Antibacterial Agents I Flashcards Preview

Infection & Immunity Block > Antibacterial Agents I > Flashcards

Flashcards in Antibacterial Agents I Deck (18):
1

Selective Toxicity

The chemotherapeutic agent should inhibit microbial growth or destroy the microbe without causing harmful effects in the host.
(Selective Toxicity = the basis for successful, effective chemotherapy)

2

Cell Wall Synthesis Inhibitors

Cell Wall Synthesis: cephalosporins, penicillins, and vancomycin

3

DNA Gyrase Inhibitors

DNA gyrase: fluoroquinolones (Cipro)
Interferes with nucleic acid metabolism

4

DNA Dependent RNA Polymerase Inhibitors

DNA dependent RNA polymerase: Rifampin
Interferes with nucleic acid metabolism

5

Protein Synthesis Inhibitors (50S)

Protein Synthesis Inhibitors (50S): macrolides (erythromycin), chloramphenicol, clindamycin

6

Protein Synthesis Inhibitors (30S)

Protein Synthesis Inhibitors (30S): tetracyclines (doxy) and aminoglycosides (genta and streptomycin)

7

Cell Membrane Agents

Cell Membrane Agents: polymyxins
Alteration of cell membrane integrity

Can cause neurotoxicity and nephrotoxicity, but have been brought back because of bacterial resistance

8

Anti-Metabolite Drugs

blockade of specific metabolic steps
Examples: sulfonamides & trimethoprim

Sulfonamides: blocks dihydropteroate synthase
Trimethoprim: blocks dihydrofolate reductase

Anti-metabolite drugs – look like biochemical compounds that microbe is using, but have affinity for enzymes and processes and compete for them and slow down bacterial growth
Do not kill them, but slow down growth

9

Bacteriocidal vs. Bacteriostatic

Cidal: killing and is irreversible action
Static: slow growth and is reversible

Protein synthesis inhibitors bind reversible and slow growth down, but aminoglycosides bind irreversibly and produce cidal effect

10

Bacteriostatic

Concentrations that inhibit growth are much lower than those that kill
Examples: macrolides, sulfonamides & tetracyclines

11

Bactericidal

Little difference between concentration that inhibits growth and that which kills

used for difficult or hard to eliminate pathogens like meningitis or in immunocompromised host; bacterial endocarditis also should use this

Examples: penicillins, cephalosporins, aminoglycosides & fluoroquinolones

12

Bactericidal Examples

Aminoglycosides
Cephalosporins
Penicillins
Metronidazole
Polymyxins
Fluroquinolones
Rifampin
Vancomycin

13

Bacteriostatic Examples

Chloramphenicol
Clindamycin
Macrolides
Sulfonamides
Tetracyclins
Trimethoprim

14

Synergism vs. Antagonism Examples

Antagonism - penicillin G + a tetracycline

Synergism -
penicillin G + gentamicin (or streptomycin)
trimethoprim + sulfamethoxazole
amoxicillin + clavulanic acid

15

Enterococcal Endocarditis Tx

Penicillin + Aminoglycoside Synergy

An example of a disease that is treated most effectively with two antibiotics is enterococcal endocarditis. The recommended treatment is with a penicillin (penicillin G or ampicillin) and an aminoglycoside (gentamicin or streptomycin).

16

Decreased Drug Entry or Accumulation

Decreased drug entry or accumulation

Loss of membrane permeability (due to alteration in porin number or structure in gram negative bacteria), OR decreased entry due to an altered transport system
decreased drug accumulation due to an efflux pump

Examples: resistance to aminoglycosides, macrolides, penicillins/cephalosporins & tetracyclines

17

Change in Affinity of Binding Sites

Change in the affinity of intracellular binding sites

Examples:
altered ribosomal binding sites for macrolides
altered PBPs for penicillins
altered target enzyme, DNA gyrase, for fluoroquinolones

18

Alternative Metabolic Pathways

Development of alternate metabolic pathways

Example: increased production of PABA by bacteria to overcome inhibition by sulfonamides