protein synthesis inhibitors Flashcards
MOA clindamycin
inhibit protein synthesis by binding only to 50S
clindamycin: bacteriostatic or bactericidal?
bacteriostatic
MOR clindamycin
presence of erm gene, which alters the 50S binding site
no activity of mef gene against clindamycin
main area of use for clindamycin
anaerobic infections peptostreptococcus actinomyces bacteriodes (use metronidazole instead) prevotella fusobacterium clostridium spp. (excluding C. difficile)
best way to test for CA MRSA resistance to clindamycin?
SSSI infections due to MRSA, give clindamycin to see if theyre susceptible or not
clindomycin have to be givenIV or PO?
no, completely and rapidly absorbed (90%)
CSF distribution clindomycin?
poor distribution
clindomycin eliminated by hemodialysis?
no
elimination mechanism for clindomycin?
primarily by liver
primary clinical use clindomycin
anaerobic infections outside of the CNS, SSSI infections due to CA MRSA
the one major adverse effect clindomycin
one of the worst inducers of C. difficile colitis
3 macrolides in clinical use
erythromycin, clarithromycin, azithromycin
improvements due to purifying erythromycin into azithromycin and clarithromycin
better bioavailability
better tissue penetration
prolonged half lives
improved tolerability
MOA macrolides
inhibit protein synthesis by binding the 50S subunit to suppress protein synthesis
macrolides: bacteriostatic or bactericidal
bacteriostatic
MOR macrolides in the US
mef gene encoding active efflux which confers a low level of resistance to macrolides