scholarly journals Oral Tolerance Failure upon Neonatal Gut Colonization with Escherichia coli Producing the Genotoxin Colibactin

2015 ◽  
Vol 83 (6) ◽  
pp. 2420-2429 ◽  
Author(s):  
Thomas Secher ◽  
Delphine Payros ◽  
Camille Brehin ◽  
Michele Boury ◽  
Claude Watrin ◽  
...  

The intestinal barrier controls the balance between tolerance and immunity to luminal antigens. When this finely tuned equilibrium is deregulated, inflammatory disorders can occur. There is a concomitant increase, in urban populations of developed countries, of immune-mediated diseases along with a shift inEscherichia colipopulation from the declining phylogenetic group A to the newly dominant group B2, including commensal strains producing a genotoxin called colibactin that massively colonized the gut of neonates. Here, we showed that mother-to-offspring early gut colonization by colibactin-producingE. coliimpairs intestinal permeability and enhances the transepithelial passage of luminal antigen, leading to an increased immune activation. Functionally, this was accompanied by a dramatic increase in local and systemic immune responses against a fed antigen, decreased regulatory T cell population, tolerogenic dendritic cells, and enhanced mucosal delayed-type hypersensitivity response. Conversely, the abolition of colibactin expression by mutagenesis abrogates the alteration of oral tolerance induced by neonatal colonization byE. coli. In conclusion, the vertical colonization byE. coliproducing the genotoxin colibactin enhances intestinal translocation and subsequently alters oral tolerance. Thus, early colonization byE. colifrom the newly dominant phylogenetic group B2, which produces colibactin, may represent a risk factor for the development of immune-mediated diseases.

2012 ◽  
Vol 78 (16) ◽  
pp. 5824-5830 ◽  
Author(s):  
Catherine M. Logue ◽  
Curt Doetkott ◽  
Paul Mangiamele ◽  
Yvonne M. Wannemuehler ◽  
Timothy J. Johnson ◽  
...  

ABSTRACTNeonatal meningitisEscherichia coli(NMEC) is one of the top causes of neonatal meningitis worldwide. Here, 85 NMEC and 204 fecalE. coliisolates from healthy humans (HFEC) were compared for possession of traits related to virulence, antimicrobial resistance, and plasmid content. This comparison was done to identify traits that typify NMEC and distinguish it from commensal strains to refine the definition of the NMEC subpathotype, identify traits that might contribute to NMEC pathogenesis, and facilitate choices of NMEC strains for future study. A large number ofE. colistrains from both groups were untypeable, with the most common serogroups occurring among NMEC being O18, followed by O83, O7, O12, and O1. NMEC strains were more likely than HFEC strains to be assigned to the B2 phylogenetic group. Few NMEC or HFEC strains were resistant to antimicrobials. Genes that best discriminated between NMEC and HFEC strains and that were present in more than 50% of NMEC isolates were mainly from extraintestinal pathogenicE. coligenomic and plasmid pathogenicity islands. Several of these defining traits had not previously been associated with NMEC pathogenesis, are of unknown function, and are plasmid located. Several genes that had been previously associated with NMEC virulence did not dominate among the NMEC isolates. These data suggest that there is much about NMEC virulence that is unknown and that there are pitfalls to studying single NMEC isolates to represent the entire subpathotype.


mBio ◽  
2013 ◽  
Vol 4 (4) ◽  
Author(s):  
Alanna M. Spees ◽  
Tamding Wangdi ◽  
Christopher A. Lopez ◽  
Dawn D. Kingsbury ◽  
Mariana N. Xavier ◽  
...  

