Antibacterial agents

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All about Antibiotics and how their action!!

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Antibacterial agents

  1. 1. ANTIBACTERIAL AGENTS I AM ANTIBACTERIA.. I AM BACTERIA …PLZ SPARE ME…. BY: MINHAZ AHMED Intgrated M.Sc 4th sem BBI11014
  2. 2. What are antibacterial agents? An antibacterial is an agent that inhibits bacterial growth or kills bacteria. often used synonymously with the term antibiotic(s). The term antibiotic was first used in 1942 by Selman Waksman.
  3. 3. WHY ANTIBACTERIALS? Bacterial conjuctivities: pink eye Bacterial Leaf Blight of soybean is caused by the bacterium Psuedomonas syringae Skin spots by bacterial activities Bacterial Canker
  4. 4. HOW ARE THEY CLASSIFIED? on the basis of chemical/biosynthetic origin into Natural (ex- penicillin)  semisynthetic  synthetic(ex-Sulfanilamide) On biological activity; according to their biological effect on microorganisms:  bactericidal agents kill bacteria, and bacteriostatic agents slow down or stall bacterial growth.
  5. 5. The bacterial cell The success of antibacterial agents owes much to the fact that they can act selectively against bacterial cells rather than animal cells.  This is largely due to the fact that bacterial cells and animal cells differ both in their structure and in the biosynthetic pathways which proceed inside them.
  6. 6. WHERE THEY WORK? Rifamycins Penicillins Cephalosporins cycloserine capsule Cell wall cytoplasm polymyxins sulfonamides Chloramphenicol Streptomycin tetracyclines Ribosomes
  7. 7. MECHANISM OF ACTIONS Inhibition of cell wall synthesis Penicillins Cephalosphorins Imipenem Meropenem Aztreonam vancomycin Inhibition of bacterial protein synthesis Aminoglycosides Chloramphenicol Macrolides Tetracycline Streptogrmins linezolid Inhibition of Nucleic Acid Synthesis Fluoroquinolones Rifampin Inhibition of Folic Acid Synthesis Sulfonamides Trimethoprim Pyrimethamine
  8. 8. Inhibition of cell wall synthesis: Penicillins, cephalosphorins, imipenem, meropenem, aztreonam, vancomycin bacteriocidal Must have beta-lactum ring in them which binds and blocks transpeptidases known as penicillin-binding proteins(PBP) which causes the final cross links between the pentapeptides of peptidoglycan layer. Mechanism of resistance: Penicillin Penicillinases: break the beta lactam ring structure ( staphylococci) Structural changes in PBP’s (MRSA), S. pneumococci cephalosporin Change in porin structure: concerns the gram negative organism
  9. 9. Inhibition of bacterial protein synthesis Aminoglycosides,Chloramphenicol,Macrolides,Tetracycline,Streptogrmins, Linezolid. Bactericidal and bacteriostatic.  The primary steps in the process that are attacked are  the formation of the 30S initiation complex (made up of mRNA, the 30S ribosomal subunit and formyl-methionyl-transfer RNA),ex Streptomycin (A-glycosides)  the formation of the 70S ribosome by the 30S initiation complex and the 50S ribosome,ex Kanamycin and tobramycin and  the elongation process of assembling amino acids into a polypeptide.ex Lincomycin, chloramphenicol. RIBOSOME
  10. 10. Erythromycin: Binds to 50S-rRNA & prevents movement along mrna
  11. 11. Mechanisms of resistance: a mutation of ribosomal binding site enzymatic modification of antibiotic an active efflux of antibiotic out of cell Streptomycin
  12. 12. Inhibition of Nucleic Acid Synthesis Fluoroquinolones(levofloxacin, norfloxacin),Rifampin Bacteriocidal Can inhibit DNA gyrase or RNA polymerase Mechanism of resistance: an alteration of alpha subunit of DNA gyrase (chromosomal) beta subunit of RNA polymerase (chromosomal) is altered
  13. 13. Quinolones are a key group of antibiotics that interfere with DNA synthesis by inhibiting topoisomerase, most frequently topoisomerase Iv and topoisomer ii (DNA gyrase) , an enzyme involved in DNA replication. DNA gyrase relaxes supercoiled DNA molecules and initiates transient breakages and rejoins phosphodiester bonds in superhelical turns of closed-circular DNA. This allows the DNA strand to be replicated by DNA or RNA polymerases.
  14. 14. Rifampicin blocks initiation of RNA synthesis by specifically inhibiting bacterial RNA polymerase. It does not interact with mammalian RNA polymerases, making it specific for Gram-positive bacteria and some Gram-negative bacteria. Mechanism of resistance: an alteration of alpha subunit of DNA gyrase (chromosomal) beta subunit of RNA polymerase (chromosomal) is altered
  15. 15. Inhibition of Folic Acid Synthesis Sulfonamides, Trimethoprim, Pyrimethamine Bacteriostatic Binds and blocks enzymes mainly pteridine synthesase, dihydrofolate reductase responsible for folic acid synthesis. What are Folic Acid? Folic acid enzymes are nessary for the synthesis of amino acids, hence necessary for bacterial protein synthesis. Folic acid
  16. 16. Sulfonamide functional group trimethoprim Pyrimethamine Pyrimethamine Mechanism of resistance: Mutations in the gene for dihydrofolate reductase decreasing binding affinity .
  17. 17. Some Side affects of antibacterial agents ANTIBACTERIAL AGENTS SIDE EFFECTS Aminoglycosides renal (kidney) toxicity, ototoxicity (hearing loss), dizziness, nausea/vomiting, nystagmus Sulfonamides nausea/vomiting, diarrhea, anorexia, abdominal pain, rash, photosensitivity, headache, dizziness Tetracyclines nausea/vomiting, diarrhea, anorexia, abdominal pain, tooth discoloration in children < 8 years, liver toxicity Quinolones nausea/vomiting, diarrhea, abdominal pain, headache, lethargy, insomnia, photosensitivity (can be severe)

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