Extended-spectrum β-lactamase-producing Escherichia coli bacteremia: Comparison of pediatric and adult populations

Background/Purpose

The prevalence of extended-spectrum β-lactamase (ESBL)-producing Escherichia coli is increasing worldwide. This study investigated the clinical features and bacteriology of pediatric patients with ESBL-producing E. coli bacteremia and compared their characteristics with those of adult patients.

Point: Should all stools be screened for Shiga toxin-producing Escherichia coli?

In October 2009, the Centers for Disease Control and Prevention recommended that clinical laboratories test all stools submitted for the detection of enteric bacterial pathogens for the presence of Shiga toxin-producing Escherichia coli (STEC). In order to do this, it is recommended that all stools be cultured for Escherichia coli O157:H7 on selective medium as well as that testing for the presence of Shiga toxin be done by immunoassay to detect non-O157 STEC (3). There are a variety of products that are FDA approved for detection of Shiga toxin. Further, it is recommended that Shiga toxin detection be done by testing overnight enrichment broth cultures of stools rather than directly examining stools for this toxin. This recommendation was made approximately 18 months ago. We have asked Mario Marcon of Nationwide's Children Hospital in Columbus, OH, to explain the rationale for his decision to follow this recommendation, while we have asked Deanna Kiska and Scott Riddell of Upstate University Hospital in Syracuse, NY, why these guidelines have not been adopted by their laboratory.     

Molecular and clinical characterization of plasmid-mediated AmpC β-lactamase-producing Escherichia coli bacteraemia: a comparison with extended-spectrum β-lactamase-producing and non-resistant E. coli bacteraemia

Plasmid-mediated AmpC β-lactamase-producing Escherichia coli (AmpC-E) bacteraemia was characterized by comparison with bacteraemia caused by extended-spectrum β-lactamase (ESBL)-producing E. coli (ESBL-E) and non-resistant E. coli (NR-E) in the era of the worldwide spread of the CTX-M-15-producing O25b-ST131-B2 clone. Of 706 bloodstream E. coli isolates collected between 2005 and 2010 in three Japanese university hospitals, 111 ESBL screening-positive isolates were analysed for AmpC and ESBL genes by PCR. A case–control study was performed in which the cases consisted of all of the patients with AmpC-E bacteraemia. Phylogenetic groups, sequence types and O25b serotype were determined. Twenty-seven AmpC-E isolates (26 of which were of the CMY-2 type) were identified, and 54 ESBL-E and 54 NR-E isolates were selected for the controls. Nineteen AmpC-E isolates were also positive for ESBL. CTX-M-14 was the most prevalent ESBL type among both the AmpC-E and ESBL-E isolates. The O25b-ST131-B2 clone was the most prevalent among the ESBL-E isolates (26%) and the second most prevalent among the NR-E isolates (13%), but only one O25b-ST131-B2 clone was found among the AmpC-E isolates. Twenty-three different sequence types were identified among the AmpC-E isolates. When compared with bacteraemia with ESBL-E, previous isolation of multidrug-resistant bacteria and intravascular catheterization were independently associated with a lower risk for AmpC-E. When compared with NR-E bacteraemia, prior use of antibiotics was the only significant risk factor for AmpC-E. Unlike the spread of the O25b-ST131-B2 clone between ESBL-E and NR-E, the AmpC-E isolates were not dominated by any specific clone.     

Juvenile polyposis coli: a facultative precancerosis with some similarities to ulcerative colitis?

We investigated the case of a 13-year-old male with juvenile polyposis (JP) to determine the extent of intraepithelial neoplasia and associated genetic changes, as well as cellular proliferation, within these polyps using immunohistochemistry with antibodies against p53, bcl-2, and Ki-67. Examination of the total proctocolectomy specimen revealed 70 polyps. The 18 largest polyps were investigated microscopically and disclosed the typical hamartomas with frequent erosions of the surface epithelium and reparative changes. Only one polyp showed focal low-grade intraepithelial neoplasia. The immunohistochemical studies revealed an expression of p53 and an abnormal Ki-67 pattern of the surface epithelium only within the neoplastic area. These findings may hint at a possible pathogenetic mechanism for the evolution of colorectal cancer in JP. As in ulcerative colitis, carcinomas in JP may develop along a dysplasia-carcinoma sequence resulting from permanent mechanical insults, inflammation, and repair rather than from an adenoma-carcinoma sequence as in familial adenomatous polyposis (FAP).     

What defines extraintestinal pathogenic Escherichia coli?

