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Yersinia Essay

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Evolutionary Insights and Effective Invasive Steps of Yersinia spp.
Author: Malvi Prakash Golwala (U53409030)
Email address: malviprakash@mail.usf.edu
Course name: Cellular Microbiology
Course number: BSC6932.079F15
Semester year: 2015

Abstract
Yersinia is a gram-negative bacteria causing plague pandemics in humans. They are facultative intracellular organisms that can very efficiently survive and replicate inside cells (1). They cause fatal plague and have destroyed millions of lives since 541 A.D (2). This review will highlight how these organisms subvert the immune system. It will elaborate on all the mechanisms and proteins utilized for the same. The main are the Yops or Yersinia outer proteins. But, there are other factors as …show more content…

Introduction
“The effects of this natural and human disaster changed Europe profoundly, perhaps more so than any other series of events. For this reason, alone, the Black Death should be ranked as the greatest biological-environmental event in history, and one of the major turning points of
WesternCivilization.”
Gottfried, R. S. 1983. The Black Death. Natural and human disaster in medieval Europe.
Yersinia rod shaped, non-motile or motile by peritrichous flagella, facultative anaerobe that exhibits a bipolar staining with methylene blue, Giemsa, etc. leading to a safety pin (3). Their pathogenicity lies within mainly 3 plasmids namely, pMT1 (Murine toxin), pPCP1 (Pesticin coagulase plasminogen activator) and in some species pYV (Yersinia virulence) (4). The genus Yersinia consists of 19 species. But, this review will only focus on three of them.
Yersinia started with the Justinian Plague between 541 and 750 A.D., going to The Black Death (1347-1351), killing almost one-third of the European population eventually causing the third pandemic between 19th until mid-20th century …show more content…

Ivy mutants showed sensitivity to not only lysozyme but also PMNs. Ivy mutants were less virulent in OF-1 mouse models of bubonic and pneumonic plague (shown in figures below).

Sensitivity to lysozyme would mean the release of peptidoglycan fragments. These are known to induce inflammatory compounds. Ivy deficient Yersinia pestis were not shown to induce inflammation as well (38-39) (as shown in figure below).

While studies were carried out for Yersinia pestis, similar were done for Yersinia pseudotuberculosis as well. When Ivy deletion was tested in Yersinia pseudotuberculosis, it did not affect inhibition of lysozyme in M. luteus, nor did it affect the virulence in orally infected mice (38) (as shown in figure below).

Yersinia pseudotuberculosis uses an alternative technique which does not include O-acetyltransferase, peptidoglycan N-deacetylase or EpsC protein which helps to provide resistance against lysozyme. Its LPS is different than from that of Yersinia pestis as well (40-44). This is probably the difference between the two species due to which Yersinia pseudotuberculosis is known to have greater resistance against antimicrobial peptides (45-46). Lysozyme resistance mechanism still remains to be

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