The future contribution of transposition to antimicrobial resistance

Bennett, PM; Hawkey, Peter M.

doi:10.1016/0195-6701(91)90026-5

Cited by 6 publications

(3 citation statements)

References 31 publications

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“…Site-specific recombination seems to play an important role in the emergence of resistance. Direct repeats are involved in the formation of resistance blocks ) and transposons, single or multiple, are also elements participating in the process of resistance gene blocks formation found in plasmids (Bennett & Hawkey 1991).…”

Section: Discussionmentioning

confidence: 99%

“…It also creates a favorable condition to the antimicrobial selection and co-selection of resistant bacteria present in the various anatomical sites ordinarily colonized (Baquero et al 1997). The reactivity and flexibility of the DNA as the basis of genetic information, and the existence of specialized genetic elements involved in DNA recombinations, as an instance of molecular parasitism (such as insertion sequences and transposons), favors the emergence of true bacterial antimicrobial resistance gene blocks, which have been identified endemically and epidemically during the last decades (Schmitt 1986, Tolmasky et al 1988, Bennett & Hawkey 1991). …”

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confidence: 99%

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Evidences of gentamicin resistance amplification in Klebsiella pneumoniae isolated from faeces of hospitalized newborns

Barros

Pinheiro

Bozza

et al. 1999

Mem. Inst. Oswaldo Cruz

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The intestinal microbiota, a barrier to the establishment of pathogenic bacteria, is also an impor using as a probe a labeled cloned insert containing aminoglycoside modifying enzyme (AME) gene sequence originated from a plasmid of a Klebsiella pneumoniae strain previously isolated in the same hospital. Further, we found indications of inactivation to other resistance genes in variants selected under similar conditions, as well as, indications of co-amplification of other AME markers (amikacin).Since the intestinal environment is a scenario of selective processes due to the therapeutic and prophylactic use of antimicrobial agents, the processes of amplification of low level antimicrobial resistance (not usually detected or sought by common methods used for antibiotic resistance surveillance) might compromise the effectiveness of antibiotic chemotherapy.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Evidences of gentamicin resistance amplification in Klebsiella pneumoniae isolated from faeces of hospitalized newborns

Barros

Pinheiro

Bozza

et al. 1999

Mem. Inst. Oswaldo Cruz

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“…TEM-1 and TEM-2, which were first described in the 1960s, are capable of destroying semisynthetic penicillins but are not as active against cephalosporins (31). The genes which encode TEM-1 and TEM-2 are located on transposable elements of the TnA family and are widely distributed among gram-negative bacteria (6). TEM ,-lactamases now account for 85% of the ,-lactamases produced by members of the Enterobactenraceae (27).…”

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confidence: 99%

Transposition of the gene encoding a TEM-12 extended-spectrum beta-lactamase

Heritage

Hawkey

Todd

et al. 1992

Antimicrob Agents Chemother

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An isolate of Klebsiella oxytoca from the blood culture of a child with leukemia was found to produce two beta-lactamases, at least one of which conferred resistance to ceftazidime. Genes encoding both enzymes were located on a single self-transmissible 100-kb plasmid, pOZ201. This plasmid was introduced into Escherichia coli UB5201 (pACYC184), and the gene encoding one beta-lactamase was transposed onto plasmid pACYC184 by exploiting a gene dosage effect. The transposable gene was found to encode a TEM-12 enzyme as determined by nucleotide sequencing. This gene was subsequently transposed onto plasmid pUB307. The transposable element encoding the TEM-12 enzyme has been designated Tn841. Both plasmids pACYC184::Tn841 and pUB307::Tn841 were shown to encode a beta-lactamase with the same isoelectric point and substrate profile as the TEM-12 beta-lactamase. Transposon Tn841, at approximately 7 kb, is larger than TnA (4.8 kb) and transposes at a lower frequency. Although it produced a resolvase which can complement the resolvase of Tn3, its transposase function was not able to complement the transposition of a TnA element which lacked transposase. The occurrence of a gene encoding an extended-spectrum beta-lactamase on a transposable element in a clinically significant bacterium is potentially a cause for concern for the spread of resistance to the extended-spectrum cephalosporins.

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