Antitubercular drugsnew

ANTITUBERCULAR DRUGS
A D I T I M A I T R A
S E N I O R R E S I D E N T
P H A R M A C O L O G Y D E P A R T M E N T
C N M C H

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INTRODUCTION
TB is caused by Mycobacterium Tuberculosis which affects most commonly
the lungs .
 TB is an airborne bacterial infection
Transmission occurs through inhalation of droplet nuclei
This chronic granulomatous disease – major health problem
1/3rd of world`s population is infected of which only 10-15% develop the
disease
 India – 2.3 million patients were suffering from India (highest contributor)
2018

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MILESTONES OF ANTI TB PROGRAMME IN INDIA
• National Tuberculosis Programme of India – 1962
•Revised National Tuberculosis Control Programme launched in 1997
•Nation wide coverage of DoT therapy 2006
•Notifiable disease 2012 -web-based TB notification system NIKSHAY was established to provide platform for
notification from both public and private sectors.
•Revised treatment guidelines 2016,2019
•NATIONAL STRATEGIC PLAN (NST) FOR TUBERCULOSIS ELIMINATION 2017–2025 – Decline burden, morbidity,
motality and elimination. DTPB Approach is- detect – treat – prevent-build

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ANTI TUBERCULAR DRUG CLASSIFICATION
1st line:High efficacy , low toxicity - routinely used
Oral:
A. Isoniazid (H)
B. Rifampicin (R)
C. PyrazinamideZ
D. Ethambutol (E)
Intramuscular:
Streptomycin (S)
2nd line- Low antitubercular efficacy and/or higher toxicity –
reserve drugs:
Oral-thiacetazone, PAS, Ehionamide, Cycloserine,
Rifabutin,Rifapentine
Injectable-kanamycin, capreomycin, amikacin,

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ALTERNATE CLASSIFICATION-WHO 2010,RNTCP 2016
Group I: most potent , best tolerated oral drugs used routinely.
Group II: potent and bactericidal, but injectable
Group III: bactericidal oral drugs; drug resistant TB should receive
one FQ.
Group IV: less effective, bacteriostatic/more toxic oral drugs for
resistant TB.
Group V: are drugs with uncertain efficacy; not recommended for
MDR-TB; may be used in extensively resistant TB (XDR-TB).

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SUBPOPULATIONS OF TB BACILLI
(a)Rapidly growing with high bacillary load as in the wall of a cavitary lesion where oxygen tension is
high and pH is neutral. These bacilli are highly susceptible to H
(b) Slow growing located intracellularly (inside macrophages) and at inflamed sites where pH is low.
They are particularly vulnerable to Z
(c) Spurters found mostly within caseous material where oxygen tension is low but pH is neutral: the
bacilli grow intermittently with occasional spurts of active metabolism. R is most active on this
subpopulation.
(d) Dormant some bacilli remain totally inactive for prolonged periods. No antitubercular drug is
significantly active against them.

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Isoniazid (Isonicotinic acid hydrazide, H)
Essential component – unless resistance or intolerability issue
Tuberculocidal – fast multiplying organisms
Acts on Extracellular as well as intracellular
 Active in acidic and alkaline medium
Acts by Oxygen dependent pathway
MOA:
 Inhibition of synthesis of mycolic acid – unique fatty acid in
mycobacterial cell wall – lipid content of mycobacteria reduced
Genes “InhA” and “KasA” are targets for INH action
 INH enters mycobacteria – converts to active metabolite by catalase
peroxidase (KatG) enzyme
Adducts with NAD and inhibits “InhA” and “KasA” Also adducts with
NADPH – DHFRase inhibition – no DNA

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ISONIAZID ( cont.)
Pharmacokinetics:
 Complete oral absorption – only impaired if isoniazid is taken with
high-fat meals
Penetrates all tissues, cavities, meninges, placenta
Extensively metabolized in liver; most important pathway being N-
acetylation by NAT2 & it is genetically determined. The rate of INH
acetylation shows genetic variation. There are either:
1. Fast acetylators: (30–40% of Indians) t½ of INH 1 hr.
2. Slow acetylators: (60–70% of Indians) t½ of INH 3 hr.
Acetylator status does not matter if INH is taken daily.
 Isoniazid induced peripheral neuritis is more common in slow
acetylators
Excretion is through glomerular filtration and secretion, predominantly
as metabolites

