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Escherichia coli intestinal infection pathotypes are characterized by distinct adhesion patterns, including the recently described clumpy adhesion phenotype. Here, we identify and characterize the genetic factors contributing to the clumpy adhesion of E. coli strain 4972. In this strain, the transcriptome and proteome of adhered bacteria were found to be distinct from planktonic bacteria in the supernatant. A total of 622 genes in the transcriptome were differentially expressed in bacteria present in clumps relative to the planktonic bacteria. Seven genes targeted for disruption had variable distribution in different pathotypes and nonpathogenic E. coli, with the pilV and spnT genes being the least frequent or absent from most groups. Deletion (Δ) of five differentially expressed genes, flgH , ffp , pilV , spnT, and yggT, affected motility, adhesion, or antibiotic stress. Δ flgH exhibited 80% decrease and Δ yggT depicted 184% increase in adhesion, and upon complementation, adhesion was significantly reduced to 13%. Δ flgH lost motility and was regenerated when complemented, whereas Δ ffp had significantly increased motility, and reintroduction of the same gene reduced it to the wild-type level. The clumps produced by Δ ffp and Δ spnT were more resistant and protected the bacteria, with Δ spnT showing the best clump formation in terms of ampicillin stress protection. Δ yggT had the lowest tolerance to gentamicin, where the antibiotic stress completely eliminated the bacteria. Overall, we were able to investigate the influence of clump formation on cell surface adhesion and antimicrobial tolerance, with the contribution of several factors crucial to clump formation on susceptibility to the selected antibiotics., Importance: The study explores a biofilm-like clumpy adhesion phenotype in Escherichia coli, along with various factors and implications for antibiotic susceptibility. The phenotype permitted the bacteria to survive the onslaught of high antibiotic concentrations. Profiles of the transcriptome and proteome allowed the differentiation between adhered bacteria in clumps and planktonic bacteria in the supernatant. The deletion mutants of genes differentially expressed between adhered and planktonic bacteria, i.e., flgH , ffp , pilV , spnT , and yggT, and respective complementations in trans cemented their roles in multiple capacities. ffp , an uncharacterized gene, is involved in motility and resistance to ampicillin in a clumpy state. The work also affirms for the first time the role of the yggT gene in adhesion and its involvement in susceptibility against another aminoglycoside antibiotic, i.e., gentamicin. Overall, the study contributes to the mechanisms of biofilm-like adhesion phenotype and understanding of the antimicrobial therapy failures and infections of E. coli ., Competing Interests: The authors declare no conflict of interest.

Background: Infections caused by avian pathogenic Escherichia coli (APEC) result in significant economic losses in poultry industry. APEC strains are known to form biofilms in various conditions allowing them to thrive even under harsh and nutrient-deficient conditions on different surfaces, and this ability enables them to evade chemical and biological eradication methods. Despite knowing the whole genome sequences of various APEC isolates, little has been reported regarding their biofilm-associated genes. A random transposon mutant library of the wild-type APEC IMT 5155 comprising 1,300 mutants was analyzed for biofilm formation under nutrient deprived conditions using Videoscan technology coupled with fluorescence microscopy. Seven transposon mutants were found to have reproducibly and significantly altered biofilm formation and their mutated genes were identified by arbitrary PCR and DNA sequencing. The intact genes were acquired from the wild-type strain, cloned in pACYC177 plasmid and transformed into the respective altered biofilm forming transposon mutants, and the biofilm formation was checked in comparison to the wild type and mutant strains under the same conditions., Results: In this study, we report seven genes i.e., nhaA, fdeC, yjhB, lysU, ecpR, AJB35136 and fdtA of APEC with significant contribution to biofilm formation. Reintroduction of AJB35136 and fdtA, reversed the altered phenotype proving that a significant role being played by these two O-antigen related genes in APEC biofilm formation. Presence of these seven genes across nonpathogenic E. coli and APEC genomes was also analyzed showing that they are more prevalent in the latter., Conclusions: The study has elucidated the role of these genes in APEC biofilm formation and compared them to adhesion expanding the knowledge and understanding of the economically significant pathogens., (© 2023. BioMed Central Ltd., part of Springer Nature.)

