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84 Cards in this Set

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chemotherapeutic agents

- chemical agents used to treat disease

- destroy pathogenic microbes or inhibit their growth within a host

- most are antibiotics

> microbial products or their derivitives that kill suceptible microbes or inhibit their growth

sources of antimicrobial drugs

1. natural products from bacteria and fungi

2. synthetic products

3. semi-synthetic products

- natural antibiotics modified to improve stability in the body

selective toxicity (definition)

the ability of a drug to kill or inhibit a pathogen while damaging the host as little as possible

therapeutic dose (definition)

the drug level required for clinical treatment

toxic dose (definition)

the drug level at which the drug becomes too toxic for the patient (ie. produces side effects)

therapeutic index (definition)

ratio of toxic dose to therapeutic dose

side effects (definition)

undesirable effects of a drug on host cells

narrow-spectrum drugs (definition)

attack only a few different pathogens

broad-spectrum drugs (definition)

attack many different pathogens

cidal agent

kills microbes

static agent

inhibits the growth of microbes

measuring the effectiveness of antimicrobial drugs

effectiveness is expressed in 2 ways:

1. minimal inhibitory concentration (MIC)

2. minimal lethal concentration (MLC)

minimal inhibitory concentration (definition)

the lowest concentration of a drug that inhibits a pathogen

minimal lethal concentration (definition)

the lowest concentration of a drug that kills a pathogen

dilution susceptability tests

- involves inoculating media containing different concentrations of a drug

- the broth or agar with the lowest concentration showing no growth in the MIC

- if broth is used, tubes showing no growth can be subcultured into drug-free medium

> the broth from which a microbe can't be recovered is the MLC

disk diffusion tests

1. disks impregnated with specific drugs are placed on agar plates inoculated with a test microbe (bacterial lawn)

2. drug diffuses from disk into agar, establishing a concentration gradient

3. observe the clear zones (no growth) around the disks (zone of inhibition)

the Kirby-Bauer method

a standardized method for the disk diffusion test

- the sensitivity/resistance is determined using tables relating zone diameter with microbial resistance

the E-test

- convenient for use with anaerobic pathogens

- similar to disk diffusion method, but uses strips rather than disks

- intersection of elliptical zone of inhibition with strip indicates MIC

mechanisms of action of antimicrobial drugs: inhibitors of cell wall synthesis

- most sensitive; high therapeutic index

- penicillin's

> most are 6-aminopenicillianic acid derivatives and differ in the side chain attached to the amino group

> most crucial feature of the molecule is the B-lactam ring

> essential for bioactivity

> many penicillin resistant organisms produce B-lactamase (penicillinase) which hydrolyzes a bond in this ring

penicillins: mode of action

1. blocks the enzyme that catalyzes transpeptidation (the formation of cross-links in peptidoglycan)

2. prevents the synthesis of complete cell walls leading to lysis of cells

3. acts only on growing bacteria that are synthesizing new peptidoglycan

4. binds to periplasmic proteins (penicillin-binding proteins aka PBP's)

5. may activate bacterial autolysins and murein hydrolases

6. stimulate bacterial holins to form holes or lesions in the plasma membrane

penicillin V

- naturally occurring

- narrow-spectrum

penicillin G

- naturally occurring

- narrow-spectrum

semi-synthetic penicillins

have a broader spectrum than naturally occurring ones

issues with penicillin

- resistance to penicillins, including semi synthetic analogs, continues to be a problem

- roughly 1-5% of adults in the US are allergic to penicillin

> the allergy can lead to a violent allergic response and death


- orginally isolated from the fungus Cephalosporium

- structually and functionally similar to penicillins

- broad-spectrum antibiotics that can be used by most patients that are allergic to penicillins

the 4 categories of cephalosporins (based on their spectrum of activity)

