Occasionally, mutations occur spontaneously in bacteria, which render them resistant to one antibiotic or another. Usually the mutation leads to a change in a receptor or binding site such as those just described, rendering the antibiotic ineffective. The changes are usually brought about by point mutations (see Chapter 11) occurring at very low frequency on chromosomal DNA. Bacteria can, however, become resistant much more rapidly by acquiring the mutant resistance-causing gene from another bacterium. This is called transmissable antibiotic resistance; it occurs mainly as a result of bacterial conjugation, and is the cause of most of the resistance problems we presently face. Transmissable resistance was first reported in Japan in the late 1950s, when multi-drug resistance in Shigella was shown to have been acquired by conjugation with resistant E. coli in a patient's large intestine. E. coli is known to transfer R (resistance) plasmids to several other gut bacteria including Klebsiella, Salmonella and Enterobacter, as well as Shigella. Whereas chromosomal mutations usually result in a modification to the drug's binding site, genes carried on plasmids code for enzymes which inactivate it, (e.g. j-lactamases) or lead to its exclusion from the cell (translocases).
There is a strong link between the use of a particular antibiotic in a locality and the incidence of resistant bacterial strains. This is because of selective pressure favouring
ANTIBIOTIC SUSCEPTIBILITY TESTING
the resistant forms of a bacterium. Fortunately this can, at least in part, be reversed, as several studies have shown, where a more restricted use of certain antibiotics over several years was followed by a reduction in the incidence of resistant bacterial forms.
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