Avian pathogenic Escherichia coli (APEC) is a major bacterial pathogen of commercial poultry contributing to extensive economic losses and contamination of the food chain. One of the initial steps in bacterial infection and successful colonization of the host is adhesion to the host cells. A random transposon mutant library ( n  = 1,300) of APEC IMT 5155 was screened phenotypically for adhesion to chicken (CHIC-8E11) and human (LoVo) intestinal epithelial cell lines. The detection and quantification of adherent bacteria were performed by a modified APEC-specific antibody staining assay using fluorescence microscopy coupled to automated VideoScan technology. Eleven mutants were found to have significantly altered adhesion to the cell lines examined. Mutated genes in these 11 "adhesion-altered mutants" were identified by arbitrary PCR and DNA sequencing. The genes were amplified from wild-type APEC IMT 5155, cloned, and transformed into the respective adhesion-altered mutants, and complementation was determined in adhesion assays. Here, we report contributions of the fdtA, rluD, yjhB, ecpR , and fdeC genes of APEC in adhesion to chicken and human intestinal cell lines. Identification of the roles of these genes in APEC pathogenesis will contribute to prevention and control of APEC infections. IMPORTANCE Avian pathogenic E. coli is not only pathogenic for commercial poultry but can also cause foodborne infections in humans utilizing the same attachment and virulence mechanisms. Our aim was to identify genes of avian pathogenic E. coli involved in adhesion to chicken and human cells in order to understand the colonization and pathogenesis of these bacteria. In contrast to the recent studies based on genotypic and bioinformatics data, we have used a combination of phenotypic and genotypic approaches for identification of novel genes contributing to adhesion in chicken and human cell lines. Identification of adhesion factors remains important, as antibodies elicited against such factors have shown potential to block colonization and ultimately prevent disease as prophylactic vaccines. Therefore, the data will augment the understanding of disease pathogenesis and ultimately in designing strategies against the infections., (Copyright © 2020 American Society for Microbiology.)

Objective: To determine the prevalence and genetic relatedness of bla CTX-M -type extended spectrum-β-lactamase (ESBL)-producing Escherichia coli at the human-animal interface in Pakistan. Materials and Methods: A total of 150 human, cattle, and poultry fecal samples (50 each) were screened for ESBL-producing E. coli using ESBL CHROMagar ® . Bacterial species confirmation as well as determination of minimum inhibitory concentrations (μg/mL) to different antibiotics was performed using the automated VITEK ® -2 compact system. Phenotypic confirmation of ESBL production was performed according to the Clinical Laboratory Standards Institute (CLSI) guidelines. Genetic analysis of bla CTX-M was carried out by PCR and DNA sequencing. Plasmids and clonal similarity of the E. coli strains were determined by PCR-based replicon typing and pulsed-field gel electrophoresis (PFGE), respectively. Results: Of 150 samples, 29 (19.3%) ESBL-producing E. coli were recovered, and majority of them originated from human ( n  = 16; 55%), followed by cattle ( n  = 9; 31%) and poultry ( n  = 4; 13.7%). bla CTX-M-15 was predominant ESBL genotype ( n  = 25; 86.2%), mainly identified from human ( n  = 15) and cattle ( n  = 9). This is also the first report of the occurrence of CTX-M-15 and CTX-M-55 in cattle and poultry E. coli isolates of Pakistan, respectively. The majority of the ESBL-producing E. coli (96.5%) showed a multidrug resistance phenotype. All isolates carried IncFII or IncFIA plasmids, and the phylogroup B1 was dominant (44.8%) followed by phylogroups A (31%), D (17.2%), and B2 (6.8%). PFGE revealed that isolates from different hosts were genetically unrelated. Conclusion: Presence of CTX-M-15-type ESBL-producing E. coli in different reservoirs is alarming and has the potential to impact both veterinary and human therapeutic treatment options.

