They’re inky black, pointy-eared, furry and, in a fierce sort of way, cute. And in May of this year, they were added to Australia’s endangered species list.
Ordinarily solitary, Tasmanian devils commune only to feast on carrion and to mate in short-lived passionate couplings during which they tear each other to ribbons. Their spine-decalcifying caterwauls — a sequence of whuffings, snarlings and growlings — have evoked satanic visions since the first European settlers arrived on the island of Tasmania more than a century ago.
“Parents used to tell their kids: ‘Don’t go out into the bush because the devil will get you,’” recalled Greg Woods, an associate professor of immunology at Menzies Research Institute in Hobart, Tasmania’s capital.
But in the past decade, the Tasmanian devil has been trapped in a purgatory of its own. Since 1996 a deadly cancer, devil facial tumor disease, has preyed on the devil. Its population plummeted to fewer than 50,000 from about 150,000, said Hamish McCallum, senior scientist with the Devil Facial Tumour Disease Program at the University of Tasmania.
The devils’ situation is dire. Yet as more has been learned about the disease, hope has appeared. Scientists have begun an experimental inoculation program, and this year, Woods identified one devil able to mount an antibody response to the tumor.
The devil, Cedric, is a three-year-old male from western Tasmania who has been living in captivity for several months. Woods inoculated Cedric and his half-brother, Clinky, who was also disease-free at the time, with irradiated — that is, dead — devil tumor cells. Although they had the same mother, Cedric and Clinky had different fathers. Woods repeated the vaccination three times.
He then administered live tumor cells to both. Cedric mounted an immune response and lived. Clinky did not develop an immune response, and he succumbed to the cancer. His father’s genetics made Clinky’s immune system more like that of the devils found in eastern Tasmania.
All mammalian immune systems rely on certain cells to recognize invaders. Demarcation of “otherness” at the cellular level is carried out in a part of the mammalian genome called the major histocompatibility complex, or MHC. An animal’s ability to fight off disease depends on this group of genes. MHC is responsible for the cell markers that flag the difference between cells that are “self” and those that are “nonself.” But the tumor’s MHC is what makes it deadly to the devil.
“The tumor has no foreign cell surface markers,” said Katherine Belov, a scientist in the Australasian Wildlife Genomics Group at the University of Sidney. “If tumor cells get into a devil, its own immune system should be able to see the cells as foreign. That doesn’t happen because the tumor’s cells look like devils’ own cells.”
Belov likened the process to genetic matching for an organ transplant: “You have to have the same genes at the MHC as your donor. If they’re different, you’ll reject the organ.”
If the tumor were a needed organ, devils would be perfect recipients. In other words, the devils’ MHC is identical to that of the tumor. The devil and the tumor are genetic clones. Not recognizing a foreign cell, the immune system does not create antibodies.
Devil facial tumor disease first showed up in a 1996 photo taken by a Dutch wildlife photographer, Christo Baars, while he was visiting at Mount William in northeastern Tasmania. Sightings of ailing devils — their lips and jaws deformed by tumors, their noses and eyes obscured by swollen, ulcerating wounds — increased in frequency, notably in the east and north. The disease is always fatal. The devils die of starvation and dehydration when the growths in their jaws and throats make eating and drinking impossible.
Until recently, scientists were at a loss to explain the cancer’s cause or mode of transmission.
“We’d predicted they’d be vulnerable to viruses” because they are an inbred population, Woods said. “That what got them was a cancer took everyone by surprise.” But this cancer, Woods and his colleagues found, was unlike any the researchers had seen before.
“In all other cancers, what you’ve got is your own cells gone haywire, whereas in this particular cancer, the cells are not from the host, they’re from a different animal,” McCallum said. “The tumor itself is the infectious agent.”
The tumor plaguing the devil is a clone, derived from one devil. When animals bite each other in the face, as they do during mating season, tumor cells are passed from host to host.
The Tasmanian devil is about the size of a corgi when fully grown and is the largest surviving carnivorous marsupial. The animal became legally protected in 1941, when farmers and settlers hunted them aggressively, believing the nocturnal scavengers were preying on livestock. Both agriculture and population growth have contributed to fragmentation of the devils’ habitat. From 1900 to the present, the human population of Tasmania increased almost threefold, to just less than 500,000. Once widespread, devil populations became more isolated, inbred and genetically similar.
Cedric was the first devil to be inoculated successfully using killed cancer cells. Woods has since found a second devil that was able to mount an immune response. Three other inoculated devils from eastern Tasmania have developed the disease, supporting Woods’s hypothesis that devils from the west have maintained greater genetic diversity.
Saving the devil from extinction has become a conservation imperative. According to McCallum, without major intervention, the devil will be extinct in five years.
Woods said he would begin the search for naturally resistant devils early next year. He posits that the devils’ best bet lies within its own genome.
Yet even if more MHC-different devils are found, Belov thinks the immunological arms race is far from over. She has already seen some evidence that the tumor is adapting.
Whereas before, the tumors were clonal, “now we’re seeing slight variation — slight chromosomal differences. They’ve begun to evolve from original clone or cell,” she said. “If it does evolve immune evasion strategies, such as turning off the MHC altogether, the tumor has potential to infect MHC-different individuals. If it down regulates its cell surface MHC — that is, switches off its MHC altogether — the tumor not only has potential to infect MHC-different individuals, but it may also cross the species barrier.”
If that happened, the most likely victim would be the devil’s closest living relative, the spotted-tail quoll. Another carnivorous marsupial indigenous to Tasmania, the quoll has a white-dotted reddish to dark chocolate brown coat and is about the size of a small house cat. Even now, it is considered an endangered species.
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