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TUBERCULOSIS
and
ANTI-
TUBERCULAR
DRUGS
G Vijay Narasimha Kumar
Asst. Professor,
Dept. of. Pharmacology
Sri Padmavathi Sch...
DEFINITION
• A chronic bacterial infection caused by Mycobacterium
tuberculosis, usually characterized pathologically by t...
• Less common strains which causes TB are
– M.africanum
– M.microti
– Mpinnipeddi
– M.cannetti
• Less pathogenic strains a...
WHY TB IS A DREADFUL DISEASE ?
REASON FOR
DREADFUL DISEASE:
• Presence of Mycolic
acid (90’c’ atoms
arranged in a ring lik...
WHY IT CAN’T BE STAINED BY NORMAL STAINS?
• Due to presence of mycolic acids and cross linked fatty
acids and other lipids...
WHY TB AFFECTS ONLY LUNGS ?
M.tuberculi
Enters
Host cell
Utilizes
Cholesterol in cell membrane (Highly oxygenases amount i...
transmission
• TB is spread through the air from one person to
another via
– Inhalation( cough droplets)
– Ingestion (self...
• Based on presence of signs and symptoms
– Active TB (only shows signs and symptoms).
– Latent TB (signs and symptoms are...
Pathogenesis
• When ever the Mycobacterium tuberculi enters body. As it is
strictly aerobic it resides in alveoli of lungs...
However, a very few no.of macrophages/some cells can process the
mycobacterial tuberculosis
The APC containing expressed M...
Activation of Monocyte Adherent Protein (MAP) on endothelium and adherence
of monocyte to MAP
Squeezing of monocytes from ...
Granuloma (Agroup of cluster of epitheloid cells surrounded by rim of
lymphocytes around them)
IN GRANULOMA
Some of macrop...
Within 10-14 days, the centre of the cellular mass undergoes into
CASEATION NECROSIS(microscopically necrosis is structure...
When infected person coughs or sneezes, the granulomas that may be present
in sputum comes in contact with air.
Lymphocyte...
SIGNS AND SYMPTOMS OF TB
INVESTIGATIONS
• Chest X- ray
• Laboratory diagnosis
– Sputum examination for AFB
– Complete haemogram (lymphocytosis and ...
• A presumptive diagnosis is commonly based on
the finding of AFB on microscopic examination
of a clinical sample (e.g., s...
•This test can often indicate disease when there is
none (false positive). Also, it can show no disease
when you may in fa...
20
Fig: Tuberculin test
Fig: Chest X-ray radiography
Showing cavity
Wheal
Complications
Prevention of TB
22
• Prevention strategies include BCG vaccination
and treatment of persons with latent
tuberculosis infe...
ANTITUBERCULA
R DRUGS
FIRST LINE AGENTS
ISONIAZID(H)
RIFAMPICIN®
PYRAZINAMIDE
ETHAMBUTOL(E)
STREPTOMYCIN(S)
SECOND LINE
AG...
ISONIAZID
Isonicotinicacid hydrazide
Catalase peroxidase (enzyme of
mycobacterium) activates
Aducts with
NAD NADP
InH a Ka...
Mechanism of action
Rifampicin
Binds with Beta subunit of
DNA dependent RNA
polymerase
Inhibition of m.R.N.A
synthesis
Tub...
PYRAZINAMIDE
MECHANISM OF ACTION
PYRAZINAMIDE
PYRAZINOIC ACID
mycolic acid synthesis Disrupts
inhibition cell
membrane
int...
ETHAMBUTOL
MECHANISM OF ACTION
Ethambutol
Inhibits Arabinosyl transferase
Inhibits Synthesis of ARABINO
GLYCANS
Inhibits c...
STREPTOMYCIN
MECHANISM OF ACTION
STREPTOMYCIN
Binds to 30S subuint of
ribosomes
Which results in production
Abnormal prote...
THIACETAZONE
• Because of its low cost and
efficacy combination with H it
was once used in 1st line drugs
for TB.
• It is ...
CYCLOSERINE
• MECHANISM OF ACTION :It is
D-alanine analogue and hence it
replaces alanine which is essential
for cell wall...
Fluoroquinolones(CIPROFLOXACIN
and OFLOXACIN):
• The fluoroquinolones are useful
new addition to the anti
tubercular drugs...
