Organization of Biogenesis Genes for Aggregative Adherence Fimbria II Defines a Virulence Gene Cluster in Enteroaggregative Escherichia coli

Abstract

Several virulence-related genes have been described for prototype enteroaggregative Escherichia coli (EAEC) strain 042, which has been shown to cause diarrhea in human volunteers. Among these factors are the enterotoxins Pet and EAST and the fimbrial antigen aggregative adherence fimbria II (AAF/II), all of which are encoded on the 65-MDa virulence plasmid pAA2. Using nucleotide sequence analysis and insertional mutagenesis, we have found that the genes required for the expression of each of these factors, as well as the transcriptional activator of fimbrial expression AggR, map to a distinct cluster on the pAA2 plasmid map. The cluster is 23 kb in length and includes two regions required for expression of the AAF/II fimbria. These fimbrial biogenesis genes feature a unique organization in which the chaperone, subunit, and transcriptional activator lie in one cluster, whereas the second, unlinked cluster comprises a silent chaperone gene, usher, and invasin reminiscent of Dr family fimbrial clusters. This plasmid-borne virulence locus may represent an important set of virulence determinants in EAEC strains.

EnteroaggregativeEscherichia colipathotype: a genetically heterogeneous emerging foodborne enteropathogen

“…Only a few EAEC fimbrial types have been genetically characterized, and certainly, the best studied are the AA fimbriae (AAFs) I, II, and III (Nataro et al, 1992;Czeczulin et al, 1997;Bernier et al, 2002). AAF I, II, and III are encoded in high-molecular-weight plasmids and are necessary for the expression of AA, in the prototype strains 17-2, 042, and 55989, respectively (Nataro et al, 1992;Elias et al, 1999;Bernier et al, 2002). Another fimbrial structure has been described in the atypical EAEC strain C1096, which adhesion is mediated by a type IV pili, encoded by genes (operon pilLMNOPQRSTUV), and located in a plasmid of the IncI1 incompatibility group (Cobeljic et al, 1996;Dudley et al, 2006a).…”

Pathogenesis of enteroaggregativeEscherichia coliinfection

“…Thus, like ETEC, EAEC apparently adheres and colonizes by virtue of antigenically heterogeneous adhesins, which will hamper any efforts to develop immunologic prophylaxis strategies. The AAF biogenesis genes feature an organization similar to genes of the Dr family of fimbrial adhesins, which are adhesins of uropathogenic E. coli and DEAC (Bilge et al, 1989;Savarino et al, 1994;Elias et al, 1999;Bernier et al, 2002). In fact, the accessory genes of the Dr family are more closely related (30-70% amino acid identity) to those of the AAFs than are the major AAF pilin subunits to each other.…”

Donor strand complementation mechanism in the biogenesis of non‐pilus systems

“…In contrast to rigid pili and fimbriae, which are complex structures often incorporating specialized carbohydrate-binding adhesin subunits, the atypical adhesins generally have a more poorly discernible morphology and are composed of only one or two major subunits of about 14-19 kDa. Reported morphologies of the atypical adhesins include: flexible and semi-rigid bundles of fimbriae (Escherichia coli AAF-I and II respectively; Savarino et al, 1994;Elias et al, 1999); fibrillar structures [Yersinia pH 6.0 antigen (Lindler and Tall, 1993) and Myf fibrillae (Iriarte et al, 1993)], as well as the amorphous capsule of Yersinia pestis F1 antigen (Lindler and Tall, 1993) or the sheath of E. coli AFA-III adhesins (Garcia et al, 1996), in which no morphological structure has been identified. In addition to a role in host cell targeting and adhesion, a number of these structures (AFA-III, pH 6.0 antigen and SEF 14/18) play important roles during internalization of adherent bacteria (Lindler and Tall, 1993;Jouve et al, 1997;Edwards et al, 2000).…”