Molecular Epidemiology of Extended-Spectrum β-Lactamase-Producing, Fluoroquinolone-Resistant Isolates of
 Klebsiella pneumoniae
 in Taiwan

Yu, Wen Liang; Jones, Ronald N.; Hollis, Richard J.; Messer, S. A.; Biedenbach, Dj; Deshpande, Lalitagauri M.; Pfaller, Michael A.

doi:10.1128/jcm.40.12.4666-4669.2002

Cited by 29 publications

(9 citation statements)

References 12 publications

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“…Therefore, special efforts should be made to control the spread of this clone. The spread of these strains is likely a result of the misapplication of primary containment measures to control infectious diseases in the hospital environment, such as changing gloves, hand washing, and proper disinfection of equipment [29,30]. The results of this study also show that resistant clones in a hospital environment are due to excessive use of cephalosporins.…”

Section: Discussionsupporting

confidence: 48%

Risk Factors Associated with Extended-Spectrum β-Lactamase-Producing Enterobacteriaceae Nosocomial Bloodstream Infections in a Tertiary Care Hospital: A Clinical and Molecular Analysis

et al. 2012

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Aim: To describe the risk factors and molecular epidemiology of nosocomial bloodstream infections caused by extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae in a tertiary care hospital. Methods: Patients with enterobacteria-positive blood cultures were included. ESBL expression in the isolates was detected using the combination disk method. Antimicrobial susceptibility testing was performed using the disk diffusion method. blaSHV, blaTEM, and blaCTX-M genes were identified in the isolated strains by PCR and sequencing. Klebsiella pneumoniae isolates were genotyped by PFGE. Results: Of the 90 isolates recovered, half were found to express ESBLs. Twenty-eight (62%) of these isolates were K. pneumoniae, 8 (18%) were Escherichia coli, 6 (13%) were Enterobacter cloacae, and 3 (7%) were Serratia marcescens. Multivariate logistic regression analysis showed that the only independent risk factor associated with infection by ESBL-producing strains was use of broad-spectrum cephalosporins. None of the isolates was resistant to imipenem. The blaSHV5 gene was detected in 84% of isolates, followed by blaCTX-M15 (27%), blaSHV2 (9%), and blaSHV12 (7%). PFGE identified six clones among the 28 ESBL-producing K. pneumoniae isolates. Conclusions: ESBL-producing K. pneumoniae clones were detected throughout the hospital. Use of broad-spectrum cephalosporins is the most important risk factor associated with the proliferation of ESBL-producing strains.

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Section: Discussionsupporting

confidence: 48%

Risk Factors Associated with Extended-Spectrum β-Lactamase-Producing Enterobacteriaceae Nosocomial Bloodstream Infections in a Tertiary Care Hospital: A Clinical and Molecular Analysis

et al. 2012

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“…Rates of ciprofloxacin resistance are reported to be very high among presumptive ESBL-producing isolates collected from Asian centers [43]. In Taiwan, concomitant ciprofloxacin resistance was observed in almost 20% of ESBL-producing K. pneumoniae isolates [44]. In the United States, outbreaks of coresistant organisms have occurred.…”

