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Mechanisms of Antibiotic Resistance and Their Dissemination of Resistance Genes in the Hospital Environment

Published online by Cambridge University Press:  02 January 2015

Bernd Wiedemann
Bernd Wiedemann*
Affiliation:
Institut für Medizinische Mikrobiologie and Immunologic der Universität, Abteilung Medizinische, Mikrobiologie für Pharmazeuten, Bonn, Federal Republic of Germany
*
Institut für Medizinische Mikrobiologie und Immunologie der Universitat, An der Immenburg AVZ II, D5300 Bonn I, Federal Republic of Germany
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Abstract

The dissemination of resistance determinants among bacterial populations depends on ecological and epidemiological properties as well as additional factors: 1) the mechanism of resistance or its specificity toward a certain drug, and 2) the genetic basis in relation to the mobility of the genetic material and its survival in bacteria. From two resistance mechanisms directed toward old-fashioned drugs, namely sulfonamides (Su) and streptomycin (Sin), we can deduce that a resistance mechanism is encoded by a special sort of genetic material. Thus the linked SmSu resistance mediated by a sulfonamide-resistant dihydropteroatsynthetase II and the aminoglycoside phosphotransferase APH-(3") is always located on very small pBPl-like plasmids. Such plasmids survive without selective pressure of drugs in Enterobacteriaceae in the bowel flora of humans and animals. Both resistance determinants can be mediated by a transposon which codes for the production of a dihydropteroatsynthetase I in connection with an aminoglycoside adenylyltransferase AAD-(3"). These two mechanisms are genetically linked as well. The basic structure is a transposon designated Tn2411, which belongs to a whole family of transposons, all including the basic structure; however, their genetic exchange and substitution leads to structures coding for many different enzymatic characters: ANT-(2") (Gentamicin resistance), CAT (Chlo-ramphenicol resistance), AAC-(6') (resistance to all modern aminoglycosides), TEM-1, OXA-1, OXA-2, or PSE (β-lactam resistance). Resistance to the modern (β-lactamase-stable antibiotics is mediated by mutation in the regulatory genes of chromosomally-determined (β-lactamases. A spread of these resistance mechanisms can be avoided as long as the responsible genes are not located on sufficient structures like small plasmids or efficient transposons.

Type
Original Articles
Information
Infection Control & Hospital Epidemiology , Volume 4 , Issue 6 , December 1983 , pp. 444 - 447
Copyright
Copyright © The Society for Healthcare Epidemiology of America 1983

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References

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