Correlation between In Vivo Biofilm Formation and Virulence Gene Expression in Escherichia coli O104:H4

Safadi, Rim Al; Abu-Ali, Galeb; Sloup, Rudolph E.; Rudrik, James T.; Waters, Christopher M.; Eaton, Kathryn A.; Manning, Shannon D.

doi:10.1371/journal.pone.0041628

Cited by 66 publications

(72 citation statements)

References 34 publications

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“…We further identified the main site of C227-11 colonization to be the cecum in both Amp-treated and ICF models, a finding that is in agreement with the findings obtained with other O104:H4 infection models (47,49,68). However, unlike Torres et al (47), we found that the O104:H4 outbreak strain clearly also colonized the small and large intestines.…”

Section: Discussionsupporting

confidence: 91%

“…is earlier than the time that it had been detected in a germfree mouse model, in which similar kidney damage was not noted in O104:H4-infected mice at 7 days p.i., though acute tubular necrosis was identified in mice euthanized on days 13 to 15 p.i. in that study (49). There have been a few publications describing acute tubular necrosis in the kidneys of STEC-infected individuals.…”

Section: Discussionmentioning

confidence: 85%

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Virulence of the Shiga Toxin Type 2-Expressing Escherichia coli O104:H4 German Outbreak Isolate in Two Animal Models

et al. 2013

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dIn May 2011, a large food-borne outbreak was traced to an unusual O104:H4 enteroaggregative Escherichia coli (EAEC) strain that produced Shiga toxin (Stx) type 2 (Stx2). We developed a mouse model to study the pathogenesis and treatment for this strain and examined the virulence of the isolate for Dutch belted rabbits. O104:H4 strain C227-11 was gavaged into C57BL/6 mice at 10 9 to 10 11 CFU/animal. The infected animals were then given water with ampicillin (Amp; 5 g/liter) ad libitum. The C227-11-infected, Amp-treated C57BL/6 mice exhibited both morbidity and mortality. Kidneys from mice infected with C227-11 showed acute tubular necrosis, a finding seen in mice infected with typical Stx-producing E. coli. We provided anti-Stx2 antibody after infection and found that all of the antibody-treated mice gained more weight than untreated mice and, in another study, that all of the antibody-treated animals lived, whereas 3/8 phosphate-buffered saline-treated mice died. We further compared the pathogenesis of C227-11 with that of an Stx-negative (Stx ؊ ) O104:H4 isolate, C734-09, and an Stx2 ؊ phage-cured derivative of C227-11. Whereas C227-11-infected animals lost weight or gained less weight over the course of infection and died, mice infected with either of the Stx ؊ isolates did not lose weight and only one mouse died. When the Stx-positive (Stx ؉ ) and Stx2 ؊ O104:H4 strains were compared in rabbits, greater morbidity and mortality were observed in rabbits infected with the Stx2 ؉ isolates than the Stx2 ؊ isolates. In conclusion, we describe two animal models for EAEC pathogenesis, and these studies show that Stx2 is responsible for most of the virulence observed in C227-11-infected mice and rabbits.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 85%

Virulence of the Shiga Toxin Type 2-Expressing Escherichia coli O104:H4 German Outbreak Isolate in Two Animal Models

et al. 2013

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“…Sci-1 and sci-2 are two gene clusters present on pheU responsible for evidence for enhanced virulence and detrimental effects caused by emerging heterogeneity among strains. 12 Transmission of EAEC is most commonly associated with contaminated food and water. In Mexico, EAEC is the most common bacterial pathogen isolated from food.…”

Section: Introductionmentioning

confidence: 99%

Animal models of enteroaggregativeEscherichia coliinfection

2013

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“…DgcT (YcdT) is a DGC that has been implicated in the production of poly-GlcNAc (PGA), which is expressed within the host and serves as biofilm matrix component and/or virulence factor in some pathogenic E. coli (48)(49)(50). We found that the dgcT gene was entirely deleted in 14 strains and disrupted by small frameshift or stop codon mutations in five additional strains (Table 2).…”

Section: Resultsmentioning

confidence: 99%

Genome-Based Comparison of Cyclic Di-GMP Signaling in Pathogenic and Commensal Escherichia coli Strains

Povolotsky

Hengge

2016

J Bacteriol

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The ubiquitous bacterial second messenger cyclic di-GMP (c-di-GMP) has recently become prominent as a trigger for biofilm formation in many bacteria. It is generated by diguanylate cyclases (DGCs; with GGDEF domains) and degraded by specific phosphodiesterases (PDEs; containing either EAL or HD-GYP domains). Most bacterial species contain multiples of these proteins with some having specific functions that are based on direct molecular interactions in addition to their enzymatic activities. Escherichia coli K-12 laboratory strains feature 29 genes encoding GGDEF and/or EAL domains, resulting in a set of 12 DGCs, 13 PDEs, and four enzymatically inactive "degenerate" proteins that act by direct macromolecular interactions. We present here a comparative analysis of GGDEF/EAL domain-encoding genes in 61 genomes of pathogenic, commensal, and probiotic E. coli strains (including enteric pathogens such as enteroaggregative, enterohemorrhagic, enteropathogenic, enterotoxigenic, and adherent and invasive Escherichia coli and the 2011 German outbreak O104:H4 strain, as well as extraintestinal pathogenic E. coli, such as uropathogenic and meningitis-associated E. coli). We describe additional genes for two membrane-associated DGCs (DgcX and DgcY) and four PDEs (the membrane-associated PdeT, as well as the EAL domain-only proteins PdeW, PdeX, and PdeY), thus showing the pangenome of E. coli to contain at least 35 GGDEF/EAL domain proteins. A core set of only eight proteins is absolutely conserved in all 61 strains: DgcC (YaiC), DgcI (YliF), PdeB (YlaB), PdeH (YhjH), PdeK (YhjK), PdeN (Rtn), and the degenerate proteins CsrD and CdgI (YeaI). In all other GGDEF/EAL domain genes, diverse point and frameshift mutations, as well as small or large deletions, were discovered in various strains. IMPORTANCEOur analysis reveals interesting trends in pathogenic Escherichia coli that could reflect different host cell adherence mechanisms. These may either benefit from or be counteracted by the c-di-GMP-stimulated production of amyloid curli fibers and cellulose. Thus, EAEC, which adhere in a "stacked brick" biofilm mode, have a potential for high c-di-GMP accumulation due to DgcX, a strongly expressed additional DGC. In contrast, EHEC and UPEC, which use alternative adherence mechanisms, tend to have extra PDEs, suggesting that low cellular c-di-GMP levels are crucial for these strains under specific conditions. Overall, our study also indicates that GGDEF/EAL domain proteins evolve rapidly and thereby contribute to adaptation to host-specific and environmental niches of various types of E. coli.

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Correlation between In Vivo Biofilm Formation and Virulence Gene Expression in Escherichia coli O104:H4

Cited by 66 publications

References 34 publications

Virulence of the Shiga Toxin Type 2-Expressing Escherichia coli O104:H4 German Outbreak Isolate in Two Animal Models

Virulence of the Shiga Toxin Type 2-Expressing Escherichia coli O104:H4 German Outbreak Isolate in Two Animal Models

Animal models of enteroaggregativeEscherichia coliinfection

Genome-Based Comparison of Cyclic Di-GMP Signaling in Pathogenic and Commensal Escherichia coli Strains

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