Section: Treatment For Infection With Esbl-producing Organismsmentioning

confidence: 99%

Extended-Spectrum β-Lactamases and Clinical Outcomes: Current Data

Ramphal

Ambrose

2006

Clinical Infectious Diseases

245

151

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Nosocomial infections caused by extended-spectrum b-lactamase (ESBL)-producing gram-negative bacteria complicate therapy and limit treatment options. However, the clinical significance of infections caused by ESBL-producing bacteria remains unclear. A critical examination of the literature provides divergent views of the effect of ESBL carriage on morbidity and mortality and suggests that ESBL production may have its most marked effect on ceftazidime. Effective strategies for the empirical and directed treatment of infections caused by ESBL-producing pathogens include the use of carbapenems and, possibly, the fourth-generation cephalosporin cefepime. Studies indicate that the use of cefepime to treat serious nosocomial infections (e.g., bacteremia, pneumonia, and urinary tract infections) is associated with high rates of microbiological and clinical success. The probability of attaining time above the minimum inhibitory concentration targets of at least 70% of the dosing interval, an important pharmacodynamic indicator of clinical success, is higher with cefepime than with other antimicrobials against Escherichia coli and Klebsiella pneumoniae strains exhibiting ESBL phenotypes. However, for non-ESBL-producing strains, there is no difference in the time above the minimum inhibitory concentration between ceftazidime and cefepime. When used appropriately in institutional settings, cefepime reduces the overall use of cephalosporins, thereby decreasing selection pressure for presumptive ESBL-producing pathogens.Infections caused by multidrug-resistant bacteria expressing extended-spectrum b-lactamases (ESBLs) pose serious challenges to clinicians. Because ESBL-producing bacteria are resistant to a broad range of b-lactams, including third-generation cephalosporins, nosocomial infections caused by these organisms complicate therapy and limit treatment options [1]. In addition, patients infected with ESBL-producing bacteria may have a higher mortality rate and may require longer hospital stays because they are generally sicker and have received more antibiotics than patients who are not infected with ESBL-producing strains. Nevertheless, the clinical significance of infections caused by ESBL-producing bacteria remains unclear, primarily because few prospective studies have been designed specifically to evaluate clin- ical outcomes among a statistically meaningful number of patients [2,3]. Studies of this kind are essential for developing consensus guidelines (which are not currently available) for the treatment of infection due to ESBL-producing bacilli.A critical examination of the literature provides divergent views of the role of ESBL carriage in death and suggests that ESBL production may have its most marked effect on ceftazidime, but this could be a geographic or enzyme-specific variation [3,4]. The present review summarizes recent reports in the medical literature related to the clinical significance of ESBL expression and describes strategies for the treatment of infections caused by ESBL-producing pathogens. ...

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“…However, three groups successfully used selective digestive decontamination with polymyxin, neomycin, and nalidixic acid (63), colistin and tobramycin (388), or norfloxacin (294) to interrupt outbreaks of infection with ESBL-producing infections that had not been completely controlled using traditional infection control measures. It should be noted that in many hospitals at least 15 to 30% of ESBL-producing organisms (20,183,206,292,435) are quinolone resistant and therefore unlikely to suppressed by use of norfloxacin prophylaxis. Additionally, multidrug-resistant isolates are unlikely to respond to selective digestive decontamination using aminoglycosides.…”

Section: Infection Control When Esbl-producing Organisms Have Not Beementioning

confidence: 99%

Extended-Spectrum β-Lactamases: a Clinical Update

2005

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SUMMARY Extended-spectrum β-lactamases (ESBLs) are a rapidly evolving group of β-lactamases which share the ability to hydrolyze third-generation cephalosporins and aztreonam yet are inhibited by clavulanic acid. Typically, they derive from genes for TEM-1, TEM-2, or SHV-1 by mutations that alter the amino acid configuration around the active site of these β-lactamases. This extends the spectrum of β-lactam antibiotics susceptible to hydrolysis by these enzymes. An increasing number of ESBLs not of TEM or SHV lineage have recently been described. The presence of ESBLs carries tremendous clinical significance. The ESBLs are frequently plasmid encoded. Plasmids responsible for ESBL production frequently carry genes encoding resistance to other drug classes (for example, aminoglycosides). Therefore, antibiotic options in the treatment of ESBL-producing organisms are extremely limited. Carbapenems are the treatment of choice for serious infections due to ESBL-producing organisms, yet carbapenem-resistant isolates have recently been reported. ESBL-producing organisms may appear susceptible to some extended-spectrum cephalosporins. However, treatment with such antibiotics has been associated with high failure rates. There is substantial debate as to the optimal method to prevent this occurrence. It has been proposed that cephalosporin breakpoints for the Enterobacteriaceae should be altered so that the need for ESBL detection would be obviated. At present, however, organizations such as the Clinical and Laboratory Standards Institute (formerly the National Committee for Clinical Laboratory Standards) provide guidelines for the detection of ESBLs in klebsiellae and Escherichia coli. In common to all ESBL detection methods is the general principle that the activity of extended-spectrum cephalosporins against ESBL-producing organisms will be enhanced by the presence of clavulanic acid. ESBLs represent an impressive example of the ability of gram-negative bacteria to develop new antibiotic resistance mechanisms in the face of the introduction of new antimicrobial agents.

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Molecular Epidemiology of Extended-Spectrum β-Lactamase-Producing, Fluoroquinolone-Resistant Isolates of Klebsiella pneumoniae in Taiwan

Cited by 29 publications

References 12 publications

Risk Factors Associated with Extended-Spectrum β-Lactamase-Producing Enterobacteriaceae Nosocomial Bloodstream Infections in a Tertiary Care Hospital: A Clinical and Molecular Analysis

Risk Factors Associated with Extended-Spectrum β-Lactamase-Producing Enterobacteriaceae Nosocomial Bloodstream Infections in a Tertiary Care Hospital: A Clinical and Molecular Analysis

Extended-Spectrum β-Lactamases and Clinical Outcomes: Current Data

Extended-Spectrum β-Lactamases: a Clinical Update

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