ABSTRACTTreatment with streptomycin enhances the growth of human commensalEscherichia coliisolates in the mouse intestine, suggesting that the resident microbial community (microbiota) can inhibit the growth of invading microbes, a phenomenon known as “colonization resistance.” However, the precise mechanisms by which streptomycin treatment lowers colonization resistance remain obscure. Here we show that streptomycin treatment rendered mice more susceptible to the development of chemically induced colitis, raising the possibility that the antibiotic might lower colonization resistance by changing mucosal immune responses rather than by preventing microbe-microbe interactions. Investigation of the underlying mechanism revealed a mild inflammatory infiltrate in the cecal mucosa of streptomycin-treated mice, which was accompanied by elevated expression ofNos2, the gene that encodes inducible nitric oxide synthase. In turn, this inflammatory response enhanced the luminal growth ofE. coliby nitrate respiration in aNos2-dependent fashion. These data identify low-level intestinal inflammation as one of the factors responsible for the loss of resistance toE. colicolonization after streptomycin treatment.IMPORTANCEOur intestine is host to a complex microbial community that confers benefits by educating the immune system and providing niche protection. Perturbation of intestinal communities by streptomycin treatment lowers “colonization resistance” through unknown mechanisms. Here we show that streptomycin increases the inflammatory tone of the intestinal mucosa, thereby making the bowel more susceptible to dextran sulfate sodium treatment and boosting theNos2-dependent growth of commensalEscherichia coliby nitrate respiration. These data point to the generation of alternative electron acceptors as a by-product of the inflammatory host response as an important factor responsible for lowering resistance to colonization by facultative anaerobic bacteria such asE. coli.


2012 ◽  
Vol 56 (7) ◽  
pp. 3898-3904 ◽  
Author(s):  
Joanne L. Platell ◽  
Darren J. Trott ◽  
James R. Johnson ◽  
Peter Heisig ◽  
Anke Heisig ◽  
...  

ABSTRACTFluoroquinolone (FQ)-resistant extraintestinal pathogenicEscherichia coli(FQrExPEC) strains from phylogenetic group B2 are undergoing epidemic spread. Isolates belonging to phylogenetic group B2 are generally more virulent than otherE. coliisolates; therefore, resistance to FQs among group B2 isolates is concerning. Although clonal expansion of sequence type 131 (ST131) is a major factor, the contribution of additional clonal groups has not been quantified. Group B2 FQrExPEC isolates from humans (n= 250) and dogs (n= 12) in Australia were screened for ST131, a recently recognized and rapidly emerging multidrug-resistant and virulent clonal group that is important in both human and companion animal medicine. Non-ST131 isolates underwent virulence genotyping, PCR-based O typing, partial multilocus sequence typing (MLST), pulsed-field gel electrophoresis (PFGE), and FQ resistance mechanism analysis. Of 49 non-ST131 isolates (45 human, 4 canine), 49% (24 human, 2 canine) represented O-type O75 and exhibited conserved virulence genotypes (F10papAallele,iha,fimH,sat,vat,fyuA,iutA,kpsMII,usp,ompT,malX, K1/K5 capsule) and MLST allele profiles corresponding with clonal complex CC14. Two clusters, each containing canine and human isolates, were identified by PFGE (differentiated by K1 and K5 capsules). Australian FQrO75 isolates exhibited commonality with an historical FQ-susceptible O75 urosepsis isolate (also CC14). The isolation from humans and dogs of highly similar FQrderivatives of the classic O75:K1/K5 (CC14) ExPEC lineage suggests recent acquisition of FQ resistance and potential cross-host-species transfer. This lineage should be targeted with ST131 in future epidemiological investigations of FQrExPEC.


2014 ◽  
Vol 63 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Toyotaka Sato ◽  
Shin-ichi Yokota ◽  
Torahiko Okubo ◽  
Masaru Usui ◽  
Nobuhiro Fujii ◽  
...  

This study aimed to investigate the genetic association between fluoroquinolone (FQ) and/or cephalosporin (CEP) resistance in Escherichia coli isolates from dogs, and the risk to human health. We characterized E. coli clinical isolates, derived from faecal samples of dogs attending veterinary hospitals, using phylogenetic grouping, determination of virulence factor (VF) prevalence, multilocus sequence typing (MLST) and O serotyping. The D group was the dominant phylogenetic group among strains resistant to FQ and/or CEP. In contrast, the dominant group among susceptible strains was group B2. Group D strains showed a significantly higher prevalence of VFs than strains belonging to groups A and B1, and were resistant to significantly more antimicrobials than group B2 strains. The phylogenetic distribution of FQ–CEP-resistant E. coli groups (FQ–CEPRECs) and FQ-resistant groups was significantly correlated (r = 0.98), but FQ–CEPRECs and CEP-resistant E. coli groups were not correlated (r = 0.58). Data from PFGE, O serotype and MLST analyses indicated that the majority of FQ-resistant strains derived from a particular lineage of phylogenetic group D: serotype O1 and sequence type (ST) 648. Some D-O1-ST648 strains carried bla CMY-2, showed multidrug resistance and possessed a higher prevalence of the VFs kspMT, ompT and PAI compared with other group D strains. Our data indicate that the emergence of FQ-CEP-resistant E. coli is based primarily on FQ-resistant E. coli. Moreover, as strains of the D-O1-ST648 lineage have been found in clinical isolates derived from humans at a relatively high frequency, our findings indicate that the spreading of D-O1-ST648 strains may cause serious difficulties in both veterinary and human clinical fields in the future.


