Resistance may develop to the AG by changes in the 30S subunit, preserving its functionality but reducing the ability of the antibiotic to bind to it. There are some cases of resistance in which the 30S subunit actually becomes altered so as to require the presence of the AG in order to function properly.
Specific AGs include Neomycin, Streptomycin, Kanamycin (these three have a limited spectrum of activity -- they are ineffective against Serratia and Pseudomonas spp.), Gentamicin, Tobramycin, Netilmicin, and Amikacin (these last two have the broadest spectrum of activity and are more effective again resistant organisms). They are poorly absorbed from the GI tract and are used only parenterally.
Therapeutics -- The AGs are used for streptococcal infections, tularemia (a plague-like infection caused by Francisella (Pasteurella) tularensis -- with ticks or the deer fly as the disease vector), plague, tuberculosis, UTI, sepsis, and meningitis (they must be given intrathecally or directly into the cerebral ventricles).
Adverse Effects
AG also exhibit a dose and duration dependent nephrotoxicity. If caught early, this effect is reversible. The AG accumulates in the PCT of the nephron, where it may reduce the reabsorptive function of that section of the nephron. It also destroys the filtering capability of the glomerulus, preventing proper filtration of plasma for urine formation. If allowed to progess, tubular necrosis may occur with permanent loss of kidney function. Baseline and periodic creatinine clearance should be performed on all patients receiveing AG antibiotics.
Rarely, AG may cause neuromuscular blockade and apnea.