Treatment of Community-Associated Methicillin-Resistant Staphylococcus aureus Infections

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Abstract
Most of infections caused by community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) isolates are skin and soft tissue infections, but serious, life-threatening infections also occur.1 To select antibiotics for initial empiric treatment of community-acquired infections for which S. aureus is a suspected etiology, physicians should be familiar with the antibiotic susceptibility patterns of S. aureus isolates in their own community. However, this information will not be readily available unless local health officials, hospital or commercial laboratories or local investigators specifically determine susceptibility rates. Most experts suggest modifying empiric therapy if more than 10–15% of community S. aureus isolates are MRSA. Microbiology laboratories should routinely test S. aureus isolates for susceptibility to macrolides, clindamycin, trimethoprim-sulfamethoxazole (TMP-SMX) and doxycycline or minocycline in addition to β-lactam antibiotics and gentamicin. Many CA-MRSA isolates are resistant to macrolides but remain susceptible to clindamycin. Clindamycin and TMP-SMX have become important in the management of staphylococcal infections. To avoid delays in selecting the most appropriate agent, isolates should be tested routinely for the inducible macrolide-lincosamide-streptogramin phenotype (MLSB) using the Clinical and Laboratory Standards Institute (formerly NCCLS)-approved method.2 This requires an additional step and expense for those laboratories using automated antibiotic susceptibility methods. However, treatment failures with clindamycin have been reported for infections caused by MRSA isolates with the inducible MLSB phenotype (D test-positive). β-Lactam antibiotics such as dicloxacillin or cephalexin for outpatients or nafcillin, oxacillin or cefazolin for inpatients are no longer appropriate antibiotics for empiric treatment or for completing treatment when CA-MRSA is a consideration or is isolated. Vancomycin is recommended for inclusion in empiric antibiotic regimens for seriously ill patients with infections that may be due to CA-MRSA. Such cases include children with septic shock, acute infective endocarditis, pneumonia with empyema or bone and joint infections complicated by septic thrombophlebitis, among others. Gentamicin is generally added to vancomycin for suspected life-threatening MRSA infections. Nafcillin/oxacillin is more rapidly bactericidal than vancomycin for methicillin-susceptible S. aureus (MSSA) isolates, and clinical data in adults suggest that nafcillin/oxacillin is superior to vancomycin for the treatment of serious MSSA infections.3 Thus for these patients, nafcillin/oxacillin is also recommended to optimally treat MSSA isolates. CA-MRSA isolates typically are susceptible to clindamycin and TMP-SMX. Clindamycin is effective in treating serious infections caused by clindamycin-susceptible CA-MRSA isolates, including osteomyelitis, septic arthritis and pleural empyema.4,5 Clindamycin is initially administered intravenously at a dose of 30–40 mg/kg/d in 3 divided doses. Clindamycin is well-absorbed by the oral route; thus treatment can be completed with oral clindamycin at the same dose. The most concerning adverse effect of clindamycin is Clostridium difficile enteritis which is a relatively rare complication In some regions of the United States, a high proportion of CA-MRSA strains are clindamycin-resistant. If the proportion of CA-MRSA isolates resistant to clindamycin exceeds 10–15%, clindamycin should not be used for empiric treatment of suspected staphylococcal infections. Simple skin and soft tissue infections account for >90% of the infections caused by CA-MRSA isolates. Optimal management of these infections is not completely clear. In several reports, β-lactam antibiotics generally were associated with a successful outcome of skin and soft tissue infections in otherwise normal children, particularly for abscesses <5 cm in diameter that underwent incision and drainage.6 Incision and drainage of abscesses without antimicrobial therapy are effective in many patients. It may be that normal host defenses along with tissue levels of an antistaphylococcal β-lactam antibiotic exceeding the minimal inhibitory concentration for a short period of time is sufficient to eradicate the organism.

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