A study shows humans are unlikely to have caused the deadly Tasmanian Devil Facial Tumour Disease. Source: AAP
HUMANS are unlikely to have caused the deadly Tasmanian Devil Facial Tumour Disease (DFTD), a new study has found.
Researchers at the University of Sydney have found the low immune gene diversity that enables the spread of the disease also existed in devils thousands of years ago.
The team examined DNA from four periods as long as 10,000 years ago, when devils also ran around on the Australian mainland.
"We found that the the immune gene diversity was actually low in Tasmania even before European arrival and also that mainland devils had low immune gene diversity," lead author Katrina Morris told AAP.
"So this wasn't caused by European settlers, it's a much longer historical trend in devils."
Devil fossils have been found in every Australian state and it is thought they became extinct on the mainland around 3000 years ago.
But it is unlikely an earlier outbreak of the facial tumour, which has wiped out more than 80 per cent of the Tasmanian population in recent years, was to blame.
"It's possible that it has occurred previously but it wouldn't really leave evidence so we can't really be sure," Ms Morris said.
"Nothing like DFTD has occurred in the last 200 years or we would have noticed that."
Ms Morris said diseases brought with the introduction of dingoes would have had a significant impact.
Devil populations have crashed several times in Tasmania in the past 200 years but DFTD did not first appear until 1996.
Dogs, this time brought by Europeans, are again thought to be the culprits.
"Since devils had this lack of immune gene diversity they were very susceptible to disease epidemics," Ms Morris said.
"So if the dogs brought anything like distemper with them they might have got into the devil population and then had quite a devastating impact and caused those population crashes."
The new study reinforces the importance of captive breeding programs which promote genetic diversity.
"They have a such a lack of immune gene diversity," Ms Morris said.
"They still do have some, though, so we need to maintain what they have left so that we don't make the problem any worse."
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