Rationale:

• Oral antimicrobials are sufficient to treat mild, uncomplicated infections due to MRSA in patients without systemic manifestation of sepsis.

Evidence:

• When the prevalence of community-associated MRSA in an area exceeds 10% to 15%, initial empiric antibiotic therapy should include drugs that have activity against community-associated MRSA for skin and soft tissue infections (91).
• Active antimicrobial therapy resulted in a greater percentage (95%) of successful outcomes in the treatment of skin and soft tissue infections due to MRSA when compared with those treated with inactive antimicrobials (87%) (92).
• For nonpurulent cellulitis, trimethoprim-sulfamethoxazole is not recommended because the likely cause, group A streptococci, is in most cases resistant to this antimicrobial agent (8; 78; 93).
• In one comparative trial cures were obtained in 37 of 42 patients treated with trimethoprim-sulfamethoxazole and 57 of 58 patients treated with vancomycin (94).
• The use of clindamycin and tetracyclines to treat MRSA is supported by observational trials (95; 96).
• When the rate of clindamycin resistance exceeds 13% in a community, consider using trimethoprim-sulfamethoxazole empirically instead (97).
• For nonpurulent cellulitis, tetracyclines are not recommended, because the likely cause, group A streptococci, are frequently resistant to this antimicrobial agent (8; 79; 98).
• A study comparing trimethoprim-sulfamethoxazole with doxycycline suggested no significant difference between these two antimicrobials in the treatment of cellulitis and soft tissue infections caused by MRSA (99).

Comments:

• Treatment of mild, uncomplicated cellulitis due to MRSA with trimethoprim-sulfamethoxazole is comparable to vancomycin. However, trimethoprim-sulfamethoxazole has not been tested in moderate to severe MRSA infection.
• Overuse of fluoroquinolones may accelerate the development of resistance to this class of antimicrobials.
• The use of moxifloxacin over levofloxacin is theoretically favored due to the lower minimum inhibitory concentrations for moxifloxacin for many organisms, which increases the mutant prevention concentration (the threshold for the development of resistance to an antimicrobial).
• A theoretical risk of ventricular arrhythmias (specifically torsades de pointes) has been proposed for the fluoroquinolone class due to QT prolongation. However, no clinical data exists at this time to indicate that it is a practical concern.