Presented by: Under the guidence of:
Mohd Muztaba Dr .Anuradha Mishra
M.Pharm 1st year
These are a group of natural and semisynthetic antibiotics
having polybasic amino groups linked glycosidically to two or
more aminosugar (strephdine2-deoxy streptamine garosamine)
Unlike penicilline which was a chance discovery
aminoglycosides are products of deliberate search for drugs
effective against gram-negative bacteria.
All aminoglycosides are produced by soil actinomycetes
MECHANISM OF ACTION
The aminoglycosides are bactericidal antibiotic
Transport of the aminoglycosides through bacterial cell wall &
cytoplasmic membrane (diffusion-outer coat-Gm –ve via porin
Irreversibly Binding to ribosomes (mostly 30s and 50s,30s
&50s interface) resulting in inhibition of protein synthesis.
MECHANISM OF RESISTANCE
Production of a transferase enzyme or enzymes inactivates the
aminoglycoside by acetylation, or phosphorylation. This is
the principal type of resistance encountered clinically
There is impaired entry of aminoglycoside into the cell. This
may be genotypic, resulting from mutation or deletion of a
proteins involved in transport and maintenance of the
electrochemical gradient; or phenotypic, eg, resulting from
growth conditions under which the oxygen-dependent
transport process described above is not functional
The receptor protein on the 30S ribosomal subunit may be
deleted or altered as a result of a mutation.
CONTRAINDICATIONS : hypersensitivity to aminoglycosides
DRUG INTERACTION :
• Inactivated by penicillins and cephalosporins when
coadministered to pateints with renal insufficiency.
• Increased incidence of ototoxicity with loop diuretics.
• Increased incidence of nephrotoxicity with other nephrotoxic
SIDE EFFECTS : nausea,vomiting,urticaria,muscles
ADVERSE EFFECTS: vertigo,myocarditis,thrombocytopenia,
leukemia,hepatic necrosis,muscle paralysis, etc.
TOXICITY : ototoxicity,nephrotoxicity
• It is older antibiotics and obtained by Streptomyces griseus,
used in past but now used for treatment of TB
• Inhibit initiation of translation by binding to 16s rRNA.
MECHANISM OF RESISTANCE
• Mutations in (16sRNA) or (ribosomal protein) which produce
alterations in the streptomycin binding site
• Partial or unidirectional cross resistance occur.
• Neither absorbed nor destroyed in git.
• Absorption from injection site in muscle is rapid.
• Distributed extracellularly, volume of distribution 0.3 L/kg
• It is not metabolized. Excreted unchanged in urine
• Plasma half life is 2-4 hrs
• Vestibular disturbances, auditory disturbances
• Hypersensitivity are rare-rashes, eosinophilia, dermatitis
• Pain at injection site
CONTRAINDICATION: pregnancy causes foetal
DOSE: Tb – 1g or 0.75 g i.m OD or thrice weekly for
Acute infection: 1g i.m OD or BD for 7-10 days
USES: TB, given with
pencillin/ampicillin/vancomycin for 4-6 weeks
• Plague: rapid cure within 7-12 days
• Tularemia: Streptomycin cures it in 7-10 days
Gentamicin is an aminoglycoside isolated from
Micromonospora purpurea . It is effective against both gram-
positive and gram-negative organisms
Gentamicin sulfate inhibits in vitro many strains of
staphylococci and coliforms and other gram-negative bacteria.
gentamicin in combination with vancomycin or a penicilline
produces a potent bactericidal effect, which in part is due to
enhanced uptake of drug that occurs with inhibition of cell wall
Resistance to gentamicin rapidly emerges in staphylococci
during monotherapy owing to selection of permeability
mutants. Ribosomal resistance is rare. Among gram-negative
bacteria, resistance is most commonly due to plasmid-encoded
Gram-negative bacteria that are gentamicin-resistant usually
are susceptible to amikacin, which is much more resistant to
modifying enzyme activity.
It is a semisynthetic aminoglycoside
It is effective against several gram negative organism
It is bactericidal effect Amikacin in highly effective against
decreased uptake and/or accumulation of the drug in bacteria
the bacterial expression of enzymes which modify the
antibiotic and thereby inactivate it
• Rt i
• Bone and joint infection
• Skin and soft tissue infection
Amphoterecin b may leads to increase nephrotoxicity and
reduce the clearance of amikacin when use in together
Increse risk of ototoxicity with potent diuretics
NEOMYCIN & KANAMYCIN
wide spectrum active against Gm-ve bacilli and some gm+ve
cocci and obtained from Streptomyces.fradiae
Antimicrobial Activity & Resistance
Drugs of the neomycin group are active against gram-positive
and gram-negative bacteria and some mycobacteria.and
streptococci are generally resistant. Mechanisms of
antibacterial action and resistance are the same as with other
The widespread use of these drugs in bowel preparation for
elective surgery has resulted in the selection of resistant
organisms and some outbreaks of enterocolitis in hospitals.
Cross-resistance between kanamycin and neomycin is
USES:Topically used in skin, eye and external ear
infections combined with bacitracin or polymyxin-B to
widen antibacterial spectrum and to prevent emergence of
Preparation of bowel before surgery 1 gm TDS
Applied topically neomycin has low sensitizing potential
However, rashes do occur.
Oral neomycin has a damaging effect on intestinal villi-
prolonged treatment can induce malabsorption syndrome with
It can decrease the absorption of digoxin and many other
drugs, as well as bile acids.
it is very similar to neomycin. It is too toxic for systemic
administration and is used topically on skin, eye, ear in the
same manner as neomycin.