BACTERIOSTATIC AGENTS
■ are antimicrobial agents that inhibit bacterial
growth but generally do not kill the organism.
EX. Chloramphenicol, dapsone, erythromycin,
clindamycin, isoniazid, rifampicin, sulfonamides and
tetracyclines
BACTERIOCIDAL AGENTS
■ are antimicrobial agents that usually kill
organisms; used for life threatening infections.
EX. Aminoglycosides (gentamicin, amikacin and
streptomycin), beta-lactams (ceftriazone, imepenem,
penicillin and cefotaxime), glycopeptides (vancomycin),
isoniazid, quinolones, bacitracin and metronidazole.
For antimicrobial agents to successfully inhibit or kill
the infecting microorganisms:
1. The antimicrobial agent must be in an active form.
- It is ensured through the pharmacodynamics
design of the drug.
2. The antibiotic must be able to achieve sufficient
concentration at the site of infection and it should be
higher than the pathogen’s MIC to be effective.
3. The antimicrobial must have selective toxicity.
Antimicrobial actions:
1. Inhibiting cell wall synthesis.
2. Inhibiting protein synthesis.
3. Inhibiting nucleic acid synthesis.
4. Destroying the cell membrane.
5. Inhibiting essential metabolites.
A. CELL WALL INHIBITORS
■ the most selective antibiotics with high
therapeutic index.
■ it inhibits transpeptidation enzymes – cell
growth stops and death often follows.
1. Penicillin
2. Cephalosporins
3. Isoniazid
4. Vancomycin
5. Carbenicillin
6. Methicillin
7. Bacitracin
Notes to remember:
 The structure of penicillin resembles the
terminal D-alanyl- D-alanine of the
peptidoglycan subunit.
 ß-lactam antibiotics: Penicillin, Cephalosporins,
Monobactams and carbapenems
 ß-lactam antibiotics differ from each other in
the basic ring structure and moieties attached
to the rings.
 Penicillinase resistant penicillin drugs:
methicillin, nafcillin and ocacillin
B. PROTEIN SYNTHESIS INHIBITOR
 Binds with 30s subunit resulting to misreading
of mRNA and interferes with aminoacyl-tRNA
binding (aminoglycosides, tetracycline)
 Binds with 50s subunits resulting to inhibition of
peptidyl transferase and inhibits peptide chain
elongation (clindamycin and erythromycin)
1. Drugs which bind to the 50s ribosomal unit:
chloramphenicol, erythromycin, lincomycin and
lindamycin
2. Drugs which to the 30s ribosomal unit:
tetracyclines, spectinomycin and minoglycosides
3. Blocks the initial step in protein synthesis -
linezolid
Notes to remember:
 Protein biosynthesis requires the sequential
binding of the 30s and 50s ribosomal subunits
to mRNA leading to translocation of the genetic
message.
 Chloramphenicol may cause temporary or
permanent depression of bone marrow leading
to aplastic anemia and leukopenia (toxic side
effect)
 Chloramphenicol and erythromycin bind to 23s
rRNA on the 50s ribosomal unit.
 High dosage of tetracycline may lead to liver
and kidney damage and yellowing of the teeth
of children.
 Aminoglycosides – gentamicin, kanamycin,
neomycin, streptomycin and tobramycin; they
have cyclohexane ring and may cause deafness
and loss of balance
 Binding of aminoglycosides to the A-binding site
on the 30s subunit prevents the attachment of
aminoacyl-tRNA resulting in mistranslation and
subsequent production of aberrant proteins.
 Tetracyclines reversibly inhibit protein synthesis
by premature release of tRNA and termination
of peptide bond formation.
 Macrolide antibiotics – erythromycin,
clindamycin and azithromycin; prevent
assembly of the 50s ribosomal subunit and
peptide chain elongation.
C. NUCLEIC ACID SYNTHESIS INHIBITORS 6. Gentamycin –Micromonosporum
1. Rifampicin – inhibits RNA polymerase B subunit purpura
synthesis 7. Netilmicin - Micromonosporum
2. Quinolones (ciprofloxacin, norfloxacin, inyoensis
levoflaxin) – interfere with DNA gyrase and 8. Spectinomycin
topoisomerase IV; highly effective for enteric
bacteria like E.coli.
3. Metronidazole – disruption of DNA; effective
against anaerobic bacteria.

D. CELL MEMBRANE INHIBITORS

1. POLYMYXIN B – Used for Gram-negative
bacteria (P.aeruginosa)
2. POLYMYXIN E – antibiotic ointments

E. ESSENTIAL METABOLITE INHIBITORS

1. Sulfamethoxazole (SMZ) – inhibits folic acid
metabolism
2. Trimethoprim (TMP) – blocks tetrahydrofolate C. Lincosamides (50s)
synthesis. 1. Lincomycin
3. Dapsone – interferes with synthesis of folic acid. 2. Clindamycin
4. Isoniazid – inhibits synthesis of cord factor D. Chloramphenicol
(mycolic acid) E. Macrolides –Erythromycin, Clarithromycin,
Azithromycin, Dirithromycin
INHIBITS DNA SYNTHESIS F. Fusidic acid
A. Quinolones
INHIBITS CELL WALL SYNTHESIS
• Nalidixic acid
A. Beta Lactam Penicillin
• Fluoroquinolones – Enoxacin, ofloxacin,
1. Natural penicillin
ciprofloxacin, norfloxacin, moxifloxacin,
2. Penicillinase resistant penicillim
galifloxacin
3. Extended Spectrum penicillin
B. Rifampicin
Cephalosporin
C. Sulfonamides
1. 1st gen
D. Trimethoprim
2. 2nd gen
INHIBITS CELL MEMBRANE 3. 3rd gen
A. Polyene Antibiotics 4. 4th gen
• Amphotericin B, Nystatin, Candicidin, Carbapenems -Imipenem
Natamycin, Griseofulvin Monobactam – Aztreonam, Tigemonam
B. Polymyxin B. Glycopeptide
C. Imidazoles Vancomycin – Streptomyces orientalis – cause
Red man syndrome
Teicoplanin
C. Bacitracin – Bacillus subtilis
INHIBITS PROTEIN SYNTHESIS
D. Cycloserine
A. Tetracycline (30s) – Tetracycline, Minocyclin,
Demecyclin, Oxytetracycline, Doxcycycline ANTIBIOTIC RESISTANCE
B. Aminoglycoside ( 30s) ■ It is a natural consequence of drug exposure
1. Streptomycin – Streptomyces griseus and results from both the use and overuse of
2. Tobramycin – Streptomyces antimicrobial agents.
tenebrarius ■ It may arose also within antibiotic-producing
3. Neomycin – Streptomyces fradiae microorganisms as a mechanism to protect
4. Kanmycin - Streptomyces them against the action of their own antibiotic
kanamycetius (autotoxicity).
5. Amikacin/Amikin – Kanamycin derived
a. Intrinsic Resistance
 It is natural to all members of a species.
 It is a result of the biochemical makeup of the
wild-type organism.
 It is passed vertically to a new cell.
 It depends on the hydrophobic or hydrophilic
nature of the antibiotic and on impermeability
of the cell wall to the antibiotic.
 It limits the spectrum of antimicrobial activity.
 All Gram-negative bacteria mediate this type of
resistance by enzymatic inactivation of
penicillin.
EX. Resistance to the glycopeptide antibiotic (Gram-
positive bacteria), the presence of porins and LPS
(Gram-negative bacteria), and secretion of ß-lactamases
by bacteria.