Antibacterial agents work by inhibiting bacterial cell growth or killing bacteria. They are classified based on their chemical origin and biological activity. They act on specific targets in the bacterial cell like the cell wall, ribosomes, or nucleic acids. Common mechanisms of action include inhibiting cell wall synthesis, bacterial protein synthesis, nucleic acid synthesis, or folic acid synthesis. Bacteria can develop resistance through mutations that prevent antibiotic binding or allow drug efflux. Side effects vary between classes but can include kidney toxicity, hearing loss, and gastrointestinal issues.

1. ANTIBACTERIAL AGENTS

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. 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.

4. 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.

5. WHERE THEY WORK?
Rifamycins
Cell wall
Penicillins
Cephalosporins
cycloserine
polymyxins
sulfonamides
Chloramphenicol
Streptomycin
tetracyclines
Ribosomes
capsule
cytoplasm

6. MECHANISM OF ACTIONS
Inhibition of cell
wall synthesis
Inhibition of
bacterial protein
synthesis
Inhibition of
Nucleic Acid
Synthesis
Inhibition of
Folic Acid
Synthesis
Penicillins
Cephalosphorins
Imipenem
Meropenem
Aztreonam
vancomycin
Aminoglycosides
Chloramphenicol
Macrolides
Tetracycline
Streptogrmins
linezolid
Fluoroquinolones
Rifampin
Sulfonamides
Trimethoprim
Pyrimethamine

7. 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
cephalosporin
Penicillinases: break the
beta lactam ring structure (
staphylococci)
Structural changes in PBP’s
(MRSA), S. pneumococci
Change in porin structure:
concerns the gram negative
organism

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. Erythromycin:
Binds to 50S-rRNA &
prevents movement
along mrna

11. Streptomycin
Mechanisms of resistance:
a mutation of ribosomal
binding site
enzymatic modification of
antibiotic
an active efflux of antibiotic
out of cell

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. 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. 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. 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. Sulfonamide functional group
trimethoprim
Pyrimethamine
Pyrimethamine
Mechanism of resistance:
Mutations in the gene for
dihydrofolate reductase
decreasing binding affinity .

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)