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Erythromycin resistant propionibacteria in antibiotic treated acne patients: association with therapeutic failure
Author(s) -
EADY E.ANNE,
COVE J.H.,
HOLLAND K.T.,
CUNLIFFE W.J.
Publication year - 1989
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.1989.tb01399.x
Subject(s) - erythromycin , clindamycin , propionibacterium acnes , medicine , antibiotics , microbiology and biotechnology , propionibacterium , acne , gastroenterology , dermatology , biology , bacteria , genetics
SUMMARY Erythromycin resistant (Em R propionibacteria were isolated from the skin surface of 51% of patients treated with oral erythromycin and 42% of patients treated with topical clindamycin compared with 3% of untreated control subject ( P < 0.001). Amongst the topical clindamycin‐treated patients, there was a higher incidence of Em R propionibacterial carriage in those patients who had previously been treated with oral erythromycin (64%) than in patients with no known previous exposure to erythromycin (20%; 0.01 > P > 0.001). Patients responding to oral erythromycin treatment carried Em R propionibacteria less frequently (24%) than patients who were not responding or who had relapsed (70%; P < 0.001). These observations suggest that the use of oral erythromycin and/or topical clindamycin encourages the development of resistant propionibacteria and that the emergence of resistant strains is associated with therapeutic failure in erythromycin‐treated patients. In total 63 resistant isolates were obtained from 52 subjects. There were 42 strains of Propionibacterium acnes , 16 strains of Propionibacterium granulosum and five strains of Propionibacterium avidum. The majority of isolates were inducibly or constitutively resistant to macrolide (e.g. erythromycin), lincosamide (e.g. clindamycin) and streptogramin B type antibiotics. Therefore, the isolates are phenotypically indistinguishable from the majority of Em R bacteria in which resistance is due to methylation of 23S ribosomal RNA.