Gentamicin belongs to the aminoglycoside antimicrobial agents. It is a bactericidal agent with a wide spectrum of activity against Gram-negative and Gram-positive organisms. It irreversibly inhibits protein biosynthesis by acting directly on the ribosome. Gentamicin binds receptors on the 30S subunit of the bacterial ribosome and inhibits protein synthesis through interference with the initiation complex, misreading of the code on the mRNA template, and causing polysomes to dissociate into nonfunctional monosomes.

Ototoxicity and nephrotoxicity are the most serious adverse effects of gentamicin. Ototoxicity is manifested as vestibular dysfunction, which may be due to destruction of hair cells. If renal failure is present, the probability of ototoxicity is greater.

Nephrotoxicity is more common with gentamicin than with any of the other aminoglycosides. It can produce acute renal insufficiency and tubular necrosis.

The amino glycoside antibiotics include gentamicin, streptomycin, neomycin, tobramycin, kanamycin, amikacin, and netilmicin. All these drugs contain amino sugars linked to an aminocyclitol ring by glycosidic bonds. They are used primarily to treat infections caused by aerobic gram-negative bacteria, where they act to interfere with protein synthesis. The aminoglycosides diffuse through channels in the outer membrane of the bacteria and enter the periplasmic space. Subsequently, the drugs are transported across the cytoplasmic membrane by an energy-dependent transport system, which requires the bacteria to utilize oxygen. Once inside the bacterium, they bind to the 30 S ribosomal subunit and block the initiation of protein synthesis. Bacteria may acquire resistance to the action of the aminoglycosides by several different mechanisms. Penetration of the drug through the pores in the outer membrane may become retarded, but resistance of this type is unimportant clinically. Natural resistance to the aminoglycoside antibiotics can be caused by the failure of the drug to penetrate the cytoplasmic membrane. As the transport mechanism requires the utilization of oxygen, this explains the resistance of anaerobic bacteria and facultative bacteria grown under anaerobic conditions. However, the importance of this mechanism on clinically-important acquired-resistance does not appear to be significant. Resistance resulting from alterations in ribosomal structure is less clinically relevant for most infections. While an alteration in ribosomal structure can prevent binding of the drug, these alterations are not widespread. The most clinically relevant mechanism for acquired-resistance to the aminoglycoside antibiotics is the plasmid-mediated elaboration of inactivating enzymes. These enzymes may phosphorylate, adenylate, or acetylate the aminoglycoside, resulting in loss of function. This has become a source of special concern with regard to enterococcal infections, many of which are highly resistant to all aminoglycosides.

Amoxicillin inhibits bacterial cell wall synthesis by interfering with the formation of cross-links between peptidoglycan polymer chains.

Macrolides, streptogramins, and clindamycin all work by inhibition of the 50S subunit of bacterial ribosomes. Tetracyclines have a similar mechanism of action, but instead affect the 30S unit of bacterial ribosomes.

Polymyxin antibiotics function by interfering with phospholipid function in bacterial cell membranes. After binding to lipopolysaccharide (LPS) in the outer membrane, polymyxins' hydrophobic tail causes damage to both the inner and outer membranes of Gram-negative bacteria.

Rifampin inhibits bacterial RNA synthesis by inhibiting RNA polymerase. This prevents the transcription of proteins within the bacterial cell, leading to cell death.

Hepatotoxicity and potential liver failure are the most serious potential adverse effects of rifampin use. Patients on this medication must establish baseline liver function tests and be monitored for liver damage. None of the other conditions listed are associated with rifampin use.

Aminoglycoside antibiotics are used to treat Gram negative bacteria. They have not been shown to be effective against Gram positive bacteria and are not antifungal. Recall the major difference between the Gram negative and positive bacteria are their cell wall composition; Gram negative have a small proportion of peptidoglycan and a high proportion of lipopolysaccharide, while Gram negative bacteria have a large proportion of peptidoglycan.

The only aminoglycoside antibiotic among those listed is streptomycin. Other examples of aminoglycosides include tobramycin and gentamicin. All aminoglycosides either end in -mycin or -micin. However, this suffix is not exclusive to aminoglycosides. It is also seen in the macrolides: erythromycin and azithromycin and both macrolides, and in lincosamides such as clindamycin.

Aminoglycoside antibiotics such as streptomycin and gentamicin have been associated with vestibular toxicity and hearing loss. Aminoglycosides remain in inner ear fluids longer than serum and can have a latent ototoxic effect, causing hearing loss even after the antibiotic has been discontinued. None of the other antibiotics listed are associated with ototoxicity.