MANAGEMENT OF TB
• Aims:
1. To kill the dividing bacteria in the lung lesions.
2. To kill the persisters so as to avoid re...
FOR NEWLY INFECTED PATIENTS
FOR PREVIOUSLY TREATED PATIENTS WITH LOW
RESISTANCE TO DRUGS
INTENSIVE PHASE
(2months)
H,R,Z,E...
MULTI DRUG RESISTANT OR HIGHLY
RESISTANT
INTENSIVE PHASE
(6months)
Z
E
AMIKACIN/KANAMYCI
N
OFLOXACIN/LEVOFLO
XACIN
CYCLOSE...
DOT’s REGIMEN OF RNTCP(REVISED NATIONAL TUBERCULOSIS
CONTROL PROGRAMME) -1997
TB in special population
• TUBERCULOSIS IN PREGNANT WOMEN:
• H, R and Z to be safe to the foetus and
recommend the standar...
Treatment of TB in MAC
• Mycobacterium avium complex (MAC) infection is common in
HIV-AIDS patients, particularly when the...
Tuberculoosis and antitubercular drugs
Tuberculoosis and antitubercular drugs
Tuberculoosis and antitubercular drugs
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Tuberculoosis and antitubercular drugs

  1. 1. TUBERCULOSIS and ANTI- TUBERCULAR DRUGS G Vijay Narasimha Kumar Asst. Professor, Dept. of. Pharmacology Sri Padmavathi School of Pharmacy
  2. 2. DEFINITION • A chronic bacterial infection caused by Mycobacterium tuberculosis, usually characterized pathologically by the formation of granulomas. The most common site of infection is the lung, but other organs such as may be involved. • Other common names included “wasting disease” and the “white plague.” AETOLOGY • TB is caused by Mycobacterium species mainly by – Mycobacterium tuberculi which is aerobic atypical rod shaped bacteria • Other strains which causes TB are – M.avium – M.bovis ( Commonly caused by consumption of unpasteurized milk) – M.hominis
  3. 3. • Less common strains which causes TB are – M.africanum – M.microti – Mpinnipeddi – M.cannetti • Less pathogenic strains are – M.abscessus – M.fortuitum – M.chelonae • Non pathogenic strains are M.smegmatis • M.tuberculi also called as Koch’s bacilli or Acid Fast bacilli
  4. 4. WHY TB IS A DREADFUL DISEASE ? REASON FOR DREADFUL DISEASE: • Presence of Mycolic acid (90’c’ atoms arranged in a ring like structure) in Mycobacterium species. • Mycolic acids  Prevents ,resists against hydrophilic and lipophilic antibiotics, loss of water, transport of various substances  Helps in evading from immune system.
  5. 5. WHY IT CAN’T BE STAINED BY NORMAL STAINS? • Due to presence of mycolic acids and cross linked fatty acids and other lipids in the cell wall of organisms ,making it impermeable to usual stain. M.tuberculi in Acid fast staining Takes up satin by carbol fuschin. Resists decolorisation by acids and alcohol. Don’t acquire 20 stain methylene blue These retain carbol fuschin hence they appear red.
  6. 6. WHY TB AFFECTS ONLY LUNGS ? M.tuberculi Enters Host cell Utilizes Cholesterol in cell membrane (Highly oxygenases amount involved in metabolism of cholesterol into) e- • The concentrations of oxygenases greater in alveoli of lungs .Hence Mycobacterium species majorly reside in alveoli of lungs. • And as it is strict aerobe strictly thrives best in tissues with high Oxygen tension such as in the apex of the lung ATP
  7. 7. transmission • TB is spread through the air from one person to another via – Inhalation( cough droplets) – Ingestion (self-swallowing of infected sputum), – Inoculation(organisms into tissue which may occur from infected postmortem tissue), – Trans placental routes( Leads to congenital TB). types of tuberculosis • Based on anatomical site – PULMONARY TB (lungs) – MILIARY TB (Liver, kidney spleen brain)
  8. 8. • Based on presence of signs and symptoms – Active TB (only shows signs and symptoms). – Latent TB (signs and symptoms are absent-DORMANT). • Based on type of tissue response and age – Primary TB or Ghon’s complex or childhood TB ( infection of an individual who has not been previously infected or immunised) – Secondary TB or Post-primary or Reinfection, or Chronic TB(infection of an individual has been previously infected or sensitized).
