Plasmid-mediated mechanisms of resistance to aminoglycoside-aminocyclitol antibiotics and to chloramphenicol in group D streptococci.
Genes conferring resistance to aminoglycoside-aminocyclitol antibiotics in three group D streptococcal strains, Streptococcus faecalis JH1 and JH6 and S. faecium JH7, and to chloramphenicol in JH6 are carried by plasmids that can transfer to other S. faecalis cells. The aminoglycoside resistance is mediated by constitutively synthesized phosphotransferase enzymes that have substrate profiles very similar to those of aminoglycoside phosphotransferases found in gram-negative bacteria. Phosphorylation probably occurs at the aminoglycoside 3'-hydroxyl group. Plasmid-borne streptomycin resistance is due to production of the enzyme streptomycin adenylyltransferase, which, as in staphylococci and in contrast to that detected in gram-negative bacteria, is less effective against spectinomycin as substrate. Resistance to chloramphenicol is by enzymatic acetylation. The chloramphenicol acetyltransferase is inducible and bears a close resemblance to the type D chloramphenicol acetyltransferase variant from staphylococci.
D000617:Aminoglycosides / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D002701:Chloramphenicol / Q000378:metabolism / Q000494:pharmacology*; D002874:Chromosome Mapping; D013293:Enterococcus faecalis / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D011815:R Factors; D013307:Streptomycin / Q000494:pharmacology
D000617:Aminoglycosides; D000900:Anti-Bacterial Agents; D002701:Chloramphenicol; D013307:Streptomycin