Will Tasmanian devils soon go extinct?

Last week, we talked about Tasmanian devil facial tumor disease, which is caused by an infectious cancer that is transmitted after a susceptible devil bites a tumor on an infected devil. After becoming infected, devils almost always die within several months. As the disease has spread through their range, devil populations have drastically declined, and there is great concern that the devils will go extinct in the near future. But not all infectious diseases that cause high host mortality will lead to host extinction, so what is special about Tasmanian devil facial tumor disease?

A while ago, I posted about the difference between pathogens with density dependent and frequency dependent transmission dynamics. To recap: when transmission is density dependent, the rate of host contacts (and thus pathogen transmission) increases with host density. When transmission is frequency dependent, the rate of host contacts (and thus pathogen transmission) does not change with host density. This means that as a host population crashes due to high mortality from an infectious disease, the transmission rates of pathogens with density dependent transmission will decline, but the transmission rates of pathogens with frequency dependent transmission will not change. Therefore, it isn’t possible for pathogens with density dependent transmission to be the cause of host extinction, because the pathogen will go extinct due to low transmission rates before the host goes extinct. (Note, however, that pathogens with density dependent transmission might cause declines in a host population that make the host population more susceptible to local extinctions due to stochastic events, like bad breeding years.)

Historically, only sexually transmitted pathogens and vector transmitted pathogens were thought to have frequency dependent transmission. And we know that Tasmanian devil facial tumor disease is not sexually transmitted or vector transmitted. However, McCallum et al. (2009) found that models with frequency dependent transmission fit mark-recapture data for devil disease dynamics better than models with density dependent transmission. How can that be? Well, it might that the number of aggressive encounters between individuals is not dependent on host density; for instance, if confrontations at carcasses continue to be likely to occur even as populations decline.

When pathogens utilize frequency dependent transmission, we know that unselective culling to reduce the number/density of susceptible hosts won’t stop a pathogen from invading a naïve host population. That’s because no matter how many individuals you cull, you won’t reduce the actual pathogen transmission rate, which is independent of host density. But what if instead of unselective culling, we try to stop the spread of Tasmanian devil facial tumor disease by selectively culling infected individuals? A culling program was undertaken to try this, but it was not effective (Lachish et al. 2010). Beeton and McCallum (2011) used epidemiological models to show that while selective culling might be effective, the rate of culling that would be necessary is just too high to be logistically possible given current resources.

Tasmanian devils have been the largest extant marsupial carnivore since the thylacine went extinct. What will happen if the Tasmanian devil goes extinct? Well, there are already documented changes in the animal communities in Tasmania that might be caused by devil declines, where the abundances of some species (e.g., feral cats) have increased and the abundances of other species (e.g., eastern quoll – so cute!) have decreased (Hollings et al. 2014). But the long term changes that will result from devil population declines (or full extinction) are hard to predict.

It’s a rough time to be a marsupial.


Beeton, N. and H. McCallum. 2011. Models predict that culling is not a feasible strategy to prevent extinction of Tasmanian devils from facial tumour disease. Journal of Applied Ecology, 48: 1315–1323.

Hollings, T., M. Jones, N. Mooney, and H. McCallum. 2014. Trophic cascades following the disease-induced decline of an apex predator, the Tasmanian devil. Conservation Biology 28(1): 63-75.

Lachish, S., H. McCallum, D. Mann, C.E. Pukk, and M.E. Jones. 2010. Evaluation of selective culling of infected individuals to control tasmanian devil facial tumor disease. Conservation Biology 24(3): 841-851.

McCallum, H., M. Jones, C. Hawkins, R. Hamede, S. Lachish, D. Sinn, N. Beeton, and B. Lazenby. 2009. Transmission dynamics of Tasmanian devil facial tumor disease may lead to disease-induced extinction. Ecology 90(12): 3379–3392.

Transmission of Tasmanian devil facial tumor disease

Tasmanian devils are threatened by one of the craziest pathogens I’ve ever heard of: an infectious cancer. You might be wondering, “How the heck can a cancer be infectious? Shouldn’t the host’s immune system recognize the parasitic cells as foreign and kill them?” Well, yeah, it should. But Tasmanian devils have very low genetic diversity in their Major Histocompatibility Complex (MHC) genes, a group of immune system genes associated with recognizing foreign/non-self materials. As a result, Tasmanian devil immune systems can’t tell that the parasitic cell line is different from the animals’ own cells. Major bummer!

So, how is this infectious cancer transmitted among Tasmanian devils? Well, you’ve probably heard that devils are very aggressive: males fight over females during the breeding season and females will fight to defend their dens. There is also fighting over carcasses. So, there’s lots of biting happening among devils, and many of these bites occur on the devils’ heads. And guess what? The infectious tumors usually occur on the faces of devils, which is why the disease is called Tasmanian devil facial tumor disease. So, people suspected for a long time that biting and transmission were linked.

Ok, now for the cool part! Hamede et al. (2013) hypothesized that the devils with the most bites on their heads would be the most likely to become infected by Tasmanian devil facial tumor disease. However, they found the opposite trend! The devils with the most bites on their heads were less likely to become infected. Hamede et al. (2013) suggested that instead of an infected biter transmitting the infectious cells to an uninfected bite recipient (more bites on devil = higher infection probability), it may be that uninfected biters become infected after biting the tumors of infected bite recipients (more bites given to other devils = higher infection probability). Devils often have open mouth wounds and the tumors often start growing inside the oral cavity, and these observations support the idea of infection resulting from biting tumors.


Dominant individuals are probably more likely to do lots of biting (as opposed to receiving many bites), so it may be that dominant individuals have higher risk of infection. This is a really cool possibility, because it suggests that some hosts (in this case the dominant individuals) in a population are “super receivers” of infection. A lot of attention has been given to disease super spreaders, like Typhoid Mary, and the super receiver concept is a neat addition to our understanding of heterogeneity in pathogen transmission rates.

Finally, I just want to point out that not all infectious cancers are transmitted by biting. For instance, there’s an infectious cancer of canines that is sexually transmitted. Crazy!


Hamede, R.K., H. McCallum, and M. Jones. 2013. Biting injuries and transmission of Tasmanian devil facial tumour disease. Journal of Animal Ecology 82: 182-190.