Hello friends. In this PPT I am talking about Anti-TB & anti leprosy drugs. If you like it, please do let me know in the comments section. A single word of appreciation from you will encourage me to make more of such videos. Thanks. Enjoy and welcome to the beautiful world of pharmacology where pharmacology comes to life. This video is intended for MBBS, BDS, paramedical and any person who wishes to have a basic understanding of the subject in the simplest way.

1. Anti-TB & anti leprosy drugs
Dr. Karun Kumar
Senior Lecturer
Dept. of Pharmacology

2. Antitubercular Drugs
• First line  High antitubercular efficacy & low
toxicity; are used routinely
• Second line  Low antitubercular efficacy or higher
toxicity or both; used as reserve drugs
• First line  Isoniazid (H), Ethambutol (E), Rifampin
(R), Streptomycin (S), Pyrazinamide (Z), Rifabutin,
Rifapentine
• Second line  Ethionamide, FQs (CLOM), PAS,
Linezolid, Injectable drugs (Kanamycin, Amikacin,
Capreomycin)

3. Classification

4. WHO & RNTCP classification
Terizidone
Rifabutin
Bedaquiline
Proteomanid
Coamoxiclav
Imipenem/
Cilastatin

5. • Group I  Most potent and best tolerated oral drugs
• Group II  Potent and bactericidal but injectable
drugs
• Group III  FQs reserved for resistant TB
• Group IV  Less effective for resistant TB
• Group V  Uncertain efficacy; not to be used for
MDR-TB; but may be used for extensively drug-
resistant TB (XDR-TB)

7. Isoniazid (H)
• Excellent antitubercular drug (tuberculocidal)
• Fast multiplying organisms are rapidly killed, but
quiescent ones are only inhibited
• MOA  Inhibition of synthesis of mycolic acids
which are unique fatty acid components of
mycobacterial cell wall.
• Adverse effects  NH (Neuritis, Hepatitis).
• Other side effects are lethargy, rashes, fever, acne
and arthralgia

8. Rifampin (Rifampicin, R)
• Bactericidal action covers all subpopulations of TB
bacilli, but acts best on slowly or intermittently
dividing ones (spurters)
• MOA  Inhibits DNA dependent RNA synthesis
• RIF (Red discoloration of urine, Induction of liver
enzymes & its toxicity, Flu like symptoms);n,v,d
• Must be given empty stomach
• Other uses  Leprosy, Prophylaxis of Meningococcal
and H. influenzae meningitis and carrier state

9. Pyrazinamide (Z)
• Weakly tuberculocidal; more lethal to intracellularly
located bacilli and to those at sites showing an
inflammatory response (pH is acidic at both these
locations)
• MOA  Similar to INH
• A/E  Pain in the joints (gout) due to hyperuricemia
Plus hepatotoxicity; Other adverse effects are
abdominal distress, arthralgia, flushing, rashes, fever
and loss of diabetes control

10. Ethambutol (E)
• Tuberculostatic and is active against MAC
• MOA  Inhibit arabinogalactan synthesis thereby
interfering with mycolic acid incorporation in
mycobacterial cell wall
• A/E  Eye toxicity (Loss of visual acuity/colour
vision, field defects due to optic neuritis); nausea,
rashes, fever, rarely peripheral neuritis;
hyperuricemia is due to interference with urate
excretion

12. Treatment of tuberculosis
• 3-4 drugs under DOTS (Directly Observed Treatment
Short course)
• Goals :-
1. Kill dividing bacilli
2. Kill persisting bacilli
3. Prevent emergence of resistance
• Intensive phase (IP)  4–5 drugs lasting 2–3 months
aimed to rapidly kill the bacilli, bringing about
sputum conversion and afford fast symptomatic relief

13. • Continuation phase (CP)  2–3 drugs lasting 4–5
months during which the remaining bacilli are
eliminated so that relapse does not occur

14. Type of
pt.
Durat
ion
IP CP
New 6 mth 2HRZE 4HRE
Prev.
treated
8 mth 2HRZES
+ 1HRZE
5
HRE

15. Multidrug-resistant (MDR) TB
• Resistance to both H and R, and may be any number
of other (1st line) drug(s)

16. Mycobacterium avium complex (MAC)
infection
• MAC is an opportunistic pathogen which causes
disseminated and multifocal disease in
immunocompromized (HIV-AIDS) patients
• Clarithromycin or Azithromycin is recommended for
prophylaxis of MAC inf. in pts. with CD4 count < 50
cells/μL
• Regimen  3 or 4 drug intensive phase of 2–6
months, followed by 2 drug maintenance phase for
at least 12 months

18. Classification of anti leprotic drugs

19. Antileprotic Drugs
• Dapsone  Inhibits PABA incorporation into folic
acid by folate synthase; leprostatic
• Well tolerated at doses 100 mg/day or less.
• Other uses  In combination with pyrimethamine,
dapsone can be used for chloroquine-resistant
malaria, toxoplasmosis and P. jirovecii infection

20. Adverse Effects
• Mild haemolytic anaemia is common
• Gastric intolerance—nausea and anorexia are
frequent in the beginning, decrease later
• Other side effects are methaemoglobinaemia,
headache, paresthesias, mental symptoms and drug
fever
• Cutaneous reactions include allergic rashes, fixed
drug eruption, hypermelanosis, phototoxicity
• Lepra reaction

21. Clofazimine
• Leprostatic; has antiinflammatory properties.
• MOA 
1. Interference with template function of DNA in M.
leprae
2. Alteration of membrane structure and its transport
function.
3. Disruption of mitochondrial electron transport
chain

22. Adverse effects
• Skin  Reddish-black discolouration of skin,
especially on exposed parts. Discolouration of hair
and body secretions may also occur. Dryness of skin
and itching is often troublesome. Conjunctival
pigmentation may create cosmetic problem
• GI symptoms  Nausea, anorexia, abdominal pain,
weight loss and enteritis with intermittent loose
stools can occur

23. Rifampin
• Most potent cidal drug for M.leprae; rapidly renders
leprosy patients noncontagious.
• Upto 99.99% M.leprae are killed in 3–7 days by 600
mg/day dose.
• Shortens the duration of T/t
• Prev. dev. of resistance to Dapsone

24. Treatment of leprosy
• Leprosy is a chronic granulomatous infection caused
by Mycobacterium leprae; primarily affecting skin,
mucous membranes and nerves
Pt. has few bacilli (non-infective) Pt. has high bacillary load (infective)