Antibiotics 1 Flashcards
Cell wall of bacteria is made up of…
Peptidoglycan
Macromolecule composed of peptides and sugars that provide a rigid support structure only found in bacteria
Peptidoglycan
Lipopolysaccharide (LPS)
Makes up which membrane?
Which kind of bacteria?
Consists of (2)?
Makes up the outer membrane of gram (-) bacteria cell wall and consists of phospholipids and polysaccharides
4 features of gram (-) bacteria that influence antibiotics
LPS
Lipid Bilayer
Hydrophilic pores
Nutrient receptors
How does LPS inhibit antibiotics?
Retards or prevents penetration of bulky, high MW antibiotics such as erythromycin
How does the lipid bilayer inhibit antibiotic action?
Penetration of water-soluble drugs is severely hindered
How do hydrophilic pores influence antibiotic action?
The pores actually allow penetration of water-soluble molecules up to 650 Daltons (like sulfonamides) but that’s it…nothing bigger
3 factors of gram + bacteria that influence antibiotic action
Teichoic and teichuronic acid
Lipid bilayer of cytoplasmic membrane
Nutrient transporters
How do teichoic and teichuronic acid influence antibiotics on gram + bacteria?
The strong anionic action affects rate of penetrations. They literally repel drugs with negative charge
How does the bilayer affect antibiotics on gram + bacteria?
Same thing…Penetration of water-soluble drugs is inhibited
How does the nutrient transporter work on either bacteria?
If a drug is similar to the nutrient normally transported, then it will go through. Otherwise, not so much
Bactericidal
Agent that will kill the bacteria. Once the organism is exposed to the drug…it dies…like real quick
Bacteriostatic
Agent will inhibit bacterial growth but will not kill it. Therapeutic success is dependent on host defense
If the drug is removed, the bacteria will grow again
Pre-emptive therapy
Treatment of high-risk patients that are infected but asymptomatic
Empirical therapy
Treatment of symptomatic patient without further testing or confirmation of the organism
Definitive therapy
Organism is identifed
Suppressive therapy
Low does therapy used as secondary prophylaxis
6 ways resistance develops
- Reduced drug entry into organism
- Increased drug export from organism
- Expression of enzymes by organism that destroy drug
- Changes in expression of enzymes that activate the drug (pro-drug)
- Impaired drug binding to the original target
- Development of new/different pathways what are not inhibited by the drug
ESKAPE bacteria
Enterococcus facecium Staph aureus Klebsiella pneumonia Acinetobacter baumannii Psuedomonas aeruginosa Enterobacter species
Daptomycin resistance mechanism
Gene mutation of mprF that results in overall increase in net positive charge of inner and outer membranes that repel antibiotics with cationic charge
Tetracycline resistance mechanism
Overexpression of an efflux pump
Metronidazole resistance mechanism
Metronidazole needs to be reduced to generate ROS. Mutation in the rdxA gene alters or decreases activation of the drug
Streptomycin resistance mechanism
Aminoglycoside-modifying enzymes chemically modify the antibiotic and alter the binding of the drug to its target
Amoxicillin resistance mechanism
Expression of beta-lactamases
TMP-SMX resistance mechanism
Expression of the drug INSENSITIVE enzymes dihydropteroate synthase and dihydrofolate reductase
Vancomycin resistance mechanism
Substitution on the peptidoglycan stem so that the agent can no longer bind to its target
