Invasiveness of Escherichia coli Is Associated with an IncFII Plasmid

Escherichia coli is one of the most prevalent pathogens, causing a variety of infections including bloodstream infections. At the same time, it can be found as a commensal, being part of the intestinal microflora. While it is widely accepted that pathogenic strains can evolve from colonizing E. coli strains, the evolutionary route facilitating the commensal-to-pathogen transition is complex and remains not fully understood. Identification of the underlying mechanisms and genetic changes remains challenging. To investigate the factors involved in the transition from intestinal commensal to invasive E. coli causing bloodstream infections, we compared E. coli isolated from blood culture to isolates from the rectal flora of the same individuals by whole genome sequencing to identify clonally related strains and potentially relevant virulence factors. in vitro invasion assays using a Caco- 2 cell intestinal epithelial barrier model and a gut organoid model were performed to compare clonally related E. coli. The experiments revealed a correlation between the presence of an IncFII plasmid carrying hha and the degree of invasiveness. In summary, we provide evidence for the role of an IncFII plasmid in the transition of colonization to invasion in clinical E. coli isolates.

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Interaction of Enteropathogenic and Shiga Toxin-Producing Escherichia coli and Porcine Intestinal Mucosa: Role of Intimin and Tir in Adherence

Infection and Immunity ◽

10.1128/iai.73.9.6005-6016.2005 ◽

2005 ◽

Vol 73 (9) ◽

pp. 6005-6016 ◽

Cited By ~ 34

Author(s):

Francis Girard ◽

Isabelle Batisson ◽

Gad M. Frankel ◽

Josée Harel ◽

John M. Fairbrother

Keyword(s):

Escherichia Coli ◽

Shiga Toxin ◽

Actin Polymerization ◽

Animal Species ◽

Ex Vivo ◽

Epec Strain ◽

E Coli ◽

In Vitro Organ Culture

ABSTRACT The ileal in vitro organ culture (IVOC) model using tissues originating from colostrum-deprived newborn piglets has proven to be an effective way to study the attaching and effacing (A/E) phenotype of porcine enteropathogenic Escherichia coli (EPEC) ex vivo. The aim of this study was to investigate the role of intimin subtype and Tir in the adherence of EPEC and Shiga-toxin-producing E. coli (STEC), isolated from different animal species, to porcine intestinal IVOC. Moreover, the role of intimin in Tir-independent adherence of the human EPEC strain E2348/69 was investigated using intimin and Tir-deficient derivatives. Our results demonstrated that A/E E. coli strains (AEEC) from various animal species and humans induce the A/E phenotype in porcine ileal IVOC and that intimin subtype influences intestinal adherence and tropism of AEEC strains. We also showed that a tir mutant of EPEC strain E2348/69 demonstrates close adherence to the epithelial cells of porcine ileal IVOC segments, with microvillous effacement but with no evidence of actin polymerization or pedestal formation, and that intimin seems to be involved in this phenotype. Overall, this study provides further evidence for the existence of one or more host-cell-encoded intimin receptor(s) in the pig gut.

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Regulatory Role of PlaR (YiaJ) for Plant Utilization in Escherichia coli K-12

Scientific Reports ◽

10.1038/s41598-019-56886-x ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 3

Author(s):

Tomohiro Shimada ◽

Yui Yokoyama ◽

Takumi Anzai ◽

Kaneyoshi Yamamoto ◽

Akira Ishihama

Keyword(s):

Escherichia Coli ◽

Genetic System ◽

Regulatory Role ◽

E Coli ◽

Warm Blooded Animal ◽

Plant Utilization ◽

K 12

AbstractOutside a warm-blooded animal host, the enterobacterium Escherichia coli K-12 is also able to grow and survive in stressful nature. The major organic substance in nature is plant, but the genetic system of E. coli how to utilize plant-derived materials as nutrients is poorly understood. Here we describe the set of regulatory targets for uncharacterized IclR-family transcription factor YiaJ on the E. coli genome, using gSELEX screening system. Among a total of 18 high-affinity binding targets of YiaJ, the major regulatory target was identified to be the yiaLMNOPQRS operon for utilization of ascorbate from fruits and galacturonate from plant pectin. The targets of YiaJ also include the genes involved in the utilization for other plant-derived materials as nutrients such as fructose, sorbitol, glycerol and fructoselysine. Detailed in vitro and in vivo analyses suggest that L-ascorbate and α-D-galacturonate are the effector ligands for regulation of YiaJ function. These findings altogether indicate that YiaJ plays a major regulatory role in expression of a set of the genes for the utilization of plant-derived materials as nutrients for survival. PlaR was also suggested to play protecting roles of E. coli under stressful environments in nature, including the formation of biofilm. We then propose renaming YiaJ to PlaR (regulator of plant utilization).

