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Chapter 12 : Chlamydial Persistence Redux

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Chlamydial Persistence Redux, Page 1 of 2

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Abstract:

The purpose of this chapter is to define what one do and do not know about chlamydial persistence with the goal of determining the extent of the role that persistence plays in chlamydial disease (if at all) and what one should do to better understand this chlamydial attribute. Out of , , , and ) causing infections in people, only two dominates: and . , which causes a form of malaria called malignant tertian malaria, is considered a major killer due to its capacity to modify the surface of infected erythrocytes such that they stick to each other and to the endothelial cells lining vessels and capillaries. may be one of only a very few bacterial pathogens that is more difficult to work with than . Environmental factors that trigger dormancy include starvation for nutrients and hypoxia. When these stress-related conditions are applied to , striking metabolic reprogramming occurs, including upregulation of stress response genes and downregulation of many central metabolism genes. Studies of persistent disease in mice indicate that persistence is a function of the capacity of the pathogen to survive in macrophages, and at least for nontyphoidal salmonellae, macrophage persistence contributes to increased disease severity in AIDS patients. The authors conclude that persistent forms may account for the insidious inflammation associated with upper genital tract disease in women, but have not been able to identify that persistent infections act as contributing factors to the disease.

Citation: Byrne G, Beatty W. 2012. Chlamydial Persistence Redux, p 265-284. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch12

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Figures

Image of FIGURE 1
FIGURE 1

Schematic diagram of the chlamydial developmental cycle. Red arrows indicate altered intracellular chlamydial development mediated by environmental factors. (A) Immunofluorescence images and schematic show mature serovar B inclusions with elementary bodies (EBs) in green (anti-OmcB), reticulate bodies (RBs) in red (anti-major outer membrane protein), and the inclusion membrane in orange (anti-incG). (B) Persistence in vitro in response to IFN-γ results in enlarged, aberrant RBs that can be maintained in this state for extended periods of time, with subsequent reversion to normal intracellular development. doi:10.1128/9781555817329.ch12.f1

Citation: Byrne G, Beatty W. 2012. Chlamydial Persistence Redux, p 265-284. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch12
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Image of FIGURE 2
FIGURE 2

Chlamydial inclusions in intestinal enterocytes of naturally infected swine. (A) Lower-magnification electron micrograph showing both a typical inclusion (indicated by arrow) with an abundance of dense EBs and inclusions containing somewhat enlarged RBs (arrowheads). (B) Higher-magnification electron micrograph showing an inclusion containing typical EBs and RBs, in addition to enlarged, aberrant RBs (arrowheads). It is interesting that both normal and abnormal developmental forms are seen, as if persistence is a stochastic event for infecting the pig intestine. Images generously provided by Andreas Pospischil, University of Zurich. doi: 10.1128/9781555817329.ch12.f2

Citation: Byrne G, Beatty W. 2012. Chlamydial Persistence Redux, p 265-284. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch12
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Image of FIGURE 3
FIGURE 3

Factors contributing to persistence of other microorganisms and potential correlates in . Attributes of other microorganisms are shown in upper panels, and potential correlates in are shown in the corresponding lower panels. Please see the text for details. doi:10.1128/9781555817329.ch12.f3

Citation: Byrne G, Beatty W. 2012. Chlamydial Persistence Redux, p 265-284. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch12
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