CLINICAL RESISTANCE TO ERYTHROMYCIN AND CLINDAMYCIN IN CUTANEOUS PROPIONIBACTERIA ISOLATED FROM ACNE PATIENTS IS ASSOCIATED WITH MUTATIONS IN 23S RIBOSOMAL-RNA
Ji. Ross et al., CLINICAL RESISTANCE TO ERYTHROMYCIN AND CLINDAMYCIN IN CUTANEOUS PROPIONIBACTERIA ISOLATED FROM ACNE PATIENTS IS ASSOCIATED WITH MUTATIONS IN 23S RIBOSOMAL-RNA, Antimicrobial agents and chemotherapy, 41(5), 1997, pp. 1162-1165
The genetic basis of erythromycin resistance in cutaneous propionibact
eria was determined by comparing the nucleotide sequences of the pepti
dyl transferase region in the 23S rRNAs from 9 susceptible and 26 resi
stant clinical isolates as well as 4 laboratory-selected erythromycin-
resistant mutants of a susceptible strain. In 13 isolates and the 4 la
boratory mutants, cross-resistance to macrolides, lincosamides, and B-
type streptogramins was associated with an A --> G transition at a pos
ition cognate with Escherichia coli 23S rRNA base 2058, These strains
were resistant to greater than or equal to 512 mu g of erythromycin pe
r ml. Two other mutations were identified, an A --> G transition at ba
se 2059 in seven strains, associated with high-level resistance to all
macrolides, and a G --> A transition at base 2057 in six strains, ass
ociated with low-level resistance to erythromycin, These mutations cor
respond to three of four phenotypic classes previously identified by u
sing MIC determinations.