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Chapter 17 : and Species

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Abstract:

Recent studies have identified previously unknown virulence mechanisms that may contribute significantly to human pathogenicity. This chapter reviews existing knowledge of virulence factors and host responses and future directions that may provide a more detailed understanding of -associated human diseases. extraintestinal diseases (peritonitis, endocarditis, pneumonia, conjunctivitis, and urinary tract infections) are more common and varied than those caused by (cellulitis, arthritis, endophthalmitis, and cholecystitis). spp., therefore, may produce different types of cytotonic enterotoxins that are functionally similar. It is plausible that the expression of various virulence factors of may be controlled by quorum sensing. The major signal molecule synthesized by the ahyI locus in was N-(butanoyl)-L-homoserine lactone (BHL), also referred to as C4-HSL, with N-acylhomoserine lactone (AHL) synthesized in relatively smaller amounts. At present, it is not possible to identify the disease-causing strains because of our incomplete understanding of virulence mechanisms. Some of the confusion surrounding enterotoxins has been resolved, and several new virulence factors have been described. The case for ’s being an enteric pathogen is less convincing than that for spp. Although species has been isolated from diarrheal patients and has been incriminated in several large water- and foodborne outbreaks, no definite virulence mechanism has been identified in most strains associated with gastrointestinal infections.

Citation: Galindo C, Chopra A. 2007. and Species, p 381-400. In Doyle M, Beuchat L (ed), Food Microbiology: Fundamentals and Frontiers, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815912.ch17

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Mitogen-Activated Protein Kinase Pathway
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Figure 17.1

Virulence factors of spp. and their effects on host cells. Aeromonads produce a single polar flagellum and several lateral flagella which aid in colonization within the host. The S layer (shown as a black line surrounding the bacterial cell) contributes to pathogenicity by allowing the bacteria to evade complement killing. Accumulation of the quorum-sensing molecule, BHL, which is synthesized by the locus, can lead to coordinated expression of virulence genes. Enolase is expressed on the bacterial cell surface and is also secreted, after which it binds to and activates plasminogen, leading to a fibrinolytic cascade and potential dissemination of the bacteria in the host. Other secreted virulence factors include the cytotonic toxins Alt (heat labile) and Ast (heat stable), which cause intestinal fluid secretion, and Act (cytotoxic enterotoxin), which exerts multiple effects on host cells. Act and the related aerolysin toxins (latter not shown) heptamerize and punch holes in host cell membranes, which leads to an influx of calcium. Act specifically can bind to galectin-3 and SNAP23, host cell molecules that are required for Act-induced host cell apoptosis. Additionally, Act binds to cholesterol, which may help aggregate the toxin on the cell surface to become internalized or bring it into contact with one or more host surface receptors through which it may signal. The newly described T3SS can directly inject pathogenicity factors, such as the AexT toxin, into host cells. The production of Act and components of the T3SS are regulated by glucose-inhibited division gene A () and DAM, which methylates specific bacterial DNA sequences. Only some of the crucial virulence factors produced by spp. are shown. Figure drawn by Erin Boyle.

Citation: Galindo C, Chopra A. 2007. and Species, p 381-400. In Doyle M, Beuchat L (ed), Food Microbiology: Fundamentals and Frontiers, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815912.ch17
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