Plague : A Flea Borne Disease Caused By The Pathogenic Agent Yersinia Pestis

Plague : A Flea Borne Disease Caused By The Pathogenic Agent Yersinia Pestis

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Plague is a flea-borne disease caused by the pathogenic agent Yersinia pestis. Of the members of genus Yersinia, Y. pestis is recognized as the most invasive and virulent bacterial pathogen, responsible for several major devastating pandemics in human history. Y. pestis ¬is believed to have evolved from Yersinia tuberculosis within the past 20,000 years. In this brief evolutionary period, the Y. tuberculosis progenitor adopted the flea as its primary vector. Transmission is typically dependent on proventricular blockage in a flea’s foregut by dense aggregates of Y. pestis—biofilm formation. Biofilm production is regulated by Y. pestis hemin storage (hms) genes, which allow successful transmission and colonization of a flea digestive tract. Additional acquired genetic factors during its evolutionary period are required for flea-borne transmission and increased virulence.
The genus Yersinia consists of gram-negative bacteria in the family enterobactericeae of the gammaproteobacteria. Yersinia consists of 17 species (Michael & Rahalison 2014), three of them being pathogenic species (Achtman et al. 1999). Y. pseudotuberculosis and Y. enterocolitica are enteric (pertaining to the intestines) food-borne and water-borne pathogens which cause relatively mild enteric diseases with side effects such as vomiting, diarrhea, stomach pain, and nausea. The third pathogenic species, Y. pestis, the causative agent of the plague, is highly virulent and responsible for several major pandemics in human history. Y. pestis is primarily a rodent pathogen; however it can be transmitted to a human host via bites from a flea vector. An infected human host can progress from the bubonic form of the disease, which causes lymph nodes to swell...

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...mT reaches Vmax, the maximum rate that enzyme can catalyze a reaction, at the ambient body temperature (below 30°C) of a flea (Bobrov et al. 2011, Sun et al. 2011 ). At higher temperature around 37°C (the ambient body temperature of a mammalian host), the DGC enzyme along with its product, c-di-GMP, is degraded by PDE. PDE activity allows Y. pestis to become increasingly more virulent and infectious after entry into the mammalian host. This increase in virulence is attributed to the degradation of the biofilm allowing the bacteria to transition from a sessile to a planktonic life style commonly associated with acute infections (Bobrov et al. 2011). Bobrov et al. (2011) demonstrated that inactivation of the PDE enzyme leads to overproduction of EPS which resulted in more than a 10-3 decrease in virulence for bubonic plague and pneumonic plague in Swiss-Webster mice.

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