Inj.

Acigent Vet

Drug Class: Antibiotic

Manufacturer: ACI Limited

Basic information

Generic Drug

Route of Administration

IM/IV

Strength / Concentration

100 mg/ml

Presentation and price

10 ml vial

45 Taka

100 ml vial

400 Taka

Dose and dosage

Sheep

1st Day: 1 ml/25 kg body weight q12 hours

From 2nd day: 1 ml/25 kg body weight q24 hours

Goat

1st Day: 1 ml/25 kg body weight q12 hours

From 2nd day: 1 ml/25 kg body weight q24 hours

Cattle

1st Day: 1 ml/25 kg body weight q12 hours

From 2nd day: 1 ml/25 kg body weight q24 hours

Horse

1st Day: 1 ml/25 kg body weight q12 hours

From 2nd day: 1 ml/25 kg body weight q24 hours


Applications: Pneumonia, bronchitis, Mastitis, Enteritis, Hemorrhagic Septicemia, Metritis, Urinary tract infection, Bacterial Enteritis, Brucellosis, salmonellosis, Septicemia, Mycoplasmosis (CRD)
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Prevention of secondary bacterial infection in viral diseases

Do not administer to animals with compromised renal function, renal insufficiency, kidney disease, or renal failure. Kidney disease impairs renal clearance of gentamicin and increases the risk of kidney injury. Use in young animals is acceptable, but higher doses may be necessary.

Gentamicin is an aminoglycoside antibiotic. Like other aminoglycosides, the action is to inhibit bacteria protein synthesis via binding to 30S ribosome. Through this action, it causes a misreading of the genetic code and inhibits bacterial protein synthesis. Another mechanism important for gram-negative bacteria is to disrupt the cell surface biofilm, particularly on gram-negative bacteria, to produce disruption, loss of cell wall integrity, and a rapid bactericidal effect. Magnesium and calcium are important to cross-bridge adjacent lipopolysaccharide molecules. Positive-charged aminoglycosides competitively displace Ca2+ and Mg2+ and destabilize the bacteria outer membrane. Therefore, death of the bacteria is caused by a cell surface effect rather than inhibition of the ribosome. This property is not as prominent for gram-positive bacteria unless administered with a cell wall–disrupting agent such as vancomycin or a beta-lactam antibiotic.

Gentamicin’s spectrum of activity includes coverage against many aerobic gram-negative and some aerobic gram-positive bacteria, including most species of E. coli, Klebsiella, Proteus, Pseudomonas, Salmonella, Enterobacter, Serratia, and Shigella, Mycoplasma, and Staphylococcus (strains of MRSA are often resistant). Several strains of Pseudomonas aeruginosa, Proteus, and Serratia that are resistant to gentamicin may still be treated with amikacin. 

Antimicrobial activity of the aminoglycosides is enhanced in an alkaline environment.
The aminoglycoside antibiotics are inactive against fungi, viruses and most anaerobic bacteria.

The following drug interactions have either been reported or are theoretical in humans or animals receiving gentamicin and may be of significance in veterinary patients:
BETA-LACTAM ANTIBIOTICS (penicillins, cephalosporins): May have synergistic effects against some bacteria; some potential for inactivation of aminoglycosides in vitro (do not mix together) and in vivo (patients in renal failure)
CEPHALOSPORINS: The concurrent use of aminoglycosides with cephalosporins is somewhat controversial. Potentially, cephalosporins could cause additive nephrotoxicity when used with aminoglycosides, but this interaction has only been well documented with cephaloridine and cephalothin (both no longer marketed).
DIURETICS, LOOP (e.g., furosemide, torsemide) or OSMOTIC (e.g., mannitol): Concurrent use with loop or osmotic diuretics may increase the nephrotoxic or ototoxic potential of the aminoglycosides
NEPHROTOXIC DRUGS, OTHER (e.g., cisplatin, amphotericin b, polymyxin B, or vancomycin): Potential for increased risk for nephrotoxicity
NEUROMUSCULAR BLOCKING AGENTS & ANESTHETICS,
GENERAL: Concomitant use with general anesthetics or neuromuscular blocking agents could potentiate neuromuscular blockade

Nephrotoxicity is the most dose-limiting toxicity. Ensure that patients have adequate fluid and electrolyte balance during therapy. Electrolyte depletion increases the risk of nephrotoxicity. Kidney injury is increased with persistently high trough concentrations. High levels of calcium and protein in the diet decrease the risk of nephrotoxicity. Ototoxicity and vestibulotoxicity also are possible but have not been often reported in animals. With high doses, neuromuscular toxicity is possible, although rare.