This polypeptide is selectively active against gram-positive bacteria. Because of severe nephrotoxicity associated with systemic administration, its use has been limited to topical application on surface lesions, usually in combination with polymyxin or neomycin.
Mupirocin (formerly pseudomonic acid) is a naturally occurring antibiotic produced by Pseudomonas fluorescens active against most gram-positive cocci, including methicillin-sensitive and methicillin-resistant S aureus and most streptococci (but not enterococci). Used topically, it can decolonize staphylococcal carriage after application to the anterior nares twice daily for 5 days. However, recurrent colonization occurs (50% at the end of 1 year), and when mupirocin is used long-term over months, resistance can emerge. High rates of mupirocin resistance have been observed in methicillin-resistant S aureus isolates from surgical intensive care unit patients, despite minimal in-hospital mupirocin use. This finding suggests the benefit of mupirocin is limited. Monthly application for 5 days each month for up to a year decreases staphylococcal colonization, which in turn lowers the risk of recurrent staphylococcal skin infections. Studies demonstrate an associated reduction in postoperative staphylococcal lung infections in colonized patients treated with mupirocin. Whether it is more effective than trimethoprim-sulfamethoxazole or dicloxacillin plus rifampin for eradication of staphylococcal nasal carriage is unknown. The IDSA recommends the use of mupirocin with chlorhexidine preferentially over oral antibacterials for methicillin-resistant S aureus decolonization. Mupirocin is equal to oral beta-lactams in the treatment of mild impetigo.
Clindamycin is active against gram-positive organisms including S pneumoniae, viridans streptococci, group A streptococci, and S aureus, though resistance has been described in all of these pathogens. Pneumococci or staphylococci with an efflux-based mechanism of resistance can be effectively treated with clindamycin. However, isolates with ribosomal methylase resistance are also resistant to clindamycin. Enterococci and most S epidermidis are resistant. Susceptibility of CA-MRSA isolates to clindamycin varies regionally. In those instances, in which CA-MRSA isolates demonstrate resistance to macrolides but susceptibility to clindamycin, additional microbiologic testing (“D” test) is advised to confirm the effectiveness of clindamycin. Clindamycin is equal to trimethoprim-sulfamethoxazole in uncomplicated skin and soft-tissue infection in emergency department patients. A dosage of 150–300 mg orally every 6 hours is generally given for bacterial infection. It is widely distributed in tissues but does not achieve therapeutic levels in cerebrospinal fluid. Excretion is primarily nonrenal.
Clindamycin is currently recommended as an alternative medication for prophylaxis against endocarditis following certain dental procedures in patients allergic to amoxicillin. Clindamycin, 300 mg orally twice daily for 7 days, can be used as an alternative to metronidazole for the therapy of bacterial vaginosis. Topical application of a 2% vaginal cream once or twice daily for 7 days or 100-mg ovules intravaginally once at bedtime for 3 days is also effective. Clindamycin is active against most anaerobes, including Prevotella, Clostridium, Peptococcus, Peptostreptococcus, and Fusobacterium organisms. However, up to 25% of B ...