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ISONIAZID ( cont.)
Resistance:
1 in 106 tubercle bacilli is inherently resistant- if given alone
Mutation of KatG ,“InhA” and “KasA”
Efflux of INH and its concentrating mechanism
Drug Interactions :
Aluminium hydroxide inhibits INH absorption.
INH retards phenytoin, carbamazepine, diazepam, theophylline and warfarin metabolism
by
inhibiting CYP2C19 and CYP3A4,

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ISONIAZID ADR: -
Most important dose-dependent toxic effects- Peripheral neuritis & variety
of neurological manifestations (paresthesias, numbness, mental
disturbances, rarely convulsions)
Pyridoxine given prophylactically (10 mg/day) prevents the neurotoxicity.
INH neurotoxicity is treated by pyridoxine 100 mg/day.
Prophylactic pyridoxine must be given to diabetics, chronic alcoholics,
malnourished, pregnant, lactating and HIV infected patients, but routine
use is not mandatory.
INH reacts with pyridoxal to form a hydrazine- inhibits generation of active
coenzyme pyridoxal phosphate. Due to formation of hydrazones, the renal
excretion of pyridoxine compounds is increased- produces a pyridoxine
deficiency state

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ISONIAZID ADR: -
Hepatitis, a major adverse effect of INH [MCQ]
Rare in children, but more common in older people and
in alcoholics (chronic alcoholism induces CYP2E1 which
generates the hepatotoxic metabolite).
 INH hepatotoxicity is due to dose-related damage to
liver cells, but is reversible on stopping the drug.
Other -lethargy, rashes, fever, acne and arthralgia.

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Rifampin (Rifampicin, R)
Obtained from Streptomyces mediterranei.
Rifampin is bactericidal to M. tuberculosis, Staph. aureus, N. meningitidis,
H. influenzae, E. coli, Klebsiella, Pseudomonas, Proteus and Legionella.
 Acts best on slowly or intermittently dividing ones (spurters)
Both extra- and intracellular organisms are affected
Only drug acts against dormant bacteria
MOA-
• Rifampin interrupts RNA synthesis
•R binds to β subunit of mycobacterial DNA-dependent RNA polymerase
(encoded by rpoB gene ) → Blocks polymerizing function
•The basis of selective toxicity is that mammalian RNA polymerase does not
avidly bind rifampin.

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Rifampin (Rifampicin, R)
RESISTANCE:
• incidence of resistant bacilli is less than 10–7
•unusual to have primary rifampin resistant tubercular infection [India only2%] .
•resistance due to mutation in the rpoB gene- reducing its affinity for the drug.
INDICATION:
1. TB [can be used safely in renal dysfunction ]mcq
2. Leprosy
3. Prophylaxis of Meningococcal and H. influenzae meningitis and carrier state.
4. Second/third choice drug for MRSA, diphtheroids and Legionella infections.
5. Combination of doxycycline and rifampin - brucellosis.

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Pharmacokinetics
I well absorbed orally, (bioavailability is ~ 70%) - food decreases absorption- R to be taken in empty stomach
It is widely distributed -penetrates intracellularly, enters tubercular cavities, caseous masses, placenta,
meninges( largely pumped out from CNS by P-glycoprotein). t½ of rifampin is variable (2–5 hours)
It is metabolized in liver to an active deacetylated metabolite which is excreted mainly in bile, some in urine also.
Rifampin and its desacetyl derivative undergo enterohepatic circulation.
Drug Interactions
Rifampin is a microsomal enzyme inducer—↑CYP450
isoenzymes(CYP3A4, CYP2D6 CYP1A2 and CYP2C)- ↑ its own metabolism
as well as that of many drugs
Contraceptive failures have occurred. It is advisable to switch over to an
oral contraceptive containing higher dose (50 μg) of estrogen or use
alternative method of contraception

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RIFAMPICIN ADVERSE REACTION
Hepatitis, a major adverse dose-related effect(infrequent with < 600 mg/ day
dose)
Generally occurs in patients with preexisting liver disease- Development of
jaundice requires discontinuation of the drug—then it is reversible.
Cutaneous syndrome: flushing, pruritus + rash (especially on face and scalp),
redness and watering of eyes.,
Flu syndrome: with chills, fever, headache, malaise and bone pain.
Abdominal syndrome: nausea, vomiting, abdominal cramps with or without
diarrhoea. Urine and secretions may become orange-red— but this is harmless.
Serious but rare reactions:
Respiratory syndrome: breathlessness which may be associated with shock and
collapse
Purpura, haemolysis, shock and renal failure.