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Role of Motility and the flhDC Operon in Escherichia coli MG1655 Colonization of the Mouse Intestine

Infection and Immunity ◽

10.1128/iai.00052-07 ◽

2007 ◽

Vol 75 (7) ◽

pp. 3315-3324 ◽

Cited By ~ 47

Author(s):

Eric J. Gauger ◽

Mary P. Leatham ◽

Regino Mercado-Lubo ◽

David C. Laux ◽

Tyrrell Conway ◽

...

Keyword(s):

Escherichia Coli ◽

Regulatory Region ◽

Flagellar Motor ◽

Wild Type ◽

E Coli ◽

Mouse Intestine ◽

Flagellum Biosynthesis ◽

Colonizing Ability

ABSTRACT Previously, we reported that the mouse intestine selected mutants of Escherichia coli MG1655 that have improved colonizing ability (M. P. Leatham et al., Infect. Immun. 73:8039-8049, 2005). These mutants grew 10 to 20% faster than their parent in mouse cecal mucus in vitro and 15 to 30% faster on several sugars found in the mouse intestine. The mutants were nonmotile and had deletions of various lengths beginning immediately downstream of an IS1 element located within the regulatory region of the flhDC operon, which encodes the master regulator of flagellum biosynthesis, FlhD4C2. Here we show that during intestinal colonization by wild-type E. coli strain MG1655, 45 to 50% of the cells became nonmotile by day 3 after feeding of the strain to mice and between 80 and 90% of the cells were nonmotile by day 15 after feeding. Ten nonmotile mutants isolated from mice were sequenced, and all were found to have flhDC deletions of various lengths. Despite this strong selection, 10 to 20% of the E. coli MG1655 cells remained motile over a 15-day period, suggesting that there is an as-yet-undefined intestinal niche in which motility is an advantage. The deletions appear to be selected in the intestine for two reasons. First, genes unrelated to motility that are normally either directly or indirectly repressed by FlhD4C2 but can contribute to maximum colonizing ability are released from repression. Second, energy normally used to synthesize flagella and turn the flagellar motor is redirected to growth.

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Role of Escherichia coli Nitrogen Regulatory Genes in the Nitrogen Response of the Azotobacter vinelandiiNifL-NifA Complex

Journal of Bacteriology ◽

10.1128/jb.183.10.3076-3082.2001 ◽

2001 ◽

Vol 183 (10) ◽

pp. 3076-3082 ◽

Cited By ~ 37

Author(s):

Francisca Reyes-Ramirez ◽

Richard Little ◽

Ray Dixon

Keyword(s):

Escherichia Coli ◽

Signal Transduction ◽

Nitrogen Control ◽

Fixed Nitrogen ◽

Nitrogen Response ◽

E Coli ◽

Nitrogen Excess

ABSTRACT The redox-sensing flavoprotein NifL inhibits the activity of the nitrogen fixation (nif)-specific transcriptional activator NifA in Azotobacter vinelandii in response to molecular oxygen and fixed nitrogen. Although the mechanism whereby the A. vinelandii NifL-NifA system responds to fixed nitrogen in vivo is unknown, the glnK gene, which encodes a PII-like signal transduction protein, has been implicated in nitrogen control. However, the precise function of A. vinelandii glnK in this response is difficult to establish because of the essential nature of this gene. We have shown previously that A. vinelandii NifL is able to respond to fixed nitrogen to control NifA activity when expressed inEscherichia coli. In this study, we investigated the role of the E. coli PII-like signal transduction proteins in nitrogen control of the A. vinelandii NifL-NifA regulatory system in vivo. In contrast to recent findings with Klebsiella pneumoniae NifL, our results indicate that neither the E. coli PII nor GlnK protein is required to relieve inhibition byA. vinelandii NifL under nitrogen-limiting conditions. Moreover, disruption of both the E. coli glnB andntrC genes resulted in a complete loss of nitrogen regulation of NifA activity by NifL. We observe that glnB ntrC and glnB glnK ntrC mutant strains accumulate high levels of intracellular 2-oxoglutarate under conditions of nitrogen excess. These findings are in accord with our recent in vitro observations (R. Little, F. Reyes-Ramirez, Y. Zhang, W. Van Heeswijk, and R. Dixon, EMBO J. 19:6041–6050, 2000) and suggest a model in which nitrogen control of the A. vinelandii NifL-NifA system is achieved through the response to the level of 2-oxoglutarate and an interaction with PII-like proteins under conditions of nitrogen excess.

