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TUBERCULOSIS
&

ANTI TUBERCULAR DRUGS
 Chronic granulomatous disease.
 Causative org M.TUBERCULOSIS.
 Incidence in India 1.8 million people develop T.B

every year of which 0.8 million are infectious.
 Mode of Transmission
 Droplet Infection
 Contact transmission
 Droplets are expelled by coughing or sneezing
 Tubercle bacilli then spread to other body organs
 Tubercle bacilli may become dormant

 Even if extend beyond the lymph nodes, TB lesion get

healed and calcified
 But in immounocomparmised or undernourished become

active
Mycobacterium Infections
Common Infection Sites
lung (primary site)
liver

brain
Kidney

bone
Less o2 tension

Symptoms
Low grade fever
Night sweats
Fatigue
Weight loss
Blood streaked productive cough

Malaise
Other acid fast bacilli
 Mycobateria other than M. tuberculosis c/s non






tuberculosis/ atypical mycobacteria
M.kanasasii- milder but chronic pulmonary disease
M.scrofulaceum – cervical lymphadenitis
M.avium complex
M.marinum- swimming pool granulomma

•Anti tubercular agents treat all forms of
mycobacterium
Different pools
 Dormant phase
 Multiplication phase
 Semi dormant phase- R
 Inside macrophages-Z
Antitubercular Therapy
Effectiveness depends upon:
 Type of infection
 Adequate dosing
 Sufficient duration of treatment

 Drug compliance
 Selection of an effective drug combination
Antitubercular Agents:
Mechanism of Action
Three Groups

 Cell wall synthesis inhibitors cycloserine, ethionamide,

isoniazid
 Protein wall synthesis inhibitors streptomycin, kanamycin,
capreomycin, rifampin, rifabutin
 Other mechanisms of action
Anti-TB drugs
 First line

 Isoniazid

H
 Rifampin
R
 Pyrazinamide Z
 Ethambutol
E
 Streptomycin S

 High efficacy
 Low toxicity

 Easily available
 Used in new cases
 All are given orally except S

(i.m.)
 All are tuberculocidal except

E(tuberculostatic)
SECOND LINE

NEWER DRUGS

 Thiacetazone

 Ciprofloxacin

 PAS

 Ofloxacin

 Ethionamide

 Clarithromycin

 Cycloserine

 Azithromycin

 Kanamycin

 rifabutin

 Amikacin
•Less efficacious

•more toxic and expensive
•Used in resistant cases
HOW DOES INH KILLS M. TUBERCULOSIS

PRODURG ACTIVATED BY CATALYSE EANZYME PEROXYDASE (katG)
UNABLE TO ENCODE ENOYL - ACP REDUCTASE OF
FATTY ACID SYNTHASE II
NO CONVERSION OF UNSATURATED FATTY ACIDS
TO SATURATED FATTY ACIDS
NO BIOSYNTHESIS OF MYCOLIC ACID

M. TUBERCULOSIS CAN NOT SURVIVE
 Resistance: Mutation in KatG gene

P.K: Dose300mg/day or 600mg 3 times weekly
 Orally well absorbed
 Effective for actively growing org.
 Distributed in pleural, peritoneal and synovial fluid
 CSF -20% in inflammed -100%
 Does not binds to serum proteins
 Metabolised in liver by N-“acetyltransferase”
 Excreted in urine
Side effects: Dose depended toxity
 Peripheral neuritis: vitamin B6(10-40mg)



Induce increase excretion of pyridoxine
Dec peripheral utilization of pyridoxine

 Hepatotoxicity
 Allergic reactions

DI:
 Aluminium hydroxide – dec. absorption
 PAS- Inhibits metabolism
 INH dec metabolism of Phenytoin
 Mech: It binds to the b subunit of bacterial “DNA

dependent RNA polymerase”
 Bacteriocidal action
 Good sterilizing and prevent resistance
 Act best on slow multiplying bacilli
Resistance : rpo B gene
P.K:
 Well absorbed orally
 Penetrates all tissues, TB cavities, Placenta and CSF
 Excreted through liver in to bile
 Under go hepatic circulation
 Metabolites excreted through faces
 Potent enzyme inducer
 600mg daily dose before breakfast
Side effect: Hepatitis
 Red orange colour Urine
 DI: More interaction it inc. metabolism of other drugs
ETHAMBUTOL : MECHANISM OF ACTION
EXACT MECHANISM : NOT KNOWN
PROBABILITIES :

