Heterogenic virulence in a diarrheagenic Escherichia coli: Evidence for an EPEC expressing heat-labile toxin of ETEC

Dutta, Sachinandan; Pazhani, Gururaja P.; Nataro, James P.; Ramamurthy, Thandavarayan

doi:10.1016/j.ijmm.2014.10.006

Cited by 44 publications

(50 citation statements)

References 44 publications

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“…A recently described hybrid enteropathogenic E. coli (EPEC)/ETEC strain harbors a π-CU pili locus, identical to the locus harbored by ETEC 700377 and ETEC 300659 (Dutta et al, 2015). Therefore, we computationally screened a set of EPEC genes in the three AN-ETEC strains in which we found π-CU pili loci; these genes were typically contained in the locus of enterocyte effacement (LEE), a pathogenicity island carried by both EPEC and enterohemorrhagic E. coli (Croxen et al, 2013).…”

Section: Resultsmentioning

confidence: 99%

“…Dutta et al reported the presence of a homolog locus of pap , which encodes the P fimbria, in an ETEC strain that also has genes that used to be part of the LEE locus in atypical EPEC strains (Dutta et al, 2015). In the current project, we identified two π-CU pili loci, one of them identical to that described by Dutta et al Our analysis was consistent in terms of the relatedness with the pap locus, but we found a higher identity with the sfp locus, which was first described in an enterohemorrhagic E. coli O157:H- strain, as is determinant in the capacity of agglutinating erythrocytes.…”

Section: Discussionmentioning

confidence: 99%

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Chaperone-Usher Pili Loci of Colonization Factor-Negative Human Enterotoxigenic Escherichia coli

Canto

O’Ryan

Pardo

et al. 2017

Front. Cell. Infect. Microbiol.

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Enterotoxigenic Escherichia coli (ETEC) is one of the most common causes of diarrhea worldwide. Among the 25 different ETEC adhesins, 22 are known as “colonization factors” (CFs), of which 17 are assembled by the chaperone-usher (CU) mechanism. Currently, there is no preventive therapy against ETEC, and CFs have been proposed as components for vaccine development. However, studies of diarrhea-causing ETEC strains worldwide indicate that between 15 and 50% of these are negative for known CFs, hindering the selection of the most widespread structures and suggesting that unknown adhesins remain to be identified. Here, we report the result of a comprehensive analysis of 35 draft genomes of ETEC strains which do not carry known adhesin genes; our goal was to find new CU pili loci. The phylogenetic profiles and serogroups of these strains were highly diverse, a majority of which produced only the heat-labile toxin. We identified 10 pili loci belonging to CU families β (1 locus), γ2 (7 loci), κ (1 locus), and π (1 locus), all of which contained the required number of open reading frames (ORFs) to encode functional structures. Three loci were variants of previously-known clusters, three had been only-partially described, and four are novel loci. Intra-loci genetic variability identified would allow the synthesis of up to 14 different structures. Clusters of putative γ2-CU pili were most common (23 strains), followed by putative β-CU pili (12 strains), which have not yet been fully characterized. Overall, our findings significantly increase the number of ETEC adhesion genes associated with human infections.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chaperone-Usher Pili Loci of Colonization Factor-Negative Human Enterotoxigenic Escherichia coli

Canto

O’Ryan

Pardo

et al. 2017

Front. Cell. Infect. Microbiol.

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“…However, some isolates do not comply with the standard pathotyping scheme (Table 2). Such strains include isolates of EPEC that carry genes for the heat-labile enterotoxin of ETEC (Dutta et al, 2015); and strains of ETEC and EAEC that secrete Shiga toxin (Zhang et al, 2007; Buchholz et al, 2011). Even Shigella dysenteriae type 1, which carries the Shiga toxin gene on its chromosome is atypical, as far as the Shigella biotype is concerned, since no other strain in this “genus” produces this toxin.…”

Section: E Coli Subtypesmentioning

confidence: 99%

Are Escherichia coli Pathotypes Still Relevant in the Era of Whole-Genome Sequencing?

Robins-Browne

Holt

Ingle³

et al. 2016

Front. Cell. Infect. Microbiol.