  9. 9. Pathogenesis • When ever the Mycobacterium tuberculi enters body. As it is strictly aerobic it resides in alveoli of lungs. • In alveoli, they will be engulfed by alveolar macrophages and with in macrophages they will be converted into phagosome • Phagosome should convert into phagolysosome but the M.tuberculi inhibits the fusion of phagosome with lysosome there by no formation of phagolysosome. • Thus the mycobacterium tuberculosis antigen becomes “Difficut to undergo Degradation”.
  10. 10. However, a very few no.of macrophages/some cells can process the mycobacterial tuberculosis The APC containing expressed MTB antigen enters lymphatic system and reaches lymphatic organs. CLONAL SELECTION Activation of TH1cells(Cell mediated Immunity) IL-1 INF-γ TNF-α Activation of INF-γ on endothelial cells of blood vessels TH1 cell
  11. 11. Activation of Monocyte Adherent Protein (MAP) on endothelium and adherence of monocyte to MAP Squeezing of monocytes from blood to site of injury. Thus monocytes entered into site of injury becomes Macrophages and increases in number. Macrophages engulf Mycobacterium tuberculosis at site of injury.Due to inhibition of Fusion of Phagolysosome, Macrophages are unable to digest Mycobacterium tuberculosis
  12. 12. Granuloma (Agroup of cluster of epitheloid cells surrounded by rim of lymphocytes around them) IN GRANULOMA Some of macrophages form Multinucleated giant cells by fusion of adjacent cells (Langhans type) Surrounding the epithelioid cells and giant cells there is a zone of lymphocytes,plasma cells, and fibroblasts. This lesion at this stage is called Hard tubercle due to absence of central necrosis.
  13. 13. Within 10-14 days, the centre of the cellular mass undergoes into CASEATION NECROSIS(microscopically necrosis is structureless esinophilic and granular material with debris) . This stage is called soft tubercle. Wide spread of Soft tubercle over various parts of alveoli and lungs causes PULMONARY TB. These soft tubercle wide spread into various parts of the body like kidney spleen, liver and bones etc.,. In those freshly infected parts Mycobacterium tuberculi diffuse out of Soft tubercle and infects which leads to formation of new granulomas. Newly formed granulomas damages tissue and degenerates tissue surrounding Extensive spread and damage of various parts of body occurs. This condition is called MILIARY TUBERCULOSIS.
  14. 14. When infected person coughs or sneezes, the granulomas that may be present in sputum comes in contact with air. Lymphocytes, fibroblasts surrounding the cluster of epitheloid cells become inactivated. And Mycobacterium tuberculi gets free from epitheloid cells Comes in contact with another person New person develops TB
  15. 15. SIGNS AND SYMPTOMS OF TB
  16. 16. INVESTIGATIONS • Chest X- ray • Laboratory diagnosis – Sputum examination for AFB – Complete haemogram (lymphocytosis and raised ERR). – Culture and drug sensitivity tests using BACTEC radiometric method ( this method used to detect live bacilli) . – D.N.A probe technology – Nucleic acid amplification test- PCR – ELISA testing for IgG antibodies ( It denotes only past infection , but not useful as diagnostic aid). – Drug susceptibility testing to anti-TB drugs. – Gene Xpert (to differentiate 10 /Multi drug resistant TB) – Fine needle aspiration cytology of an enlarged peripherallymph node is quite helpful for confirmation of diagnosis – INF- ɣTESTS • T.SPOT • Quantiferon TB gold intube • Sputum collection • Tuberculin test
  17. 17. • A presumptive diagnosis is commonly based on the finding of AFB on microscopic examination of a clinical sample (e.g., sputum/pus). • When this is not possible, a probable diagnosis may be made using imaging (X-ray/scans) and/or a tuberculin skin test (Mantoux test). • Tuberculin skin test, which yields a delayed hypersensitivity type response (a small, raised, blanched wheal) to an extract made from M. tuberculosis (purified protein derivative; PPD). • TUBERCULIN SKIN TEST: Purified protein derivative (PPD), 0.1ml Intradermally, conc. 0.002mg/ml. If a raised bump of more than 5 mm (0.2 in) appears at the site 48 hours later, the test may be positive.
  18. 18. •This test can often indicate disease when there is none (false positive). Also, it can show no disease when you may in fact have TB (false negative). Interpretation • 0–4 mm Negative • 5–9 mm Doubtful (may be due to atypica mycobacteria) • 10 mm or more Positive • In HIV infected individuals, 5 mm is considered positive. • Tuberculin negative patients should be vaccinated with BCG. • False-negative tuberculin tests (i.e. negative skin tests occurring in patients with tuberculosis).