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Escherichia coli O157:H7 Colonization in Cattle following Systemic and Mucosal Immunization with Purified H7 Flagellin

Infection and Immunity ◽

10.1128/iai.01452-07 ◽

2008 ◽

Vol 76 (6) ◽

pp. 2594-2602 ◽

Cited By ~ 59

Author(s):

Tom N. McNeilly ◽

Stuart W. Naylor ◽

Arvind Mahajan ◽

Mairi C. Mitchell ◽

Sean McAteer ◽

...

Keyword(s):

Escherichia Coli ◽

Bacterial Colonization ◽

Primary Source ◽

Rectal Administration ◽

Intestinal Epithelial ◽

E Coli ◽

Source Of Infection ◽

Antibody Isotypes ◽

Nasal Secretions

ABSTRACT Escherichia coli O157:H7 is an important pathogen of humans. Cattle are most frequently identified as the primary source of infection, and therefore, reduction in E. coli O157:H7 prevalence in cattle by vaccination represents an attractive strategy for reducing the incidence of human disease. H7 flagella have been implicated in intestinal-epithelial colonization of E. coli O157:H7 and may represent a useful target for vaccination. In this study, calves were immunized either systemically with H7 flagellin by intramuscular injection or mucosally via the rectum with either H7 or H7 incorporated into poly(dl-lactide-co-glycolide) microparticles (PLG:H7). Systemic immunization resulted in high levels of flagellin-specific immunoglobulin G (IgG) and IgA in both serum and nasal secretions and detectable levels of both antibody isotypes in rectal secretions. Rectal administration of flagellin resulted in levels of rectal IgA similar to those by the intramuscular route but failed to induce any other antibody response, whereas rectal immunization with PLG:H7 failed to induce any H7-specific antibodies. Following subsequent oral challenge with E. coli O157:H7, reduced colonization rates and delayed peak bacterial shedding were observed in the intramuscularly immunized group compared to nonvaccinated calves, but no reduction in total bacterial shedding occurred. Rectal immunization with either H7 or PLG:H7 had no effect on subsequent bacterial colonization or shedding. Furthermore, purified H7-specific IgA and IgG from intramuscularly immunized calves were shown to reduce intestinal-epithelial binding in vitro. These results indicate that H7 flagellin may be a useful component in a systemic vaccine to reduce E. coli O157:H7 colonization in cattle.

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THE ROLE OF PENICILLIN-INDUCED BACTERIAL VARIANTS IN EXPERIMENTAL PYELONEPHRITIS

Journal of Experimental Medicine ◽

10.1084/jem.125.4.607 ◽

1967 ◽

Vol 125 (4) ◽

pp. 607-618 ◽

Cited By ~ 15

Author(s):

Richard H. Winterbauer ◽

Laura T. Gutman ◽

Marvin Turck ◽

Ralph J. Wedgwood ◽

Robert G. Petersdorf

Keyword(s):

Escherichia Coli ◽

Renal Medulla ◽

Round Cell ◽

Histologic Response ◽

E Coli ◽

Round Cell Infiltration ◽

Kidney Liver

1. After injection into the renal medulla of rats Escherichia coli 06 variants reverted rapidly in vivo in the absence of penicillin. These variants had previously been shown to be stable in vitro. 2. Variants failed to survive following intramedullary injection when animals were receiving penicillin. 3. Late reversion of variants also failed to occur in animals treated with penicillin for only 1 or 2 days. 4. Variants survived and reverted more readily when injected in the renal medulla, compared with liver and spleen. Classical bacteria injected into the kidney, liver, and spleen were recovered in approximately equal numbers. 5. The histologic response to nonreverting variants, medium not containing variants, and killed variants was similar and was characterized by a fibrotic reaction with moderate round cell infiltration. 6. In contrast, the histologic response to reverting variants and to classical E. coli was characterized by an intense, acute, polymorphonuclear leukocytosis typical of acute pyelonephritis.

