The epidemiology of animal-borne illness is more complex than once believed.
In the wake of the recent Ebola virus epidemic in West Africa, a reevaluation of the ways plague spreads through prairie dog colonies in the western United States has yielded insights that could help explain outbreaks of plague, Ebola, and other diseases that can be transmitted by animals to humans. These include West Nile Virus disease and MERS (Middle East Respiratory Syndrome). The study, led by Dan Salkeld and Mike Antolin of Colorado State University and described in the journal BioScience, suggests that even deadly diseases may persist unnoticed in a population for years as smoldering infections, rather than jump from another species immediately before an outbreak. Moreover, the investigations commonly launched after a human outbreak can yield misleading information about which host species were actually responsible.
For instance, it seems that grasshopper mice and coyotes, which scavenge plague-killed black-tailed prairie dogs, may speed transmission of the plague-causing bacterium by acquiring and spreading the fleas that spread the disease. Thus, fleas can transmit plague faster than was once thought. According to Salkeld and colleagues, the disease can persist in wider prairie dog populations through repeated dispersal and reinvasion despite local outbreaks that can kill 95%-100% of the members of affected colonies. The authors state that this "slow, smoldering, cryptic disease transmission in animal populations prior to outbreaks in humans is... a hypothetical explanation for the persistence of pathogens." These pathogens, in turn, emerge only as a result of "complex multifaceted ecological interactions" that may involve several species.
Oversimplification of the ways animal-borne diseases spread may lead to serious scientific errors, caution the authors: "If disease outbreaks are sporadic and difficult to predict, a bias toward studies of the pathogen's ecology during the peaks or aftermaths of the outbreaks will naturally arise." In the case of Ebola virus, they argue, sampling of "fruit bats after human outbreaks may have biased subsequent investigations toward bat-Ebola virus ecology," resulting in researchers' possibly overlooking other species that could be involved, including nonhuman primates and ungulates. According to the authors: "A misplaced focus on a single animal host species may nullify efforts to create useful early warning monitoring programs."
The authors acknowledge that avoiding such biases constitutes a significant undertaking that will require a broadly epidemiological approach to studying diseases that are resident in wild animals. To this end, they encourage careful disease monitoring in its "ecological context before, during, and after outbreaks that occur in humans or animal species of conservation concern."