  19. 19. 20 Fig: Tuberculin test Fig: Chest X-ray radiography Showing cavity Wheal
  20. 20. Complications
  21. 21. Prevention of TB 22 • Prevention strategies include BCG vaccination and treatment of persons with latent tuberculosis infection who are at high risk of developing active disease. • BCG was derived from an attenuated strain of M. bovis. • Efficacy is between 0-80%. • BCG vaccine is recommended for routine use at birth in countries with high tuberculosis prevalence. • Bacillus Calmette-Guérin (BCG)
  22. 22. ANTITUBERCULA R DRUGS FIRST LINE AGENTS ISONIAZID(H) RIFAMPICIN® PYRAZINAMIDE ETHAMBUTOL(E) STREPTOMYCIN(S) SECOND LINE AGENTS THIOCETAZONE(T) PARAAMINOSALICYLIC ACID(PAS) ETHIONAMIDE(ET) CYCLOSERINE(C) AMIKACIN(A) KANAMYCIN AND CAPREOMYCIN (K) NEWER DRUGS (FLUOROQUINOLON E MACROLIDE ANTIBIOTICS,LINE ZOLID,RIFAPENTIN, RIFABUTIN)
  23. 23. ISONIAZID Isonicotinicacid hydrazide Catalase peroxidase (enzyme of mycobacterium) activates Aducts with NAD NADP InH a Kas a dihydrofolate reductase Inhibition of Inhibition of Mycolic acid DNA synthesis Bactericidal action • Resistance : – Mycobacteria may develops resistance towards H due to change in genes coding for catalase peroxidase. – Alteration in Kas a and Inh a and in structure of efflux pumps of bacteria. • Pharmacokinetics: – Orally well absorbed – Well distributed – Metabolized in Liver by – Based on acylation • Slow acetylators (Half life- 3h) • Fast acetylators( Half life-1h) – Excreted through urine • Adverse effects: – GI disturbances, – Hepatotoxicity – Peripheral Neuritis – Hypersensitivity reactions
  24. 24. Mechanism of action Rifampicin Binds with Beta subunit of DNA dependent RNA polymerase Inhibition of m.R.N.A synthesis Tuberculocidal effect • PHARMACOKINETICS: – Orally well absorbed – High protein bound – Distributed to all parts – Metabolized in liver into desacetyl rifampicin which undergoes entero- hepatic circulation. – Excreted largely in feces and small in urine. – Enzyme inducer for • HIV protease inhibitors • NNRTI’s • Azole antifungals,Sulphonyl ureas,Phenytoin, Warfarin, Theophylline Carbamazepine. • ADVERSE EFFECTS: – Patients with hepatic disease are prone to hepatitis – Allergic reactions-Pruritis – GI disturbances – Flulike symptoms RIFAMPICIN
  25. 25. PYRAZINAMIDE MECHANISM OF ACTION PYRAZINAMIDE PYRAZINOIC ACID mycolic acid synthesis Disrupts inhibition cell membrane integrity Tuberculocidal effect • Pyrazinoic acid Highly effective in acid environment and inflammatory conditions • PHARMACOKINETICS: – Rapidly absorbed from GI tract – It is widely distributed in the body and achieves a concentration in the CSF equal to the plasma levels. – Deaminated in theliver. – Degradation products and he free drug are eliminated in urine • ADVERSE EFFECTS: – Hyperuricemia (precipitating gout) – Metallic state – Sulfurous eructation's – Toxic hepatitis (Not dose related) – Arthralgia,nausea,vomiting,anorex ia,malaise, – Rarely photosensitivity reaction • Used in both Extrapulmonary and pulmonary TB
  26. 26. ETHAMBUTOL MECHANISM OF ACTION Ethambutol Inhibits Arabinosyl transferase Inhibits Synthesis of ARABINO GLYCANS Inhibits cell wall synthesis • Only tuberculostatic among all first line Anti tubercular agents. • Suppress the emergence of resistance • Hastens sputum conversion • PHARMACOKINETICS: – 70% is absorbed – Penetrates into erythrocytes, gets deposited, and released into circulation – 50% of oral dose excreted unchanged in urine with in 24h – 15% excreted in the form of two metabolites – Accumulates in presence of renal damage • ADVERSE EFFECTS: – Retrobulbular optic neuritis on prolonged therapy which results in decrease visual acuity. – Others are Nausea,headache,anorexia,allergic reactions,and confusion • If any visual disturbances are seen in the patient,Ethambutol should be removed from patient’s regimen