ETHAMBUTOL
BLOCKS
ARABINOSYL TRANSFERASE (ENCODED BY emb)

NO POLYMERIZATION REACTION OF ARABINOGLYCAN

INTERFERANCE IN CELL WALL SYSNTHESIS
 Included as 4th drug
 Oral BV -80%
 Wide distribution
 Daily dose 800-1000mg or 1600mg thrice a week

Side effects:
 25mg for 9 months cause retrobulbar neuritis
impairing visual acuity
 Dec renal urease excretion- gouty arthritis
 Synthetic analogue of nicotinamide acid
 ACTIVE IN ACIDIC PH (5.5)
 Excellent action against intracellular bacilli
 Active against old non- replicating bacilli due to their

low membrane potential and disruption of membrane
potentil by pyrazinoic acid and acidic pH
PZA : MECHANISM OF ACTION
PZA enter through passive diffusion
Bac. Pyrazinamidase

Pyrazinoic acid

inhibit myobacterial fatty acid synthase -I

INTERFERANCE IN CELL WALL SYSNTHESIS
 Well absorbed Orally
 Wide distribution

 Metabolized by liver
 Excreted through urine
 Half life 9-10hrs

Side effects: Hepatotoxicity
 Daily dose 1500mg or 2000mg thrice in week
SULPHATE

 FIRST ANTI TUBERCULAR DRUG
 DISCOVERED BY WAKSMAN IN 1943

 ISOLATED FROM Streptomyces griseus
 IM 1000 MG

 CONTAINS N - METHYL- L- GLUCOSAMINE
 CONTAINS STREPTIDINE
 BACTERICIDAL
 ACTIVE AGAINST EXTRACELLULAR BACILLI
 Seldom use
 Cause gastric irritation, peripheral neuritis, optic






neuritis
It block mycolic acids
Tuberculostatic
Acts on extracellular and intra cellular organism
Recommended dose 1g/day
 It was once used as first line drug



Low cost, more efficacy
In combination with INH

 But now it was used as 2nd line drug



Ototoxicity, hepatotoxicity,
life threatening hypersensivity reaction

 Tuberculostatic drugs

 150mg once daily in combination with INH
 It is structural analogue of PABA
 Bacteriostatic
 Effect against only M. Tuberculosis
 Fir second due to poor compliance

 Cause crystalueria
 Hypersensivity reaction
 Dose 8-12g/day orally in 3 divided doses
 Rifabutin is structural analogue of rifampicin
 Same mech, resis, spectrum
 Less enzyme inducer
 Better activity on M.avium complex

 It used alone or combination with PZA in latent

tubercular infection

ADR: Neutopenia
Skin rashes
 National Tuberculosis Progamme 1997
 To dec therapeutic failure
 Patient poor compliance
 Directly Observed treatment Strategy (DOTS)
 Intensive phase
 Continuous phase
 Intensive phase: period of 2-3months
 Rapidly kill the bacteria
 To minimize the chance for devp. Resistances
 Bring about sputum conversion
 Symptomatic relief

 Continuous phase: 4-6months
 Remaining bacilli eliminated
 Minimize the chance of relapse
Special Terms
 Fresh case
 Open case
 Defaulter
 Treatment failure
Regime
TB category

Intensive Contin..
phase
phase

Total
duration

New smear +Ve
New smear –Ve but serious ill
New seriously ill
extrapulmonary TB

2(HRZE)

6

II

2(HRZES) 5(HRE)

Smear +ve retreatment group
Treatment failure/relapse

+ 1(HRZE)3

I
4(HR)

8

II
New smear –Ve pulmonary TB
but not serious ill
Extra pulmonary TB

2(HRZ)

4(HR)

6
MDR TB
 Resistance to both H and R with or without
resistance to other drugs.
 Incidence of H resistance = 10-6
 Incidence of R resistance =10–8
 Incidence of resistance to both = 10–14
 Therapy depends on earlier regime
 Dosage
 Regularity
 Presence of associated diseases-HIV/AIDS,
Diabetes, Leukaemia
 MDR:
 For INH : RMP+ PZA+ ETB for 12mon
 For RMP: INH+PZA+ETB for 12months
 For Both : PZA+ETB+S+ ciprofloxacin for 12-18months
 Chemoprophylaxis: closed contact to infected patients

or neonate of TB mother
 INH 300mg/day (5mg/kg/day children) for 6-12month
 INH (5mg/kg/day)+RMP(10mg/kg/day) for 6months
 In pregnancy
 All drugs are safe except E
 In hepatic dysfunction
 Z is contraindicated
 In renal dysfunction
 S is contraindicated