Escherichia coli (E. coli) exhibits considerable physiological and metabolic versatility and includes a variety of non-pathogenic, commensal variants, which belong to the normal gut flora of humans and warm-blooded animals. Additionally, several pathogenic variants have been identified which cause various types of intestinal or extraintestinal infections in humans and animals. In contrast to intestinal pathogenic E. coli (IPEC), which are obligate pathogens, extraintestinal pathogenic E. coli (ExPEC) are facultative pathogens which belong to the normal gut flora of a certain fraction of the healthy population where they live as commensals. Comparative genomics and epidemiological studies have been applied to study genomic diversity, markers, and phenotypic traits that may support discrimination of different E. coli pathotypes. Whereas IPEC are often epidemiologically and phylogenetically distinct from ExPEC and non-pathogenic, commensal strains, many ExPEC and non-pathogenic E. coli share large genomic fractions. Furthermore, extraintestinal infections of elderly or immunocompromised patients can be caused by E. coli variants which differ in their geno- and phenotypes from archetypal ExPEC. Thus, strain typing based on the detection of a limited number of ExPEC virulence/fitness-related genes may be ambiguous. A limited number of ExPEC-dominated clonal complexes can be identified in the E. coli population by multi locus sequence typing. Nevertheless, ExPEC and non-pathogenic E. coli cannot be clearly discriminated by molecular epidemiological approaches. Increased knowledge of the phylogeny, virulence and fitness traits, and host factors contributing to host susceptibility of the different groups of ExPEC variants is required for a better understanding of the biological basis of ExPEC infections.     

Bloodstream infection with extended-spectrum beta-lactamase–producing Escherichia coli: The role of virulence genes

BackgroundExtraintestinal pathogenic Escherichia coli (ExPEC) strains hold the responsibility for the majority of E. coli infections. Numerous extraintestinal virulence factors (VFs) were possessed by ExPEC which are involved in the pathogenesis of infection. However, the effect of comorbidities or infection syndrome in the association of VFs and mortality remains inconclusive.MethodThis study addressed whether specific sequence type (ST) and VFs of extended-spectrum beta-lactamase–producing E. coli (ESBL-EC) are associated with different outcomes in patients with bloodstream infection. 121 adults from southern Taiwan with ESBL-EC bloodstream infections were enrolled during a 6-year period. Demographic data, including infection syndromes, underlying disease and outcomes, were collected. The virulence factors in isolates were analyzed by PCR and multilocus sequence typing analyses were also performed.ResultPositivity for the virulence genes iha, hlyD, sat, iutA, fyuA, malX, ompT, and traT was associated with ST131 positivity (P < 0.05). Some ESBL-EC virulence genes associated with urinary tract infection (UTI) were revealed. Positivity for ST405 and the virulence genes iroN and iss were significantly associated with increased 30-day mortality (death within 30 days) on univariate analysis (P < 0.05). Independent risk factors of 30-day mortality in bacteremic patients with UTI included underlying chronic liver disease and malignancy. ST131 was borderline associated with 30-day mortality. Independent risk factors associated with 30-day mortality among bacteremic patients without UTI included comorbidities and iroN positivity.ConclusionIn bacteremic patients with UTI, and the ST131 clone was borderline associated with mortality. Positivity for the virulence gene iroN may be linked to mortality in bacteremic patients without UTI.     

Diversity of Escherichia coli Strains Producing Extended-Spectrum β-Lactamases in Spain: Second Nationwide Study

