The first case of mammalian extinction due to an exotic disease – an alarm bell for conservation efforts?

An interesting article that we accepted last month for PLoS ONE describes a very fine DNA detective work to put forth the hypothesis of mammalian extinction due to an introduced infectious disease. The research published on November 6 suggests that a century ago the black rat species, which led to the emergence of the bubonic plague in Medieval Europe and considered one of the worst invasive species on the planet, sheltered a parasitic disease that eliminated two immunologically naive rat species native to the Christmas Island in the Indian Ocean.

Alex Greenwood from the Old Dominion University in Norfolk, Virginia, and colleagues brilliantly attempted to solve the mystery of the mammalian extinctions. They collected samples from 21 historical rat specimens from Christmas Island stored at natural history museums across the United Kingdom. These researchers analyzed preserved remains of black rats, the extinct species, and the crosses of the two. The century old specimens were then analyzed for genetic signatures of crossbreeding as well as for the presence of Trypanosoma lewisi, the close relative of the sleeping sickness pathogen, T. evansii.

The interesting part of the story is that the authors argue they did not find any evidence of hybridization between black rats and Christmas Island rats. They emphasize that mere invasion does not necessarily lead to extinction and, that on Christmas Island, the Christmas Island shrew survived until 1985 even in the presence of black rats, arguing against general competitive exclusion or predation. Therefore, it appears that their data are more consistent with disease as a reason for extinction rather than competition.

The authors speculate that the extinction of Christmas Island rats (Rattus macleari) was due to a trypanosome pathogen present in fleas carried by black rats introduced to the island (Rattus rattus). The study presents acceptable evidence for the presence of trypanosome infection in the Christmas Island rats after black rats have been introduced to the island, but not before.

However, if we consider some of the arguments, the scenario becomes little implausible - Trypanosome diseases do not normally have short and acute progression and T. lewisi (which the authors tested for) is not reported to be acutely pathogenic in rats. The other question could be - what is the reason to believe that the Christmas Island rats would reveal a different pathology compared with the black rats which were putatively carrying the disease? Nevertheless, it is possible that R. macleari would have been immunologically naïve to black rat pathogens which acted more deadly in a naïve host compared to its natural host or to a host adapted to it. But the next argument could be - why the Christmas Island rats were not killed by some other pathogen (for example a rodent virus) introduced by the black rats? Also, it is possible that the authors missed a possible interspecific ecological competition that might have served as an important extinction force. But no one knows ways to test that!

Leaving this debate to the scientific community (and the PLoS ONE readership at large) to choose among different explanations, I thought the paper was indeed worthy of publication because some of the emerging and re-emerging infectious diseases could possibly serve as a strong force to future extinctions, especially of the wildlife that are increasingly threatened and we thus have a warning bell in the form of this important study.