Drug acting on cell wall of gram positive bacteria:March 2009
Gentamycin
Ciprofloxacin
Tetracycline
Vancomycin
Ans. D: VancomycinVancomycins bind to the peptides of the peptidoglycan monomers and block both the formation of gycosidic bonds between the sugars by the transgycosidase enzymes and the formation of the peptide cross-links by the transpeptidase enzymes. This results in a weak cell wall and osmotic lysis of the bacterium.The fluoroquinolones (norfloxacin, lomefloxacin, fleroxacin, ciprofloxacin, enoxacin, trovafloxacin, gatifloxacin, etc.) work by inhibiting one or more of a group of enzymes called topoisomerase, enzymes needed for supercoiling, replication and separation of circular bacterial DNA.For example, DNA gyrase is a topoisomerase that catalyzes the negative supercoiling of the circular DNA found in bacteria. Topoisomerase IV, on the other hand, is involved in the relaxation of the supercoiled circular DNA, enabling the separation of the interlinked daughter chromosomes at the end of bacterial DNA replication.In gram-positive bacteria, the main target for fluoroquinolones is DNA gyrase (topoisomerase II), an enzyme responsible for supercoiling of bacterial DNA during DNA replication; in gram-negative bacteria, the primary target is topoisomerase IV, an enzyme responsible for relaxation of supercoiled circular DNA and separation of the inter-linked daughter chromosomes.The tetracyclines (tetracycline, doxycycline, demeclocycline, minocycline, etc.) block bacterial translation by binding reversibly to the 30S subunit and distoing it in such a way that the anticodons of the charged tRNAs cannot align properly with the codons of the mRNA.The aminoglycosides (streptomycin, neomycin, netilmicin, tobramycin, gentamicin, amikacin, etc.) bind irreversibly to the 30S subunit of bacterial ribosomes.