Nucleotide sequences of CAZ-2, CAZ-6, and CAZ-7 beta-lactamase genes

Chanal, C.; Poupart, M C; Sirot, D.; Labia, Roger; Sirot, J.; Cluzel, R

doi:10.1128/aac.36.9.1817

Cited by 58 publications

(34 citation statements)

References 11 publications

(8 reference statements)

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“…Nucleotide sequence analysis showed that it differed from the TEM-2 sequence by four substitutions leading to the amino acid replacements Glu3Lys-104, Arg3Ser-164, Ala3Thr-237, and Glu3Lys-239 (positions are numbered in accordance with the system of Ambler et al [3]) and by one silent mutation at position 925 (A3G) (according to Sutcliffe's numbering system [41]). These substitutions are identical to those previously described for TEM-24, except for the cytidine at position 682, which is identical to the bla TEM-2 gene, instead of the silent mutation (C3T) as described previously (10).…”

Section: Resultsmentioning

confidence: 58%

Coexistence of SHV-4- and TEM-24-Producing Enterobacter aerogenes Strains before a Large Outbreak of TEM-24-Producing Strains in a French Hospital

Mammeri¹,

Laurans²,

Eveillard³

et al. 2001

J Clin Microbiol

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In 1996, a monitoring program was initiated at the teaching hospital of Amiens, France, and carried out for 3 years. All extended-spectrum ␤-lactamase (ESBL)-producing Enterobacter aerogenes isolates recovered from clinical specimens were collected for investigation of their epidemiological relatedness by pulsed-field gel electrophoresis and enterobacterial repetitive intergenic consensus PCR (ERIC-PCR) and determination of the type of ESBL harbored by isoelectric focusing and DNA sequencing. Molecular typing revealed the endemic coexistence, during the first 2 years, of two clones expressing, respectively, SHV-4 and TEM-24 ESBLs, while an outbreak of the TEM-24-producing strain raged in the hospital during the third year, causing the infection or colonization of 165 patients. Furthermore, this strain was identified as the prevalent clone responsible for outbreaks in many French hospitals since 1996. This study shows that TEM-24-producing E. aerogenes is an epidemic clone that is well established in the hospital's ecology and able to spread throughout wards. The management of the outbreak at the teaching hospital of Amiens, which included the reinforcement of infection control measures, failed to obtain complete eradication of the clone, which has become an endemic pathogen.

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Section: Resultsmentioning

confidence: 58%

Coexistence of SHV-4- and TEM-24-Producing Enterobacter aerogenes Strains before a Large Outbreak of TEM-24-Producing Strains in a French Hospital

Mammeri¹,

Laurans²,

Eveillard³

et al. 2001

J Clin Microbiol

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“…The change Arg-1643Ser has been found previously in TEM-5, TEM-7, TEM-8, TEM-9, TEM-10, TEM-12, TEM-24, and TEM-26 (6,11,19). Dramatic changes in the hydrolysis of ceftazidime and aztreonam occurred when we introduced the mutation Ser-164.…”

Section: Discussionmentioning

confidence: 82%

“…In our work, the strains harboring such mutations required higher MICs of ceftazidime and aztreonam. The Ala-2373Thr change, found in TEM-5 and TEM-24 (6,29), is apparently neutral in relation to the tested antibiotics except for amoxicillin, which had a decreased MIC. This decrease of activity for penicillins has been shown previously by Healey et al (10).…”

Section: Discussionmentioning

confidence: 91%

“…This effect could be increased by the higher promoter strength of the natural bla TEM-2 gene from Tn1 (7). The change Glu-1043Lys was identified previously in TEM-3, TEM-4, TEM-6, TEM-8, TEM-9, TEM-14, TEM-15, TEM-16, TEM-17, TEM-18, TEM-24, and TEM-26 (6,11,19), and the change Glu-2403Lys was identified in TEM-5, TEM-10, and TEM-24 (6,11). These changes at positions 104 and 240 consistently decreased susceptibility to ceftazidime and aztreonam.…”

Section: Discussionmentioning

confidence: 99%

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Single amino acid replacements at positions altered in naturally occurring extended-spectrum TEM beta-lactamases

Blázquez

Morosini

Negri

et al. 1995

Antimicrob Agents Chemother

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By directed mutagenesis, we constructed a set of seven TEM-1 derivatives containing single replacements in each one of the amino acids substituted in naturally occurring extended-spectrum TEM ␤-lactamases. The exact contribution of each mutation to the resistance phenotype was determined. In addition, mutant enzyme production and stabilities were studied. Five of seven mutations determined to some extent variations in cephalosporin and/or monobactam activity. Dramatic changes in the hydrolysis of ceftazidime and aztreonam occurred when a serine was at position 164. Changes at positions 104, 238, and 240 showed more leaky variation in activity towards cephalosporins and aztreonam. Replacements at positions 237 and 265 caused no variation in susceptibility to cephalosporins. Interestingly, the change from Gln to Lys at position 39 found in TEM-2, classically considered a neutral change, slightly but consistently increased the MIC of ceftazidime and aztreonam. The in vitro construction of mutations appearing in naturally occurring TEM-␤-lactamases, studied in the same genetic context, may help to understand the evolution of extended-spectrum ␤-lactamases.The production of TEM-type ␤-lactamases is the most prevalent mode of resistance to ␤-lactam antibiotics. TEM-1 ␤-lactamase is considered a broad-spectrum enzyme because it hydrolyzes both penicillins and cephalosporins (4). TEM-1, however, cannot efficiently inactivate new extended-spectrum cephalosporins, such as cefotaxime and ceftazidime, and monobactams, such as aztreonam. Molecular variants of TEM-1, termed extended-spectrum ␤-lactamases, emerged and disseminated probably as a consequence of the introduction of these extended-spectrum ␤-lactam antibiotics.After years of intensive study of molecular variations involved in substrate profile alterations of TEM enzymes, it is now known that clinically resistant variants are the result of amino acid substitutions in one of several well-defined positions or of combinations of two to five of these substitutions (for a review, see reference 11). Figure 1 shows the modified positions in these resistant variants and the amino acids by which they are substituted in naturally occurring TEM-type ␤-lactamases. For each position, the replacement is with a particular amino acid, the only exception being Arg-164, which can be replaced by either Ser or His. Several authors constructed TEM-1 derivatives containing some of the abovedescribed single mutations by either oligonucleotide-directed mutagenesis (10, 30) or subcloning of fragments containing those mutations (28). Biochemical and microbiological studies have been performed with some of these mutants. Nevertheless, none of these publications includes a comparative study of the variations in ␤-lactamase phenotype and stability resulting from all seven single mutations corresponding to the seven positions modified in naturally occurring ␤-lactamases. In addition, the microbiological activities were, in each one of these studies, measured in a different genetic context (prom...

