Antibacterial agents, also known as antibiotics, are used to inhibit or kill bacteria. They are classified based on their chemical origin and biological activity. Antibiotics work by interfering with bacterial cell wall synthesis, protein synthesis, nucleic acid synthesis, or folic acid synthesis. Common mechanisms of action include inhibiting bacterial transpeptidases, binding to the bacterial ribosome, inhibiting DNA gyrase or RNA polymerase, and blocking enzymes involved in folic acid synthesis. However, bacteria can develop resistance through mutations or other changes that prevent antibiotics from working effectively. Potential side effects depend on the specific antibiotic but may include kidney or liver toxicity, hearing loss, or gastrointestinal issues.

1. ANTIMICROBIAL AGENTS
I AM
ANTIBACTERIA..
I AMBACTERIA
…PLZ SPARE
ME….
BY: Mohsin shah
Demonstrater
Khyber Medical
University

8. What are antibacterial agents?
An antibacterial is an agent that inhibits bacterial growth or kills
bacteria.
often usedsynonymously withthe term antibiotic(s).
Theterm antibiotic wasfirst usedin 1942 by SelmanWaksman.

9. WHY ANTIBACTERIALS?
Bacterial Leaf Blight of
soybeanis caused by the
bacterium Psuedomonas
syringae
Bacterial
Canker
Bacterial conjuctivities: pink eye Skinspots by bacterial activities

10. HOW ARE THEYCLASSIFIED?
on the basisof chemical/biosynthetic origininto
Natural (ex- penicillin)
 semisynthetic
 synthetic(ex-Sulfanilamide)
On biological activity; according to their biological effecton
microorganisms:
 bactericidal agents kill bacteria,
and bacteriostatic agents slow down or stall bacterialgrowth.

11. The bacterial cell
Thesuccessof antibacterial agentsowes much to the fact thatthey canact
selectively
against bacterial cells rather than animalcells.
 Thisis largely due to the factthat
bacterial cells and animal cells differ both in their structure and in the biosynthetic
pathways which proceed insidethem.

12. WHERE THEY WORK
Rifamycins
Cellwall
Penicillins
Cephalosporins
cycloserine
polymyxins
sulfonamides
Chloramphenicol
Streptomycin
tetracyclines
Ribosomes
capsule
cytoplasm

13. MECHANISM OF ACTIONS
Inhibition of
cell wall
synthesis
Inhibition of
bacterial
protein
synthesis
Inhibition
of Nucleic
Acid
Synthesis
Inhibition
of Folic
Acid
Synthesis
Penicillins
Cephalosphori
ns
Imipenem
Meropenem
Aztreonam
vancomycin
Aminoglycosid
es
Chlorampheni
col
Macrolides
Tetracycline
Streptogrmins
linezolid
Fluoroquinolon
es
Rifampin
Sulfonamide
s
Trimethoprim
Pyrimethami
ne

14. 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:
Penicilli
n
cephalosporin
Penicillinases: break
the beta lactam ring
structure (
staphylococci)
Structuralchangesin PBP’s
(MRSA), S. pneumococci
Change in porin
structure: concerns the
gram negative
organism

16. Inhibition of bacterial protein synthesis
Aminoglycosides,Chloramphenicol,Macrolides,Tetracycline,Streptogrmins, Linezolid.
Bactericidal and bacteriostatic.
 Theprimary steps in the processthat 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

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

18. Streptomyc
in
Mechanisms of resistance:
amutation of ribosomal
binding site
enzymatic modification of
antibiotic
an active efflux of antibiotic
out of cell

19. 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

20. Quinolones are akeygroup of antibiotics that interfere with DNAsynthesis by
inhibiting topoisomerase, most frequently topoisomerase Iv and topoisomer ii (DNA
gyrase) , an enzyme involved in DNAreplication. DNAgyrase relaxes supercoiled
DNAmolecules and initiates transient breakagesand rejoins phosphodiester bonds
in superhelical turns of closed-circular DNA.Thisallows the DNAstrand to be
replicated by DNAor RNApolymerases.

21. Rifampicin blocks initiation of RNAsynthesis by specifically inhibiting
bacterial RNApolymerase. 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

22. 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.
Folicacid

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

24. SomeSideaffects 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)