Susceptibility Flashcards
B-lactam antibiotics
Penicillins
Cephalosporins
Carbapenems
Monobactams
B-lactam antibiotics mechanism of attack
B-lactam is 4 membered ring that takes the place of the normal structure in transpeptidase reaction, disrupting the formation of the cell wall
Resistance to B-lactam
Caused by bacterial enzymes that destroy the antibiotic
Ex. altered targets (PBP), decreased intracellular uptake
Streptomycin Gentamicin Neomycin Kanamycin Amikacin Trobramycin
Aminoglycoside antibiotics
Aminoglycoside antibiotics mechanism of attack
Binds specifically to 16S ribosomal unit @ the A binding site in the 30S ribosomal unit, prevents the docking of aminoacyl transfer RNA, causing it to be misread, leaving org unable to synthesize proteins vital to growth
1st, 2nd, 3rd gen cephalosporins
B-lactam ring is 6-member dihydrothiazine ring, allowing more resistance to hydrolysis than 5-member ring
Basic structure has more modifiable sites to increase action against bacteria
Differences in 1st, 2nd, 3rd gen cephalosporins
Alterations of positions R1 & R2
What effect does a bacteriostatic antibiotics have on the microbe?
Inhibits microbial growth, doesn’t kill it
What effect does a bactericidal antibiotic have on the microbe?
The antimicrobial agent actually kills the organism
CLSI recommendations for selective reporting for Group A
Antimicrobial agents that are done & reported routinely
CLSI recommendations for selective reporting for Group B
Reported only if an organism shows resistance to A agents/patients cannot tolerate A agents/infection is not responding/or it is a multi organism infection
CLSI recommendations for selective reporting for Group C
Broad-spectrum activity, orgs resistant to A & B agents
CLSI recommendations for selective reporting for Group D
Urine antimicrobials
Quinoline group affect on microbes.
Inhibition of DNA gyrase by binding to the A subunit of DNA gyrase. Enzymes needed are topoisomerases I, II, III, IV
Specifically targets the topoisomerase I & II & prevents the supercoiling of DNA by inhibiting synthesis
Members of quinoline group
Nalidixic acid, cinozacin, farehoxacin, ciproflaxacin
Cinoxacin, loracarbef, nitrofurantoin, sulfixoxazole, trimethoprim
Group D antibiotics
Ceftazidime, Kanamycin, netilmicin, tobramycin, tetracycline, chloramphenicol
Group C antibiotics
Mezlocillin, ticarcillin, amoxicillin group, cephalosporins other than ceftazidime, amikacin, T/S
Group B antibiotics
Group A antibiotics
Ampicillin, cefazolin, cephalothin, gentamicin
Purpose of MBC
For immunosuppressed patients or very serious infections
The synergistic combination of the antimicrobial & patient’s own immune system is weak
To just inhibit the microbe may not sufficient & bactericidal levels are needed
Calculate MBC
- From growth well, dilute organism to 1:1000 (.01 mL in 10mL saline)
- 0.01 mL aliquot is plated from a clear well
- 18 hours - growth plate = # of colonies x 10^4
MBC end point is calculated if 99.9% killing has occurred
Important criteria for Kirby-Bauer disk diffusion
Lawn correct conc. of microbe on media Select appropriate disks Press lightly on surface within 15 mins of inoculation Incubate 16-18 hrs NO CO2 unless required Standardized depth of media
Susceptible
A regression analysis plot is used by CLSI & US FDA to develop zone interpretation criteria
Resistant
Antimicrobial will most likely be ineffective