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Increasing clindamycin resistance among methicillin-resistant Staphylococcus aureus in 57 northeast United States military treatment facilities

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PEDIATRIC INFECTIOUS DISEASE JOURNAL
卷 24, 期 7, 页码 622-626

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/01.inf.0000171175.76673.64

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community-acquired; methicillin-resistant Staphylococcus aureus; Staphylococcus aureus; clindamycin; double disk diffusion test; trimethoprim-sulfamethoxazole

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Background: Increasing community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) has led many to use clindamycin for CA-MRSA disease, whereas others suggest caution because of inducible clindamycin resistance and rely on drugs such as trimethoprim-sulfamethoxazole (TMP-SMX). Aim: To analyze the change in antibiotic susceptibility pattern of S. aureus isolates from 2001 to 2004 in a closed health care system, a period during which clindamycin and TMP-SMX use increased 99 and 62%, respectively. Methods: S. aureus cultures from 57 military hospitals and clinics from 2001 2002 and 2003-2004 were compared for body site and antibiotic sensitivity, particularly the potentially inducible clindamycin-susceptible erythromycin-resistant pattern. A portion was evaluated by a double disk diffusion test (D test). Results: Numbers of S. aureus-positive cultures obtained from wound sites rose significantly in both pediatric (138 to 215, P < 0.001) and adult (715 to 972, P < 0.001) isolates, with a rise in MRSA in children (6 of 138 to 60 of 215, P < 0.001) and in adults (161 of 715 to 324 of 972, P < 0.001). Clindamycin resistance increased among pediatric S. aureus isolates (1 of 207 to 13 of 327, P < 0.05), whereas > 96% remained TMP-SMX-susceptible. Five methicillin-susceptible S. aureus (MSSA), 2 MRSA of 41 pediatric and 36 MSSA, 43 MRSA of 437 adult S. aureus specimens were D test-positive. Conclusions: In late 2004, most S. aurelis from our region are still P-lactam-susceptible. Most of the MRSA are still susceptible to clindamycin and do not appear to have inducible resistance. We must closely monitor the rates of constitutive and inducible clindamycin resistance as well as consider treatment alternatives that may slow the rate of clindamycin resistance.

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