|Systematic (IUPAC) name|
|Legal status||POM (UK)|
|Routes||IV, IM, topical|
|Bioavailability||limited oral bioavailability|
|ATC code||D06 J01 S01 S02 S03 QA07 QG01 QG51 QJ51|
|Mol. mass||477.596 g/mol|
| (what is this?)
Gentamicin is an aminoglycoside antibiotic, used to treat many types of bacterial infections, particularly those caused by Gram-negative organisms. However, gentamicin is not used for Neisseria gonorrhoeae, Neisseria meningitidis or Legionella pneumophila. Gentamicin is also ototoxic and nephrotoxic, with this toxicity remaining a major problem in clinical use.
It is synthesized by Micromonospora, a genus of Gram-positive bacteria widely present in the environment (water and soil). To highlight their specific biological origins, gentamicin and other related antibiotics produced by this genus (verdamicin, mutamicin, sisomicin, netilmicin, retymicin) generally have their spellings ending in ~micin and not in ~mycin. Gentamicin is a bactericidal antibiotic that works by binding the 30S subunit of the bacterial ribosome, interrupting protein synthesis.
Like all aminoglycosides, when gentamicin is given orally, it is not systemically active. This is because it is not absorbed to any appreciable extent from the small intestine. It is administered intravenously, intramuscularly or topically to treat infections. It appears to be completely eliminated unchanged in the urine. Urine must be collected for many days to recover all of a given dose because the drug binds avidly to certain tissues.
E. coli has shown some resistance to gentamicin, despite being Gram-negative. Reluctance to use gentamicin for empirical therapy has led to increased use of alternative broad-spectrum antibiotics, which some experts suggest has led to the prevalence of antibiotic-resistant bacterial infections by MRSA and other so-called "superbugs".
Gentamicin is one of the few heat-stable antibiotics that remain active even after autoclaving, which makes it particularly useful in the preparation of some microbiological growth media. It is used during orthopaedic surgery when high temperatures are required for the setting of cements (e.g. hip replacements).
Spectrum of activity 
Active against a wide range of human bacterial infections, mostly Gram-negative bacteria including Pseudomonas, Proteus, Serratia, and the Gram-positive Staphylococcus. Gentamicin is not used for Neisseria gonorrhoeae, Neisseria meningitidis or Legionella pneumophila bacterial infections (because of the risk of the patient going into shock from lipid A endotoxin found in certain Gram-negative organisms). Gentamicin is also useful against Yersinia pestis, its relatives, and Francisella tularensis (the organism responsible for Tularemia seen often in hunters and/or trappers). Some Enterobacteriaceae, Pseudomonas spp., enterococci, Staphylococcus aureus and other staphylococci are resistant to Gentamicin Sulfate, USP to varying degrees.
Side effects 
These aminoglycosides are toxic to the sensory cells of the ear, but they vary greatly in their relative effects on hearing versus balance. Gentamicin is a vestibulotoxin, and can cause permanent loss of equilibrioception, caused by damage to the vestibular apparatus of the inner ear, usually if taken at high doses or for prolonged periods of time, but there are well documented cases in which gentamicin completely destroyed the vestibular apparatus after three to five days. A small number of affected individuals have a normally harmless mutation in their mitochondrial RNA (m1555 A>G), that allows the gentamicin to affect their cells. The cells of the ear are particularly sensitive to this, sometimes causing complete hearing loss. However, gentamicin is sometimes used intentionally for this purpose in severe Ménière's disease, to disable the vestibular apparatus. These side effects are most common when the drug is administered via drops directly to the eye.
Gentamicin can also be highly nephrotoxic, particularly if multiple doses accumulate over a course of treatment. For this reason gentamicin is usually dosed by body weight. Various formulae exist for calculating gentamicin dosage. Also trough and peak serum levels of gentamicin are monitored during treatment, generally before and after the third dose is infused.
Gentamicin, like other aminoglycosides, causes nephrotoxicity by inhibiting protein synthesis in renal cells. This mechanism specifically causes necrosis of cells in the proximal tubule, resulting in acute tubular necrosis which can lead to acute renal failure.
Side effects of gentamicin toxicity vary from patient to patient. Side effects may become apparent shortly after or up to months after gentamicin is administered. Symptoms of gentamicin toxicity include:
- Balance difficulty
- Bouncing, unsteady vision
- Ringing in the ears (tinnitus)
- Difficulty multi-tasking, particularly when standing
Psychiatric symptoms related to gentamicin can occur. These include anorexia, confusion, depression, disorientation and visual hallucinations. Immediate professional help should be sought if any of these symptoms or others appear after administration of aminoglycosides. General medical practitioners should refer patients with such symptoms to an otolaryngologist, commonly known as an 'ear, nose, and throat doctor', for comprehensive tests.
A number of factors and determinants should be taken into account when using gentamicin, including differentiation between empirical and directed therapy which will affect dosage and treatment period. Many medical practitioners freely administer gentamicin as an antibiotic without advising patients of the severe and permanent potential ramifications of its use. Gentamicin is well known to be a cheap, low-cost yet old medicine when compared with modern alternatives, and is typically US$3–6 per dosage less than modern alternatives.
Many people recover from gentamicin toxicity naturally over time if the drug is discontinued, but they recover slowly and usually incompletely. Sometimes the toxicity of gentamicin can still increase over months after the last dose. Upon cessation of gentamicin therapy symptoms such as tinnitus and imbalance may become less pronounced. Sensori-neural hearing loss caused by gentamicin toxicity is permanent however.
Production and usage in research 
Gentamicin is produced by the fermentation of Micromonospora purpurea. It was discovered in 1963 by Weinstein, Wagman et al at Schering Corporation in Bloomfield, N.J. working with source material (soil samples) provided by Rico Woyciesjes. Subsequently it was purified and the structures of its three components determined by Cooper, et al also at the Schering Corporation. It was initially used as a topical treatment for burns at the Atlanta and San Antonio burn units and was introduced into IV usage in 1971. It remains a mainstay for use in sepsis.
Gentamicin is also used in molecular biology research as an antibacterial agent in tissue and cell culture, to prevent contamination of sterile cultures.
- Moulds, Robert and Jeyasingham, Melanie (October 2010). "Gentamicin: a great way to start". Australian Prescriber (33): 134–135.
- Hendriks JGE, van Horn JR, van der Mei HC, and Busscher, HJ (2004). "Backgrounds of antibiotic-loaded bone cement and prosthesis-related infection". Biomaterials 25 (3): 545–556. doi:10.1016/S0142-9612(03)00554-4. PMID 14585704.
- Gentamicin: Drug Information Provided by Lexi-Comp: Merck Manual Professional
- Goljan, Edward F. (2011). Rapid Review Pathology 3rd ed. Philadelphia, PA: Elsevier. p. 241. ISBN 978-0-323-08438-3.
- "Gentamicin spectrum of bacterial susceptibility and Resistance". Retrieved 15 May 2012.
- Gentamicin Toxicity at the American Hearing Research Foundation
- Sundin DP, Sandoval R, Molitoris BA: Gentamicin Inhibits Renal Protein and Phospholipid Metabolism in Rats: Implications Involving Intracellular Trafficking. J Am Soc Nephrol 12:114-123, 2001
- AJ Giannini, HR Black. Psychiatric, Psychogenic and Somatopsychic Disorders Handbook. Garden City, NY. Medical Examination Publishing Co.,1978. Pp.136-137. ISBN 0-87488-596-5.
- Weinstein, Marvin; Wagman (1963). "Gentamicin, A New Antimicrobial Complex from Micromonospora". J Med Chem 6: 463–464.