Vancomycin and Bacitracin
Penicillin and Cephalosporin
3. What does Cell Death require?
Action of Autolysin
4. What are three mechanisms of resistance to Penicillin?
Lack of accessibility to target (Gram Negative)
Production of Penicillinases (Beta-Lactamase)
Alterations in Penicillin Binding Proteins
6. What is the standard reference of Penicillin?
Penicillin G
7. Is oral use of Penicillin G indicated?
Not, it is inactivated at low pH
10. Which type of penicillin is acid stable?
Penicillin V
11. Should you use sulfonamides on a patient with 6-glucose phosphate dehydrogenase deficiency?
No, it could produce acute hemolytic anemia
13. Why are long-acting sulfonamides not available in the US any longer?
Due to the high incidence of Stevens-Johnson syndrome
14. What is the mechanism of Trimethoprim?
It is a selective inhibitor of Dihydrofolate reductase
16. Which types of bacteria are targeted by Trimethoprim?
Both Gram - and Gram +
Its Broad Spectrum
17. Which chemotherapeutic agents are inhibitors of cell wall synthesis?
Penicillin
Cephalosporin
Vancomycin
Bacitracin
Cycloserine
20. What log cell kill is required to cure microbial infections?
2 (99% of population is killed)
22. What types of bacteria do sulfonamides target?
Broad-Spectrum - Gram + and Gram -
23. What is the mechanism of action of sulfonamides?
They are structural analogs and competitive antagonists of PABA (Para-Aminobenzoic Acid)
25. How do sulfonamides not interfere with host metabolism?
Mammalian cells use preformed folic acid.
27. How is resistance to sulfonamides presented?
Increased synthesis of PABA
Alterations in enzyme that utilizes PABA
Increased capacity to destroy or inactive the drug
Development of an alternative metabolic pathway for synthesis of essential metabolites
30. What condition must be considered when prescribing sulfonamides and chloramphenicol?
Glucose-6-Phosphate Dehydrogenase Deficiency (May produce Hemolysis)
31. What are six mechanisms of resistance from chemotherapeutic agents?
1) Absence of Target (Ergosterol's absent)
2) Alterations in Target (Pen. Binding Protein Alterations)
3) Low concentration at target (Interference with membrane passage)
4) Lack of metabolic activation (Antifungal Flucytosine -> Fluorouracil)
5) Inactivation (Penicillinases)
6) Escape from Effect (Alternate Metabolic Pathways)
32. What type of resistance occurs in the absence of selective pressure?
De Novo (Intrinsic) Resistance
33. When is a microorganism said to be resistant?
When the concentration of the drug required to weaken or kill the microorganism is greater than can be tolerated by the host.
34. What generally happens when you add two bacteriocidal agents?
Generally results in a synergistic effect.
35. What generally happens when you combine 1 bacteriocidal and 1 bacteriostatic agent?
Generally results in antagonism