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Category: Bacterial Pathogenesis
Free-Living and Host-Associated Protozoa as Training Camps for Intracellular Pathogens, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555815851/9781555814694_Chap09-1.gif /docserver/preview/fulltext/10.1128/9781555815851/9781555814694_Chap09-2.gifAbstract:
Protozoa ingest bacteria as a nutrient source, while macrophages do the same except as a defensive mechanism for the host. There is extensive evidence for a symbiotic relationship between protozoa and bacteria in which bacteria are ingested but remain inside the protozoa and survive without damaging the protozoa. The ability to survive within protozoa is dependent upon warding off the insults within the phagolysosome. Survival within and self-liberation from protozoa create new opportunities for the pathogen. The first of these is gene acquisition, whereby surviving bacteria can acquire the DNA of bacteria that have succumbed to digestive processes inside protozoa. Secondly, the constant insult to the pathogen can lead to new gene expression patterns in which some genes are overexpressed, repressed genes become expressed, and cryptic genes yield novel gene products. The bulk of this chapter is devoted to these possibilities, with Salmonella enterica serving as a new model pathogen and rumen protozoa (RPz) functioning as the conduit for changes in the pathogen. The original protozoan-pathogen model was based on free-living protozoa that were inhaled. The model for a detergent is dioctylsulfosuccinate (DSS), although this compound has a narrow therapeutic index for some species. The expression of invasin has little impact upon Salmonella virulence, but the possibility remains that this type of transfer could occur. Eliminating amoebae, including pathogenic ones such as Entamoeba histolytica and Leishmania, is of benefit to society, while removing RPz is at the very least not harmful to ruminants.
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Cartoon depiction of the mechanistic basis of the enhancement of the virulence of DT104 bacteria engulfed by RPz. The left side represents DT104 while the right side represents serovar Typhimurium lacking SGI1. (A) Bacteria are ingested by protozoa and engulfed within the phagosome. (B) Within the phagosome, hilA expression is activated by a low oxygen concentration and/or SO13. HilA promotes the production of virulence proteins. (C) Following bacterial egress from the protozoa, the pathogens can invade the ileum and eventually enter extraintestinal destinations. (D) As depicted, more DT104 bacteria can navigate through this maze and enter the systemic circulation. Not drawn to scale.
Cartoon depiction of the intraprotozoan transfer of plasmids between Salmonella and protozoan-sensitive pathogens. The left side depicts the transfer of a ceftriaxone resistance plasmid from Klebsiella (K) to Salmonella strain DT104 (D), as recently documented ( 79 ). The right side illustrates a proposed scenario in which pathogen X transfers a virulence plasmid to Salmonella. (A) Bacteria are ingested by protozoa and engulfed within the phagosome. (B) Within the phagosome, the pathogens are crowded together. (C) The protozoan-sensitive pathogen is lysed and donates its plasmid to Salmonella. (D) Following egress from the protozoa, Salmonella now expresses either a cephamycinase (Cmy) that can neutralize ceftriaxone (Cftrx) (left side) or a new virulence protein (Vp) (right side). Not drawn to scale.