2015 ◽  
Vol 59 (6) ◽  
pp. 3574-3577 ◽  
Author(s):  
Shuhei Ueda ◽  
Bui Thi Kim Ngan ◽  
Bui Thi Mai Huong ◽  
Itaru Hirai ◽  
Le Danh Tuyen ◽  
...  

ABSTRACTWe examined whetherEscherichia coliisolates that produce CTX-M-9-type extended-spectrum β-lactamases (ESBL) are transferred between humans and chickens in a Vietnamese community. The phylogenetic group compositions, sequence types, antimicrobial resistance profiles, the prevalence of plasmid antibiotic resistance genes, and the plasmid replicon types generally differed between the human and chickenE. coliisolates. Our results suggest that transmission of theblaCTX-M-9-positiveE. colibetween humans and poultry was limited.


2017 ◽  
Vol 119 (7) ◽  
pp. 1633-1647
Author(s):  
Kaotar Nayme ◽  
Abouddihaj Barguigua ◽  
Brahim Bouchrif ◽  
Idrissa Diawara ◽  
Fatima El Otmani ◽  
...  

Purpose The purpose of this paper is to assess the occurrence of the extended-spectrum β-lactamases (ESBLs) and AmpC β-lactamase genes in 144 Escherichia coli isolates recovered from 160 vegetable salad samples. Design/methodology/approach Among the 144 E. coli isolates recovered from 160 vegetable salads, 17 (12 percent) ceftazidime-resistant isolates were screened for ESBL production with the double disk-diffusion test. The ESBL-producing isolates were characterized for antimicrobial resistance, the presence of virulence genes and plasmid-mediated quinolone resistance (PMQR) determinants. The isolates were also subjected to phylogenetic group typing. The existence of plasmid AmpC genes and mutations in the regulatory region of the chromosomal AmpC gene was assessed using polymerase chain reaction (PCR) and sequencing. All β-lactamase isolates were further characterized by pulsed-field gel electrophoresis to determine the genetic relatedness. Findings Overall, 17 (12 percent) of the 144 E. coli isolates studied were ceftazidime resistant. Among the 17 isolates, 13 (77 percent) were multidrug resistant and four (23.5 percent) were ESBL producers. The bla CTX-M14 was the only gene detected. Of the 12 AmpC-producing isolates, three (18 percent) harbored plasmid-encoded AmpC and sequencing analysis of the chromosomal AmpC genes revealed mutations in the promoter/attenuator region. PMQR determinants were detected in 9 (52 percent) isolates. A was the most prevalent phylogenetic group (56 percent), followed by groups B1 (31 percent), D (6 percent), and B2 (6 percent). PCR showed that six (50 percent) ESBL/AmpC-producing E. coli isolates carried one and/or two virulence genes. Pulsed-field gel electrophoresis showed no epidemiological relationship between these isolates. Originality/value This study places vegetable salads within the spectrum of ecological niches that may be vehicles for antibiotic-resistant bacteria/genes with clinical interest and these findings are worthy of attention as their spread to humans by ingestion cannot be dismissed.


2012 ◽  
Vol 194 (23) ◽  
pp. 6640-6641 ◽  
Author(s):  
Kihyun Lee ◽  
Hana Yi ◽  
Yong-Joon Cho ◽  
Jeonghwan Jang ◽  
Hor-Gil Hur ◽  
...  

ABSTRACTEscherichia coliAI27 is a putatively commensal strain isolated from feces of a pig. Here we report the draft genome sequence ofE. coliAI27. This is the first porcine strain in the phylogenetic group B1 whose genome sequence has been determined.


