Prevalence and Characteristics of the O122 Pathogenicity Island in Typical and Atypical Enteropathogenic Escherichia coli Strains

Abstract

The presence of the pathogenicity island (PAI) O122 genes, efa1 (lifA), sen, pagC, nleB, and nleE, in typical and atypical enteropathogenic Escherichia coli (EPEC) strains was investigated. The simultaneous occurrence of all genes was statistically associated with diarrhea due to atypical EPEC. Detection of the complete PAI O122 could aid in the identification of potential pathogenic strains of atypical EPEC.Enteropathogenic Escherichia coli (EPEC) and Shiga toxin (Stx)-producing E. coli (STEC) are important human enteropathogens (9). EPEC is further subgrouped into typical (tEPEC) and atypical (aEPEC) EPEC (8, 21). tEPEC strains are major causative agents of acute diarrhea in infants in developing countries, whereas aEPEC strains affect children and adults worldwide (5,7,9,21). The main difference between tEPEC and aEPEC is the presence of the EPEC adherence factor (EAF) plasmid in tEPEC (8,21). This plasmid encodes the bundle-forming pilus (BFP), which mediates localized adherence to intestinal cells (9), which is an essential property to differentiate tEPEC from aEPEC strains (1,7,21).Formation of the attaching-and-effacing (AE) lesion is the major virulence mechanism of EPEC and an additional virulence property of enterohemorrhagic E. coli (EHEC) strains, a subset of STEC strains (9). This lesion consists of intimate bacterial adherence to the intestinal epithelial cells, cytoskeleton remodeling, and microvillus effacement (9). The genes encoding the AE lesion are located in a pathogenicity island (PAI) known as the locus of enterocyte effacement (LEE) (9). Despite the recognized importance of AE lesion formation, other putative virulence genes among AE-producing E. coli strains have been described. Efa1 (EHEC factor for adherence) is an adhesin originally described in some EHEC strains (16). The efa1 gene is almost identical to lifA, an EPEC gene encoding lymphostatin (LifA) (13). LifA inhibits the proliferation of mitogen-activated lymphocytes and the synthesis of proinflammatory cytokines (13). Efa1/LifA contributes to EPEC adherence to epithelial cells and is critical for intestinal colonization by Citrobacter rodentium, which is an AE lesion-producing bacterial pathogen of mice (12). Although, in the prototype EHEC O157:H7 strain EDL933, efa1 (lifA) lacks the 3Ј region (efaC), the adherence ability of this strain is preserved (20).efa1 (lifA) is outside the LEE and inside PAI O122 (16). This island also harbors genes which are very similar to pagC of Salmonella enterica serovar Typhimurium, sen of Shigella flexneri, and two C. rodentium non-LEE genes, nleB and nleE. PagC is required for bacterial survival within macrophages and is immunogenic to humans, while sen encodes an S. flexneri enterotoxin (10). NleB is linked to colonization and disease in mice (11), and NleE induces polymorphonuclear (PMN) transepithelial migration and is involved in the blockage of 24). Afset et al. (2) found that, of 182 virulence genes searched for among aEPEC strains, 12 were statistically associated with diarrhea, includi...

Pathogenicity Island O-122 in enteropathogenic Escherichia coli strains is associated with diarrhea severity in children from Lima Peru

“…These results differ from those reported by Vieira, where complete PAI O-122 was found in 32.5% of EPEC strains isolated from patients with diarrhea and was more prevalent in t-EPEC than in a-EPEC (48.9% versus 17.8%, respectively). Considering t-EPEC and a-EPEC strains together, the presence of complete PAI O-122 was similar among strains isolated from diarrhea (8.6%) and control (9.6%), different than the data reported by Vieira where EPEC and a-EPEC strains with complete PAI O-122 were significantly associated with diarrhea (32.5% and 22.4%) than control strains (10.5% and 6.5) respectively (Vieira et al, 2010). …”

“…However, its association with diarrhea is controversial (Afset et al, 2006). Vieira et al, have shown that typical and atypical EPEC strains may harbor a complete ( pagC, senA, nleB, nleE and lifA/efa-1 all together) or incomplete PAI O-122; a strong association between the presence of a complete PAI O-122 and diarrhea was observed only in a-EPEC strains (Vieira et al, 2010). It is unknown if incomplete PAI O-122 could also be associated with diarrhea.…”

Norwegian Sheep Are an Important Reservoir for Human-Pathogenic Escherichia coli O26:H11

“…However, group C isolates from four other sheep flocks had MLVA profiles (6-3-0-8-3-4-1 or 6-3-0-8-3-7-1) previously described for human E. coli O26, but these isolates were from patients infected in Brazil (39). Although the group C isolates lacked typical EHEC genes such as stx, ehxA, and espK, their virulence gene profile (eae, nleB, efa1, lpfA R141 , and lpfA O113 ) indicates that these E. coli O26:H11 isolates cannot be considered nonpathogenic to humans (1,16,57).…”

“…In contrast, yjaA was absent from all isolates. Previous clinical studies have shown that the presence of OI-122 genes and absence of yjaA were associated with diarrhea in patients infected with aEPEC (1,57). Recently, a close relationship between the presence of the nleB gene and highly virulent EHEC and EPEC strains was found (16).…”

“…However, during human infection these stx-negative bacteria may represent a suitable target for transduction by stx-carrying phages released from other Stx-producing E. coli bacteria (38). It is also important to emphasize that even if the ovine EHEClike O26:H11 isolates do not gain stx-carrying phages, they have to be considered human pathogens due to their virulence gene profile (1,16,57). Although the PFGE profiles were very heterogeneous among E. coli O26:H11 isolates, a few isolates from sheep and patients showed identical PFGE profiles, and these were all assigned to group A or B.…”