Antibacterial Agents I Flashcards Preview

Infection & Immunity Block > Antibacterial Agents I > Flashcards

Flashcards in Antibacterial Agents I Deck (18)
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1
Q

Selective Toxicity

A

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
Q

Cell Wall Synthesis Inhibitors

A

Cell Wall Synthesis: cephalosporins, penicillins, and vancomycin

3
Q

DNA Gyrase Inhibitors

A

DNA gyrase: fluoroquinolones (Cipro)

Interferes with nucleic acid metabolism

4
Q

DNA Dependent RNA Polymerase Inhibitors

A

DNA dependent RNA polymerase: Rifampin

Interferes with nucleic acid metabolism

5
Q

Protein Synthesis Inhibitors (50S)

A

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

6
Q

Protein Synthesis Inhibitors (30S)

A

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

7
Q

Cell Membrane Agents

A

Cell Membrane Agents: polymyxins
Alteration of cell membrane integrity

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

8
Q

Anti-Metabolite Drugs

A

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
Q

Bacteriocidal vs. Bacteriostatic

A

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
Q

Bacteriostatic

A

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

11
Q

Bactericidal

A

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
Q

Bactericidal Examples

A
Aminoglycosides
Cephalosporins
Penicillins
Metronidazole
Polymyxins
Fluroquinolones
Rifampin
Vancomycin
13
Q

Bacteriostatic Examples

A
Chloramphenicol
Clindamycin
Macrolides
Sulfonamides
Tetracyclins
Trimethoprim
14
Q

Synergism vs. Antagonism Examples

A

Antagonism - penicillin G + a tetracycline

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

15
Q

Enterococcal Endocarditis Tx

A

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
Q

Decreased Drug Entry or Accumulation

A

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
Q

Change in Affinity of Binding Sites

A

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
Q

Alternative Metabolic Pathways

A

Development of alternate metabolic pathways

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