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“…PCR was performed on plasmids extracted from the transconjugants and from the non-ESBLproducing P. mirabilis strain which was resistant to imipenem with primers J (forward, 5Ј-CTTATTCCCTTTTTTGCGGC-3Ј) and E (reverse, 5Ј-GGTCTGACAGTTACCAATGC-3Ј) (8) at positions 236 and 1079 of the TEM family gene ␤-lactamase according to Sutcliffe numbering (25). The sequence of the gene encoding the ␤-lactamase with a pI of 5.4 produced by the P. mirabilis strain was identical to that of TEM-1b (16,25), and the sequence of the gene encoding the ␤-lactamase with a pI of 6.5 was identical to that of the extended-broad-spectrum ␤-lactamase TEM-24b (8,17).…”

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confidence: 81%

Evidence of In Vivo Transfer of a Plasmid Encoding the Extended-Spectrum β-Lactamase TEM-24 and Other Resistance Factors among Different Members of the Family Enterobacteriaceae

et al. 2001

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The epidemiological study of several multidrug-resistant Enterobacteriaceae isolated from five patients demonstrated in vivo dissemination of a 100-kb plasmid encoding the extended-spectrum ␤-lactamase TEM-24 from a clonal strain of Enterobacter aerogenes to different strains of Klebsiella pneumoniae, Escherichia coli, Proteus vulgaris, Proteus mirabilis, and Serratia marcescens.In France, plasmid-mediated extended-spectrum beta-lactamases (ESBLs) have been mostly described from strains of Klebsiella pneumoniae (1,2,3,6,7,15), but more recently infections caused by strains of Enterobacter spp. producing the TEM-24 ESBL have increased (5,14,24). The same phenomenon was observed in our University Hospital (2,000 beds, in Dijon, France). In 1996, 1997, and 1998 we isolated, respectively, 16, 37, and 50 Enterobacter aerogenes strains producing TEM-24 among totals of 78, 70, and 70 nonrepetitive ESBLproducing strains. All these strains were analyzed by pulsedfield gel electrophoresis (PFGE). During our continuous survey we found that five patients were cocolonized or coinfected with different multidrug-resistant species of enterobacteria. Following the use of imipenem, two strains of Proteus mirabilis and E. aerogenes resistant to this molecule were recovered from one patient. We report here the epidemiological study and the ␤-lactamase characterization of all the strains isolated from the five patients.The origins of the strains are given in Table 1. The detection of ESBL production was performed by the double-disk synergy test (19) but with a quarter of the disk containing third-generation cephalosporin for Proteus sp. (9).Analyses of chromosomal DNAs by PFGE were performed as described previously (15) but with a pulse range from 40 to 5 s for 20 h at 180 V for strains of E. aerogenes, K. pneumoniae, Serratia marcescens, and Escherichia coli. For P. mirabilis and Proteus vulgaris, we used a pulse range from 25 to 5 s for 20 h at 180 V ( Fig. 1 and 2). A single profile was found for the strains of E. aerogenes, similar to that of the epidemic strain described in 1996 (24). For the other enterobacteria, strains from the same species (ESBL or not ESBL producing) isolated from the same patient shared concordant PFGE patterns, suggesting their clonal origin. Nevertheless, the strains of the same species isolated from the five patients were not related. This result excluded the possibility that resistant strains of K. pneumoniae, E. coli, or P. vulgaris were disseminated between the patients or that there was a common source of contamination.A large plasmid of about 100 kb was isolated by the method of Birnboim and Doly from the ESBL-producing strains (4). The restriction patterns obtained after digestion of the plasmid by EcoRI were very similar. The plasmid was easily transferred

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Nucleotide sequences of CAZ-2, CAZ-6, and CAZ-7 beta-lactamase genes

Cited by 58 publications

References 11 publications

Coexistence of SHV-4- and TEM-24-Producing Enterobacter aerogenes Strains before a Large Outbreak of TEM-24-Producing Strains in a French Hospital

Coexistence of SHV-4- and TEM-24-Producing Enterobacter aerogenes Strains before a Large Outbreak of TEM-24-Producing Strains in a French Hospital

Single amino acid replacements at positions altered in naturally occurring extended-spectrum TEM beta-lactamases

Evidence of In Vivo Transfer of a Plasmid Encoding the Extended-Spectrum β-Lactamase TEM-24 and Other Resistance Factors among Different Members of the Family Enterobacteriaceae

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