Molecular Darwinian Evolution of Virulence in Yersinia pestis

Abstract

The genus Yersinia consists of 15 species (www.bacterio.cict.fr/xz/yersinia.html), and only three of them, Y. pestis, Y. pseudotuberculosis, and Y. enterocolitica, are pathogenic to mammals, including humans. The Y. pseudotuberculosis-Y. pestis evolutionary linkage diverged from Y. enterocolitica between 41 and 186 million years ago, while Y. pestis diverged from Y. pseudotuberculosis within the last 1,500 to 20,000 years (1, 65). In accordance with this evolutionary cascade, wide genetic diversity exists between Y. pseudotuberculosis and Y. enterocolitica, while very close genetic similarity is found between Y. pseudotuberculosis and Y. pestis. Y. pseudotuberculosis causes only nonfatal gastrointestinal disease in mammalian hosts, including humans, and the disease is transmitted by the food-borne route. Y. pestis causes plague, which is one of the most deadly diseases (47). Three pandemics of plague have been recorded in human history and have claimed hundreds of thousands of lives (47). Plague is a typical enzootic disease (an infection of the animal population[s] in one or more confined natural foci without the need for external inputs), and epidemics of rodent plague are restricted in various enzootic plague foci especially in Asia, the Americas, and Africa (80). Compared to its progenitor Y. pseudotuberculosis, Y. pestis utilizes a radically different mechanism of transmission in rodent reservoirs that relies primarily upon biting by flea vectors. This review deals with how genetic changes (gene inactivation, loss, and acquisition) and remodeling of gene regulation encourage Y. pestis to switch from an enteric lifestyle to a mammalian blood-borne lifestyle that relies on vector-borne transmission.