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•Rifabutin related to rifampin in structure and mechanism of action
•Less active against M tuberculosis, and more active against MAC
•Only place of rifabutin in the treatment of TB is as a substitute for R - to ↓drug interactions due to
strong enzyme inducing property of R. (Rifabutin is a much weaker inducer of CYP enzymes than
R) Esp important in HIV coinfected patients of TB who receive a protease inhibitor (PD) and/or a
non-nucleoside reverse transcriptase inhibitor (NNRTI) whose metabolism is markedly induced by R
rendering them ineffective. The primary indication of rifabutin is for prophylaxis and treatment of
MAC infection( 300 mg/day)in HIV-AIDS patients
•ADR: gastrointestinal intolerance, rashes ,granulocytopenia, myalgia and uveitis
RIFABUTIN

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 Rifampin congener,
t1/2 of rifapentine (13-15 hr) is longer than that of rifampin, so that it can
be given once or twice weekly.
 Only indication of rifapentine (600 mg once/twice weekly) is in the
continuation phase of treatment of TB, as a substitute of daily rifampin. It
is not suitable for use during the intensive phase.
 Once weekly rifapentine combined with INH has also been employed to
treat latent TB.
RIFAPENTIN

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Pyrazinamide (Z)
Chemically similar to INH
More active in acidic medium.
More lethal to intracellularly located bacilli and to those at sites showing an inflammatory response
By killing the residual intracellular bacilli it has good ‘sterilizing’ activity. Its inclusion has enabled duration of
treatment to be shortened and risk of relapse to be reduced.
Mechanism of action:
It converted inside the mycobacterial cell into an active
metabolite pyrazinoic acid (POA)by an enzyme
(pyrazinamidase) encoded by the pncA gene.
POA gets accumulated in acidic medium and probably
inhibits mycolic acid synthesis, but by interacting with a
different fatty acid synthase. Pyrazinoic acid - disrupt
mycobacterial cell membrane and its transport function.
Resistance : mostly due to mutation in the pncA gene.

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PK:
absorbed orally, widely distributed, has good penetration in CSF( highly useful
in meningeal TB) extensively metabolized in liver and excreted in urine.
plasma t½ is 6–10 hours.
ADR:
Hepatotoxicity is the most important dose related adverse effect.
Less common in the Indian population than in western countries.
Daily dose is now limited to 25–30mg/kg which produces only a low incidence
of hepatotoxicity. It is contraindicated in patients with liver disease.
Safety during pregnancy is uncertain.
Hyperuricaemia is common & due to inhibition of uric acid secretion in kidney
Other :abdominal distress, arthralgia, flushing, rashes, fever and loss of
diabetes control: repeated blood glucose monitoring is warranted in diabetics.
Pyrazinamide (Z)

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ETHAMBUTOL ( E )
 Ethambutol is selectively tuberculostatic
Fast multiplying bacilli are more susceptible.
 Hasten the rate of sputum conversion and to prevent development of resistance(primary purpose)
Mechanism of action of E –
Resistance develops slowly and is most commonly associated with mutation in embB gene.
It is safe during pregnancy. It is not hepatotoxic.
Ethambutol is used in MAC infection as well

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ETHAMBUTOL ( E )
SIDE EFFECTS :
Loss of visual acuity/colour vision, field defects due to optic neuritis
- most important ( due to effect on amacrine & bipolar cells of
retina) [mcq]
Dose and duration of therapy dependent toxicity.
Early recognition & stoppage of the drug-visual toxicity reversible.
Patients should be instructed to stop the drug at the first indication
of visual impairment. Young children now allowed with due
precaution.
Contraindicated in patients with optic neuritis.
other S/E:
nausea, rashes, fever, rarely peripheral neuritis , hyperuricemia
Caution required in patients with renal disease.

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STREPTOMYCIN (S)
 Aminoglycoside antibiotic, tuberculocidal, labelled as a
‘supplemental’ 1st line drug.
 Acts only on extracellular bacilli (because of poor penetration
into cells). It penetrates tubercular cavities, but does not cross to
the CSF.

