career and has set up an Australian Wildlife Genomics Group at the University of Sydney to study the immune systems of wallabies, koalas, opossums, platypuses and now devils.

She led the MHC characterisation and then the immune genes characterisations for the opossum genome project and worked on the platypus genome as well. (The platypus genome has now been completed and submitted to Nature for publication.)

She is also part of the Tamar wallaby project, the sequencing for which has been completed and assembly about to begin.

Marsupial and monotreme genomes can tell us an awful lot about our own evolution, especially in Belov's specialty of the evolution of the immune system.

"When we characterised all of the immune genes in the opossum genome we were really surprised to find they were comparable to humans, unlike the genomes of, say, birds. So they do have an immune system that looks like it going to be on par. That's really changing the way we understand the immune system in marsupials."

For the devil, Belov and her team are hoping to be able to survey more animals, particularly those in areas of Tasmania other than the east coast. She is working with Dr Jeremy Austin at the Centre for Ancient DNA at the University of Adelaide to look at MHC diversity in the past to try to understand what has happened.

"Perhaps there was a disease that swept through the population that selected this MHC type. It would be nice to see if we can find when the diversity levels dropped."

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