Antibiotic Targets and modes

Antibiotic Targets and modes

1. Act on the Cell Wall

   • relatively inexpensive
   • non-toxic (can be administered in high doses)
   • Penicillin
     • contains bete-Lactam ring.
     • beta-lactam inhibits the cross link between peptidoglycan between NAM and NAG in the bacterial cell wall
       • the bete-lactam ring binds with the enzyme that produces these linkages
         • the enzyme that hydrolises these bonds continue to work making the cell wall weak, the osmotic pressure will continue to rise eventually causing the cell to burst and die
     • Blocks the division of the bacteria
   • usually on gram positive as there is a single cell wall

2. Target Ribosomes

   • targets protein synthesis
     • Streptomycin
       • cannot be administered orally but instead by regular intramuscular injections
       • binds to the 30s subunits of the bacterial ribosome, this misleads the DNA codon eventually causing inhibition of protein synthesis
         • by binding to the 30s subunit it interferes with the 50s subunit whcih associates with mRNA. as a result an unstable mRNA strand is produced meaning the incorect AA acids are coded for and therefore the worn proteing are produced causing cell death
       • can be used on both gran negative and positive making it a broad spectrum antibiotic
       • bacterial ribosomes are different than that of humans meaning that it has specific toxicity

3. Inhibit Nucleic Acid Synthesis

   • Qunilones
     • broad spectrum
     • prevent DNA from unwinding and duplicating
     • targets DNA gyrasa (topoisomerase) which causes the DNA to unwind during DNA replication.
       • used to treat certain infections (UTIs) caused by gram negative bacteria
     • enter cells via pores therefore often used to treat intracellular infections

4. Anti-metabolites

   • Sulfonamides
     • humans require folic acid but the get it through diet and we do not synthesis it therefor this is effective against organismis that rely on folic acid synthesis
       • selective toxicity
     • competitive inhibition of dihydropterate synthetase (DHPS)
       • DHPS catalyses tconversion of PABA to dihydropterate in folate synthesis pathway
         • inhibit the production of folic acid an important metabolite in DNA synthesis therefor cells are unable to divide
   • inhibits the use of a metabolite which is part of normal metabolism
   • can have a toxic effect on cells such as halt growth and cell division (sometimes used in cancer treatments)