scholarly journals Association of Atypical Enteropathogenic Escherichia coli with Diarrhea and Related Mortality in Kittens

2017 ◽  
Vol 55 (9) ◽  
pp. 2719-2735 ◽  
Author(s):  
Victoria E. Watson ◽  
Megan E. Jacob ◽  
James R. Flowers ◽  
Sandra J. Strong ◽  
Chitrita DebRoy ◽  
...  

ABSTRACTDiarrhea is responsible for the death of approximately 900,000 children per year worldwide. In children, typical enteropathogenicEscherichia coli(EPEC) is a common cause of diarrhea and is associated with a higher hazard of death. Typical EPEC infection is rare in animals and poorly reproduced in experimental animal models. In contrast, atypical EPEC (aEPEC) infection is common in both children and animals, but its role in diarrhea is uncertain. Mortality in kittens is often attributed to diarrhea, and we previously identified enteroadherent EPEC in the intestines of deceased kittens. The purpose of this study was to determine the prevalence and type of EPEC in kittens and whether infection was associated with diarrhea, diarrhea-related mortality, gastrointestinal pathology, or other risk factors. Kittens with and without diarrhea were obtained from two shelter facilities and determined to shed atypical EPEC at a culture-based prevalence of 18%. In contrast, quantitative PCR detected the presence of the gene for intimin (eae) in feces from 42% of kittens. aEPEC was isolated from kittens with and without diarrhea. However, kittens with diarrhea harbored significantly larger quantities of aEPEC than kittens without diarrhea. Kittens with aEPEC had a significantly greater severity of small intestinal and colonic lesions and were significantly more likely to have required subcutaneous fluid administration. These findings identify aEPEC to be prevalent in kittens and a significant primary or contributing cause of intestinal inflammation, diarrhea, dehydration, and associated mortality in kittens.

2010 ◽  
Vol 78 (3) ◽  
pp. 927-938 ◽  
Author(s):  
Mônica A. M. Vieira ◽  
Tânia A. T. Gomes ◽  
Antonio J. P. Ferreira ◽  
Terezinha Knöbl ◽  
Alain L. Servin ◽  
...  

ABSTRACT In rabbit ligated ileal loops, two atypical enteropathogenic Escherichia coli (aEPEC) strains, 3991-1 and 0421-1, intimately associated with the cell membrane, forming the characteristic EPEC attachment and effacement lesion of the brush border, induced a mucous hypersecretion, whereas typical EPEC (tEPEC) strain E2348/69 did not. Using cultured human mucin-secreting intestinal HT29-MTX cells, we demonstrate that apically aEPEC infection is followed by increased production of secreted MUC2 and MUC5AC mucins and membrane-bound MUC3 and MUC4 mucins. The transcription of the MUC5AC and MUC4 genes was transiently upregulated after aEPEC infection. We provide evidence that the apically adhering aEPEC cells exploit the mucins' increased production since they grew in the presence of membrane-bound mucins, whereas tEPEC did not. The data described herein report a putative new virulence phenomenon in aEPEC.


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.


2019 ◽  
Vol 87 (10) ◽  
Author(s):  
Tracy H. Hazen ◽  
David A. Rasko

ABSTRACT Enteropathogenic Escherichia coli (EPEC) is a leading cause of moderate to severe diarrhea among young children in developing countries, and EPEC isolates can be subdivided into two groups. Typical EPEC (tEPEC) bacteria are characterized by the presence of both the locus of enterocyte effacement (LEE) and the plasmid-encoded bundle-forming pilus (BFP), which are involved in adherence and translocation of type III effectors into the host cells. Atypical EPEC (aEPEC) bacteria also contain the LEE but lack the BFP. In the current report, we describe the complete genome of outbreak-associated aEPEC isolate E110019, which carries four plasmids. Comparative genomic analysis demonstrated that the type III secreted effector EspT gene, an autotransporter gene, a hemolysin gene, and putative fimbrial genes are all carried on plasmids. Further investigation of 65 espT-containing E. coli genomes demonstrated that different espT alleles are associated with multiple plasmids that differ in their overall gene content from the E110019 espT-containing plasmid. EspT has been previously described with respect to its role in the ability of E110019 to invade host cells. While other type III secreted effectors of E. coli have been identified on insertion elements and prophages of the chromosome, we demonstrated in the current study that the espT gene is located on multiple unique plasmids. These findings highlight a role of plasmids in dissemination of a unique E. coli type III secreted effector that is involved in host invasion and severe diarrheal illness.