The prevalence of extended-spectrum β-lactamase (ESBL)-producing Escherichia coli (ESBLEC) in Spain increased 8-fold from 2000 to 2006. ESBL type, clonal relationship, antimicrobial susceptibility, and clinical data about infections caused by ESBLEC are evaluated in a second nationwide study developed in 2006. From 1008 clinical isolates obtained over 2 months from 44 hospitals, 254 were used for further analysis. ESBL production was evaluated by synergy testing, PCR, and sequencing. Antimicrobial activity was evaluated by microdilution. The clonal relationship was evaluated by repetitive extragenic palindromic-PCR (REP-PCR). The O25b subtype and the new afa operon {"type":"entrez-nucleotide","attrs":{"text":"FM955459","term_id":"218921801","term_text":"FM955459"}}FM955459 were determined by triplex PCR in isolates producing CTX-M-15. Multilocus sequence typing was performed on these isolates. A total of 72% of all ESBLs were of the CTX-M type, 26.8% were of the SHV type, and 1.2% were of the TEM type. The most prevalent ESBLs were CTX-M-14 (119 isolates), SHV-12 (68 isolates), CTX-M-15 (37 isolates), and CTX-M-9 (21 isolates). By REP-PCR, 214 clones were detected. All but five CTX-M-15 ESBLEC isolates corresponded to the international O25b/ST131 clone. This clone had not been detected in the first study (published in 2000). Epidemiological and clinical features were studied in 304 representative patients. A total of 60% of the patients were older than 60 and had nonfatal underlying diseases, and 55% had recently received antibiotics. Urinary tract infections accounted for 71% of cases, and 9% were bacteremic. There has been a significant increase in the prevalence of ESBLEC in Spain, with most of these strains being CTX-M-producing isolates, including the pandemic O25b-ST131. SHV-12-producing E. coli remains an important cause of community-acquired infection.Extended-spectrum β-lactamase (ESBL)-producing Escherichia coli (ESBLEC) has emerged worldwide as a significant cause of both community and healthcare-associated infections (13). Moreover, the role of this microorganism as a cause of nosocomial infection is also increasing (15). The type of ESBL expressed by this microorganism has changed in recent years. The classic SHV and TEM types have often been substituted by members of the CTX-M family (3).The epidemiology of ESBLEC is a complex and evolving phenomenon. A few years ago most ESBLEC strains were clonally unrelated, and the rapid emergence of ESBL was related to the dissemination of mobile genetic elements (14). Nevertheless, both plasmid and bacterial transmission between humans has been demonstrated (17). Recently, the international spread of the O25b-ST131 clone producing CTX-M-15 and other β-lactamases has been described (6, 11). For these reasons, the development of studies directed at discovering the epidemiology of ESBLs in a specific area is recommended.In 2000, the first nationwide study of ESBLEC was developed in Spain (GEIH-BLEE 2000) (8). The prevalence of ESBL production among E. coli isolates was determined to be 0.5%, with CTX-M-9, SHV-12, and CTX-M-14 being the most commonly found ESBLs. No CTX-M-15-producing E. coli strain was isolated. A nationwide study designed along similar lines was developed in 2006 (GEIH-BLEE 2006) because of perceived important changes in the epidemiology of ESBLEC. In 6 years, the prevalence of ESBLEC increased to 4.04% (range, 0.4 to 20.3%) in Spain (7). The distributions of origins of infection between community-acquired, healthcare-associated, and nosocomial strains were 32, 36, and 30%, respectively. The changes in ESBL type, clonal relationship, susceptibility to antimicrobial agents, and relevant clinical data pertaining to ESBLEC in Spain are discussed here.     

Untersuchungen zum Aminosäurestoffwechsel von Bacterium coli

Zusammenfassung Es wird über das Verhalten von Escherichia coli in Nährböden mit einem Gehalt an verschiedenen Aminosäuren berichtet. Dabei treten nach der Bebrütung in der Kulturflüssigkeit zusätzliche Aminosäuren auf und ein Peptid, das nach einem stets übereinstimmenden R_f-Wert zu urteilen, immer gleichartig zusammengesetzt zu sein scheint. Untersuchungen dazu sind noch im Gange.     

Unusual “Flesh-Eating” Strain of Escherichia coli

We report an exceptional case of life-threatening Escherichia coli-induced necrotizing fasciitis. A combined host-pathogen genetic analysis explained the phenotype: the host displayed a susceptibility to intravascular coagulation, and the strain was capable of producing a necrotic toxin (cytotoxic necrotizing factor 1), showing how E. coli can be a dermonecrotic pathogen.     

Avian pathogenic, uropathogenic, and newborn meningitis-causing Escherichia coli: how closely related are they?

Avian pathogenic Escherichia coli (APEC), uropathogenic E. coli (UPEC), and newborn meningitis-causing E. coli (NMEC) establish infections in extraintestinal habitats (extraintestinal pathogenic E. coli; ExPEC) of different hosts. As diversity, epidemiological sources, and evolutionary origins of ExPEC are so far only partially defined, we screened a collection of 526 strains of medical and veterinary origin of various O-types for assignment to E. coli reference collection (ECOR) group and virulence gene patterns. Results of ECOR typing confirmed that human ExPEC strains mostly belong to groups B2, followed by group D. Although a considerable portion of APEC strains did also fell into ECOR group B2 (35.1%), a higher amount (46.1%) belonged to group A, which has previously been described to also harbour strains with a high pathogenic potential for humans. The number of virulence-associated genes of single strains ranged from 5 to 26 among 33 genes tested and high numbers were rather related to K1-positive and ECOR B2 strains than to a certain pathotype. With a few exceptions (iha, afa/draB, sfa/foc, and hlyA), which were rarely present in APEC strains, most chromosomally located genes were widely distributed among all ExPEC strains irrespective of host and pathotype. However, prevalence of invasion genes (ibeA and gimB) and K1 capsule-encoding gene neuC indicated a closer relationship between APEC and NMEC strains. Genes associated with ColV plasmids (tsh, iss, and the episomal sit locus) were in general more prevalent in APEC than in UPEC and NMEC strains, indicating that APEC could be a source of ColV-located genes or complete plasmids for other ExPEC strains. Our data support the hypothesis that (a) poultry may be a vehicle or even a reservoir for human ExPEC strains, (b) APEC potentially serve as a reservoir of virulence-associated genes for UPEC and NMEC, (c) some ExPEC strains, although of different pathotypes, may share common ancestors, and (d) as a conclusion certain APEC subgroups have to be considered potential zoonotic agents. The finding of different evolutionary clusters within these three pathotypes implicates an independently and parallel evolution, which should be resolved in the future by thorough phylogenetic typing.     

