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Gentamicin- and clindamycin-resistant Staphylococcus aureus.

Abstract

From 1975 through 1978 isolates from 21 of 230 (9%) Staphylococcus aureus bacteremias were resistant to gentamicin and clindamycin. Gentamicin- and clindamycin-resistant S aureus (GCRS) accounted for 23% of all S aureus isolates from 1977 compared with 2 to 6% in the two years immediately preceding, and the year following 1977. When compared with patients with gentamicin- and clindamycin-sensitive S aureus (GCSS) from 1977, GCRS were more often isolated from patients who acquired their infections in the hospital, particularly in the intensive care unit. A significant association existed between prior or concurrent therapy with gentamicin and/or clindamycin and the isolation of GCRS. Infection with GCRS was associated with a 73% mortality rate versus 28% with GCSS. GCRS were susceptible to oxacillin, cephalothin, tetracycline, and vancomycin. GCRS were resistant to kanamycin and tobramycin but were susceptible to amikacin (median MIC of GCRS, 4.0 microgram/ml). Multiple bacteriophage types of S aureus were involved, and resistance appeared to be plasmid-mediated. A survey of antibiotic usage showed that in comparison to January 1977, a mikacin usage increased and gentamicin usage decreased in March 1979. Because of the popularity of the combination of clindamycin and gentamicin for therapy of life-threatening infections, clinicians should be aware of potential gentamicin- and clindamycin-resistance in S aureus.

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BibTeXRIS

J D Semel, G M Trenholme, S Levin. Gentamicin- and clindamycin-resistant Staphylococcus aureus.. https://doi.org/10.1097/00000441-198007000-00001

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Induction of clindamycin resistance in erythromycin-resistant, clindamycin susceptible and methicillin-resistant clinical Staphylococcal isolates.

OBJECTIVES: To demonstrate the in vitro ability of erythromycin to induce clindamycin in erythromycin resistant and clindamycin susceptible clinical isolates of Staphylococci. METHODS: We studied 291 clinical isolates of erythromycin-resistant (ER-R) clindamycin-susceptible Staphylococci (CL-S) at Almana General Hospitals, Al-Khobar, Dammam, Saudi Arabia during the period from June 2004 to May 2005. The isolates included 70 Staphylococcus aureus, 81 Methicillin Resistant Staphylococcus aureus (MRSA) and 140 coagulase-negative Staphylococci (CNS). We examined these isolates for inducible clindamycin resistance (ICR) by erythromycin induction test using double disc susceptibility test (D-test). Strains producing ICR show flattening of the clindamycin disc zone adjacent to the erythromycin disc. RESULTS: Of the 291 ER Staphylococci studied, 82 (28%) demonstrated constitutive clindamycin resistance [2 (2.9%) S. aureus, 43 (53%) MRSA and 37 (26%) CNS]. Inducible clindamycin resistance was demonstrated in 113 (38.8%) of Staphylococcal isolates, including 84 (28.9%) from adult patients and 29 (10%) from pediatric patients. The incidence of ICR was 49 (70%) for S. aureus, 35 (43%) for MRSA and 29 (20.7)% for CNS. Overall, 96 (33%) of the isolates remained susceptible to clindamycin and were negative for clindamycin induction [19 (27%) S. aureus, 3 (3.7%) MRSA and 74 (52.8%) CNS]. CONCLUSION: We conclude that a significant number of ER-R CL-S staphylococcal isolates studied were positive for ICR. These isolates should be reported as clindamycin resistant. Given the high rate of inducible resistance to clindamycin in the staphylococcal isolates, we recommend that microbiology laboratories perform erythromycin induction test on all ER-R CL-S staphylococcal isolates prior to reporting clindamycin susceptibility.

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