Drug-induced photosensitivity can be caused by tetracyclines (doxycycline, tigecycline), sulfonamides and quinolones. Although tigecycline can be used in bacteremia caused by MRSA, it acts by inhibiting protein synthesis (by binding to the 30S ribosomal subunit), not by the creation of transmembrane channels. Sulfamethoxazole acts by inhibiting folate synthesis, and quinolones inhibit topoisomerase II and IV. Neither drug class creates transmembrane channels. Daptomycin can cause pruritus and a rash in certain susceptible individuals, but it is not known to induce photosensitivity.
Mucocutaneous necrosis occurs in Stevens-Johnson syndrome (SJS), which is a complications of medical treatment with sulfonamides (e.g., TMP/SMX). Sulfamethoxazole inhibits folate synthesis; it does not create transmembrane channels. Although TMP/SMX has proven useful in dermal MRSA infections, it is not effective in MRSA bacteremia.
Elevations in creatine phosphokinase (CPK) and rhabdomyolysis are known adverse effects of daptomycin. Serum creatine kinase should therefore be monitored and treatment discontinued if muscle-related complications occur (e.g., muscle pain). Symptoms usually resolve within 2–3 days after discontinuation of the drug. Concurrent use of daptomycin and statins (HMG-CoA reductase inhibitors) may result in increased risk of myopathy or rhabdomyolysis. Daptomycin is used as an alternative to vancomycin to treat MRSA bacteremia. Daptomycin should not be used in patients with concomitant S. aureus pneumonia because it is inactivated by surfactant and has low lung penetration. In addition to promptly initiating the appropriate antimicrobial therapy, the source of infection should be determined and controlled (e.g., removal of an indwelling catheter).
Ototoxicity is a common complication of treatment with aminoglycosides, vancomycin, and certain macrolides. Although vancomycin is a first-line treatment for MRSA bacteremia, it acts by inhibiting peptidoglycan formation in the cell wall rather than creating transmembrane channels. Aminoglycosides inhibit protein synthesis by binding to the 30S ribosomal subunit and macrolides block the peptidyl transferase at the ribosomal 50S subunit. Aminoglycosides and macrolides are not used to treat bacteremia caused by MRSA because resistance is common.