E.coli DNA抗肿瘤免疫的实验研究

目的探讨 E.coli DNA抗肿瘤免疫的效果及免疫作用机制。方法纯化提取大肠埃希菌染色体 DNA(E.coliDNA)进行抗肿瘤治疗及免疫学指标测定。结果 E.coli DNA体内多种途径给药均可抑制肿瘤生长 ,增强正常小鼠 NK细胞杀伤活性 ,在荷瘤小鼠亦测出 NK/ MΦ 细胞的杀伤活性增强 ,对荷瘤所致的 NK细胞功能下降有提高作用 ,还可诱生荷瘤小鼠体内 γ- IFN,调节其 TNF- α水平。结论 E.coli DNA具有抗肿瘤免疫特性 ,为微生物 DNA制剂开发应用于抗肿瘤治疗提供了科学依据。     

MMS-induced mutagenesis and DNA repair in Escherichia coli dnaQ49: Contribution of UmuD′ to DNA repair

dnaQ-encoded epsilon subunit of DNA polymerase III, possesses 3′,5′ exonuclease (proofreading) activity, and is a fidelity factor of polymerase III holoenzyme. It is assumed that during SOS-induced mutagenesis, UmuD′, UmuC and RecA may suppress DnaQ proofreading activity, and allow for translesional DNA synthesis at the cost of fidelity of replication. In this report SOS-dependent, MMS-induced mutagenesis and DNA repair were tested in E. coli dnaQ49 strains. Bacteria were transformed with various pDNAs harboring compilation of the umuD(D′)C genes, and the influence of plasmids on mutagenesis (argE3 → Arg⁺) and DNA repair was tested. DNA damage and repair were tested in plasmid DNA grown in MMS-treated bacteria and isolated either immediately after MMS treatment, or after starving the cells (MFD conditions) for 30 and 60 min, then nicking activity of Fpg protein on plasmid DNAs was analyzed. It has been found that (i) repair of MMS-induced lesions depends on umuD′C, umuD′ (and to much less degree, on umuDC) genes encoded in pDNA; (ii) MMS-induced mutations, in contrast to DNA repair, are highest in the cells transformed with pDNA harboring umuDC, and lowest or zero in cells with plasmids harboring umuD′C. It is postulated that UmuD′C or UmuD′ proteins play a role in the repair of damaged DNA and/or in maintenance of DNA integrity. The kinetics of these processes (perhaps due to introducing too many of the lessions) seems to be different in E. coli dnaQ⁺ and dnaQ cells, and probably this is a reason that (iii) MMS-induced mutations in dnaQ49 strains are not subject to MFD.     

Colonisation with Escherichia coli resistant to “critically important” antibiotics: a high risk for international travellers

Antimicrobial resistance among community-acquired isolates of Escherichia coli is increasing globally, with international travel emerging as a risk for colonisation and infection. The aim was to determine the rate and duration of colonisation with resistant E. coli following international travel. One hundred and two adult hospital staff and contacts from Canberra, Australia, submitted perianal/rectal swabs before and following international travel. Swabs were cultured selectively to identify E. coli resistant to gentamicin, ciprofloxacin and/or third-generation cephalosporins. Those with resistant E. coli post-travel were tested monthly for persistent colonisation. Colonisation with antibiotic-resistant E. coli increased significantly from 7.8% (95% confidence interval [CI] 3.8–14.9) pre-travel to 49% (95% CI 39.5–58.6) post-travel. Those colonised were more likely to have taken antibiotics whilst travelling; however, travel remained a risk independent of antibiotic use. Colonisation with resistant E. coli occurred most frequently following travel to Asia. While over half of those carrying resistant E. coli post-travel had no detectable resistant strains two months after their return, at least 18% remained colonised at six months. Colonisation with antibiotic-resistant E. coli occurs commonly after international travel, and can be persistent. Medical practitioners should be aware of this risk, particularly when managing patients with suspected Gram-negative sepsis.