Evolution and spread of SHV extended-spectrum β-lactamases in Gram-negative bacteria

Heritage, John; M’Zali, Fatima; Gascoyne-Binzi, Deborah; Hawkey, Peter M.

doi:10.1093/jac/44.3.309

Cited by 93 publications

(66 citation statements)

References 74 publications

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“…(This activity was never confirmed in later studies with purified enzyme.) Reviews focusing on the SHV-type ␤-lactamases summarizing kinetic properties of ␤-lactamases of this family have been published (162,399).…”

Section: Diversity Of Esbl Types Shvmentioning

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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Section: Diversity Of Esbl Types Shvmentioning

confidence: 99%

Extended-Spectrum β-Lactamases: a Clinical Update

2005

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“…A number of SHV variants with ESBL activity have been described thereafter [26]. Most of them have a Gly238Ser substitution in common.…”

Section: Shvmentioning

confidence: 99%

Extended-spectrumβ-Lactamases: Implications for the Clinical Laboratory and Therapy

2008

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“…Isolates of the Enterobacteriaceae family have historically recruited narrow-spectrum Ambler class A ␤-lactamases of the TEM and SHV lineages, which were associated with nosocomial outbreaks in the 1980s (24). Continued evolution under strong selective pressure led to a broadening of the hydrolytic spectrum, as exemplified by the global spread of TEM and SHV derivatives (10). More recently, CTX-M class A enzymes have appeared globally and are of particular concern in Europe (14).…”

mentioning

confidence: 99%

Cephalosporin MIC Distribution of Extended-Spectrum-β-Lactamase- and pAmpC-Producing Escherichia coli and Klebsiella Species

Kohner¹,

Robberts²,

Cockerill³

et al. 2009

J Clin Microbiol

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The acquisition of ␤-lactamases in members of the Enterobacteriaceae family poses a challenge to antimicrobial susceptibility testing in the clinical laboratory. We correlated the distribution of the MICs for Klebsiella spp. and Escherichia coli with the presence of extended-spectrum ␤-lactamase (ESBL) and plasmid-mediated AmpC ␤-lactamase (pAmpC) genes. A total of 264 isolates were subjected to cefazolin, ceftriaxone, cefotaxime, ceftazidime, cefepime, and aztreonam agar dilution MIC determination; ESBL screening and confirmatory testing by the methods of the Clinical and Laboratory Standards Institute (CLSI); and for isolates for which the MICs of extended-spectrum cephalosporins were >1 g/ml or the MICs of cefpodoxime were >4 g/ml, PCR amplification and sequencing of the ESBL and pAmpC genes. PCR was positive for 73/81 isolates (45 isolates with an ESBL gene alone, 24 isolates with a pAmpC gene alone, with 4 isolates with both genes). Compared to PCR, confirmatory testing by the CLSI method yielded a sensitivity and a specificity of 98.0 and 96.3%, respectively; there were six false-positive results and one false-negative result. No distinction in the MIC distribution was apparent between isolates with the ESBL gene and isolates with the pAmpC gene. A substantial percentage of the isolates with PCR-confirmed ESBL and/or pAmpC genes fell within the current CLSI susceptible category. For a ceftazidime, ceftriaxone, or cefotaxime MIC of >2 g/ml, a dichotomy existed between isolates with and without ESBL and pAmpC genes in most cases. This suggests that the presence of the ESBL and the pAmpC enzymes may yield similar MICs of extended-spectrum cephalosporins, many of which fall within the current nonresistant categories. Lowering of the current CLSI breakpoints for cephalosporins appears to be warranted.

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Evolution and spread of SHV extended-spectrum β-lactamases in Gram-negative bacteria

Cited by 93 publications

References 74 publications

Extended-Spectrum β-Lactamases: a Clinical Update

Extended-Spectrum β-Lactamases: a Clinical Update

Extended-spectrumβ-Lactamases: Implications for the Clinical Laboratory and Therapy

Cephalosporin MIC Distribution of Extended-Spectrum-β-Lactamase- and pAmpC-Producing Escherichia coli and Klebsiella Species

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