Clinical resistance to erythromycin and clindamycin in cutaneous propionibacteria isolated from acne patients is associated with mutations in 23S rRNA.

The genetic basis of erythromycin resistance in cutaneous propionibacteria was determined by comparing the nucleotide sequences of the peptidyl transferase region in the 23S rRNAs from 9 susceptible and 26 resistant clinical isolates as well as 4 laboratory-selected erythromycin-resistant mutants of a susceptible strain. In 13 isolates and the 4 laboratory mutants, cross-resistance to macrolides, lincosamides, and B-type streptogramins was associated with an A-->G transition at a position cognate with Escherichia coli 23S rRNA base 2058. These strains were resistant to > or = 512 microg of erythromycin per ml. Two other mutations were identified, an A-->G transition at base 2059 in seven strains, associated with high-level resistance to all macrolides, and a G-->A transition at base 2057 in six strains, associated with low-level resistance to erythromycin. These mutations correspond to three of four phenotypic classes previously identified by using MIC determinations.

Sequential antibiotic therapy for acne promotes the carriage of resistant staphylococci on the skin of contacts.

The selection of a predominantly resistant staphylococcal skin flora in acne patients during antibiotic treatment has been extensively documented. This study sought to determine whether antibiotic therapy for acne had any effect on skin carriage of resistant coagulase-negative staphylococci (CNS) by close contacts of treated patients. Bacterial samples were obtained using a scrub wash technique from facial skin of 41 contacts (parents, siblings or partners) of patients who had been treated with at least three different antibiotics over a minimum period of 2 years. Samples were also obtained from 41 control subjects who had no known contact with any antibiotic treated acne patient. None of the contacts or controls had received any antibiotic therapy in the preceding two years. The number, percentage and prevalence of CNS resistant to each of seven antibiotics was estimated by plating serial ten-fold dilutions of wash fluid directly onto antibiotic-containing and antibiotic-free medium. Significantly more contacts than controls carried strains resistant to erythromycin, clindamycin, fusidic acid, trimethoprim and chloramphenicol as well as more multiply resistant strains (P < 0.05, chi 2). The number and percentage of staphylococci resistant to tetracycline, erythromycin, clindamycin, fusidic acid and chloramphenicol were also significantly raised (P < 0.05, Mann-Whitney U-test) in contacts. Only aminoglycoside resistance was not increased by any of the above criteria. These observations provide evidence that sequential antibiotic therapy for acne exerts selective pressure for increased skin carriage of resistant CNS not only in patients but also in their close contacts.