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9. tb

  • 2.  Chronic granulomatous disease.  Causative org M.TUBERCULOSIS.  Incidence in India 1.8 million people develop T.B every year of which 0.8 million are infectious.  Mode of Transmission  Droplet Infection  Contact transmission
  • 3.  Droplets are expelled by coughing or sneezing  Tubercle bacilli then spread to other body organs  Tubercle bacilli may become dormant  Even if extend beyond the lymph nodes, TB lesion get healed and calcified  But in immounocomparmised or undernourished become active
  • 4. Mycobacterium Infections Common Infection Sites lung (primary site) liver brain Kidney bone Less o2 tension Symptoms Low grade fever Night sweats Fatigue Weight loss Blood streaked productive cough Malaise
  • 5. Other acid fast bacilli  Mycobateria other than M. tuberculosis c/s non     tuberculosis/ atypical mycobacteria M.kanasasii- milder but chronic pulmonary disease M.scrofulaceum – cervical lymphadenitis M.avium complex M.marinum- swimming pool granulomma •Anti tubercular agents treat all forms of mycobacterium
  • 6. Different pools  Dormant phase  Multiplication phase  Semi dormant phase- R  Inside macrophages-Z
  • 7. Antitubercular Therapy Effectiveness depends upon:  Type of infection  Adequate dosing  Sufficient duration of treatment  Drug compliance  Selection of an effective drug combination
  • 8. Antitubercular Agents: Mechanism of Action Three Groups  Cell wall synthesis inhibitors cycloserine, ethionamide, isoniazid  Protein wall synthesis inhibitors streptomycin, kanamycin, capreomycin, rifampin, rifabutin  Other mechanisms of action
  • 9. Anti-TB drugs  First line  Isoniazid H  Rifampin R  Pyrazinamide Z  Ethambutol E  Streptomycin S  High efficacy  Low toxicity  Easily available  Used in new cases  All are given orally except S (i.m.)  All are tuberculocidal except E(tuberculostatic)
  • 10. SECOND LINE NEWER DRUGS  Thiacetazone  Ciprofloxacin  PAS  Ofloxacin  Ethionamide  Clarithromycin  Cycloserine  Azithromycin  Kanamycin  rifabutin  Amikacin •Less efficacious •more toxic and expensive •Used in resistant cases
  • 11. HOW DOES INH KILLS M. TUBERCULOSIS PRODURG ACTIVATED BY CATALYSE EANZYME PEROXYDASE (katG) UNABLE TO ENCODE ENOYL - ACP REDUCTASE OF FATTY ACID SYNTHASE II NO CONVERSION OF UNSATURATED FATTY ACIDS TO SATURATED FATTY ACIDS NO BIOSYNTHESIS OF MYCOLIC ACID M. TUBERCULOSIS CAN NOT SURVIVE
  • 12.  Resistance: Mutation in KatG gene P.K: Dose300mg/day or 600mg 3 times weekly  Orally well absorbed  Effective for actively growing org.  Distributed in pleural, peritoneal and synovial fluid  CSF -20% in inflammed -100%  Does not binds to serum proteins  Metabolised in liver by N-“acetyltransferase”  Excreted in urine
  • 13. Side effects: Dose depended toxity  Peripheral neuritis: vitamin B6(10-40mg)   Induce increase excretion of pyridoxine Dec peripheral utilization of pyridoxine  Hepatotoxicity  Allergic reactions DI:  Aluminium hydroxide – dec. absorption  PAS- Inhibits metabolism  INH dec metabolism of Phenytoin
  • 14.  Mech: It binds to the b subunit of bacterial “DNA dependent RNA polymerase”  Bacteriocidal action  Good sterilizing and prevent resistance  Act best on slow multiplying bacilli Resistance : rpo B gene
  • 15. P.K:  Well absorbed orally  Penetrates all tissues, TB cavities, Placenta and CSF  Excreted through liver in to bile  Under go hepatic circulation  Metabolites excreted through faces  Potent enzyme inducer  600mg daily dose before breakfast
  • 16. Side effect: Hepatitis  Red orange colour Urine  DI: More interaction it inc. metabolism of other drugs
  • 17. ETHAMBUTOL : MECHANISM OF ACTION EXACT MECHANISM : NOT KNOWN PROBABILITIES : ETHAMBUTOL BLOCKS ARABINOSYL TRANSFERASE (ENCODED BY emb) NO POLYMERIZATION REACTION OF ARABINOGLYCAN INTERFERANCE IN CELL WALL SYSNTHESIS
