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Antimicrobial Medications Study Guide

Terms in this set (37)

Antibiotics
chemical substance produced by certain microbes that inhibit or kill other microbes
Synthetic drugs
(man-made) derived from dyes or chemicals that inhibit or kill microbes
Antimicrobial Drugs
chemicals that inhibit or kill microbes. Includes both antibiotics and synthetic drugs.
What are the characteristics of an ideal antimicrobial drug?
Kill infectious agent w/o harm to host

Reach infectious agent

Not predispose to other infections or allergies (penicillin allergy, causing yeast infection)

Remains active long enough to act (half life of drug)

Safely excreted or inactivated by host

Easily administers
Name the 4 most common genera of bacteria and fungus that produce antibiotics.
Penicillium spp.

Cephalosporium spp.

Bacillus spp.

Streptomyces spp.
Narrow-spectrum
effective against a limited array of different microbial types.
Broad-spectrum
active against a wide range of different microbes.
Describe the situation in which you would use each type. (narrow-spectrum vs broad-spectrum)
As a doctor, when you don't know which bacteria you are dealing with you would use a Broad-spectrum. Whereas if you know exactly what to target you would use a narrow spectrum for more efficacy.
List some common adverse effects of antimicrobial medications.
-Allergic reactions (fever and rash up to anaphylactic shock)

-Toxic effects (kidney damage, deafness, aplastic anemia)

-Suppression of normal microbiota (the normal microbiota protect host and protect against pathogenic microbes)
List the 5 mechanism of antimicrobial drug actions.
1. Cell Wall Synthesis
2. Protein Synthesis
3. Nucleic Acid Synthesis
4. Metabolic Pathway
5. Cell Membrane Integrity
Cell Wall Synthesis
prevent synthesis, damage, or break down cell wall.

Lead to cell lysis. Prevents cell from forming peptidoglycan. Humans don't have cell walls.
Protein Synthesis
Target is 70s ribosome.

Prevents translation.

Humans have 80s ribosome.

Some very slight toxicity because humans have 70s ribosome in eukaryotic mitochondria.
Nucleic Acid Synthesis
targets enzymes for nucleic acid synthesis.

Impedes replication or transcription of DNA.

Bacteria replicate DNA at a much faster rate so it affects them greater.

But still toxic to humans because we undergo DNA replication too.
Metabolic Pathways
most common is folic acid synthesis (most microbes make their own folic acid, humans get it from diet).

Humans don't undergo folic acid synthesis so we are unaffected by this target.
Cell Membrane Integrity
Damage leads to loss of selective permeability. Leads to cell death.

Antifungals do this by targeting ergosterol.

This can also destroy human cell membranes. Most are topical use only for humans because of the potential damage to cell membranes (have extreme list of side effects).

Except antifungals can be taken orally.
In vivo
Process occurring in a living thing, ex: patient drug trials
In vitro
process occurring in an artificial environment, ex: test tubes, culture media
Describe the Kirby-Bauer test.
Kirby-Bauer test determines the susceptibility of an organism to an antibiotic. It is a "sensitivity test".
What is the zone of inhibition?
area around disk where bacteria didn't grow.
What is resistant, intermediate and susceptible?
Resistant: bacteria grew. No effect on bacteria.

Intermediate: may or may not work.

Susceptible: bacteria doesn't grow. Growth was inhibited.
How do you determine which drug is susceptible?
The zone of inhibition (preferably wide/thick) is measured and compared to the measured value to see if it is susceptible. Zone size is dependent on bacteria.
Describe the tube dilution test.
Serial dilutions of drug are done. Then inolculate with bacteria, and then incubate.
Minimal inhibitory concentration (MIC)
minimal amount of drug to inhibit bacterial growth. The tubes are examined for turbidity, the first tube that is clear is the MIC.
Minimal Lethal Concentration (MLC)
minimum concentration of drug to kill bacterial cells. The clear tubes are subcultured.
Define the therapeutic index.
A comparison of the amount of a therapeutic agent that causes the therapeutic effect to the amount that causes toxicity. (determines if a drug is safe to use in a patient).
How do you calculate the therapeutic index?
Calculated: Toxic dose(of patient)/MIC

A wider range/higher TI number is better.

Smaller TI number means higher potential for toxic drug reaction.
What criteria is used to determine which drug to use for that particular patient?
-patient's health
-preexisting medical condition (liver, kidney disease)
-potential drug adverse effects
-nature and spectrum of drug (narrow/broad spectrum)
What are the reasons for failed antimicrobial drug therapy in the patient?
-In vivo results don't match in vitro test
-Drug can't get to infection site
-Resistant cells present
-Multi-pathogenic infection
-Lack of compliance (could be unaffordable)
How is antimicrobial drug resistance acquired and how is the information stored in the cell?
-spontaneous mutation
-gene transfer, plasmid-extrachromosomal DNA, Easy horizontal transfer between unrelated bacteria.
-uses pili. Resistance can be passed on quickly.
4 mechanisms of drug resistance.
Drug-inactivating enzymes

Alter target molecule

Decrease uptake of drug

Increase elimination of drug
Drug-inactivating enzymes
destroy or inactivate drug before it starts working
Alter target molecule
decreases binding(receptor) sites of drug, changes binding site.
Decrease uptake of drug
decrease drug permeability by changing membrane proteins.

Drug can't get into cell,

drugs bind to surface molecules.
Increase elimination of drug
increase efflux pumps or change pumps to pump drugs out faster,

resistant to variety of drugs simultaneously

(drug doesn't stay long enough to work)
Describe 3 ways in which you can minimize the development of drug resistance. Why is this important?
Use antimicrobial drugs only when necessary

Use proper concentration

Use for proper length of time
Describe the mechanism of antiviral drug actions.
1. Prevent virus entry

2. Interfere with viral uncoating (prevent viral nucleic acid from separating from capsid, thus can't replicate

3. Interfere with nucleic acid synthesis/block transcription and translation (damage to rapidly replicating genome-side effects

4. Prevent genome integration (prevent insertion of viral DNA into host chromosomes)

5. Prevent viral assembly/release
Mechanism of Antiviral drugs
-not affected by antimicrobial drugs
-disrupt viral metabolism-disrupt host metabolism
-target infectious cycle of virus
-can't eliminate latent viral infections
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