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Bloodstream Infections Caused by Extended-Spectrum-β-Lactamase- Producing Escherichia coli: Risk Factors for Inadequate Initial Antimicrobial Therapy

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.00063-08 ◽

2008 ◽

Vol 52 (9) ◽

pp. 3244-3252 ◽

Cited By ~ 72

Author(s):

Mario Tumbarello ◽

Michela Sali ◽

Enrico Maria Trecarichi ◽

Fiammetta Leone ◽

Marianna Rossi ◽

...

Keyword(s):

Risk Factors ◽

Escherichia Coli ◽

Antimicrobial Therapy ◽

Bloodstream Infections ◽

Disease Epidemiology ◽

E Coli ◽

Infectious Disease Epidemiology ◽

Extended Spectrum ◽

Initial Antimicrobial Therapy

ABSTRACT Extended-spectrum-β-lactamase (ESBL)-producing strains of Escherichia coli are a significant cause of bloodstream infections (BSI) in hospitalized and nonhospitalized patients. We previously showed that delaying effective antimicrobial therapy in BSI caused by ESBL producers significantly increases mortality. The aim of this retrospective 7-year analysis was to identify risk factors for inadequate initial antimicrobial therapy (IIAT) (i.e., empirical treatment based on a drug to which the isolate had displayed in vitro resistance) for inpatients with BSI caused by ESBL-producing E. coli. Of the 129 patients considered, 56 (43.4%) received IIAT for 48 to 120 h (mean, 72 h). Independent risk factors for IIAT include an unknown BSI source (odds ratios [OR], 4.86; 95% confidence interval [CI], 1.98 to 11.91; P = 0.001), isolate coresistance to ≥3 antimicrobials (OR, 3.73; 95% CI, 1.58 to 8.83; P = 0.003), hospitalization during the 12 months preceding BSI onset (OR, 3.33; 95% CI, 1.42 to 7.79; P = 0.005), and antimicrobial therapy during the 3 months preceding BSI onset (OR, 2.65; 95% CI, 1.11 to 6.29; P = 0.02). IIAT was the strongest risk factor for 21-day mortality and significantly increased the length of hospitalization after BSI onset. Our results underscore the need for a systematic approach to the management of patients with serious infections by ESBL-producing E. coli. Such an approach should be based on sound, updated knowledge of local infectious-disease epidemiology, detailed analysis of the patient's history with emphasis on recent contact with the health care system, and aggressive attempts to identify the infectious focus that has given rise to the BSI.

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Pathogenic Escherichia coli – virulence mechanisms

Medycyna Weterynaryjna ◽

10.21521/mw.5522 ◽

2016 ◽

Vol 72 (6) ◽

pp. 352-357

Author(s):

Katarzyna Półtorak ◽

Kinga Wieczorek ◽

Jacek Osek

Keyword(s):

Bloodstream Infections ◽

Epidemiological Data ◽

Intestinal Epithelial ◽

Bacterial Strains ◽

Internal Organs ◽

E Coli ◽

Cellular Processes ◽

Pathogenic Escherichia Coli ◽

Different Strains

E. coli are the predominant microorganisms in the human gastrointestinal tract. In most cases, they exist as harmless comensals, and some of them are beneficial to their host in balancing gut flora and absorption of nutrients. However, there are pathogenic strains that cause a broad range of diseases in humans and animals, from diarrhea to bloodstream infections. Among bacterial strains causing these symptoms, seven pathotypes are now recognized: enteropathogenic E. coli (EPEC), shiga toxin-producing E. coli (STEC), enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC), enteroaggregative E. coli (EAEC), diffusely adherent E. coli (DAEC), and adherent-invasive E. coli (AIEC). Several different strains cause diverse diseases by means of virulence factors that facilitate their interactions with the host, including colonization of the intestinal epithelial surfaces, crossing of the mucosal barriers, invasion of the bloodstream and internal organs or producing toxins that affect various cellular processes. Pathogenic E. coli are commonly studied in humans, animals, food and the environment, in developed and developing countries. The presented paper reviews recent information concerning the pathogenic mechanisms of E. coli, the role of animals and food in the transmission chain and a short overview of epidemiological data.

