The first drug active against tuberculosis isolated in isolated in 1943. Its scarcity lead to a land mark trial  that not only revolutionised treatment but was the first true clinical randomised controlled trial in the context of post war fair shares for all. It is rarely used now except for drug resistant tuberculosis and for vestibular ablation.
IM 15mg/kg to max 1g daily with reduced dose if under 50kg, over 40 years or with renal impairment to total accumulative dose 100g
- Impairment neuromuscular transmission
Aminoglycoside ototoxicity is associated with a genetic susceptibility in a third to a half of all cases. Most commonly mitochondrial – shows bacterial origin. Screening patients likely to need repeated courses eg CFs, chemotherapy patients, preterm neonates is feasible, but cost:benefit ratio? Consider costs of deafness, cochlear implant etc.
- Enhanced ototoxicity with ototoxic diuretics eg furosemide.
Monitor drug levels in renal failure. Can cause hearing loss through exposure in pregnancy
Inhibits bacterial ribosomal protein formation.
- ↑ Streptomycin Treatment of Pulmonary Tuberculosis: A Medical Research Council Investigation. BMJ. 1948;2:769–782 doi:10.1136/bmj.2.4582.769. As this download is corrupted as of 23 June 2009 see also Editorial on Article, Editorial continued
- ↑ Yoshioka A. Use of randomisation in the Medical Research Council's clinical trial of streptomycin in pulmonary tuberculosis in the 1940s. BMJ (Clinical research ed.) 1998;317(7167):1220-3.
- ↑ Donald PR, Doherty E, Van Zyl FJ. Hearing loss in the child following streptomycin administration during pregnancy. The Central African journal of medicine. 1991 Aug; 37(8):268-71.