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Trimethoprim resistance controlled by a combination of plasmid and chromosomal genes

Published online by Cambridge University Press:  14 April 2009

S. G. B. Amyes  and
J. T. Smith
S. G. B. Amyes
Affiliation:
Microbiology Section, Department of Pharmaceutics, The School of Pharmacy, University of London, 29/39 Brunswick Square, London WC1N 1AX
J. T. Smith
Affiliation:
Microbiology Section, Department of Pharmaceutics, The School of Pharmacy, University of London, 29/39 Brunswick Square, London WC1N 1AX

Summary

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R388s is a mutant of the R factor, R388. Unlike its parent R388s does not confer trimethoprim resistance, though it does confer sulphonamide resistance and the ability to transfer. It is shown that when bacteria harbour R388s mutations to trimethoprim resistance occurred at a high frequency (3·5 × 10−4), whereas such mutations never occurred when the host lacked the R factor. Bacteria harbouring R388s did not mutate to resistance to any other antibiotics at a detectable frequency.

The expression of trimethoprim resistance in bacteria possessing R388s appears to require two genes, one located on the R factor and the other situated presumably on the chromosome. The mechanism of trimethoprim resistance in these bacteria is probably due to reduced permeability and is thus quite unlike the insusceptible target site mechanism of the parent R factor, R388.

Type
Research Article
Information
Genetics Research , Volume 29 , Issue 1 , February 1977 , pp. 35 - 45
Copyright
Copyright © Cambridge University Press 1977

References

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