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        Isoniazine (Isonicotinic Acid Hydrazide) (H)          § Tuberculocidal
 Inhibition of synthesis of mycolic acids which are unique FA component of mycobacterial cell wall.
 Two gene product labelled ‘InhA’ and ‘KasA’ which function in mycolic acid synthesis are target of INH action.
 Peripheral neuritis
 Paresthesias
 Numbness
 Mental disturbances
 Convulsions
These are due to interference with production of active coenzyme pyridoxal phosphate from pyridoxine.
Pyridoxine given prophylactically (10 mg/day) prevents neurotoxicity even in higher doses.
 Hepatitis
 Lethargy, Rashes, Fever and Arthalgia
 TB
 Completely absorbed orally and penetrate all body tissue, TB cavity, Placenta and meninges
                Rifampicin (R)              § Bactericidal- on slowly dividing
 Rifampicin interrupts RNA synthesis by binding to B- subunit of mycobacterial DNA- dependent RNA polymerase (encoded by rpoB gene) and blocking its polymerizing function.
 Hepatitis
 Flu syndrome- Chills, fever, headache, malaise and bone pain
 Cutaneous syndrome- flushing, pruritus, rash, redness and watering of eyes
 Abdominal syndrome- N, V, abdominal cramps, Diarrhea
 TB- widely distributed in body, penetrate intracellularly, enter TB cavity, caseous mass and placenta; though crosses meninges- pumped out by P- glycoprotein
 Leprosy and ENL
 Prophylaxis of Meningococcal and H. influenzae meningitis and carrier state.
 MRSA, Dipheroides, Legionella infections
 Brucellosis- Doxycycline + Rifampicin is DOC
 Q fever
 Mycetoma
Pyrazinamide (Z) Tuberculocidal
 MOA is not well understood
 Like INH it is also converted inside mycobacterial cell into an active metabolite pyrazinoic acid by and enzyme (Pyrazinamidase) encoded by pncA gene.
 This metabolite gets accumulated in acidic medium and probably inhibits mycolic acid synthesis, but by interacting with a different FA synthase.
 Disrupts mycobacterial CM and its transport function.
 Hepatotoxicity
 Hyperurecemia, gout, polyarthalgia- due to inhibition of uric acid secretion in kidney
 Rashes, fever, flushing
 Abdominal distress
 Loss of diabetic control- repeated BG monitoring is warranted
TB- good penetration in CSF, highly useful in meningeal TB
Ethambutol (E) Tuberculostatic- fast multiplying bacteria
 MOA not fully understood
 Inhibit arabinosyl transferases involved in arabinogalactan synthesis thereby interfering with mycolic acid incorporation in mycobacterial cell wall.
 Optic neuritis- Loss of visual acuity/ color vision, field of vision
 Fever
 Rashes
 Nausea
 Peripheral neuritis
 Hyperurecemia- due to defective urate excretion
TB- penetrate meninges incompletely
Streptomycin (S)
 Tuberculocidal but less effective than INH or Rifampicin
 Acts only on extracellular bacilli due to poor penetration
 Penetrate tubercular cavity, but
do not cross BBB
 In case of S-resistance it must be stopped at earliest.
 Due to narrow margin of safety its use is restricted to maximum of 2 month.
 Also labelled as supplemental 1st line
TB- Resistance developed rapidly when used alone in TB
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