Drugs of choice are: isoniazid, rifampin, ethambutol, along with streptomycin and pyrazinamide. Less well tolerated, second-line agents include: p-aminosal-icylic acid, cycloserine, viomycin, ka-namycin, amikacin, capreomycin, ethi-onamide.
Isoniazid is bactericidal against growing M. tuberculosis. Its mechanism of action remains unclear. (In the bacterium it is converted to isonicotinic acid, which is membrane impermeable, hence likely to accumulate intracellu-larly.) Isoniazid is rapidly absorbed after oral administration. In the liver, it is inactivated by acetylation, the rate of which is genetically controlled and shows a characteristic distribution in different ethnic groups (fast vs. slow acetylators). Notable adverse effects are: peripheral neuropathy, optic neuritis preventable by administration of vitamin B6 (pyridoxine); hepatitis, jaundice.
Rifampin. Source, antibacterial activity, and routes of administration are described on p. 274. Albeit mostly well tolerated, this drug may cause several adverse effects including hepatic damage, hypersensitivity with flu-like symptoms, disconcerting but harmless red/orange discoloration of body fluids, and enzyme induction (failure of oral contraceptives). Concerning rifabutin see p. 274.
Ethambutol. The cause of its specific antitubercular action is unknown. Ethambutol is given orally. It is generally well tolerated, but may cause dose-dependent damage to the optic nerve with disturbances of vision (red/green blindness, visual field defects).
Pyrazinamide exerts a bactericidal action by an unknown mechanism. It is given orally. Pyrazinamide may impair liver function; hyperuricemia results from inhibition of renal urate elimination.
Streptomycin must be given i.v. (pp. 278ff) like other aminoglycoside antibiotics. It damages the inner ear and the labyrinth. Its nephrotoxicity is comparatively minor.
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