Bacterial biofilm formation is a widespread phenomenon and a complex process requiring a set of genes facilitating the initial adhesion, maturation, and production of the extracellular polymeric matrix and subsequent dispersal of bacteria. Most studies on Escherichia coli biofilm formation have investigated nonpathogenic E. coli K-12 strains. Due to the extensive focus on laboratory strains in most studies, there is poor information regarding biofilm formation by pathogenic E. coli isolates. In this study, we genotypically and phenotypically characterized 187 human clinical E. coli isolates representing various pathotypes (e.g., uropathogenic, enteropathogenic, and enteroaggregative E. coli ). We investigated the presence of biofilm-associated genes ("genotype") and phenotypically analyzed the isolates for motility and curli and cellulose production ("phenotype"). We developed a new screening method to examine the in vitro biofilm formation ability. In summary, we found a high prevalence of biofilm-associated genes. However, we could not detect a biofilm-associated gene or specific phenotype correlating with the biofilm formation ability. In contrast, we did identify an association of increased biofilm formation with a specific E. coli pathotype. Enteroaggregative E. coli (EAEC) was found to exhibit the highest capacity for biofilm formation. Using our image-based technology for the screening of biofilm formation, we demonstrated the characteristic biofilm formation pattern of EAEC, consisting of thick bacterial aggregates. In summary, our results highlight the fact that biofilm-promoting factors shown to be critical for biofilm formation in nonpathogenic strains do not reflect their impact in clinical isolates and that the ability of biofilm formation is a defined characteristic of EAEC. IMPORTANCE Bacterial biofilms are ubiquitous and consist of sessile bacterial cells surrounded by a self-produced extracellular polymeric matrix. They cause chronic and device-related infections due to their high resistance to antibiotics and the host immune system. In nonpathogenic Escherichia coli , cell surface components playing a pivotal role in biofilm formation are well known. In contrast, there is poor information for their role in biofilm formation of pathogenic isolates. Our study provides insights into the correlation of biofilm-associated genes or specific phenotypes with the biofilm formation ability of commensal and pathogenic E. coli Additionally, we describe a newly developed method enabling qualitative biofilm analysis by automated image analysis, which is beneficial for high-throughput screenings. Our results help to establish a better understanding of E. coli biofilm formation., (Copyright © 2017 American Society for Microbiology.)

Background: Drug resistance is a major problem in Escherichia coli isolated from surgical wound infections. In this study, we evaluated relationship between phylogenicity and drug resistance., Methodology: A total of 29 multi-drug resistant (MDR) E. coli isolates of known drug resistance genes and integron profile were selected for the present study. Triplex PCR was conducted for phylogenetic classification of these isolates into four established phylogenetic groups: A, B1, B2 and D. Statistical analysis was done to determine the association of different drug resistance genes and integrons with the phylogenetic groups., Results: Most of the isolates (44.8%) belonged to phylogenetic group A followed by group B2 and D (24.1% each) and group B1 (6.9%)., Conclusions: There is a definitive relationship between drug resistance and various phylogenetic groups of E. coli infecting wounds. A shift towards phylogenetic group A might be observed with an increasing drug resistance profile.

Escherichia coli are one of the leading causes of infection in wounds. Emerging multiple drug resistance among E. coli poses a serious challenge to antimicrobial therapy for wounds. This study was conducted to ascertain a baseline profile of antimicrobial resistance in E. coli isolates infecting surgical wounds. A total of 64 pus samples from hospitalized patients were screened and 29 (45.3%) were found to have E. coli, which were identified biochemically and confirmed by molecular methods. Using the disc diffusion method, antimicrobial resistance was observed toward tetracycline (100%), cefradine (100%), nalidixic acid (93.1%), ampicillin (86.2%), gentamicin (86.2%), cefixime (82.8%), ceftriaxone (82.8%), aztreonam (82.8%), ciprofloxacin (75.9%), streptomycin (72.4%), cefoperazone (65.5%), chloramphenicol (58.6%) and amikacin (58.6%). In an effort to find relevant genes, 11 different genes were targeted by PCR. Among these, the mutated gyrA gene was found to be the most prevalent (82.8%), followed by the TEM (72.4%), catP (68.9%), catA1 (68.9%), tetB (62.1%), blt (58.6%), bla(CTX-M-15) (27.6%), bla(TEM) (20.7%), bla(OXA) (17.2%), tetA (17.2%) and aadA1 (13.8%) genes. The presence of integrons was also studied among these isolates. The prevalence of class 1 integrons was the highest (44.8%), followed by class 2 (27.6%). Three (10.3%) isolates carried both class 1 and class 2 integrons (first report from E. coli infecting wounds). The high incidence of integrons points toward their facilitation for carriage of antimicrobial resistance genes; however, in nearly 37% isolates, no integrons were detected, indicating the significance of alternative mechanisms of gene transfer. Another salient finding was that all isolates were multidrug-resistant E. coli.