130

120

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The empirical and pragmatic nature of diagnostic microbiology has given rise to several different schemes to subtype E.coli, including biotyping, serotyping, and pathotyping. These schemes have proved invaluable in identifying and tracking outbreaks, and for prognostication in individual cases of infection, but they are imprecise and potentially misleading due to the malleability and continuous evolution of E. coli. Whole genome sequencing can be used to accurately determine E. coli subtypes that are based on allelic variation or differences in gene content, such as serotyping and pathotyping. Whole genome sequencing also provides information about single nucleotide polymorphisms in the core genome of E. coli, which form the basis of sequence typing, and is more reliable than other systems for tracking the evolution and spread of individual strains. A typing scheme for E. coli based on genome sequences that includes elements of both the core and accessory genomes, should reduce typing anomalies and promote understanding of how different varieties of E. coli spread and cause disease. Such a scheme could also define pathotypes more precisely than current methods.

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“…Delivery of heat-labile (LT) and/or heat-stable (ST) enterotoxins and release of lipopolysaccharide (LPS) to the intestine are critical virulence traits for the onset of the diarrhea. Moreover, ETEC and other diarrheagenic E. coli strains (e.g., enteropathogenic E. coli [EPEC] and verocytotoxigenic E. coli [VTEC]) may obtain additional virulence factors via horizontal gene transfer (4,5). Formation of attachment and effacing (A/E) lesions on intestinal cells is related to the presence of intimin (eae gene) secreted by EPEC/ETEC (6).…”

mentioning

confidence: 99%

Oral Administration of a Select Mixture of Bacillus Probiotics Affects the Gut Microbiota and Goblet Cell Function following Escherichia coli Challenge in Newly Weaned Pigs of Genotype MUC4 That Are Supposed To Be Enterotoxigenic E. coli F4ab/ac Receptor Negative

Zhang

Zhu

Zhou

et al. 2017

Appl Environ Microbiol

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Structural disruption of the gut microbiota and impaired goblet cell function are collateral etiologic factors in enteric diseases. Low, moderate, or high doses of a Bacillus licheniformis-B. subtilis mixture (BLS mix) were orally administered to piglets of genotype MUC4 that are supposed to be F4-expressing enterotoxigenic Escherichia coli strain (F4 ϩ ETEC) F4ab/ac receptor negative (i.e., MUC4-resistant piglets) for 1 week before F4 ϩ ETEC challenge. The luminal contents were collected from the mucosa of the colon on day 8 after F4 ϩ ETEC challenge. The BLS mix attenuated E. coli-induced expansion of Bacteroides uniformis, Eubacterium eligens, Acetanaerobacterium, and Sporobacter populations. Clostridium and Turicibacter populations increased following F4 ϩ ETEC challenge in pigs pretreated with low-dose BLS mix. Lactobacillus gasseri and Lactobacillus salivarius populations increased after administration of BLS mix during E. coli infection. The beneficial effects of BLS mix were due in part to the expansion of certain Clostridium, Lactobacillus, and Turicibacter populations, with a corresponding increase in the number of goblet cells in the ileum via upregulated Atoh1 expression, in turn increasing MUC2 production and thus preserving the mucus barrier and enhancing host defenses against enteropathogenic bacteria. However, excessive BLS mix consumption may increase the risk for enteritis, partly through disruption of colonic microbial ecology, characterized by expansion of Proteobacteria and impaired goblet cell function in the ileum. Our findings suggest that oral administration of BLS mix reprograms the gut microbiota and enhances goblet cell function to ameliorate enteritis.IMPORTANCE The present study is important for improving our understanding of the protective role of probiotics against Escherichia coli infection in piglets. Structural disruption of the gut microbiota and impaired goblet cell function are collateral etiologic factors in enteric diseases. In this study, low, moderate, or high doses of a Bacillus licheniformis-B. subtilis mixture (BLS mix) were orally administered to MUC4-resistant piglets for 1 week before the F4-expressing ETEC strain (F4 ϩ ETEC) challenge. Our findings suggest that oral administration of BLS mix reprograms the gut microbiota and enhances goblet cell function to ameliorate enteritis. KEYWORDS

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Heterogenic virulence in a diarrheagenic Escherichia coli: Evidence for an EPEC expressing heat-labile toxin of ETEC

Cited by 44 publications

References 44 publications

Chaperone-Usher Pili Loci of Colonization Factor-Negative Human Enterotoxigenic Escherichia coli

Chaperone-Usher Pili Loci of Colonization Factor-Negative Human Enterotoxigenic Escherichia coli

Are Escherichia coli Pathotypes Still Relevant in the Era of Whole-Genome Sequencing?

Oral Administration of a Select Mixture of Bacillus Probiotics Affects the Gut Microbiota and Goblet Cell Function following Escherichia coli Challenge in Newly Weaned Pigs of Genotype MUC4 That Are Supposed To Be Enterotoxigenic E. coli F4ab/ac Receptor Negative

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