Aminoglycosides are a class of antibiotics that include streptomycin, kanamycin, and gentamicin. They work by binding to the 30S ribosomal unit in bacteria and preventing proper protein synthesis. This results in misreading of the genetic code and incorporation of incorrect amino acids into proteins. Aminoglycosides are bactericidal, derived from actinomycetes, and have poor oral absorption so they must be given intravenously or intramuscularly. Common side effects include nephrotoxicity and ototoxicity. Gentamicin and tobramycin are effective against pseudomonas and enterobacteriaceae but can cause nephrotoxicity, while amikacin and sis

2. Aminoglycosides
Tetra cyclines
Macrolids
Chloramphenicol

3.  Structure
Glycosidic
Aminosugar
- O -
Aminocyclitol
2-deoxystreptamine
- O-
Aminosugar
Streptomycin
Streptidine
- O -
Strepose
aminosugar
- O -
N-methyl-Lglucosamine
aminosugar
Streptobiosamine

4. Aminoglycosides Penetrate Bact. Cell Wall To Periplasmic Space
Transport Across Cytoplasmic Membrane
(Oxygen Dependent)
Bind To 30s Ribosomal Units
Prevent Formation of ‘Initiation Complex’
Misreading of Genetic Code on mRNA
Incorrect Amino Acids into Peptide Chain
Inhibits Protein Synthesis

5.  All
derived from an actinomycete or are
semisynthetic derivatives
 Bactericidal
 Are

action
highly polar compounds
GIT poor absorption so IV/IM
 More
active in alkaline pH

6. • STREPTOMYCIN (1944)
• KANAMYCIN (1957 )
• GENTAMICIN (1964)
• AMIKACIN
• SISOMICIN
• NEOMYCIN
• NEITILMICIN
• FRAMYCETIN
• TOBRAMYCIN 1967

7.  Suffix-“Mycin”-
Streptomyces
 “Micin’-Micromonospora

8.  Half
life 1-3hr.
 Concentration
 Single
depended killing
daily dose result in higher tissue
concentration
 Interval
8-12hr

9. 1. Plasmid Mediated Bacterial Transferase
Enzymes
2. Deletion of Porin Channels
3. Alteration of Receptor Protein on 30s
Ribosomal Unit

10. • Very Poor Oral Bioavailability
• Poor Distribution
• Do Not Cross BBB
• Excreted Through Kidney
• Excretion is directly proportion to creatine
clearence

11. • AEROBIC G-ve BACILLI
• ENTEROBACTERIACEAE
• NOT EFFECTIVE AGAINST :
G +ve BACILLI
G –ve COCCI
ANAEROBES

12. OTOTOXICITY:AG causes impairment of 8th cranial nerve.,
accumulate in the endolymph and perilymph of
the inner ear leading to vestibular and cochlear
damage.
• Irrversible
NEUROMUSCULAR BLOCKADE

13. NEPHROTOXICITY
Inhibition of intracellular Phospholipase A2 in renal
brush border
Leads to lysosomal distension ,rapture
Release acid hydrolases & AG
Free drug binds to other cellular organelles
Leading to degeneration and necrosis

14. 
Spectrum :
Y. Pestis, Brucella, F.Tularensis, M.Tuberculosis


TOXICITY : Vestibular > Auditory
Lowest Nephrotoxicity
USES :
•
•
•
•
Tuberculosis
SABE
Plague
Tularemia & Brucellosis

15. 


Spectrum :
Pseudomonas, Proteus, E. Coli, Klebsiella, Enterobacteria &
Seretia.
TOXICITY :
More Nephrotoxic
USES :
• Respiratory Infection in Critically Ill Pt.
• Pelvic Infection
• SABE
• UTIs
• Pseudomonal Infections
• Infected Wounds, Burns, & Conjunctivitis

16. 
Clinically & PK similar to Gentamicin

Susceptible to Aminoglycoside Inactivating
Enzymes

Used Interchangeably with Gentamicin

17. 
Semi synthetic Derivative of SISOMYCIN

Resistant to Inactivating Enzymes

Lesser Ototoxicity

Used in Gentamicin Resistant Infections

18. 
Identical To Gentamicin

2-4 times More Active Against Pseudomonas &
Proteus

Ototoxicity & Nephrotoxicity < Gentamicin

Reserve Alternative to ‘G’

19. 
RESISTANT TO BACTERIAL ENZYMES

USED against Gentamicin & Tobramycin
Resistant Infections

USES:
• Multi drug Resistant TB
• Hospital Acquired Infections

Hearing loss > Vestibular loss

20. 
HIGHLY TOXIC

UESE
• Infected Wounds, Ulcers, Burn
• External Ear & Eye Infections
• Preoperative Intestinal Antiseptic
• Hepatic Coma