Background: Wastewater is a major source of Antibiotic-Resistant Bacteria (ARB) and a hotspot for the exchange of Antibiotic-Resistant Genes (ARGs). The occurrence of Carbapenem-Resistant Bacteria (CRB) in wastewater samples is a major public health concern. Objectives: This study aimed to analyze Antibiotic resistance in bacteria from wastewater sources in Pakistan. Methods: We analyzed 32 bacterial isolates, including 18 Escherichia coli, 4 Klebsiella pneumoniae, and 10 other bacterial isolates using phenotypic antibiotic susceptibility assay and whole-genome sequencing. This study identified the ARGs, plasmid replicons, and integron genes cassettes in the sequenced isolates. One representative isolate was further sequenced using Illumina and Oxford nanopore sequencing technologies. Results: Our findings revealed high resistance to clinically important antibiotics: 91% of isolates were resistant to cefotaxime, 75% to ciprofloxacin, and 62.5% to imipenem, while 31% showed non-susceptibility to gentamicin. All E. coli isolates were resistant to cephalosporins, with 72% also resistant to carbapenems. Sequence analysis showed a diverse resistome, including carbapenamases (blaNDM-5, blaOXA-181), ESBLs (blaCTX-M-15, blaTEM), and AmpC-type β-lactamases (blaCMY). Key point mutations noticed in the isolates were pmrB_Y358N (colistin) and ftsI_N337NYRIN, ftsI_I336IKYRI (carbapenem). The E. coli isolates had 11 different STs, with ST410 predominating (28%). Notably, the E. coli phylogroup A isolate 45EC1, (ST10886) is reported for the first time from wastewater, carrying blaNDM-5, blaCMY-16, and pmrB_Y358N with class 1 integron gene cassette of dfrA12-aadA2-qacEΔ1 on a plasmid-borne contig. Other carbapenamase, blaNDM-1 and blaOXA-72, were detected in K. pneumoniae 22EB1 and Acinetobacter baumannii 51AC1, respectively. The integrons with the gene cassettes encoding antibiotic resistance, and the transport and bacterial mobilization protein, were identified in the sequenced isolates. Ten plasmid replicons were identified, with IncFIB prevalent in 53% of isolates. Combined Illumina and Oxford nanopore sequencing revealed blaNDM-5 on an IncFIA/IncFIC plasmid and is identical to those reported in the USA, Myanmar, and Tanzania. Conclusions: These findings highlight the environmental prevalence of high-risk and WHO-priority pathogens with clinically important ARGs, underscoring the need for a One Health approach to mitigate ARB isolates. [ABSTRACT FROM AUTHOR]

Background: Multidrug resistance (MDR) in the family Enterobacteriaceae is a perniciously increasing threat to global health security. The discovery of new antimicrobials having the reversing drug resistance potential may contribute to augment and revive the antibiotic arsenal in hand. This study aimed to explore the anti-Enterobacteriaceae capability of bioactive polyphenols from Punica granatum (P. granatum) and their co-action with antibiotics against clinical isolates of Enterobacteriaceae predominantly prevalent in South Asian countries. Methods: The Kandhari P. granatum (Pakistani origin) extracts were tested for anti-Enterobacteriaceae activity by agar well diffusion assay against MDR Salmonella enterica serovar Typhi, serovar Typhimurium and Escherichia coli. Predominant compounds of active extract were determined by mass spectrometry and screened for bioactivity by agar well diffusion and minimum inhibitory concentration (MIC) assay. The active punicalagin was further evaluated at sub-inhibitory concentrations (SICs) for coactivity with nine conventional antimicrobials using a disc diffusion assay followed by time-kill experiments that proceeded with SICs of punicalagin and antimicrobials. Results: Among all P. granatum crude extracts, pomegranate peel methanol extract showed the largest inhibition zones of 25, 22 and 19 mm, and the MICs as 3.9, 7.8 and 7.8 mg/mL for S. typhi, S. typhimurium and E. coli, respectively. Punicalagin and ellagic acid were determined as predominant compounds by mass spectrometry. In plate assay, punicalagin (10 mg/mL) was active with hazy inhibition zones of 17, 14, and 13 mm against S. typhi, S. typhimurium and E. coli, respectively. However, in broth dilution assay punicalagin showed no MIC up to 10 mg/mL. The SICs 30 μg, 100 μg, and 500 μg of punicalagin combined with antimicrobials i.e., aminoglycoside, β-lactam, and fluoroquinolone act in synergy against MDR strains with % increase in inhibition zone values varying from 3.4 ± 2.7% to 73.8 ± 8.4%. In time-kill curves, a significant decrease in cell density was observed with the SICs of antimicrobials/punicalagin (0.03–60 μg/mL/30, 100, 500 μg/mL of punicalagin) combinations. Conclusions: The P. granatum peel methanol extract exhibited antimicrobial activity against MDR Enterobacteriaceae pathogens. Punicalagin, the bacteriostatic flavonoid act as a concentration-dependent sensitizing agent for antimicrobials against Enterobacteriaceae. Our findings for the therapeutic punicalagin-antimicrobial combination prompt further evaluation of punicalagin as a potent activator for drugs, which otherwise remain less or inactive against MDR strains. [ABSTRACT FROM AUTHOR]

