Antimicrobial Drugs

Chapter 20

 

 

 

History of Chemotherapy

u  Chemotherapy

 

u  Antimicrobial drugs

–  Selective toxicity

 

u  Alexander Fleming (1929)

–  Penicillin

 

u  Antibiotic

 

–  Produced by

u Molds

–  Penicillium and Cephalosporium

u Bacteria

–  Streptomyces and Bacillus

 

 

 

Spectrum of Antimicrobial Activity

u  Broad spectrum vs. narrow spectrum

 

u Tetracyline vs. penicillin

 

u Disadvantage of broad spectrum

–  Superinfection
u Ex. Candida albicans

 

 

 

Major Modes of Action
(Fig 20.2)

 

 

 

Antimicrobial Action

u  Inhibition of peptidoglycan synthesis

–   No peptidoglycan

–   Weak cell wall

u Cell lysis

–  Only actively growing cells

–  Selectively toxic

–  Example:

u  Penicillin

 

 

 

 

Antimicrobial Action

u  Inhibition of protein synthesis

–  Selective toxicityΰdifference in ribosomes

u Bacteria= 70S ribosome (50S and 30S portions)

u Ribosomes are key players in protein synthesis

u Chloramphenicol (bacteriostatic and broad spectrum)

–  50S portion
–  Inhibits formation of peptide bonds

u Tetracycline (bacteriostatic and broad spectrum)

–  30S portion
–  Interference with attachment of tRNA, which carries aa

u Streptomycin (bacteriocidal and broad spectrum)

–  30S portion
–  Changes shape of 30S portion and genetic code read wrong

u Erythromycin (bacteriostatic and Gram + only)

–  50S portion
–  Prevents translocation

 

 

 

 

Antimicrobial Action

u  Injury to plasma membrane

–  Changes cell permeability

–  Loss of metabolites or cell bursting

–  EX) polymyxin B (Neosporin) attaches to phospholipids (bacteriocidal and Gram neg.)

–  EX) amphotericin B combines with sterols in fungal membranes (Fungicidal)

u Targets ergosterol—a sterol specific to fungi

u Can be toxic to kidney cells of humans, however

u Administered in liposomes

u  Inhibition of nucleic acid synthesis

–  More difficult to find b/c of lack of selective toxicity

–  EX) Rifampin inhibits mRNA synthesis (bacteriocidal and Mycobacterium tuberculosis)

 

 

 

Antimicrobial Action

u  Inhibition of synthesis of essential metabolites

–  Essential enzymes are competitively inhibited

–  EX)sulfanilamide (bacteriostatic and broad spectrum)

u Microbes normally produce folic acid from a para-aminobenzoic acid (PABA) substrate and an enzyme

u When sulfanilamide is present the enzyme binds to it instead

u Humans get folic acid from food

 

 

 

 

 

 

 

 

 

Mechanisms of Drug Resistance

u  Destruction or inactivation of antibiotic

–  Production of an acid perhaps

u  Some organisms can prevent some drugs from penetrating them

–  Gram negative’s have this ability with some antibiotics

u  Alteration of target site

–  Some cells can alter their structures so antibiotics won’t work on them

u  Rapid efflux

–  Some cells have systems for pumping the antibiotic back out of the cell

 

 

 

Resistance

u    Resistance is usually hereditary

u    Can also be passed via horizontal gene transfer

–   Plasmids* and conjugation

u    Replacement of sensitive bacteria in a population by resistant bacteria*

u    Misuse of antibiotics can lead to increased resistance

–   Lack of prescriptions

–   Improper use (headaches and viruses)

u CDC estimates percentage of wrong prescriptions

–  30% ear infections, 50% sore throats, 100% colds

–   Weak forms select for resistant bacteria

–   Not taken long enough

–   Use to promote animal growth

u Animal feed supplements

 

 

 

 

 

Drug Combinations

u  In case the organism is resistant to one drug why not use two at same time

u  Synergism:  drug assistance

–  EX) penicillin and Streptomycin for bacterial endocarditis

u Penicillin disrupts cell wall and Streptomycin gets in faster

u  Antagonism:  One drug makes other ineffective

–  EX) penicillin and Tetracycline

u Tet interferes with Penicillin

 

 

 

Chemotherapeutic Future

u  Modify existing drugs

–  Extend spectrum

–  Prevent resistance

u  New targets of activity

u  Antibiotics from plants or animals

–  EX)magainin from frogs or cecropin from moths

u  Triplex agents

–  DNA that will selectively bind to site on DNA or mRNA where pathogenic protein is coded and prevent the production of the pathogenic protein

–  Prevent production rather than destroy product

–  Problem with penetration