  • 18.  Included as 4th drug  Oral BV -80%  Wide distribution  Daily dose 800-1000mg or 1600mg thrice a week Side effects:  25mg for 9 months cause retrobulbar neuritis impairing visual acuity  Dec renal urease excretion- gouty arthritis
  • 19.  Synthetic analogue of nicotinamide acid  ACTIVE IN ACIDIC PH (5.5)  Excellent action against intracellular bacilli  Active against old non- replicating bacilli due to their low membrane potential and disruption of membrane potentil by pyrazinoic acid and acidic pH
  • 20. PZA : MECHANISM OF ACTION PZA enter through passive diffusion Bac. Pyrazinamidase Pyrazinoic acid inhibit myobacterial fatty acid synthase -I INTERFERANCE IN CELL WALL SYSNTHESIS
  • 21.  Well absorbed Orally  Wide distribution  Metabolized by liver  Excreted through urine  Half life 9-10hrs Side effects: Hepatotoxicity  Daily dose 1500mg or 2000mg thrice in week
  • 22. SULPHATE  FIRST ANTI TUBERCULAR DRUG  DISCOVERED BY WAKSMAN IN 1943  ISOLATED FROM Streptomyces griseus  IM 1000 MG  CONTAINS N - METHYL- L- GLUCOSAMINE  CONTAINS STREPTIDINE  BACTERICIDAL  ACTIVE AGAINST EXTRACELLULAR BACILLI
  • 23.  Seldom use  Cause gastric irritation, peripheral neuritis, optic     neuritis It block mycolic acids Tuberculostatic Acts on extracellular and intra cellular organism Recommended dose 1g/day
  • 24.  It was once used as first line drug   Low cost, more efficacy In combination with INH  But now it was used as 2nd line drug   Ototoxicity, hepatotoxicity, life threatening hypersensivity reaction  Tuberculostatic drugs  150mg once daily in combination with INH
  • 25.  It is structural analogue of PABA  Bacteriostatic  Effect against only M. Tuberculosis  Fir second due to poor compliance  Cause crystalueria  Hypersensivity reaction  Dose 8-12g/day orally in 3 divided doses
  • 26.  Rifabutin is structural analogue of rifampicin  Same mech, resis, spectrum  Less enzyme inducer  Better activity on M.avium complex  It used alone or combination with PZA in latent tubercular infection ADR: Neutopenia Skin rashes
  • 27.  National Tuberculosis Progamme 1997  To dec therapeutic failure  Patient poor compliance  Directly Observed treatment Strategy (DOTS)  Intensive phase  Continuous phase
  • 28.  Intensive phase: period of 2-3months  Rapidly kill the bacteria  To minimize the chance for devp. Resistances  Bring about sputum conversion  Symptomatic relief  Continuous phase: 4-6months  Remaining bacilli eliminated  Minimize the chance of relapse
  • 29. Special Terms  Fresh case  Open case  Defaulter  Treatment failure
  • 30. Regime TB category Intensive Contin.. phase phase Total duration New smear +Ve New smear –Ve but serious ill New seriously ill extrapulmonary TB 2(HRZE) 6 II 2(HRZES) 5(HRE) Smear +ve retreatment group Treatment failure/relapse + 1(HRZE)3 I 4(HR) 8 II New smear –Ve pulmonary TB but not serious ill Extra pulmonary TB 2(HRZ) 4(HR) 6
  • 31. MDR TB  Resistance to both H and R with or without resistance to other drugs.  Incidence of H resistance = 10-6  Incidence of R resistance =10–8  Incidence of resistance to both = 10–14  Therapy depends on earlier regime  Dosage  Regularity  Presence of associated diseases-HIV/AIDS, Diabetes, Leukaemia
  • 32.  MDR:  For INH : RMP+ PZA+ ETB for 12mon  For RMP: INH+PZA+ETB for 12months  For Both : PZA+ETB+S+ ciprofloxacin for 12-18months  Chemoprophylaxis: closed contact to infected patients or neonate of TB mother  INH 300mg/day (5mg/kg/day children) for 6-12month  INH (5mg/kg/day)+RMP(10mg/kg/day) for 6months
  • 33.  In pregnancy  All drugs are safe except E  In hepatic dysfunction  Z is contraindicated  In renal dysfunction  S is contraindicated