Urinary tract infections (UTIs) are predominantly caused by uropathogenic Escherichia coli (E. coli). There is rapid increase in antimicrobial resistance in UTIs, also declared as a serious health threat by World Health Organization (WHO). Present study was designed to investigate the antimicrobial resistance status with specific focus on ESBLs and carbapenemases in local uropathogenic E. coli (UPEC) isolates. E. coli isolates were characterized from patients of all ages visiting diagnostic laboratories for urine examination. Demographic data was also recorded for each patient. Antibiograms were developed to observe antibiotic resistance in UPEC using Kirby Bauer disc diffusion technique. Double Disc Synergy test (DDST) was used for phenotypic ESBL test. ESBLs and carbapenemases genes were detected in UPEC using PCR. The PCR results were confirmed by sequencing. The UPEC isolates under study exhibited 78%, 77%, 74%, 72% and 55% resistance against cefotaxime, amoxicillin, erythromycin, ceftriaxone and cefixime, respectively. Resistance against colistin and meropenem was observed in 64% and 34% isolates, respectively. Phenotypic DDST identified 48% isolates as ESBLs producers. Genotypic characterization identified 70%, 74.4% and 49% prevalence of CTXM-1, TEM-1 and CTXM-15 genes respectively. One isolate was observed exhibiting co-existence of all ESBL genes. TEM-1 + CTXM-1 and TEM-1 + CTXM-1 + CTXM-15 + OXA-1 gene patterns were dominant among ESBLs. For carbapenem-resistance, 14% isolates indicated the presence of KPC whereas GES and VIM was detected in 7% and 3.4% isolates, respectively. In conclusion, our results present a high prevalence of extensively drug resistant UPEC isolates with a considerable percentage of ESBL producers. These findings propose the need of continuous surveillance for antimicrobial resistance and targeted antimicrobial therapy. [ABSTRACT FROM AUTHOR]

Objectives: Production of extended spectrum beta -lactamases (ESBLs) by clinical isolates of pathogenic E. coli is a very serious therapeutic threat. This study was aimed to investigate the prevalence of ESBLs and associated drug resistance in E. coli isolates from urine and pus, and to report the drift from 2005 to 2009-10. Methodology: Among 173 E. coli isolates, 82 were phenotypically detected as ESBL producers by standard cefotaxime / clavulanic acid and ceftazidime / clavulanic acid disc diffusion tests. Antimicrobial resistance of all ESBL producers was assessed by disc diffusion method. Presence of CTX-M, TEM, SHV and OXA groups was investigated by PCR. Results: The prevalence of ESBL producing E. coli increased significantly from 33.7% in 2005 to 60.0% in 2009-10 (urine: 31.8% to 62.9%; pus: 41.1% to 55.5%). Resistance to cefotaxime, ceftazidime, ciprofloxacin, gentamicin, nalidixic acid, ticarcillin-clavulanic acid, and trimethoprim-sulfamethoxazole was above 85% in both sets of isolates. Imipenem and Fosfomycin resistance was non-existent in 2005 but ranged from 3-15% in 2009-10. Remarkable increase from 9.5% to 64.7% in urinary tract isolates and from 0 to 55% in pus isolates was observed in colistin sulphate resistance. The dissemination of genes encoding ESBLs was: CTX-M 3.5%; TEM 10.7%; both CTX-M and TEM 3.5% in 2005, and CTX-M 42.5%; TEM 48.1%; both CTX-M and TEM 29.6% in 2009-10. Conclusions: Our results showed very rapid emergence of multidrug resistant ESBL producing E. coli in Pakistan posing a very serious threat in the treatment of nosocomial and community acquired infections. [ABSTRACT FROM AUTHOR]