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Costs of Bloodstream Infections Caused by Escherichia coli and Influence of Extended-Spectrum-β-Lactamase Production and Inadequate Initial Antibiotic Therapy

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.00143-10 ◽

2010 ◽

Vol 54 (10) ◽

pp. 4085-4091 ◽

Cited By ~ 112

Author(s):

Mario Tumbarello ◽

Teresa Spanu ◽

Rossella Di Bidino ◽

Marco Marchetti ◽

Matteo Ruggeri ◽

...

Keyword(s):

Escherichia Coli ◽

Hospital Costs ◽

Bloodstream Infections ◽

Antimicrobial Treatment ◽

Accounting System ◽

Esbl Production ◽

E Coli ◽

Extended Spectrum ◽

Hospital Stays

ABSTRACT Escherichia coli is the leading cause of bloodstream infections (BSIs) caused by Gram-negative bacteria. The increasing prevalence of antibiotic-resistant E. coli strains, particularly those producing extended-spectrum β-lactamases (ESBLs), increases the odds that empirically prescribed antimicrobial therapy for these infections will be inadequate, but the economic impact of this risk has not been fully evaluated. In the present retrospective 1-year analysis of 134 consecutive E. coli BSIs in our hospital, we explored the clinical and economic impacts of (i) inadequate initial antimicrobial treatment (IIAT) (i.e., empirical treatment with drugs to which the isolate had displayed in vitro resistance) of these infections and (ii) ESBL production by the bloodstream isolate. Cost data were obtained from the hospital accounting system. Compared with the 107 (79.8%) adequately treated patients, the 27 (20.1%) who received IIAT had a higher proportion of ESBL BSIs (74.0% versus 15.8%), longer (+6 days) and more costly (+EUR 4,322.00) post-BSI-onset hospital stays, and higher 21-day mortality rates (40.7% versus 5.6%). Compared with the 97 non-ESBL infections, the 37 (27.6%) ESBL BSIs were also associated with longer (+7 days) and more costly (+EUR 5,026.00) post-BSI-onset hospital stays and increased 21-day mortality (29.7% versus 6.1%). These findings confirm that the hospital costs and mortality associated with E. coli BSIs are significantly increased by ESBL production and by IIAT.

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Macrophage Class A Scavenger Receptor-Mediated Phagocytosis of Escherichia coli: Role of Cell Heterogeneity, Microbial Strain, and Culture Conditions In Vitro

Infection and Immunity ◽

10.1128/iai.68.4.1953-1963.2000 ◽

2000 ◽

Vol 68 (4) ◽

pp. 1953-1963 ◽

Cited By ~ 160

Author(s):

Leanne Peiser ◽

Peter J. Gough ◽

Tatsuhiko Kodama ◽

Siamon Gordon

Keyword(s):

Escherichia Coli ◽

Host Defense ◽

Bacterial Strain ◽

Chinese Hamster Ovary Cells ◽

Culture Conditions ◽

E Coli ◽

Class A

ABSTRACT Macrophage class A scavenger receptors (SR-AI and SR-AII) contribute to host defense by binding polyanionic ligands such as lipopolysaccharide and lipoteichoic acid. SR-A knockout (SR-A−/−) mice are more susceptible to endotoxic shock and Listeria monocytogenes infection in vivo, possibly due to decreased clearance of lipopolysaccharide and microorganisms, respectively. We have used flow cytometry to analyze the role of SR-A and other scavenger-like receptors in phagocytosis of bacteria in vitro. Chinese hamster ovary cells stably transfected with human SR-A bound Escherichia coli and Staphylococcus aureus but ingested few organisms. Primary human monocyte-derived macrophages (Mφ) bound and ingested E. coli more efficiently, and this was partially but selectively blocked by the general SR inhibitor, poly(I). A specific and selective role for SR-A was shown, since bone marrow culture-derived Mφ from SR-A−/− mice ingested fewer E. coli organisms than did wild-type cells, while uptake of antibody-opsonized E. coli was unaffected. SR-A-dependent uptake of E. colivaried with the bacterial strain; ingestion of DH5α and K1 by SR-A−/− Mφ was reduced by 30 to 60% and 70 to 75%, respectively. Phagocytosis and endocytosis via SR-A were markedly down-modulated when Mφ were plated on serum-coated tissue culture plastic compared to bacteriologic plastic, where cell adhesion is mediated by SR-A and CR3, respectively. This paper demonstrates that SR-A can bind and ingest bacteria directly, consistent with a role in host defense in vivo, and highlights the importance of the source of the Mφ, bacterial strain, and culture conditions on receptor function in vitro.

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