Trimethoprim‐Sulfamethoxazole Activity and Pharmacodynamics against Glycopeptide‐Intermediate Staphylococcus aureus

Abstract

All GISA strains were susceptible to TMP-SMX. In addition, it appears that TMP-SMX may have concentration-dependent antibacterial activity against these organisms. As an option in the management of GISA infection, TMP-SMX merits further study.

Trimethoprim-Sulfamethoxazole or Clindamycin for Community-Associated MRSA (CA-MRSA) Skin Infections

“…2,7,8 The importance of TMP-SMX dosing in CA-MRSA skin infections has not yet been validated in the clinical setting, and this study suggests these prescribers might not have been familiar with the pharmacokinetic-pharmacodynamic literature for TMP-SMX. It is possible that TMP-SMX, dosed at 2 double-strength tablets twice daily, might be superior to clindamycin, but that cannot be determined from this study.…”

Management of cutaneous lesions associated with an emerging epidemic: community-acquired methicillin-resistant Staphylococcus aureus skin infections

“…8,9,16,19,34,36,51 MRSA should be confirmed by culture because vancomycin is less rapidly bacteriocidal and less efficacious than the beta-lactams (such as cefazolin) and the semisynthetic penicillinase-resistant penicillins (such as oxacillin and nafcillin) against MSSA. 51 In patients who fail or cannot tolerate vancomycin, potential alternative antibiotics include linezolid (Zyvox) 9,23,27,51,54,[56][57][58][59] ; dactomycin (Cubicin), which recently received Food and Drug Administration marketing approval for this indication; quinupristin/dalfopristin (Synercid) 27,51,54,57 ; and teicoplanin (Targocid). 27,37 Is there a role for topical antimicrobial agents in the management of CAMRSA?…”

Question 1: Co-trimoxazole dosing dilemma: what is the right dose?

“…Co-trimoxazole interrupts folic acid synthesis and formation of thymidine. Although it exhibits concentration-dependent activity against Staphylococcus aureus ,9 there are no in vitro pharmacodynamic studies of co-trimoxazole activity against P. jirovecii , a major barrier to dose optimisation. Animal models show that co-trimoxazole reduces the burden but does not eliminate P. jirovecii 10…”