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.
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.