Genetic differences between<i>Escherichia coli</i>O26 strains isolated in Brazil and in other countries

Peixoto, Jean Charles da Cunha; Bando, Sílvia Yumi; Ordonez, Joana; Botelho, Beatriz Amoroso; Trabulsi, Luíz Rachid; Moreira-Filho, Carlos Alberto

doi:10.1111/j.1574-6968.2001.tb10571.x

Cited by 22 publications

(3 citation statements)

References 28 publications

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“…In fact, these serotypes and others with properties similar to those of O128:H2 are not true atypical EPEC or STEC serotypes but rather are heterogeneous serotypes that include different clones or genetic lineages. For example, we have recently shown by random amplified polymorphic DNA that O26:H11 Stx-producing strains isolated in Europe and North America are genetically different from Stx-negative strains of the same serotype isolated in Brazil ( 18 ). Although this kind of study has not been done with serotype O128:H2, this serotype is also heterogeneous since it includes different ribotypes with distinct virulence characteristics (L.R.…”

Section: Serotypesmentioning

confidence: 99%

Typical and Atypical EnteropathogenicEscherichia coli

Trabulsi

Keller

Gomes

2002

Emerg. Infect. Dis.

635

723

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Typical and atypical enteropathogenic Escherichia coli (EPEC) strains differ in several characteristics. Typical EPEC, a leading cause of infantile diarrhea in developing countries, is rare in industrialized countries, where atypical EPEC seems to be a more important cause of diarrhea. For typical EPEC, the only reservoir is humans; for atypical EPEC, both animals and humans can be reservoirs. Typical and atypical EPEC also differ in genetic characteristics, serotypes, and virulence properties. Atypical EPEC is more closely related to Shiga toxin–producing E. coli (STEC), and like STEC these strains appear to be emerging pathogens.

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Section: Serotypesmentioning

confidence: 99%

Typical and Atypical EnteropathogenicEscherichia coli

Trabulsi

Keller

Gomes

2002

Emerg. Infect. Dis.

635

723

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“…Recent findings in Brazil of E. coli O26 containing the H8 antigen belonging to EHEC and stx-negative strains led to the inclusion of this antigen in this study (45). Furthermore, antigen H11 and nonpathogenic antigen H32, commonly isolated in food products, were also tested (18,(45)(46)(47). Investigation of the H antigen revealed that all strains were positive for fliC H11 .…”

Section: Discussionmentioning

confidence: 99%

Genetic Diversity and Pathogenic Potential of Attaching and Effacing Escherichia coli O26:H11 Strains Recovered from Bovine Feces in the United States

