Evolution and epidemiology of MLS resistance.
Within the framework of this symposium, it is not feasible to present an exhaustive description of the present state of knowledge regarding the sensitivity and resistance of bacterial species to macrolides, lincosamides and streptogramins (MLS). This paper is limited to a description of the evolution of different types of resistance in the light of decisive factors described in previous papers, in order to deduce, if at all possible, trends in future strategy in therapeutics. Only acquired resistance lends itself to epidemiological study, in contrast to natural resistance which is, by definition, characteristic of a species or a genus, and not liable to change. Three groups will therefore be studied in turn: Staphylococcus aureus, streptococci and Bacteroides fragilis. There is as yet insufficient accumulated data to draw conclusions regarding the epidemiology and evolution of MLSB resistance observed in Clostridium perfringens and Corynebacterium diphtheriae, or regarding the high-level resistance to erythromycin due to enzymatic inactivation recently described in Escherichia coli.
D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001439:Bacteroides / Q000187:drug effects / Q000235:genetics*; D001442:Bacteroides Infections / Q000453:epidemiology; D005075:Biological Evolution; D004352:Drug Resistance, Microbial; D006801:Humans; D055231:Lincosamides; D018942:Macrolides; D010641:Phenotype; D013045:Species Specificity; D013203:Staphylococcal Infections / Q000453:epidemiology; D013210:Staphylococcus / Q000187:drug effects / Q000235:genetics*; D013211:Staphylococcus aureus / Q000235:genetics; D013290:Streptococcal Infections / Q000453:epidemiology; D013291:Streptococcus / Q000187:drug effects / Q000235:genetics*; D013297:Streptococcus pyogenes / Q000235:genetics; D013329:Structure-Activity Relationship; D014769:Virginiamycin / Q000494:pharmacology*
D000900:Anti-Bacterial Agents; D055231:Lincosamides; D018942:Macrolides; D014769:Virginiamycin