A suppressor in the genome of phage T4 inhibiting phenotypic expression of mutations in genes 46 and 47.
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Although the qualitative aspects of antibiotic resistance are increasingly well understood, our understanding of the quantitative aspects has always lagged. Deficiency of understanding or of investigation affects the methods used to characterize the phenotypes of organisms from clinical sources, delays acquisition of knowledge of the importance of quantitative diversity in patient management, and introduces error into epidemiological studies of the prevalence of resistance. This, in turn, gives rise to a devaluation of the work done in diagnostic laboratories in relation to the technology of sensitivity testing, to the interpretation of their results for clinicians, including those used in clinical trials, and to the statistical analyses of resistance trends used inter alia as a guide to empirical antibiotic therapy and to test the efficacy of methods of control. There is a need to bring about a shift of opinion of those who provide funds, in relation to the role of clinical microbiologists and infectious diseases clinicians in defining and solving these problems.
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Streptomyces glaucescens strain GLAO (=ETH 22794) produces hydroxystreptomycin and has a high natural resistance to hydroxystreptomycin, dihydrostreptomycin and streptomycin. The wild-type strain gives rise spontaneously to streptomycin-sensitive (StrS-) variants at a frequency of 0 . 2 to 1 . 4%. These mutants lack streptomycin phosphotransferase activity responsible for the wild-type resistance to streptomycin group antibiotics and are unable to produce detectable amounts of hydroxystreptomycin. Mapping experiments showed that the strS marker lies between the chromosomal markers lys-2 and ura-3 on the linkage map of S. glaucescens. The molecular basis for instability of this marker is as yet unknown.
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A small plasmid of 4.4 kb encoding resistance to streptomycin (Smr) was detected in a multiresistant Staphylococcus hyicus culture from a piglet with exudative epidermitis. The plasmid-encoded properties were determined by interspecies protoplast transformation experiments. This plasmid was further characterised by restriction endonuclease analysis and a preliminary restriction map was constructed. The plasmid from S. hyicus that conferred streptomycin resistance was designated as pSAI-1. It showed some structural homology with the streptomycin-chloramphenicol resistance plasmid pSK68 from S. aureus of human origin. The MIC of streptomycin in resistance mediated by pSAI-1 was about 10 times higher than the MICs in resistance mediated by Smr plasmids from human S. aureus strains.
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