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Abstract:

The first reported outbreak of Enteroaggregative (EAEC) diarrhea occurred in Serbia, where 19 newborns in a nursery developed watery diarrhea. Recently, EAEC has been implicated as an important agent of diarrhea in industrialized countries as well. In a large prospective study of adults and children with diarrhea in the United Kingdom, researchers found that EAEC was strongly associated with diarrheal illness and was the second most commonly implicated bacterial pathogen after . Importantly, in that study, EAEC was defined by positivity by an assay with an empirically derived DNA probe rather than by the more inclusive HEp-2 adherence assay. A double-blind, placebo-controlled crossover trial of ciprofloxacin versus placebo in a study population demonstrated improvement in diarrhea and intestinal symptoms in patients with human immunodeficiency virus (HIV) and EAEC infections when they were treated with antibiotics. The basic strategy of EAEC infection appears to comprise colonization of small-bowel and large-bowel mucosal surfaces, followed by elaboration of enterotoxins. A role for Pet in EAEC infection is supported by the observation that an EAEC strain mutated in the Pet-encoding gene is unable to elicit damage to the colonic mucosa in the organ culture model. AggR was initially found to induce expression of AA fimbriae (AAF)/I and AAF/II, but the author's laboratory has noted that many strains carrying the gene do not express any known adhesin of AAF.

Citation: Nataro J. 2004. Enteroaggregative , p 101-110. In Scheld W, Murray B, Hughes J (ed), Emerging Infections 6. ASM Press, Washington, DC. doi: 10.1128/9781555816995.ch7
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Figure 1

AA in the HEp-2 assay. EAEC is defined by the characteristic pattern of adherence after 3 h of incubation in the presence of viable HEp-2 cells. Bacteria adhere to the surfaces of the cells as well as to the glass substratum in a characteristic stacked brick phenotype.

Citation: Nataro J. 2004. Enteroaggregative , p 101-110. In Scheld W, Murray B, Hughes J (ed), Emerging Infections 6. ASM Press, Washington, DC. doi: 10.1128/9781555816995.ch7
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Image of Figure 2
Figure 2

Genetics of EAEC virulence. Most EAEC strains harbor a ca. 60-MDa plasmid designated pAA, which encodes the adhesin of AAF in many isolates. The plasmid may also encode the toxins Pet and EAST1. pAA also encodes the transcriptional activator AggR, which induces the expression of genes encoding AAF, as well as additional as yet cryptic loci on pAA itself and on the bacterial chromosome. Three chromosomal loci have been identified in EAEC, including the yersiniabactin island (similar to that of ), the Pic-ShET1 island, and a cryptic island under AggR control.

Citation: Nataro J. 2004. Enteroaggregative , p 101-110. In Scheld W, Murray B, Hughes J (ed), Emerging Infections 6. ASM Press, Washington, DC. doi: 10.1128/9781555816995.ch7
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