In the midst of a human pandemic, we have some good news about wildlife: our new study, published today in Science, shows that Tasmanian devils are likely to survive despite the infectious cancer that has ravaged their population.
The Tasmanian devils have been ravaged by a strange transmissible cancer. Tumor on the devil’s face, or DFTD for short, was first discovered in 1996 in northeastern Tasmania. Transmitted by bite, DFTD has spread throughout most of the state, reaching the West Coast in the last two or three years. This has led to a drop of at least 80% in the total devil’s population.
Ten years ago, we thought there was a real chance that DFTD would do that bring the Tasmanian devil to extinction. Our concern arose not only because the cancer was almost inevitably deadly, but also because the rate of transmission did not seem to slow down, even when the devils became very rare.
Our new study has some good news: from pioneering application of genomic analysis commonly used for viruses, we found that the curve flattened and the rate of infection growth slowed. This means that while the disease probably does not disappear, neither the Tasmanian devils.
Genomics is a relatively new field of science, which uses the vast amounts of available data from modern genetic sequencing techniques to answer some of the most difficult and important questions in biology.
The genomic approach we used is called philodynamics. He uses complex mathematical analysis of small changes in DNA to reconstruct the evolution and spread of the tumor through devil populations. This is the same method used for tracking the COVID-19 pandemic, and was first developed for influenza virus testing. Viruses have small genomes and develop rapidly. This is the first time the method has been used for a pathogen with a much more complex and slow-growing genome.
Screening more than 11,000 genes, we found the R number (the average number of secondary cases for each primary case, now known from COVID-19) has dropped from about 3.5 at the peak of the epidemic to about one now. This suggests that some steady state has been reached and the disease and the devils now coexist.
This finding supports a an article we published last year, in which we came to a similar conclusion using mathematical models based on marking and recapturing Tasmanian devils in one place of study, without taking into account genetics.
Our new study is based on samples collected in Tasmania from the early 2000s. Given the very different nature of the two methods, agreement between the results gives us more confidence in our conclusions.
This article, in addition to a few that we published recently, shows that there have been rapid evolutionary changes in Tasmanian devils and in the tumors themselves since the advent of this transmissible cancer. Already the frequencies of gene variants known to be associated with immune function in humans they have increased in populations of Tasmanian devils, suggesting that devils evolve and adapt to the threat.
We now also know that a relatively small number of genes have a great influence about whether the devils get infected and whether they survive if they do.
Finally, and perhaps most encouraging of all, we now saw tumors shrink and disappear – something that was unheard of when the disease first appeared. Moreover, we also know that there is strong genetic basiswhich again suggests that devils adapt genetically to their enemy.
Together, all of these findings show that wild Tasmanian devils can evolve very quickly – in just five generations or so – in response to this disease. This has profoundly encouraging consequences for their likely future survival.
There is still much to learn about the evolution of devils and their tumors. But in the meantime our results provide a warning that the strategy for reintroducing captive animals to supplement sick wild devil populations is likely to be counterproductive.
When devils from populations that have never been exposed to the disease interbreed with wild animals in diseased populations, the evolution we observe in wild populations is likely to slow or even reverse, threatening those populations.
Moreover, the delay in the rate of disease transmission may be due in part to the reduced density of the devil’s population, leading to less bites. An artificial increase in population density may accelerate the transmission of the disease, contrary to the expected effect.
With the growing body of evidence showing that extinctions are unlikely even in the next 100 years, we have time to think carefully about management strategies. In particular, models can be developed to assess evolutionary and epidemiological consequences of reintroduction or translocation.
One possibility is to breed captive devils who have the right genes to increase their chances of surviving the disease. More broadly, our study emphasizes the vital importance of taking evolutionary considerations into account in the management of endangered species. Now we have the genomic tools for this.
Many thanks to Andrew Storfer of Washington State University, Menna Jones and Rodrigo Hamede of the University of Tasmania, and Paul Hohenlohe of the University of Idaho for their contributions to this article and the research he describes.