Chapter 13 : Pathogenic Mechanisms and Virulence Factors of Group B Streptococci

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Pathogenic Mechanisms and Virulence Factors of Group B Streptococci, Page 1 of 2

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Although group B streptococci (GBS) commonly colonize the lower gastrointestinal tract and vaginal epithelium of healthy adults, they remain a potentially devastating pathogen to susceptible infants. As the newborn is quantitatively and qualitatively deficient in host defenses, including phagocytes, complement, and specific antibody, an environment exists in which a variety of potential GBS virulence factors are unveiled. The complex interactions between the bacterium and the newborn host that lead to disease manifestation can be divided into several important categories. This chapter reviews GBS pathogenic mechanisms involved in adherence to epithelial surfaces, cellular invasion of epithelial and endothelial barriers, direct injury to host tissues, avoidance of immunologic clearance, and induction of the sepsis syndrome. Special attention is focused on recent molecular genetic discoveries, including the sequencing of three complete GBS genomes, which have led to the identification of specific virulence determinants implicated in the pathogenesis of newborn infection.

Citation: Nizet V, Rubens C. 2006. Pathogenic Mechanisms and Virulence Factors of Group B Streptococci, p 152-168. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch13

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Bacterial Cell Wall
Cell Wall Proteins
Tumor Necrosis Factor alpha
Mobile Genetic Elements
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Intracellular invasion of host cells by GBS. (A) Primary cultures of human chorionic epithelial cells. (B) Respiratory epithelial cells of an infant macaque following infection by intraamniotic inoculation. (C) Immortalized cultures of human brain microvascular endothelial cells. In each case, intracellular GBS are found within membrane-bound vacuoles (v). Host cytoskeletal changes in panel C suggest that the organism elicits its own endocytotic uptake.

Citation: Nizet V, Rubens C. 2006. Pathogenic Mechanisms and Virulence Factors of Group B Streptococci, p 152-168. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch13
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Image of FIGURE 2

CPS synthesis operons of type III and V GBS and type 14 (14). Functional organization of the loci is indicated at top. Block arrows indicate ORFs with their gene designations below. Promoter locations are indicated (→), as are transcriptional terminators (Ω), intergenic regions (IGR), and insertion elements (IS). For the type V and 14 sequences, solid black indicates >40% identity and solid gray indicates 20 to 40% identity with the respective type III GBS homologue. Diagonal hatching, no homology; white, unrelated to CPS production.

Citation: Nizet V, Rubens C. 2006. Pathogenic Mechanisms and Virulence Factors of Group B Streptococci, p 152-168. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch13
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Virulence attributes of group B streptococci implicated in neonatal infection

Role in virulence demonstrated by animal studies with isogenic, factor-deficient mutants.

Citation: Nizet V, Rubens C. 2006. Pathogenic Mechanisms and Virulence Factors of Group B Streptococci, p 152-168. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch13

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