Background: Uropathogenic E.coli (UPEC) are among major pathogens causing urinary tract infections. Virulence factors are mainly responsible for the severity of these emerging infections. This study was planned to investigate the distribution of virulence genes and cytotoxic effects of UPEC isolates with reference to phylogenetic groups (B2, B1, D and A) to understand the presence and impact of virulence factors in the severity of infection in Faisalabad region of Pakistan. Methods: In this study phylogenetic analysis, virulence gene identification and cytotoxicity of 59 uropathogenic E. coli isolates obtained from non-hospitalized patients was studied. Results: Among 59 isolates, phylogenetic group B2 (50%) was most dominant followed by groups A, B1 (19% each) and D (12%). Isolates present in group D showed highest presence of virulence genes. The prevalence hlyA (37%) was highest followed by sfaDE (27%), papC (24%), cnf1 (20%), eaeA (19%) and afaBC3 (14%). Highly hemolytic and highly verotoxic isolates mainly belonged to group D and B2. We also found two isolates with simultaneous presence of three fimbrial adhesin genes present on pap, afa, and sfa operons. This has not been reported before and underlines the dynamic nature of these UPEC isolates. Conclusions: It was concluded that in local UPEC isolates from non-hospitalized patients, group B2 was more prevalent. However, group D isolates were most versatile as all were equipped with virulence genes and showed highest level of cytotoxicity. [ABSTRACT FROM AUTHOR]

The mitotic spindle contains many bundles of microtubules (MTs) including midzones and kinetochore fibers, but little is known about how bundled structures are formed. Here, we show that the chromosomal passenger complex (CPC) purified from Escherichia coli undergoes liquid-liquid demixing in vitro. An emergent property of the resultant condensates is to generate parallel MT bundles when incubated with free tubulin and GTP in vitro. We demonstrate that MT bundles emerge from CPC droplets with protruding minus ends that then grow into long and tapered MT structures. During this growth, we found that the CPC in these condensates apparently reorganize to coat and bundle the resulting MT structures. CPC mutants attenuated for liquid-liquid demixing or MT binding prevented the generation of parallel MT bundles in vitro and reduced the number of MTs present at spindle midzones in HeLa cells. Our data demonstrate that an in vitro biochemical activity to produce MT bundles emerges after the concentration of the CPC and provides models for how cells generate parallel-bundled MT structures that are important for the assembly of the mitotic spindle. Moreover, these data suggest that cells contain MT-organizing centers that generate MT bundles that emerge with the opposite polarity from centrosomes. [ABSTRACT FROM AUTHOR]

Pathogenic bacteria, such as enteropathogenic Escherichia coli (EPEC) and enterotoxigenic E. coli (ETEC), cause diarrhea in mammals. In particular, E. coli colonizes and infects the gastrointestinal tract via type 1 fimbriae (T1F). Here, the major zymogen granule membrane glycoprotein 2 (GP2) acts as a host cell receptor. GP2 is also secreted by the pancreas and various mucous glands, interacting with luminal type 1 fimbriae-positive E. coli. It is unknown whether GP2 isoforms demonstrate specific E. coli pathotype binding. In this study, we investigated interactions of human, porcine, and bovine EPEC and ETEC, as well as commensal E. coli isolates with human, porcine, and bovine GP2. We first defined pathotype- and host-associated FimH variants. Second, we could prove that GP2 isoforms bound to FimH variants to various degrees. However, the GP2-FimH interactions did not seem to be influenced by the host specificity of E. coli. In contrast, soluble GP2 affected ETEC infection and phagocytosis rates of macrophages. Preincubation of the ETEC pathotype with GP2 reduced the infection of cell lines. Furthermore, preincubation of E. coli with GP2 improved the phagocytosis rate of macrophages. Our findings suggest that GP2 plays a role in the defense against E. coli infection and in the corresponding host immune response. IMPORTANCE Infection by pathogenic bacteria, such as certain Escherichia coli pathotypes, results in diarrhea in mammals. Pathogens, including zoonotic agents, can infect different hosts or show host specificity. There are Escherichia coli strains which are frequently transmitted between humans and animals, whereas other Escherichia coli strains tend to colonize only one host. This host specificity is still not fully understood. We show that glycoprotein 2 is a selective receptor for particular Escherichia coli strains or variants of the adhesin FimH but not a selector for a species-specific Escherichia coli group. We demonstrate that GP2 is involved in the regulation of colonization and infection and thus represents a molecule of interest for the prevention or treatment of disease. [ABSTRACT FROM AUTHOR]