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Chapter 4 :

Authors: J. Michael Janda1, Sharon L. Abbott2
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Affiliations: 1: Microbial Diseases Laboratory California Department of Health Services, Richmond, California; 2: Enteric Bacteriology Microbial Diseases Laboratory California Department of Health Services, Richmond, California
Content Type: Monograph
Publication Year: 2006

Category: Bacterial Pathogenesis

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Abstract:

This chapter discusses six pathogenic or putative pathogenic groups of diarrheal that are incapable of causing infection outside the gastrointestinal (GI) tract in detail. Commonly used acronyms for these groups are enteroinvasive (EIEC), enterotoxigenic (ETEC), enteropathogenic (EPEC), Shiga toxin-producing (STEC, also known as enterohemorrhagic (EHEC), enteroaggregative (EAEC), and diffuse adhering (DAEC). strains involved in extraintestinal infections are related by the presence of specific virulence traits, and extraintestinal pathogenic (ExPEC) has been proposed for these strains. Molecular studies where DNA containing the alpha-hemolysin gene of one isolate has been recombined into a nonhemolytic fecal isolate have resulted in the recipient developing enhanced virulence in the rat peritonitis model. Production of cytotoxic necrotizing factor (CNF), a recently described virulence-associated factor, may also be associated with bacteremic strains. The K1 capsule is the major virulence determinant in strains, causing neonatal meningitis. GI disease involves the oral ingestion of pathogenic strains, with their subsequent colonization and infection of the small intestine and/or colon. Susceptibility testing of cysteine-requiring auxotrophs isolated from the urinary tract or other extraintestinal sites does not require supplementation for accurate results.

Citation: Janda J, Abbott S. 2006. , p 23-58. In The Enterobacteria, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817541.ch4
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Escherichia coli
Citation: Janda J, Abbott S. 2006. , p 23-58. In The Enterobacteria, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817541.ch4
/content/10.1128/9781555817541.chap4.fig4-1
Figure 1.

Schematic representation of adherence patterns representing EPEC (localized), EAEC (aggregative), and DAEC (diffuse) types.

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Image of Figure 1.
Figure 1.

Schematic representation of adherence patterns representing EPEC (localized), EAEC (aggregative), and DAEC (diffuse) types.

Citation: Janda J, Abbott S. 2006. , p 23-58. In The Enterobacteria, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817541.ch4
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Figure 2.

(Right) Normal Y1 sheet; (left) Y1 cells exposed to heat-labile toxin (LT) for 24 h.

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Image of Figure 2.
Figure 2.

(Right) Normal Y1 sheet; (left) Y1 cells exposed to heat-labile toxin (LT) for 24 h.

Citation: Janda J, Abbott S. 2006. , p 23-58. In The Enterobacteria, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817541.ch4
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Figure 3.

(A) Normal Vero cell sheet; (B) Vero cells exposed to Shiga toxin (Stx) for 48 h.

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Image of Figure 3.
Figure 3.

(A) Normal Vero cell sheet; (B) Vero cells exposed to Shiga toxin (Stx) for 48 h.

Citation: Janda J, Abbott S. 2006. , p 23-58. In The Enterobacteria, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817541.ch4
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Figure 4.

Pellicle formation by three EAEC strains in Mueller-Hinton broth. The strongest reaction is indicated at the far left (with autoagglutination), and the weakest reaction is at the right.

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10.1128/9781555817541/fig4-4.gif
Image of Figure 4.
Figure 4.

Pellicle formation by three EAEC strains in Mueller-Hinton broth. The strongest reaction is indicated at the far left (with autoagglutination), and the weakest reaction is at the right.

Citation: Janda J, Abbott S. 2006. , p 23-58. In The Enterobacteria, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817541.ch4
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