Showing papers by "Shiri Navon-Venezia published in 2005"

Multidrug-resistant Acinetobacter baumannii.

Abstract: To understand the epidemiology of multidrug-resistant (MDR) Acinetobacter baumannii and define individual risk factors for MDR, we used epidemiologic methods, performed organism typing by pulsed-field gel electrophoresis (PFGE), and conducted a matched case-control retrospective study. We investigated 118 patients, on 27 wards, in whom MDR A. baumannii was isolated from clinical cultures. Each case-patient had a control without MDR A. baumannii and was matched for hospital length of stay, ward, and calendar time. The epidemiologic investigation found small clusters of up to 6 patients each with no common identified source. Ten different PFGE clones were found, of which 2 dominated. The PFGE pattern differed within temporospatial clusters, and antimicrobial drug susceptibility patterns varied within and between clones. Multivariate analysis identified the following significant risk factors: male sex, cardiovascular disease, having undergone mechanical ventilation, and having been treated with antimicrobial drugs (particularly metronidazole). Penicillins were protective. The complex epidemiology may explain why the emergence of MDR A. baumannii is difficult to control.

Update on pseudomonas aeruginosa and acinetobacter baumannii infections in the healthcare setting

Abstract: Summary The emergence and spread of multidrug-resistant P. aeruginosa and A. baumannii and their genetic potential to carry and transfer diverse antibiotic resistance determinants pose a major threat in hospitals. The complex interplay of clonal spread, persistence, transfer of resistance elements, and cell‐cell interaction contribute to the difficulty in treating infections caused by these multidrug-resistant strains. In the absence of new antibiotic agents, new modalities of treatment should be developed.

High Levels of Antimicrobial Coresistance among Extended-Spectrum-β-Lactamase-Producing Enterobacteriaceae

Abstract: We compared the susceptibility of 312 extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae isolates with that of 1,216 ESBL nonproducers. Of ESBL producers, 25% were susceptible to gentamicin, 30% to trimethoprim-sulfamethoxazole, 41% to ciprofloxacin, and 60% to piperacillin-tazobactam. ESBL nonproducers were more often susceptible to these agents. ESBL-producing Enterobacteriaceae represent a major source of resistance to various antibiotics.

Extended-Spectrum Beta-Lactamases among Enterobacter Isolates Obtained in Tel Aviv, Israel

Abstract: Enterobacter spp. are leading nosocomial pathogens (26) that commonly cause pneumonia (25) and that are the most frequent gram-negative organisms causing bloodstream infections in intensive care units (14, 33). More than one-third of the Enterobacter sp. isolates in intensive care units reporting to the National Nosocomial Infection Surveillance System (26) are resistant to extended-spectrum cephalosporins. Moreover, treatment with extended-spectrum cephalosporins may lead to the emergence of resistance to these antimicrobial agents among susceptible strains of Enterobacter spp. (8, 19, 35). Emergence of resistance results in increased rates of mortality, longer hospital stays, and higher hospital charges (9, 10). The resistance of Enterobacter spp. to beta-lactam antibiotics is most frequently mediated by hyperproduction of chromosomal AmpC beta-lactamase, caused either by induction or, more likely, by selection of derepressed mutants (1). In the last decade, the production of plasmid-mediated extended-spectrum beta-lactamases (ESBLs) has been recognized as an additional important emerging mechanism of resistance among members of the family Enterobacteriaceae (3, 17), including clinical isolates of Enterobacter spp. (31). The most common ESBLs found in clinical isolates of Enterobacter spp. belong to the TEM-, SHV-, and CTX-M-derived β-lactamases (2, 5, 36). However, other ESBLs have recently been reported in Enterobacter spp., including IBC-1, which was detected in an Enterobacter cloacae isolate in Greece (15, 18); VEB-1, which was found in clinical isolates of E. cloacae and Enterobacter sakazakii in Bangkok, Thailand (16); and SFO-1, which was detected in E. cloacae isolates in Japan (24). The prevalence of ESBLs among members of the family Enterobacteriaceae may vary significantly between geographical areas (40). For example, Schwaber et al. (34) recently reported that less than 2% of 152 U.S. isolates of Enterobacter spp. were confirmed to produce ESBLs. In sharp contrast, we recently investigated the occurrence of the ESBL-producing phenotype among members of the family Enterobacteriaceae at the Tel Aviv Sourasky Medical Center, Tel Aviv, Israel, and found that 22% of the Enterobacter clinical isolates in our institution had this phenotype (27). To understand the widespread occurrence of the ESBL phenotype in Enterobacter spp. at the Tel Aviv Sourasky Medical Center, we examined the genetic relatedness between these ESBL producers and characterized the ESBL enzyme families produced by these strains.

