Here’s a "shorter" (😅) tweetorial…why do we use a combination of beta-lactam + vancomycin for cellulitis or MSSA bacteremia?
If vancomycin covers both strep and staph, why not use it alone? Let’s dive in! 🧵 #medsky #pharmsky #EMsky #MedEd #IDsky #AMSky #nursesky
If vancomycin covers both strep and staph, why not use it alone? Let’s dive in! 🧵 #medsky #pharmsky #EMsky #MedEd #IDsky #AMSky #nursesky
Comments
however for MSSA, we might've heard that vancomycin is less effective than beta-lactams (BL) and should rarely be used as monotherapy...
why is this the case? let’s briefly explore! 👇 2/
MSSA produces penicillin-binding proteins (PBPs) highly susceptible to β-lactam (BL) abx eg penicillins & cephalosporins
BLs directly bind PBPs...inhibiting bacterial cell wall synthesis quickly & effectively...leading to rapid bacterial killing 3/
but this MOA is slower & less efficient than BL!
This diff in bactericidal activity is why vanco has slower killing compared to BL esp against staph. Thus why BL preferred over vanco for MSSA 4/
https://pubmed.ncbi.nlm.nih.gov/22011388/
https://pubmed.ncbi.nlm.nih.gov/17984229/
https://pubmed.ncbi.nlm.nih.gov/17173215/
5/
MRSA carries mecA gene...which encodes for an altered PBP2a that has low affinity for BL...making it resistant to penicillins & cephalosporins
...but MRSA still requires peptidoglycan synthesis which vancomycin effectively inhibits by binding to different site D-Ala-D-Ala 6/
thus MRSA requires alternative treatments like vancomycin, daptomycin, or linezolid with other MOA aside from PBP target! 7/