1. cephalothin

2. cefoxitin

3. cefoperazone

4. ceftriaxone


- glycopeptide antibiotic

- inhibit cell wall synthesis

- binds to the D-alanyl-D-alanine terminal sequence of peptidoglycan


- glycopeptide antibiotics

- inhibit cell wall synthesis

protein synthesis inhibitors

- many antibiotics bind specifically to the bacterial ribosome

> binding can be to the 30S (small) or 50S (large) ribosomal subunit

- other antibiotics inhibit a step in protein synthesis

> aminoacyl-tRNA binding, peptide bond formation, mRNA reading, translocation

aminoglycoside antibiotics

- large group all with a cyclohexane ring and amino sugars

- bactericidal

aminoglycoside antibiotic mechanism

1. bind to the 30S ribosomal subunit

2. the ribosome incorportates the incorrect amino acids

3. the protein cannot fold correctly

tetracyclines: structure

all have a 4 ring structure to which a variety of side chains are attached


- broad-spectrum

- bacteriostatic

- sometimes used to treat acne

tetracyclines: mechanism

1. combine with the 30S ribosomal subunit

2. inhibits binding of aminoacyl-tRNA molecules to the A site of the ribosome


contain 12- to 22-carbon lactone rings linked to one or more sugars

macrolides (e.g Erythromycin)

- broad-spectrum

- usually bacteriostatic

- used for patients allergic to penicillin

macrolides (e.g Erythromycin): mechanism

1. binds to the 23S rRNA of the 50S ribosomal subunit

2. inhibits peptide chain elongation

how is the mechanism by which aminoglycosides block synthesis similar to that of the tetracyclines?

(3 ways)

1. both act on the 30S subunit

2. aminoglycosides cause tRNA mismatching

3. tetracyclines block tRNA entry

lincosamines: mechanism

interferes with protein synthesis in microbes

lincosamines are produced by

the Streptomyces bacteria

lincosamines antibiotic activity

- broad-spectrum against anaerobic microbes

- less activity against aerobes

why are lincosamines used sparingly

they can support (indirectly) the growth of C. diff which can result in other disease states

chloramphenicol was originally isolated from

Streptomyces venezuelae but is now chemically synthesized

chloramphenicol: mechanism

1. binds to 23S rRNA on the 50S ribosomal subunit

2. inhibits peptidyl transferase reaction

when is chloramphenicol used and why

only used in life-threatening situations because it is seriously toxic and has numerous side effects

metabolic antagonists act as


- antagonize or block the functioning of metabolic pathways by competitively inhibiting the use of metabolites by key enzymes

metabolic antagonists are

structural analogs

- molecules that are structurally similar to, and compete with, naturally occurring metabolic intermediates

- block normal cellular metabolism

sulfonamides or sulfa drugs: structure

- structurally related to sulfanilamide, a p-aminobenzoic acid (PABA) analog

> PABA is used for the synthesis of folic acid and is made by many pathogens

sulfa drugs are

selectively toxic due to the competitive inhibition of folic acid synthesis enzymes

trimethoprim is a

synthetic antibiotic that interferes with folic acid production

antibiotic activity of trimethoprim

- broad-spectrum

trimethoprim can be combined with

sulfa drugs

- to increase the efficacy of the treatment

- the combination blocks 2 steps in the folic acid pathway

side effects of trimethoprim

1. abdominal pain

2. photo sensitivity reactions

nucleic acid synthesis inhibition: mechanisms

1. block DNA replication

- inhibition of DNA polymerase

- inhibition of DNA helicase

2. block transcription

- inhibition of RNA polymerase

nucleic acid synthesis inhibition

drugs not as selectively toxic as other antibiotics because bacteria and eukaryotes do not differ greatly in the way they synthesis nucelic acids


- broad-spectrum, bactericidal, synthetic drugs containing the 4-quinolone ring

quinolones: mechanism

act by inhibiting bacterial DNA-gyrase and topoisomerase II

antifungal drugs

- fewer effective agents because of similarity of eukaryotic fungal cells and human cells