2012 ◽  
Vol 56 (6) ◽  
pp. 2888-2893 ◽  
Author(s):  
Nan-Yao Lee ◽  
Ching-Chi Lee ◽  
Wei-Han Huang ◽  
Ko-Chung Tsui ◽  
Po-Ren Hsueh ◽  
...  

ABSTRACTA retrospective study was conducted at two medical centers in Taiwan to evaluate the clinical characteristics, outcomes, and risk factors for mortality among patients treated with a carbapenem for bacteremia caused by extended-spectrum-beta-lactamase (ESBL)-producing organisms. A total of 251 patients with bacteremia caused by ESBL-producingEscherichia coliandKlebsiella pneumoniaeisolates treated by a carbapenem were identified. Among these ESBL-producing isolates, rates of susceptibility to ertapenem (MICs ≤ 0.25 μg/ml) were 83.8% and 76.4%, respectively; those to meropenem were 100% and 99.3%, respectively; and those to imipenem were 100% and 97.9%, respectively. There were no significant differences in the critical illness rate (P= 0.1) or sepsis-related mortality rate (P= 0.2) for patients with bacteremia caused by ESBL-producingK. pneumoniae(140 isolates, 55.8%) andE. coli(111 isolates, 44.2%). Multivariate analysis of variables related to sepsis-related mortality revealed that the presence of severe sepsis (odds ratio [OR], 15.9; 95% confidence interval [CI], 5.84 to 43.34;P< 0.001), hospital-onset bacteremia (OR, 4.65; 95% CI, 1.42 to 15.24;P= 0.01), and ertapenem-nonsusceptible isolates (OR, 5.12; 95% CI, 2.04 to 12.88;P= 0.001) were independent risk factors. The patients receiving inappropriate therapy had a higher sepsis-related mortality than those with appropriate therapy (P= 0.002), irrespective of ertapenem, imipenem, or meropenem therapy. Infections due to the ertapenem-susceptible isolates (MICs ≤ 0.25 μg/ml) were associated with a more favorable outcome than those due to ertapenem-nonsusceptible isolates (MICs > 0.25 μg/ml), if treated by a carbapenem. However, the mortality for patients with bacteremic episodes due to isolates with MICs of ≤0.5 μg/ml was similar to the mortality for those whose isolates had MICs of >0.5 μg/ml (P= 0.8). Such a finding supports the rationale of the current CLSI 2011 criteria for carbapenems forEnterobacteriaceae.


2004 ◽  
Vol 53 (11) ◽  
pp. 1137-1144 ◽  
Author(s):  
Jan E Afset ◽  
Lars Bevanger ◽  
Pål Romundstad ◽  
Kåre Bergh

The aim of the present case control study was to investigate the prevalence of atypical enteropathogenic Escherichia coli (EPEC) and its possible role in causing diarrhoea among children < 5 years of age in Norway. Stool specimens received in the laboratory from children with suspected gastroenteritis (n = 251) were, in addition to routine testing, analysed for the presence of EPEC by PCR of the eae, bfpA and stx genes. Specimens from healthy children (n = 210) recruited from Maternal and Child Health Centres were analysed for EPEC only. EPEC isolates (eae +, stx −) were classified as typical (bfpA +) or atypical (bfpA −), and were tested for O : K serogroup. Information on duration of diarrhoea was recorded in a questionnaire and from referral forms. Atypical EPEC was diagnosed in 37 patients (14.7 %) compared to 21 (10.0 %) of the healthy controls [Odds ratio (OR) = 1.4, P = 0.3]. Only three isolates, all from patients, belonged to EPEC serogroups. One patient had typical EPEC. Twenty (22.5 %) of 89 patients with diarrhoea lasting ⩾14 days had atypical EPEC. The association between atypical EPEC and prolonged diarrhoea (OR = 2.1, P = 0.04) was caused by a high prevalence among female patients (40.6 %). In conclusion, atypical EPEC was found to be slightly more prevalent in patients than controls, without any overall significant association with diarrhoea. However, a significant association was observed with diarrhoea lasting 14 days or more, a finding that may indicate a role for atypical EPEC in prolonged disease.


