streptomycin
Summary
Streptomycin is an aminoglycoside antibiotic that inhibits bacterial protein synthesis by binding the 30S ribosomal subunit, causing misreading of mRNA. It is historically important as the first effective drug against tuberculosis and is still used in select cases of TB, plague, and tularemia. Like other aminoglycosides, it carries risk of nephrotoxicity and ototoxicity.
Detail
Streptomycin is a bactericidal aminoglycoside antibiotic derived from Streptomyces griseus. Mechanism: it irreversibly binds the 30S ribosomal subunit, causing misreading of the genetic code and inhibition of translocation, leading to production of nonfunctional or truncated proteins and ultimately bacterial cell death. Like other aminoglycosides, it requires oxygen-dependent uptake into bacterial cells, making it ineffective against anaerobes.
Clinical uses: Historically the first drug effective against Mycobacterium tuberculosis (used in combination therapy for drug-resistant TB). Also used for treatment of plague (Yersinia pestis), tularemia (Francisella tularensis), and as part of combination therapy for enterococcal or streptococcal endocarditis (synergy with cell wall-active agents like penicillin).
Pharmacokinetics: Poor oral absorption, so given parenterally (IM/IV). Does not cross into CSF well. Renally excreted.
Adverse effects: Nephrotoxicity (reversible), ototoxicity (vestibular and auditory, can be irreversible), neuromuscular blockade (especially with anesthetics or myasthenia gravis), and teratogenicity (ototoxic to fetus, contraindicated in pregnancy). Aminoglycosides show synergy with beta-lactams/vancomycin because cell wall-active drugs facilitate aminoglycoside entry into bacteria.
Resistance mechanisms: Aminoglycoside-modifying enzymes (acetyltransferases, phosphotransferases, adenylyltransferases), decreased uptake, or altered ribosomal binding site (streptomycin resistance often due to a single point mutation in the ribosomal protein S12, unlike other aminoglycosides which show cross-resistance).
High-yield boards points: First anti-TB drug historically; requires aerobic environment for uptake (mnemonic: aminoglycosides = 'mean' GNRs, ineffective for anaerobes); ototoxicity mnemonic 'mycin = kills the ear'; used with cell-wall inhibitors for synergistic bactericidal effect in endocarditis.
Sources
- Katzung's Basic and Clinical Pharmacology
- First Aid for the USMLE Step 1
- Goodman & Gilman's The Pharmacological Basis of Therapeutics
- Sanford Guide to Antimicrobial Therapy
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