An aminoglycoside is a molecule composed of a sugar group and an amino group. [MeshName|Aminoglycosides]

Several aminoglycosides function as antibiotics that are effective against certain types of bacteria. They include amikacin, gentamicin, kanamycin, neomycin, netilmicin, paromomycin, rhodostreptomycin [Massachusetts Institute of Technology. "Bacterial 'Battle For Survival' Leads To New Antibiotic." ScienceDaily 27 February 2008. 28 February 2008 .] , streptomycin, tobramycin, and apramycin.

Anthracyclines are another group of aminoglycosides. These compounds are used in chemotherapy.


Aminoglycosides that are derived from bacteria of the "Streptomyces" genus are named with the suffix "-mycin", while those which are derived from "Micromonospora" are named with the suffix "-micin".

This nomenclature system is not specific for aminoglycosides. For example vancomycin is a glycopeptide antibiotic and erythromycin, which is produced from a defunct species of "Streptomyces" along with its synthetic derivatives clarithromycin and azithromycin are macrolides - all of which differ in their mechanisms of action.

Mechanism of action

Aminoglycosides work by binding to the bacterial 30S ribosomal subunitcite web |url= |title=Aminoglycosides: Bacteria and Antibacterial Drugs: Merck Manual Professional |format= |work= |accessdate=] cite web |url= |title=Aminoglycosides |format= |work= |accessdate=] (some work by binding to the 50S subunit)Fact|date=August 2008, inhibiting the translocation of the peptidyl-tRNA from the A-site to the P-site and also causing misreading of mRNA, leaving the bacterium unable to synthesize proteins vital to its growth. They kill bacteria by inhibiting protein synthesis as they bind to the 16S rRNA and by disrupting the integrity of bacterial cell membrane. [Aminoglycosides versus bacteria--a description of the action, resistance mechanism, and nosocomial battleground. J Biomed Sci. 2008 Jan;15(1):5-14. ] However, their exact mechanism of action is not fully known.

There is a significant relationship between the dose administered and the resultant plasma level in blood. TDM, therapeutic drug monitoring, is necessary to obtain the correct dose. These agents exhibit a post-antibiotic effect in which there is no or very little drug levels detectable in blood, but there still seems to be inhibition of bacterial re-growth. This is due to strong, irreversible binding to the ribosome, and remains intracellular long after plasma levels drop. This allows a prolonged dosage interval. Depending on their concentration they act as bacteriostatic or bacteriocidial agents.

The protein synthesis inhibition of aminoglycosides does not usually produce a bactericidal effect, let alone a rapid one as is frequently observed on susceptible Gram-negative bacilli. Aminoglycosides competitively displace cell biofilm-associated Mg2+ and Ca2+ that link the polysaccharides of adjacent lipopolysaccharide molecules. "The result is shedding of cell membrane blebs, with formation of transient holes in the cell wall and disruption of the normal permeability of the cell wall. This action alone may be sufficient to kill most susceptible Gram-negative bacteria before the aminoglycoside has a chance to reach the 30S ribosome [Lorian, Victor. "Antibiotics in Laboratory Medicine". Williams & Wilkins Press, 1996 (pp.589-590)] ."

Traditionally, the antibacterial properties of aminoglycosides were believed to result from inhibition of bacterial protein synthesis through irreversible binding to the 30S bacterial ribosome. This explanation, however, does not account for the potent bactericidal properties of these agents, since other antibiotics that inhibit the synthesis of proteins (such as tetracycline) are not bactericidal. Recent experimental studies show that the initial site of action is the outer bacterial membrane. The cationic antibiotic molecules create fissures in the outer cell membrane, resulting in leakage of intracellular contents and enhanced antibiotic uptake. This rapid action at the outer membrane probably accounts for most of the bactericidal activity.2 Energy is needed for aminoglycoside uptake into the bacterial cell. Anaerobes have less energy available for this uptake, so aminoglycosides are less active against anaerobes.Aminoglycosides are useful primarily in infections involving aerobic, gram-negative bacteria, such as "Pseudomonas", "Acinetobacter", and "Enterobacter". In addition, some "Mycobacteria", including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. The most frequent use of aminoglycosides is empiric therapy for serious infections such as septicemia, complicated intraabdominal infections, complicated urinary tract infections, and nosocomial respiratory tract infections. Usually, once cultures of the causal organism are grown and their susceptibilities tested, aminoglycosides are discontinued in favor of less toxic antibiotics.

Streptomycin was the first effective drug in the treatment of tuberculosis, though the role of aminoglycosides such as streptomycin and amikacin has been eclipsed (because of their toxicity and inconvenient route of administration) except for multiple drug resistant strains.

Infections caused by gram-positive bacteria can also be treated with aminoglycosides, but other types of antibiotics are more potent and less damaging to the host. In the past the aminoglycosides have been used in conjunction with beta-lactam antibiotics in streptococcal infections for their synergistic effects, particularly in endocarditis. One of the most frequent combinations is ampicillin (a beta-lactam, or penicillin-related antibiotic) and gentamicin. Often, hospital staff refer to this combination as "amp and gent" or more recently called "pen and gent" for penicillin and gentamicin.

Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses.

Experimentation with aminoglycosides as a treatment of cystic fibrosis (CF) has shown some promising results. CF is caused by a mutation in the gene coding for the "cystic fibrosis transmembrane conductance regulator" ("CFTR") protein. In approximately 10% of CF cases the mutation in this gene causes its early termination during translation, leading to the formation of is truncated and non-functional CFTR protein. It is believed that gentamicin distorts the structure of the ribosome-RNA complex, leading to a mis-reading of the termination codon, causing the ribosome to "skip" over the stop sequence and to continue with the normal elongation and production of the CFTR protein. The treatment is still experimental but showed improvement in cells from CF patients with susceptible mutations. [cite journal |author=Wilschanski M, Yahav Y, Yaacov Y, "et al" |title=Gentamicin-induced correction of CFTR function in patients with cystic fibrosis and CFTR stop mutations |journal=N. Engl. J. Med. |volume=349 |issue=15 |pages=1433–41 |year=2003 |month=October |pmid=14534336 |doi=10.1056/NEJMoa022170 |url=]


The toxicity of these agents are dose-related, and therefore every individual can get these side effects provided the dose is sufficiently high enough. Because of their potential for ototoxicity and nephrotoxicity (kidney toxicity), aminoglycosides are administered in doses based on body weight. Vestibular damage, hearing loss and tinnitus are irreversible, so care must be taken not to achieve a sufficiently high dose. Concomitant administration of a cephalosporin may lead to increased risk of nephrotoxicity while administration with a loop diuretic increases the risk of ototoxicity. Blood drug levels and creatinine are monitored during the course of therapy, as there is a highly variable dose to plasma level in blood. Serum creatinine measurements are used to estimate how well the kidneys are functioning and as a marker for kidney damage caused by these drugs. They may react with and prolong the actions of neuromuscular agents. Impaired renal function necessitates a reduced dose.Fact|date=February 2007

Routes of administration

Since they are not absorbed from the gut, they are administered intravenously and intramuscularly. Some are used in topical preparations for wounds. Oral administration can be used for gut decontamination (e.g. in hepatic encephalopathy).


External links

* [ MedlinePlus drug information] - Aminoglycosides (Systemic)
* [ Science Daily Bacterial 'Battle for Survival'] - Rhodostreptomycin

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