> many have a low therapeutic index and are toxic

- fungi are able to degrade many compounds including drugs

- it is easier to treat superficial mycoses than systemic infections

treating superficial mycoses (ex. Candida, atheletes foot)

- topical and oral

- mechanisms:

1. disrupts membrane permeability and inhibit sterol synthesis

2. disrupts mitotic spindle; may inhibit protein and DNA synthesis

treating systemic mycoses

- difficult to control and can be fatal

- 3 common drugs:

1. amphotericin B

> binds sterols in membrane

2. 5-flucytosine

> disrupts RNA functions

3. fluconazole

treating mycoses: amphotericin B

1. binds to ergosterol and damages membranes

2. administered orally

3. stays in suspension

4. poorly absorbed

5. stable in GI tract

6. for GI tract infections

treating mycoses: nystatin

1. binds to ergosterol and damages membranes

2. administered IV

3. serious side effects

4. for systemic infections

antiviral drugs: drug development

- drug development has been slow because it is difficult to specifically target viral replication

- drugs currently used inhibit virus-specific enzymes and life cycle processes

antiviral drugs: amantidine

- used to prevent influenza infections

- blocks penetration and uncoating of influenza virus

antiviral drugs: adenine arabinoside (vidarabine)

- inhibits herpes virus enzymes involved in DNA and RNA synthesis and function

antiviral drugs: tamiflu

- anti-influenza agent

- a neuraminidase inhibitor

> essential for release of new particles from infected cell

- not a cure

- leads to resistant viruses

- prescribed prophylactically

anti-HIV drugs: azidothymidine (AZT)

nucleoside reverse transcriptase inhibitors

anti-HIV drugs: ritonavir

- viral protease inhibitor

> mimic peptide bond that is normally attacked by the protease

anti-HIV drugs: fusion inhibitors

prevent HIV entry into the cell

most effective HIV drugs

drug cocktails to curtail resistance

1. infection begins with HIV fusion

fusion inhibitors block this step

2. once inside a host cell, HIV uncoats and its reverse transcriptase forces the host to make DNA from the viral RNA

RT inhibitors block this step

3. the viral DNA is transcribed and translated into a linear polypeptide that is cut to release viral proteins

protease inhibitors block this step

4. viral DNA is added to the host DNA by the action of a viral integrase

integrase inhibitors block this step

why is malaria, like AIDS, now treated with several drugs simultaneously?

many strains of the malaria parasite are resistant to drugs that used to be effective. Now single drugs are no longer effective. Furthermore, the use of multiple drugs require multiple mutations to occur simultaneously which is hoped to reduce the chance of resistance of occurring again

antiprotozoan drugs: mechanism

the mechanism of antiprotozoan drugs is not known

what special considerations must to taken into account when treating infections caused by protozoan parasites?

protozoan parasites are geographically endemic, and each variety may need it's own drug

ability of a drug to reach the site of infection depends on:

mode of administration: oral, topical, or parenteral (non oral)

factors influencing the ability of a drug to reach concentrations exceeding the MIC

1. amount administered

2. route of administration

3. speed of uptake

4. rate of clearance (elimination) from the body

drugs resistance is an increasing problem because...

1. once resistance originates in a population, it can be transmitted to other bacteria

2. a particular type of resistance mechanism is not confirmed to a single class of drugs

drug resistance mutants arise...

spontaneously and are then selected

microbes in ______ or ______ may be growing ______ and not be _______

abscesses, biofilms, slowly, susceptible

development of a resistant strain of bacteria

1. a population of microbial cells that contains both drug-sensitive cells and drug-resistant cells is exposed to the drug

2. drug-sensitive cells are inhibited by the exposure to the drug

3. the remaining drug-resistant cells grow over time

4. resulting in a population of (mostly) drug-resistant cells

overcoming drug resistance

1. give drug in appropriate concentrations to destroy susceptible

2. give 2 or more drugs at the same time

3. use drugs only when necessary