CTX-M-2 and a new CTX-M-39 enzyme are the major extended-spectrum beta-lactamases in multiple Escherichia coli clones isolated in Tel Aviv, Israel

Abstract: The rate of occurrence of the extended-spectrum beta-lactamase (ESBL)-producing phenotype among Escherichia coli isolates in Tel Aviv is 12% (22). The aim of this study was to understand the molecular epidemiology of E. coli ESBL producers and to identify the ESBL genes carried by them. We studied 20 single-patient ESBL-producing E. coli clinical isolates. They comprised 11 distinct nonrelated pulsed-field gel electrophoresis (PFGE) genotypes: six isolates belonged to the same PFGE clone, four other clones included two isolates each, and six unrelated clones included only one isolate. All isolates produced various beta-lactamases with pIs ranging from 5.2 to 8.2, varying within similar PFGE clones. The most prevalent ESBL gene was bla(CTX-M); 16 isolates carried bla(CTX-M-2) and three carried a new ESBL gene designated bla(CTX-M-39). Three strains carried bla(SHV) (two bla(SHV-12) and one bla(SHV-5)), and two strains carried inhibitor-resistant ESBL genes, bla(TEM-33) and bla(TEM-30); 18 strains carried bla(TEM-1) and eight strains carried bla(OXA-2). Plasmid mapping and Southern blot analysis with a CTX-M-2 probe demonstrated that bla(CTX-M-2) is plasmid borne. The wide dissemination of ESBLs among E. coli isolates in our institution is partly related to clonal spread, but more notably to various plasmid-associated ESBL genes, occurring in multiple clones, wherein the CTX-M gene family appears almost uniformly. We report here a new CTX-M gene, designated bla(CTX-M-39), which revealed 99% homology with bla(CTX-M-26), with a substitution of arginine for glutamine at position 225.

Erroneous Reporting of Coagulase-Negative Staphylococci as Kocuria spp. by the Vitek 2 System

Abstract: Misidentification of coagulase-negative staphylococci (CoNS) may delay appropriate treatment. We investigated 20 clinical isolates identified as Kocuria spp. by the Vitek 2 system. All were identified as CoNS by 16S rRNA gene sequencing (18 Staphylococcus epidermidis, 1 Staphylococcus haemolyticus). Four Kocuria isolates were shown to be identical to CoNS from the same patient by pulsed-field gel electrophoresis. Isolates identified by Vitek 2 as Kocuria most likely represent misidentified CoNS, and if clinically indicated, should be investigated further by genomic methods.

Antibodies raised against N'-terminal Pseudomonas aeruginosa flagellin prevent mortality in lethal murine models of infection

Abstract: The goal of this study was to investigate if antibodies raised against N'-terminal Pseudomonas aeruginosa (Pa) flagellin could afford protection in two lethal mouse models of Pa infection. To that end, rabbit polyclonal antibodies were generated against the N'-terminal domains (amino acids 1-156) of recombinant Pa01 or Salmonella muenchen flagellins, termed anti-N'-fla-b and anti-N'-fla-Sm, respectively. In vitro, anti-N'-fla-b but not anti-N'-fla-Sm IgG specifically recognized recombinant and Pa endogenous flagellin type b proteins, total bacterial lysates of Pa type b, and inhibited Pa01 invasion into A549 cells. In vivo, administration of anti-N'-fla-b afforded a remarkable improvement in survival in lethal peritonitis (90% vs. 12% in control; p<0.001) and burn infection (83% vs. 8-17% in control groups; p<0.005) Pa models. These findings would suggest that the N'-terminal domain of Pa flagellin harbors critically important bioactive domains and that an antibody-targeted, neutralization approach directed at this region could provide a novel therapeutic strategy to combat Pa infection.

Evaluation of an Accelerated Protocol for Detection of Extended-Spectrum β-Lactamase-Producing Gram-Negative Bacilli from Positive Blood Cultures

Abstract: We evaluated a protocol for the accelerated detection of extended-spectrum β-lactamases (ESBLs) in gram-negative bloodstream pathogens. Two hundred eighty-three blood culture bottles were subjected to direct ESBL testing by inoculating samples directly from blood culture bottles onto agar plates containing cefotaxime and ceftazidime disks, with and without clavulanate. Standard ESBL testing in accordance with the NCCLS guidelines after subculturing on agar plates was performed in parallel. Results of the direct ESBL testing were reported 2.3 days sooner and were comparable to those of the standard NCCLS method with sensitivity, specificity, and positive and negative predictive values of 100, 98, 94, and 100%, respectively.

Multidrug-resiistant Acinetobacter baumannii

Abstract: To understand the epidemiology of multidrug-res istant {MDR) Acinetobacter baumannii and define individual risk factors for multidrug resistance, we used epidemiologic methods, performed organism typing by pulsed-field gel electrophoresis (PFGE), and conducted a matched casecontrol retrospective study. We investigated 118 patients, on 27 wards in Israel, in whom MDR A. baumannii \Nas isolated from clinical cultures. Each case-patient had a control without MDR ,4. baumannii and was matched for hospital length of stay, ward, and calendar time. The epidemiologic investigation found small clusters of up to 6 patients each with no common identified source. Ten different PFGE clones were found, of which 2 dominated. The PFGE pattern differed w\Xh temporospatial clusters, and antimicrobial drug susceptibility patterns varied within and between clones. Multivariate analysis identified the following significant risk factors: male sex, cardiovascular disease, having undergone mechanical ventilation, and having been treated with antimicrobial drugs (particularly metronidazole). Penicillins were protective. The complex epidemiology may explain why the emergence of MDR A. baumannii is difficult to control.