2011 ◽  
Vol 55 (6) ◽  
pp. 2986-2988 ◽  
Author(s):  
Gisele Peirano ◽  
Paul C. Schreckenberger ◽  
Johann D. D. Pitout

ABSTRACTAn NDM-1 carbapenemase-producingEscherichia coliisolate of sequence type 131 (ST131) that belonged to phylogenetic group B2 was obtained from a patient with a urinary tract infection who returned to the United States after a recent hospitalization while visiting India. NDM-1-producingE. coliST131 had significantly more virulence factors than NDM-1-producingE. coliST101, previously isolated from a patient in Canada. The presence of NDM β-lactamases in a very successful and virulentE. colisequence type is of concern.


2012 ◽  
Vol 80 (8) ◽  
pp. 2655-2666 ◽  
Author(s):  
Vanessa Martinez-Jéhanne ◽  
Christophe Pichon ◽  
Laurence du Merle ◽  
Olivier Poupel ◽  
Nadège Cayet ◽  
...  

ABSTRACTUropathogenicEscherichia coli(UPEC) strains are a leading cause of infections in humans, but the mechanisms governing host colonization by this bacterium remain poorly understood. Previous studies have identified numerous gene clusters encoding proteins involved in sugar transport, in pathogen-specific islands. We investigated the role in fitness and virulence of thevpeoperon encoding an EII complex of the phosphotransferase (PTS) system, which is found more frequently in human strains from infected urine and blood (45%) than inE. coliisolated from healthy humans (15%). We studied the role of this locusin vivo, using the UPECE. colistrain AL511, mutants, and complemented derivatives in two experimental mouse models of infection. Mutant strains displayed attenuated virulence in a mouse model of sepsis. A role in kidney colonization was also demonstrated by coinfection experiments in a mouse model of pyelonephritis. Electron microscopy examinations showed that thevpeBCmutant produced much smaller amounts of a capsule-like surface material than the wild type, particularly when growing in human urine. Complementation of thevpeBCmutation led to an increase in the amount of exopolysaccharide, resistance to serum killing, and virulence. It was therefore clear that the loss ofvpegenes was responsible for all the observed phenotypes. We also demonstrated the involvement of thevpelocus in gut colonization in the streptomycin-treated mouse model of intestinal colonization. These findings confirm that carbohydrate transport and metabolism underlie the ability of UPEC strains to colonize the host intestine and to infect various host sites.


2017 ◽  
Vol 11 (04) ◽  
pp. 306-313 ◽  
Author(s):  
Xiaoqiang Liu ◽  
Haixia Liu ◽  
Yinqian Li ◽  
Caiju Hao

Introduction: Escherichia coli is not only a commensal organism in humans and animals, but also a causative agent of diarrhea and extraintestinal infections. Information about the relationship between population structure, virulence gene profiles, and fluoroquinolone resistance of E. coli in dogs and cats in China is limited. Methodology: A total of 174 pathogenic and commensal E. coli isolates were evaluated in terms of phylogenetic group, virulence gene profile, sequence types (STs), and fluoroquinolone susceptibility. Results: A total of 46.6% of isolates belonged to phylogenetic group B2. Isolates displayed high resistance to tetracycline (82.2%), amoxicillin/clavulanic acid (73.6%), gentamicin (62.1%), and enrofloxacin (60.9%). fimH (81.6%) was the most prevalent virulence gene, and 83.9% of isolates contained one or more investigated virulence genes. The majority of the investigated virulence genes were more prevalent in fluoroquinolone-susceptible isolates and pathogenic isolates. Multilocus sequence typing (MLST) showed that E. coli isolates analyzed were assigned to 65 STs. Among of them, pathogenic-resistant and pathogenic-susceptible isolates had 44 and 10 STs, respectively, while there were 8 and 3 STs in the commensal resistant and susceptible isolates, respectively. Conclusions: Phylogenetic group B2 was the dominant group, accounting for 46.6% of the isolates. Pathogenic isolates and fluoroquinolone-susceptible isolates possessed more virulence genes. Pathogenic isolates and fluoroquinolone-resistant isolates exhibited high population diversity, and pandemic clone ST131 appeared in 9.8% of isolates.


Sign in / Sign up

Export Citation Format

Share Document