Ison

Delannoy

Bugarel

et al. 2015

Appl Environ Microbiol

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c Escherichia coli O26 has been identified as the most common non-O157 Shiga toxin-producing E. coli (STEC) serogroup to cause human illnesses in the United States and has been implicated in outbreaks around the world. E. coli has high genomic plasticity, which facilitates the loss or acquisition of virulence genes. Attaching and effacing E. coli (AEEC) O26 strains have frequently been isolated from bovine feces, and there is a need to better characterize the relatedness of these strains to defined molecular pathotypes and to describe the extent of their genetic diversity. High-throughput real-time PCR was used to screen 178 E. coli O26 isolates from a single U.S. cattle feedlot, collected from May to July 2011, for the presence or absence of 25 O26 serogroupspecific and virulence-associated markers. The selected markers were capable of distinguishing these strains into molecularly defined groups (yielding 18 unique marker combinations). Analysis of the clustered regularly interspaced short palindromic repeat 1 (CRISPR1) and CRISPR2a loci further discriminated isolates into 24 CRISPR types. The combination of molecular markers and CRISPR typing provided 20.8% diversity. The recent CRISPR PCR target SP_O26-E, which was previously identified only in stx 2 -positive O26:H11 human clinical strains, was identified in 96.4% (161/167 [95% confidence interval, 99.2 to 93.6%]) of the stx-negative AEEC O26:H11 bovine fecal strains. This supports that these stx-negative strains may have previously contained a prophage carrying stx or could acquire this prophage, thus possibly giving them the potential to become pathogenic to humans. These results show that investigation of specific genetic markers may further elucidate our understanding of the genetic diversity of AEEC O26 strains in bovine feces. Escherichia coli O26 has been identified as the most common non-O157 Shiga toxin-producing E. coli (STEC) serogroup to cause human illnesses resulting in hemorrhagic colitis and hemolytic-uremic syndrome (HUS) in the United States and in Europe (1-3). In an effort to ensure a safer food supply, in 2012, the U.S. Department of Agriculture Food Safety and Inspection Service (FSIS) expanded the list of serogroups designated adulterants in raw nonintact beef and products that will become nonintact beef to include non-O157 STEC serogroups O26, O45, O103, O111, O121, and O145 (4).Cattle have been implicated as a reservoir for E. coli O26, and cattle likely serve as an important source of contamination of raw agriculture products that come into contact with contaminated manure, including beef, dairy, and produce (5, 6). Additionally, E. coli O26 is a highly diverse serogroup, and strains can vary from highly pathogenic to avirulent, nonpathogenic variants (7-10). Furthermore, this distribution of molecularly defined E. coli O26 pathogroups within bovine feces has not been fully described.In E. coli, most virulence factors are located on potentially mobile elements (phages, plasmids, and pathogenicity islands), which can rapidly be excha...

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“…The typical and atypical EPEC strains selected for this study belong to the classical EPEC serogroups. We selected 10 aEPEC strains (two O26:H11, four O55:H7, one O111ab:H9, one O111:HNM, and two O119:H2) characterized by the eae ϩ EAF Ϫ genetic profile and expression of LAL in HEp-2 cells (6-h adherence assay) in previous studies (19,22,(26)(27)(28)(29). For comparison, three tEPEC strains (eae ϩ EAF ϩ ) belonging to the classical serogroups (O55:H6, O111:H2, and O119:H6) were also studied (19,26,27).…”

Section: Methodsmentioning

confidence: 99%

Late Establishment of the Attaching and Effacing Lesion Caused by Atypical Enteropathogenic Escherichia coli Depends on Protein Expression Regulated by Per

et al. 2015

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c Enteropathogenic Escherichia coli (EPEC) is classified as typical (tEPEC) or atypical (aEPEC) based on the presence or absence of the E. coli adherence factor plasmid (pEAF), respectively. The hallmark of EPEC infection is the formation of the attaching and effacing (A/E) lesions on the gut mucosa. We compared the kinetics of A/E lesion formation induced by aEPEC and tEPEC. The examination of infected HEp-2 cells clearly demonstrated delayed A/E lesion formation by aEPEC in comparison to tEPEC. This delay was associated with the expression of locus of enterocyte effacement (LEE)-encoded virulence factors (i.e., intimin and EspD). Indeed, the insertion of a plasmid containing perABC, a transcriptional regulator of virulence factors involved in A/E formation, into aEPEC strains increased and accelerated the formation of A/E lesions. Interestingly, the enhanced expression and translocation of LEE-encoded proteins, such as those expressed in LEE5 (intimin) and LEE4 (EspD), in aEPEC (perABC) was independent of bacterial adhesion. The secretion kinetics of these two proteins representing LEE5 and LEE4 expression correlated with A/E lesion formation. We conclude that the lack of Per in the regulation network of virulence genes is one of the main factors that delay the establishment of A/E lesions induced by aEPEC strains.

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Genetic differences betweenEscherichia coliO26 strains isolated in Brazil and in other countries

Cited by 22 publications

References 28 publications

Typical and Atypical EnteropathogenicEscherichia coli

Typical and Atypical EnteropathogenicEscherichia coli

Genetic Diversity and Pathogenic Potential of Attaching and Effacing Escherichia coli O26:H11 Strains Recovered from Bovine Feces in the United States

Late Establishment of the Attaching and Effacing Lesion Caused by Atypical Enteropathogenic Escherichia coli Depends on Protein Expression Regulated by Per

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