PubMed · 8869352
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E J Minton, J T Macfarlane. 1996. Antibiotic resistant Streptococcus pneumoniae.. https://doi.org/10.1136/thx.51.suppl_2.s45
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OBJECTIVES: The dissemination of cephamycin resistance in Enterobacteriaceae and its correlation with a transposon-like DNA element consisting of a specific tnpA-bla(CMY-2)-blc-sugE structure were investigated. METHODS: A total of 140 enterobacterial isolates belonging to 17 species (10 genera) of Enterobacteriaceae phenotypically characterized as putative AmpC-producers were evaluated. The isolates were examined by PCR analysis, DNA-DNA hybridization and nucleotide sequencing. RESULTS: The bla(CMY-2)-carrying element was detected in 34 isolates from 10 species (9 genera), including all 14 Salmonella and 4 Shigella isolates as well as 7 of the 10 Escherichia coli isolates tested. The remaining 9 isolates were from 112 isolates of the other 14 species tested. The genetic structure of the bla(CMY-2)-carrying element was identical in 29 isolates, while in 3 E. coli and 2 Citrobacter isolates an additional insertion sequence IS1 was found inserted at various nucleotide positions close to the 3' end, either within or downstream, of tnpA. In 12 of the 14 representative isolates examined, the bla(CMY-2)-carrying element was found inserted in the finQ gene of various-sized plasmids with highly conserved 8 bp direct repeats flanking the junction regions. Among the other 106 non-CMY-2-producing isolates, plasmid-mediated ampC genes were found only in one isolate of Enterobacter aerogenes which carried a bla(DHA-1)-like gene. CONCLUSIONS: bla(CMY-2) is the most prevalent plasmid-mediated ampC gene among Enterobacteriaceae. All the bla(CMY-2) genes identified in the present study were associated with a specific transposon-like element that may be responsible for the spread of bla(CMY-2) among Enterobacteriaceae.
The treatment of bacterial infections is increasingly complicated by the ability of bacteria to develop resistance to antimicrobial agents. Antimicrobial agents are often categorized according to their principal mechanism of action. Mechanisms include interference with cell wall synthesis (eg, beta-lactams and glycopeptide agents), inhibition of protein synthesis (macrolides and tetracyclines), interference with nucleic acid synthesis (fluoroquinolones and rifampin), inhibition of a metabolic pathway (trimethoprim-sulfamethoxazole), and disruption of bacterial membrane structure (polymyxins and daptomycin). Bacteria may be intrinsically resistant to > or =1 class of antimicrobial agents, or may acquire resistance by de novo mutation or via the acquisition of resistance genes from other organisms. Acquired resistance genes may enable a bacterium to produce enzymes that destroy the antibacterial drug, to express efflux systems that prevent the drug from reaching its intracellular target, to modify the drug's target site, or to produce an alternative metabolic pathway that bypasses the action of the drug. Acquisition of new genetic material by antimicrobial-susceptible bacteria from resistant strains of bacteria may occur through conjugation, transformation, or transduction, with transposons often facilitating the incorporation of the multiple resistance genes into the host's genome or plasmids. Use of antibacterial agents creates selective pressure for the emergence of resistant strains. Herein 3 case histories-one involving Escherichia coli resistance to third-generation cephalosporins, another focusing on the emergence of vancomycin-resistant Staphylococcus aureus, and a third detailing multidrug resistance in Pseudomonas aeruginosa-are reviewed to illustrate the varied ways in which resistant bacteria develop.
Replicon typing of plasmids carrying bla(CTX-M) or bla(CMY) beta-lactamase genes indicates a predominance of I1 and A/C replicons among bla(CMY)-carrying plasmids and five different plasmid scaffolds associated with the different types of bla(CTX-M) genes (I1, FII, HI2, K, and N). These results demonstrate the association of certain beta-lactamase genes with specific plasmid backbones.