3-Antibiotics Flashcards
chemotherapy
treat of dz with use of chemicals to kill/impair growth of microorgs
-antimicrobial or antibacterial
selective toxicity
leveraging biochem diff b/t host and pathogen to kill/inhib without harming host
bacteriotstatic
no overt killing
-therapeutic success dep on host immunity, buy time for host
-non life threatening
bactericidal
overt killing
use when immune sys not counted on to combat pathogen
-immunocomp patients, life threatening dz
broad spectrum
cover large variety of bacteria
-useful for life threatening to cover unknown cause of infection
can disrupt normal microbiota
ampicillin
narrow spectrum
cover only small subset of bacteria
-avoid disrupting normal microbiota
-have to id causative agent to be confident
methicillin
antibiotic synergism
combo two antib with enhanced bactericidal activity when used together
trimethoprim + sulfonamide
antibiotic antagonism
combo of antib that one interferes with activity of other
therapy progression
- empiric- treatment while waiting for lab results
- targeted-
- adjusted
antibiotic naturally occuring?
thru random mutation or acquisition of genetic elements carrying resistnace
antibiotic use
LEADS to resistance not causes
bc enriches spread of bacteria
causes of resistance crisis
- overuse and inapprop prescribing
- extensive use in agriculture
- lack of discovery/development
what can physicians do
- follow protocols
- use diagnostics
- only prescribe when needed
4.
when are antibs necessary
- surgery
- chronic conditions
- organ transplants
- dialysis
- cancer therapy
minimum inhibitory concentration
MIC
to test susceptibilty- lowest antib concentratin that inhibits growth
in broth culture, culture on agar (kirby bauer, E test)
minimum bactericidal concentration
lowest amount that kills 99.9%
agar based methods
MIC
- bacteria spread evenly on agar
- paper disc with antib (kirby bauer disk diffusion) OR paper strip with concentration gradient
- allow grow for 24-48 hr
- measure zone of inhibition
broth culture MIC and MBC
multi tubes with decreasing amount of antibs
-can visually see minimum concnetration that worked
then do MBC to see how many actually died (rather than just inhibited)
breakpoint tables
MIC values compared
-specific to each org/antib
categorized as suspectible, intermed, resistant
susceptible
therapeutic success is likely
-inhibits growth is usually achieved
intermed
resistant
dec influx + active efflux
mechanism
drug pumped out
or not come in by dec porin permeabilty
targetting
mechanism
-modify
-bypass
-protect
-or just no target in general
inactivating
mechanism
cell wall active
disrupt peptidoglycan synthesis
-effective vs actively dividing bact
membrane active
disrupts membrane integrity
-vs resting and actively dividing bact
beta-lactam antibs
beta lactam ring
-irreversibly bind transpeptidase and prevent cross linking
penicillin
cephalosporins
penicillins
cephalosporins
beta-lactam resistance mechanisms
- dec uptake by mutating prins
- antibiotic degrad
3.
beta-lactamase inhibitors
irrev bind and inhibit action of susceptible beta-lactamase
-inactive the resistant mech
always given with beta-lactams
vancomycin
prevents crosslinking and polymerization of peptid chain by bind D-ala
-but NOT a beta-lactam
resistance by changing D-ala to D-lactate
bacitracin
inhib peptid syn by interfere with dephos the lipid carrier (bactoprenol)
-no more new NAM-NAG units added
tetracyclines
aminoglycosides
macrolides
quinolones
inhibit DNA replication via gyrases
ciprofloxacin, levofloxacin
rifampin/rifabutin
metronidazole
