A review of plague persistence with special emphasis on fleas.
Sylvatic plague is highly prevalent during infrequent epizootics that ravage the landscape of western North America. During these periods, plague dissemination is very efficient. Epizootics end when rodent and flea populations are decimated and vectored transmission declines. A second phase (enzootic plague) ensues when plague is difficult to detect from fleas, hosts or the environment, and presents less of a threat to public health. Recently, researchers have hypothesized that the bacterium (Yersinia pestis) responsible for plague maintains a continuous state of high virulence and thus only changes in transmission efficiency explain the shift between alternating enzootic and epizootic phases. However, if virulent transmission becomes too inefficient, strong selection might favor an alternate survival strategy. Another plausible non-exclusive hypothesis, best supported from Asian field studies, is that Y. pestis persists (locally) at foci by maintaining a more benign relationship within adapted rodents during the long expanses of time between outbreaks. From this vantage, it can revert to the epizootic (transmission efficient) form. Similarly, in the United States (US), enzootic plague persistence has been proposed to develop sequestered within New World rodent carriers. However, the absence of clear support for rodent carriers in North America has encouraged a broader search for alternative explanations. A telluric plague existence has been proposed. However, the availability of flea life stages and their hosts could critically supplement environmental plague sources, or fleas might directly represent a lowlevel plague reservoir. Here, we note a potentially pivotal role for fleas. These epizootic plague vectors should be closely studied with newer more exacting methods to determine their potential to serve as participants in or accomplices to a plague persistence reservoir.
Wimsatt
Jeffrey
J
Center for Comparative Medicine and Department of Biology, University of Virginia, Charlottesville, USA. jhw5b@virginia.edu
Biggins
Dean E
DE
D000818:Animals; D004197:Disease Reservoirs; D054884:Host-Pathogen Interactions; D007303:Insect Vectors / Q000254:growth & development / Q000382:microbiology; D010930:Plague / Q000382:microbiology / Q000635:transmission*; D012376:Rodent Diseases / Q000382:microbiology / Q000469:parasitology; D012589:Sciuridae / Q000382:microbiology / Q000469:parasitology; D005423:Siphonaptera / Q000254:growth & development / Q000382:microbiology; D014774:Virulence; D015010:Yersinia pestis / Q000472:pathogenicity* / Q000502:physiology