Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. For the treatment of clinical infection by S aureus, cloxacillin or cephalexin is used. In streptococcal infections, cephalexin is preferred. If not effective, penicillin and clindamycin in combination are effective. Consider staphylococcal infection in every flare of atopic dermatitis.
Cephalexin is a first-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. It has bactericidal activity against rapidly growing organisms. Its primary activity is against skin flora; it is used for skin infections or prophylaxis in minor procedures.
Cephalexin suspension includes mauve granules (125 mg/5 mL) and peach granules (250 mg/5 mL).
Penicillin VK (Beepen-VK, Betapen-VK, Veetids)
Penicillin VK inhibits the biosynthesis of cell wall mucopeptide. It is bactericidal against sensitive organisms when adequate concentrations are reached, and it is most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.
Clindamycin is a lincosamide for the treatment of serious skin and soft tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). It inhibits bacterial growth, possibly by blocking the dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Mupirocin (Bactroban, Bactroban Nasal, Centany)
Mupirocin is used as a topical treatment for bacterial skin infections such as furuncle, impetigo, and open wounds. It is also useful in the treatment of methicillin-resistant Staphylococcus aureus (MRSA) infection.
Trimethoprim/sulfamethoxazole (Bactrim, Bactrim DS, Cotrim)
Sulfamethoxazole disrupts bacterial folic acid synthesis and growth via inhibition of dihydrofolic acid formation; trimethoprim inhibits dihydrofolic acid reduction to tetrahydrofolate, resulting in the inhibition of enzymes of the folic acid pathway.