Antibiotic resistance patterns of aerobic coryneforms and furazolidone-resistant Gram-positive cocci from the skin surface of the human axilla and fourth toe cleft.

Samples of skin surface bacteria from 28 healthy subjects plated directly on to selective and non-selective media revealed that the proportion of aerobic coryneforms and furazolidone-resistant Gram-positive cocci (FURECs) resistant to erythromycin was significantly greater in the fourth toe cleft than in the axilla (P < 0.05). There were more erythromycin-resistant bacteria than tetracycline-resistant bacteria at both sites (P = 0.001 for the toe cleft; P < 0.01 for the axilla). In total, 160 distinct isolates were obtained, of which 42 were FURECs and 118 were aerobic coryneforms. Of these, 153 (96%) were resistant to erythromycin and 66 (41%) to tetracycline. All except seven of the tetracycline-resistant strains were also resistant to erythromycin. The resistant isolates belonged to a variety of species. CDC group ANF corynebacteria were most numerous and composed 31% of all isolates. The majority (76%) of FURECs were identified as Micrococcus luteus. MIC determinations on selected strains revealed that tetracycline-resistant FURECs were sensitive to doxycycline and minocycline, as were most tetracycline-resistant coryneforms. Nine coryneform isolates were cross-resistant to all three tetracyclines. Only a minority of erythromycin-resistant FURECs (21%) demonstrated a macrolide-lincosamide-streptogramin type B (MLS)-resistant phenotype with inducible or constitutive cross-resistance to clindamycin and the type B streptogramin, pristinamycin IA. Twenty-nine erythromycin-resistant FURECs had a novel phenotype distinct from MLS and macrolide-streptogramin type B resistance. In contrast, most coryneforms (79%) were MLS resistant. Among the remainder, two unusual erythromycin resistance phenotypes were apparent, both of which differed from the unusual phenotype in FURECs. This study has revealed that the non-staphylococcal aerobic flora of skin contains a considerable reservoir of tetracycline and erythromycin resistance determinants. The three unusual macrolide resistance phenotypes may be associated with novel resistance mechanisms.

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.