  27. 27. STREPTOMYCIN MECHANISM OF ACTION STREPTOMYCIN Binds to 30S subuint of ribosomes Which results in production Abnormal proteins Accumulates in mycobacterium Destruction of mycobacterium • PHARMACOKINETICS: – Not absorbed orally and must be given in IM. Well absorbed when instilled in intrapleurally – It doesn’t cross BBB. However, high concentrations are seen in CSF during meningeal inflammation. – It is mainly concentrated in kidneys, liver, and skeletal tissues. – It crosses Placental barrier, – Excreted unchanged by GFR. And approximately 50-60% of drug is eliminated in urine in active form within 24h. • ADVERSE EFFECTS: – Pain at the site of injection – 8th cranial nerve damage – Neuromuscular blockade – Nephrotoxicity and ototoxicity – Super infections with Staphylococcus aureus and candida
  28. 28. THIACETAZONE • Because of its low cost and efficacy combination with H it was once used in 1st line drugs for TB. • It is orally active , rapidly diffuses into various body tissues ,Partly metabolized in liver and about 40% excreted unchanged in urine with t1/2 12h. • It is no longer used now because of its Exfoliative dermatitis Stevens-Jhonson syndrome ototoxicity and life-threatening hypersensitivity reactions (Hepatitis, neutropenia, thrombocytopenia). PARA-AMINO SALICYLIC ACID(PAS) • It is chemically as well as in mechanism of action related to Sulfonamides.It is not active against other bacteria and the reason may be due to the difference in the affinity of folate synthetase of TB and other bacteria. • Absorbed completely by oral route and distributed all over the body except CSF,about 50% PAS is aceylated and competes with acetylation of H- Prolongs its t1/2.Excreted rapidly by Glomerular filtration and tubular secretion. • Patient acceptibility is poor because of frequent anorexia, nausea and epigastric pain and other adverse effects are blood dyscrasias, fever rash, etc.,. SECOND LINE AGENTS These alternative drugs that are useful in cases of resistance to 1st line drugs
  29. 29. CYCLOSERINE • MECHANISM OF ACTION :It is D-alanine analogue and hence it replaces alanine which is essential for cell wall synthesis. • PHARMACOKINETICS: Rapidly absorbed from gut,distributed through out the body (csf and plasma concentrations are equal in meningitis condition).50% of orally administered dose gets excreted in urine in unchanged form and 65% is excreted by kidneys within 72h. • Broad spectrum antibiotic and it is tuberculostatic. • It is effective against tubercle bacilli resistant to H or S and against atypical mycobacterium. • ADVERSE EFFECTS: – Peripheral neuropathy, – Ataxia – Delusions, Nervousnessetc.,. ethionamide • MECHANISM OF ACTION: Blocks the synthesis of mycolic acids and it is a tuberculostatic drug. • PHARMACOKINETICS: ABSORPTION is similar to H, Metabolized in liver and only 1% excreted unchanged in urine • Because of its Intense gastric irritation and neurological toxicity(optic and peripheral neuritis) and hepatotoxicity, it is rarely used, as in recommended dose of 1mg/kg. • ADVERSE EFFECTS: • Purpura, • GI disturbances • Toxic hepatitis • Miscellaneous: Gynecomastia, Mennorhagia etc.,.
