miscellaneous abx Flashcards
Vancomycin (Vancocin) administration/metabolism
IV (poor oral absorption)
- widely distributed and does penetrate the CSF when the meninges are inflamed
- 90% of vancomycin is eliminated by renal excretion, adjust dose with renal failure
Vancomycin (Vancocin) MOA
inhibits bacterial cell wall synthesis by binding to the D- alanyl-D-alanine portion of the peptidoglycan pentapeptide, bactericidal
how does resistance to Vancomycin develop?
bacterial enzymes that can induce alterations in the cell wall precursors so that vancomycin can’t bind as well
i.e. Vancomycin resistant enterococci replace D-alanyl-D- alanine with D-alanyl-D lactate or D-alanyl-D-serine
vanco spectrum
MRSA, MSSA, S. epidermidis, Streptococci, Corynebacterium diptheria, Clostridium spp. (the only anaerobe effective against)
NOT against G-s
vanco uses
serious staph infections
G+ infections in pts allergic to PCNs/cephs (tx w. aminoglycoside for synergism)
C. diff colitis (oral vanco)
staph meningitis in a PCN-allergic pt, if caused by S. pneumo include with a 3rd gen ceph
vanco SEs
-Ototoxicity and Nephrotoxicity: (rare)m ore common when given in combo with another ototoxic abx (i.e. amino glycoside)
-“Red man” or “Red Neck” syndrome – If vancomycin is infused too rapidly
is can cause flushing of the face, neck and torso due to histamine release.
minor: Injection site irritation, and chills and fever
Clindamycin (Cleocin)
- oral and parental, distributed widely EXCEPT does not penetrate well into the CNS even with inflammation of the meninges
- does have good abscess penetration
clindamycin MOA: similar to ??
imilar to erythromycin and chloramphenicol – binds to 50 S ribosomal subunit and inhibits bacterial protein synthesis; bacteriostatic
resistance to clindamycin develops how?
- Mutations in the 50 S bacterial ribosomal subunit which prevents Clindamycin binding
- Modification of the binding site by the enzyme methylase that prevent clindamycin binding
- Enzymatic inactivation of clindamycin
- Bac resistant to clindamycin are usually resistant to
erythromycin. (similar mech)
clindamycin spectrum
most Staph aureus strains (has activity against some community acquired MRSA), Strept. Pneumoniae, but enterococci are resistant.
- NOT useful against G- AEROBES
- is active against G- and G+ anaerobes (B. fragilis and C. perfringens)
clindamycin uses
- anaerobic infections (abscesses)- NOT brain abscesses
- used in combo w. amino glycoside/ceph to tx deep wounds
- *ppx against endocarditis in valvular heart dis. pts who are having dental procedures
- alternative to PCN/ceph in allergic pts
- PCP and toxoplasma gondii (+pyrimethamine) in AIDS pt
clindamycin SEs
C. diff-induced Pseudomembranous colitis (tx w. oral Vancomycin, Metronidazole, and Cholestyramine (not orally w. vanco: antagonistic effect)
Nitrofurantoin (Furadantin, Macrobid, Macrodantin)
- Rapidly absorbed after oral admin, metabolized/excreted by glomerular filtration and tubular secretion (40% of free drug is found in the urine), often so quickly drug effects not seen!
- don’t use in renal failure
- reduced forms can damage DNA, both bactericidal and static
- admin w. acidifying agent (more active @ pH
nitrofurantoin spectrum?
resistance development??
- G+ and G- bac
- NOT effective against Pseudomonas and many Proteus strains (resistant)
- Bac resistance takes a long time to develop and there is no cross resistance with other abx
nitrofurantoin uses
-tx UTIS and for ppx for recurrent UTIs (used of UTIs caused by E. coli resistant to TMP-SMX and FQs)
nitrofurantoin SEs
- GI: anorexia, N/V
- hemolytic anemia (rare, seen in pts w. G6PD deficiency)
- neurological, pulmonary fibrosis, chronic active hepatitis, allergic reactions
- contraindicated in renal failure, caution w. preggos