2013 ◽  
Vol 62 (10) ◽  
pp. 1531-1534 ◽  
Author(s):  
Hanan Sakkejha ◽  
Lisa Byrne ◽  
Andy J. Lawson ◽  
Claire Jenkins

Historically, enteropathogenic Escherichia coli (EPEC) are a well-known cause of outbreaks of infantile diarrhoea associated with morbidity and mortality in England. The aim of this study was to provide an update on the microbiology and epidemiology of strains of EPEC in England between 2010 and 2012. A wide range of E. coli serogroups were identified, with the most common being E. coli O145, O49 and O157. Few isolates (9 %) had additional virulence factors (specifically bfp, vtx2f and espT genes) and the majority were classified as atypical EPEC. The majority of cases (86 %) were among children. This included a significantly higher percentage (17.4 %) of cases aged 0–12 months when compared with cases of other common gastrointestinal pathogens (P<0.001). No outbreaks were reported during this period; however, the data indicated that EPEC are still an important cause of sporadic cases of infantile diarrhoea in England.


2013 ◽  
Vol 81 (10) ◽  
pp. 3662-3671 ◽  
Author(s):  
Sandrine Tchaptchet ◽  
Ting-Jia Fan ◽  
Laura Goeser ◽  
Alexi Schoenborn ◽  
Ajay S. Gulati ◽  
...  

ABSTRACTDysregulated immune responses to commensal intestinal bacteria, includingEscherichia coli, contribute to the development of inflammatory bowel diseases (IBDs) and experimental colitis. Reciprocally,E. coliresponds to chronic intestinal inflammation by upregulating expression of stress response genes, includinggadAandgadB. GadAB encode glutamate decarboxylase and protectE. colifrom the toxic effects of low pH and fermentation acids, factors present in the intestinal lumen in patients with active IBDs. We hypothesized thatE. coliupregulatesgadABduring inflammation to enhance its survival and virulence. Using real-time PCR, we determinedgadABexpression in luminalE. colifrom ex-germfree wild-type (WT) and interleukin-10 (IL-10) knockout (KO) (IL-10−/−) mice selectively colonized with a commensalE. coliisolate (NC101) that causes colitis in KO mice in isolation or in combination with 7 other commensal intestinal bacterial strains.E. colisurvival and host inflammatory responses were measured in WT and KO mice colonized with NC101 or a mutant lacking thegadABgenes (NC101ΔgadAB). The susceptibility of NC101 and NC101ΔgadABto killing by host antimicrobial peptides and their translocation across intestinal epithelial cells were evaluated using bacterial killing assays and transwell experiments, respectively. We show that expression ofgadABin luminalE. coliincreases proportionately with intestinal inflammation in KO mice and enhances the susceptibility of NC101 to killing by the host antimicrobial peptide cryptdin-4 but decreases bacterial transmigration across intestinal epithelial cells, colonic inflammation, and mucosal immune responses. Chronic intestinal inflammation upregulates acid tolerance pathways in commensalE. coliisolates, which, contrary to our original hypothesis, limits their survival and colitogenic potential. Further investigation of microbial adaptation to immune-mediated inflammation may provide novel insights into the pathogenesis and treatment of IBDs.


2015 ◽  
Vol 198 (5) ◽  
pp. 846-856 ◽  
Author(s):  
Claudia F. Martinez de la Peña ◽  
Leon De Masi ◽  
Shahista Nisa ◽  
George Mulvey ◽  
Jesse Tong ◽  
...  

ABSTRACTEnteropathogenicEscherichia coli(EPEC) remains a significant cause of infant diarrheal illness and associated morbidity and mortality in developing countries. EPEC strains are characterized by their ability to colonize the small intestines of their hosts by a multistep program involving initial loose attachment to intestinal epithelial cells followed by an intimate adhesion phase. The initial loose interaction of typical EPEC with host intestinal cells is mediated by bundle-forming pili (BFP). BFP are type 4b pili (T4bP) based on structural and functional properties shared with T4bP expressed by other bacteria. The major structural subunit of BFP is called bundlin, a T4b pilin expressed from thebfpAgene in the BFP operon, which contains three additional genes that encode the pilin-like proteins BfpI, BfpJ, and BfpK. In this study, we show that, in the absence of the BFP retraction ATPase (BfpF), BfpI, BfpJ, and BfpK are dispensable for BFP biogenesis. We also demonstrate that these three minor pilins are incorporated along with bundlin into the BFP filament and contribute to its structural integrity and host cell adhesive properties. The results confirm that previous findings in T4aP systems can be extended to a model T4bP such as BFP.IMPORTANCEBundle-forming pili contribute to the host colonization strategy of enteropathogenicEscherichia coli. The studies described here investigate the role for three minor pilin subunits in the structure and function of BFP in EPEC. The studies also suggest that these subunits could be antigens for vaccine development.


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