streptomycin

Streptomycin is an aminoglycoside antibiotic produced by the bacterium Streptomyces griseus. It was discovered in 1943 by Selman Waksman and Albert Schatz and became the first antibiotic widely used to treat tuberculosis. It is typically administered by intramuscular or intravenous injection due to poor oral absorption.

The drug binds irreversibly to the 30S ribosomal subunit in bacteria, causing misreading of messenger RNA and disruption of protein synthesis. This action is bactericidal and requires active bacterial uptake, which is enhanced by cellular respiration and, in some cases, prior cell-wall damage. Streptomycin exhibits activity primarily against aerobic Gram-negative bacteria and certain mycobacteria, including Mycobacterium tuberculosis, and is used in combination regimens to prevent resistance.

Clinical use has shifted over time. Historically a cornerstone of tuberculosis therapy, streptomycin is now mostly a second-line agent for drug-resistant tuberculosis and is employed in specific infections such as plague and tularemia. It is rarely used as monotherapy because resistance can develop rapidly.

Pharmacokinetics and safety considerations include poor gastrointestinal absorption, with administration by injection; distribution mainly to extracellular fluid and limited penetration into the central nervous system; renal excretion necessitates dose adjustment in renal impairment. Adverse effects include ototoxicity (both cochlear and vestibular) and nephrotoxicity, as well as a potential for neuromuscular blockade in susceptible individuals. Risk of toxicity increases with prolonged use or high trough levels. Resistance mechanisms involve aminoglycoside-modifying enzymes and mutations in the 30S ribosomal binding site, and cross-resistance can occur with other aminoglycosides.