Speer, Brenda S. and Shoemaker, Nadja B. and Salyers, Abigail A. (1992) Bacterial resistance to tetracycline: mechanisms, transfer, and clinical significance. Clinical Microbiology Reviews, 5 (4). pp. 387-399. ISSN 0893-8512. PMCID PMC358256. http://resolver.caltech.edu/CaltechAUTHORS:SPEcmr92
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Tetracycline has been a widely used antibiotic because of its low toxicity and broad spectrum of activity. However, its clinical usefulness has been declining because of the appearance of an increasing number of tetracycline-resistant isolates of clinically important bacteria. Two types of resistance mechanisms predominate: tetracycline efflux and ribosomal protection. A third mechanism of resistance, tetracycline modification, has been identified, but its clinical relevance is still unclear. For some tetracycline resistance genes, expression is regulated. In efflux genes found in gram-negative enteric bacteria, regulation is via a repressor that interacts with tetracycline. Gram-positive efflux genes appear to be regulated by an attenuation mechanism. Recently it was reported that at least one of the ribosome protection genes is regulated by attenuation. Tetracycline resistance genes are often found on transmissible elements. Efflux resistance genes are generally found on plasmids, whereas genes involved in ribosome protection have been found on both plasmids and self-transmissible chromosomal elements (conjugative transposons). One class of conjugative transposon, originally found in streptococci, can transfer itself from streptococci to a variety of recipients, including other gram-positive bacteria, gram-negative bacteria, and mycoplasmas. Another class of conjugative transposons has been found in the Bacteroides group. An unusual feature of the Bacteroides elements is that their transfer is enhanced by preexposure to tetracycline. Thus, tetracycline has the double effect of selecting for recipients that acquire a resistance gene and stimulating transfer of the gene.
|Additional Information:||Copyright © 1992 by the American Society for Microbiology. This work was supported in part by grant AI 22383 from the National Institutes of Health. We thank Frank Tally, Marilyn Roberts, Joe O'Sullivan, and Prabha Fernandez for helpful criticisms and suggestions and for sharing unpublished data with us.|
|PubMed Central ID:||PMC358256|
|Usage Policy:||No commercial reproduction, distribution, display or performance rights in this work are provided.|
|Deposited By:||Archive Administrator|
|Deposited On:||18 Sep 2008 05:07|
|Last Modified:||03 Apr 2017 22:52|
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