Introduction Yersinia pestis is a bacterium that causes the bubonic plague, in which one of its well-known symptoms is swollen lymph nodes called buboes to appear on the body (Perry and Fetherson 1999). Yersinia pestis evolved from clones of Y. pseudotuberculosis within the last 1,500 to 20,000 years, where it evolved separate times in China (Achtman et al. 1999). Yersinia pestis is spread through fleas feeding on infected and uninfected blood as well as open wound contact with infected blood (Titball et al. 2003).
Symptoms and Proximate Causes Initially, after two to six days of infection, victims start to develop fever, headache, chills and buboes that appear around the body (Perry and Fetherson 1999). Buboes are swollen lymph glands
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pestis isolates are the most diverse. (Morelli et al. 2010) The boom of the rodent population in China triggered the evolution of Y. pestis from Y. pseudotuberculosis. This boom of the rodent population may have been since the beginnings in agriculture in China (Achtman et al. 1999). The increase in food supplies for rats as well as growing human populations in China lead to opportunities for Y. pestis to evolve for transmission to human hosts (Achtman et al. 1999). Flea-borne transmission evolved within the last 20,000 years, where Y. pestis evolved to adapt to the flea gut in order to colonize the flea where it can serve as a vector for transmission to mammalian hosts (Achtman et al. 1999). Prior to the end of the 18th century, arthropod ectoparasites were common in humans and were responsible for historical outbreaks of disease (Drancourt et al. 2006). Drancourt et al. (2006) also assert that in areas where there are little anthropophilic rodents, such as Kurdistan in the 19th century, spread of the bubonic plague was mainly through arthropod ectoparasites rather than from rats.
Evolutionary Mechanisms In order to adapt to the new flea vector, Y. pestis evolved several mechanisms where it could be transmitted through arthopods from a food and water-borne pathogen (Hinnebusch 2005; Titball et al. 2003). According to Hinnebusch (2005), Y. pestis developed the Yersinia murine toxin which is a phospholipase D that enhances survival in the midgut as a