Antimicrobial Resistance Flashcards
Bactericidal
directly kills susceptible bacteria
host responses NOT needed
Bacteriostatic
inhibits bacterial growth and relies on host defences (immune system) to clear the bacteria
won’t use for certain infections since it doesn’t directly kill
Narrow spectrum antibiotics
active against a small group of bacteria
Broad spectrum antibiotics
active against a much wider variety of bacteria
Resistance
when an organism no longer responds to a therapy OR is associated with failure in vivo
no longer has clinical impact
patient will not improve
Sensitive/Susceptible
when an organism responds to an antimicrobial and has activity in vivo
patient will get better when using this antibiotic
Antimicrobial Targets (4)
interferes with:
1) bacterial cell membrane
2) nucleic acid
-DNA –> RNA –> protein
3) protein synthesis
-RNA –> protein
4) potential for organism to obtain things they need to grow - folate synthesis
Bacterial cell membrane synthesis antibiotic mechanism
beta-lactam antibiotics
beta-lactam ring is the central component of all beta-lactam antibiotics
inhibits synthesis of bacterial cell membrane synthesis
transpeptidase enzyme crosslinks the
peptidoglycans NAG and NAM
beta-lactam antibiotics
bind to transpeptidase enzyme complex and blocks this reaction
Beta-lactam antibiotics (many)
Active in both gram positive AND gram negatives
penicillins (Group A strep, Group B strep, syphillis)
amoxicillin (common in peds)
cephalosporins
minocyclines
carbapenems
Penicillins
narrowest
penicillinG
penicillinV
cloxacillin
amoxicillin
peperacillin
Cephalosporins
1st gen - broader
-ampicillin
2nd gen - broader
-cefazolin
3rd gen - very broad
-ceftazidime
-ceftriaxone
-cefixime
Carbapenems
BROADEST
multi drug resistant organisms, last resort
Ertapenem
Meropenem
Glycopeptides
non Beta-Lactam
cell wall active agents
bacteriocidal
vancomycin, teicoplanin
act on the cell wall of GRAM POSITIVE organisms
-C. difficile
-MRSA
stops the extension of the peptidoglycan unit of the bacterial cell wall
interferes with D-Ala, D-Ala binding
Protein synthesis inhibitors
binds parts of the ribosomes (make proteins from nucleic acids)
antibiotics bind the 30S and 50S subunits of ribosomes to stop protein synthesis
tetracyclines - 30S
e.g. doxycycline
macrolides - 50S
-e.g. azithromycin
Nucleic acid inhibitors
fluoroquinolones
bind to nuclear enzymes (topoisomerase an gyrase) inhibiting DNA replication
fluoroquinolones
excellent drugs with a broad spectrum of activity
good tissue penetration
used to used for UTIs, stopped, can use again
CAP
Metabolic Inhibitors
prevent acquisition or generation of things like folate
Trimethoprim/Sulfamethoxazole (Septra, Bactrim)
-inhibitors of the active form of folic acid (tetrahydrofolic acid)
Trimethoprim - structural analogue of DHF (dihydrofolic acid) and competitive inhibitor of dihydrofolate reductase
Sulfamethoxazole - Structural analogue of PABA and competitively inhibits synthesis of DHF
Intrinsic resistance
bug is already always resistance to the antibiotic
like how skin is waterproof
Inducible resistance
acquired
has to get it from somewhere
from other bacteria, the environment, or sub-optimal exposure (not finishing dose as prescribed, taking when not needed, skipping doses*** - like a punching bag making the bug stronger)
Antibiotic Susceptibility Testing
done in vitro (in glass)
interpretations:
S = susceptible/sensitive (organism doesn’t grow)
I = intermediate
R = resistant (organisms grows, don’t use)
several methods are done to test the sensitivity of the organism to antibiotics
Resistance Detection
Antibiotic disc
Zone of inhibition (in mm)
Bigger the zone=more susceptible
Use guidelines to interpret the zone of inhibition as S, I or R
Micro-Broth Dilution
different concentrations of antibiotics from L of the plate to the R
suspension of bacteria added to the plate and incubated
last well before growth is seen is the Minimum Inhibitory Concentration (MIC)
bacteria makes liquid go cloudy (turbidity)
Bacterial Resistance Types (2)
1) inherited
2) acquired - another bug that’s shared DNA with bug to give it phenotype that’s resistant
What bacterial characteristic contributes to bacterial resistance?
short replication times