  30. 30. Fluoroquinolones(CIPROFLOXACIN and OFLOXACIN): • The fluoroquinolones are useful new addition to the anti tubercular drugs. Ciprofloxacin,Ofloxacin and sparfloxacin are active against M.tuberculosis as well as M.avium complex. • They penetrate cells and kill mycobacteria lodged in macrophages also. • Because of their good tolerability,they are being increasingly included combination regimens against MDR TB and MAC infection HIV patients. • The generally employed doses are ciprofloxacin 1500 mg/ day and ofloxacin 800mg/ day in 2 divided doses. Sparfloxacin is more active against mycobacteria in vitro, but has been used clinically to a lesser extent. Macrolide antibiotics (CLARITHROMYCIN AND AZITHROMYCN: • These newer macrolide antibiotics are most active against nontubercular mycobacteria including MAC, M. fortuitum, M. Kansasii and M. marinum. • Clarithromycin has been used to a greater extent because its MIC values are lower, but azithromycin may be equally efficacious due to its higher tissue and intracellular levels. • combination with other drugs. In AIDS patients, life-long therapy is required-may cause ototoxicity NEWER DRUGS
  31. 31. MANAGEMENT OF TB • Aims: 1. To kill the dividing bacteria in the lung lesions. 2. To kill the persisters so as to avoid relapse and ensure total cure 3. To prevent emergence of drug resistance And based on treatment is given PATIENT NEWLY AFFECTED PATIENTS ACTIVE TB LATENT TB PREVIOUSLY TREATED PATIENTS AND BASED ON DRUG SENSITIVITY TEST LESS SENSITIVE MORE SENSITIVE
  32. 32. FOR NEWLY INFECTED PATIENTS FOR PREVIOUSLY TREATED PATIENTS WITH LOW RESISTANCE TO DRUGS INTENSIVE PHASE (2months) H,R,Z,E+VitB6 CONTINUOUS PHASE (4months) H,R+VIT B6 INTENSIVE PHASE (3months) HRZES HRZE + Pyridoxine 100mg/day CONTINUOUS PHASE (5months) HRZ + Pyridoxine 100mg/day
  33. 33. MULTI DRUG RESISTANT OR HIGHLY RESISTANT INTENSIVE PHASE (6months) Z E AMIKACIN/KANAMYCI N OFLOXACIN/LEVOFLO XACIN CYCLOSERINE ETHIONAMIDE+ PYRIDOXINE CONTINUOUS PHASE (12-18months) E OFLOXACIN/LEVOFLOXA CIN CYCLOSERINE ETHIONAMIDE+ PYRIDOXINE For H resistance: R+Z+E for 12Months For R resistance: H+Z+E for 12Months For both H+R resistance: Z+E+S(Et)+CIROFLOXACIN(OR OFLOXACIB OR LEVOFLOXACIN),for 12-18 Months
  34. 34. DOT’s REGIMEN OF RNTCP(REVISED NATIONAL TUBERCULOSIS CONTROL PROGRAMME) -1997
  35. 35. TB in special population • TUBERCULOSIS IN PREGNANT WOMEN: • H, R and Z to be safe to the foetus and recommend the standard 6 month (2HRZ + 4HR) regimen for pregnant women with TB. E can be added during late but not early pregnancy. S is contraindicated. • India, it is advised to avoid Z, and to treat pregnant TB patients with 2 HRE + 7HR (total 9 months). Treatment of TB should not be withheld or delayed because of pregnancy. • TREATMENT OF BREASTFEEDING WOMEN : • All antiTB drugs are compatible with breastfeeding; full course should be given to the mother, but the baby should be watched. The infant should receive BCG vaccination and isoniazid prophylaxis. • In case of M. tuberculosis infection, drugs used are the same as in non-HIV cases, but the duration is longer and at least 4 drugs are used. • Initial therapy with 2 month HRZE is started immediately on the diagnosis of TB, and is followed by a continuation phase of HR for 7 months (total 9 months). • Alternatively, 3 drugs (HRE) are given for 4 months in the continuation phase. Pyridoxine 25-50 mg/ day is routinely given along with H to counteract its neurological side effects, which are more likely in AIDS patients. • MDR-TB in HIV-AIDS patients should be treated for a total of 18-24 months or for 12 months after sputum smear negativity. Tb in hiv
  36. 36. Treatment of TB in MAC • Mycobacterium avium complex (MAC) infection is common in HIV-AIDS patients, particularly when the CD4 count drops to < 100 cells/J.IL • Clarithromycin/ azithromycin are the most active drugs against MAC. A favoured regimen consists of an intensive phase of at least 4 drugsclarithromycin/ azithromycin + ethambutol rifabutin + one FQ / clofazimine/ ethionamide given for 2-6 months (duration is response based) . • Followed by 2 drug maintenance phase with clarithromycin/ azithromycin + ethambutol/ one FQ/ rifabutin for at least 1 2 months or eYen lifelong. • However, any additional benefit of the initial 4 drug intensive phase is unproven. Clarithromycin inhibits the metabolism of rifabutin.
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Tuberculoosis and antitubercular drugs

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