 Resistance developed rapidly when streptomycin was used alone
It is not hepatotoxic
lower margin of safety (ototoxicity and nephrotoxicity)
Contraindicated in pregnancy

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BEDAQUILINE
Diaaryl quinoline acts by a novel mechanism-targets mycobacterial ATP synthase, and enzyme
essential for supply of energy to mycobacterium TB
Use of BDQ for MDR-TB reduced the time for sputum to become culture negative .
Exhibits strong bactericidal and sterilizing activity against M. tuberculosis by killing both rapidly
multiplying as well as dormant bacilli
Bedaquiline (BDQ) MOA: inhibits mycobacterial ATP synthase-limiting energy production within
mycobacterial cell. The human ATP synthase is 20,000 fold less sensitive to BDQ than is the
mycobacterial enzyme.[mcq]
Resistance to BDQ primarily by mutation of ATP synthase enzyme & by acquisition of BDQ efflux
from the bacilli. no cross resistance between BDQ and any 1 line or 2nd line anti-TB drug occurs.

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Bedaquiline PK: well absorbed orally; fatty meal improves absorption, highly plasma protein bound ,extensively
distributed in tissues.
Metabolism occurs in liver, mainly by CYP3A4 - drug interactions occur with CYP3A4 inducers and inhibitors.
The terminal t½ of BDQ is very long ( 160 days), probably due to redistribution from tissues.
It is excreted mainly in faeces.
Recommendations regarding use of BDQ are:
 It should be used only for pulmonary MDR-TB adults (18 yr)
Women patients should be nonpregnant and willing to remain so during BDQ use
Cardiac fitness desirable
BDQ dose: maximum of 24 weeks in a dose of 400 mg/day for 2 weeks followed by 200 mg 3 times a week for the next
22 weeks.
Adverse effects of BDQ : nausea, headache. arthralgia and prolongation of QT interval, hepatotoxicity(with other QT
prolonging drug)
BEDAQUILINE

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DELAMANID
Nitroimidazole class drug-new drug
MOA: blocks mycolic acid synthesis & release NO
DOSE: 100mg BD for 24 weeks
INDICATION: MDR, XDR, MIXED PATTERN RESISTANT TB
ADR: QT prolongation, GI disturbances
recommendations regarding use of delamanid are:
 It should be used only for pulmonary MDR-TB adults (18 yr)
Women patients should be nonpregnant and willing to remain so during BDQ use
 Cardiac screening

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Diagnostic tests for TB

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Presumptive TB cases ( previously k/a suspected )
Presumptive pulmonary TB refers to a person with any of the symptoms or signs suggestive of TB:
• cough >2 weeks, • fever >2 weeks, • significant weight loss, • haemoptysis, • any abnormalities in chest X-ray
Presumptive TB cases in paediatric patients, where loss of body weight is defined that loss of >5% body weight as
compared to highest weight recorded in the last 3 months. The history of unexplained or no weight gain in the past 3
months and symptomatic child contact with any form of active TB in the last 2 years may be significant.
Presumptive DRTB cases as follows:
• TB patients who have failed treatment with first-line anti-tubercular drugs (ATD)
• Paediatric TB non-responder
• TB patients who are contacts of DRTB
• TB patients who are found positive on any follow-up sputum smear examination during treatment with first-line ATD
• Previously treated TB cases
• TB patients with HIV co-infection.

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Goals Of Antitubercular Chemotherapy
(a) Kill dividing bacilli- patient is non-contagious to the community: transmission of TB is
interrupted,affords quick symptom relief.
(b) Kill persisting bacilli To effect cure and prevent relapse.
(c) Prevent emergence of resistance - bacilli remain susceptible to the drugs.
PHASES OF TB TREATMENT:
All regimens have an initial intensive phase with 4–5 drugs lasting 2–3 months aimed to
rapidly kill the bacilli, bringing about sputum conversion and afford fast symptomatic relief.
This is followed by a continuation phase with 2–3 drugs lasting 4–5 months during which the
remaining bacilli are eliminated so that relapse does not occur.

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CASE DEFINITIONS
1.Microbiologically confirmed TB case -presumptive TB patient with biological specimen positive for
acid-fast bacilli, or positive for mycobacterium TB on culture, or positive for TB through Quality
Assured Rapid Diagnostic molecular test.
2. Clinically diagnosed TB case -presumptive TB patient who is not microbiologically confirmed, but has
been diagnosed with active TB by a clinician on the basis of X-ray abnormalities, histopathology or
clinical signs with a decision to treat the patient with a full course of anti-TB treatment.
Microbiologically confirmed or clinically diagnosed cases of TB are classified according to
1. Anatomical site of disease
2. History of previous TB
3. Drug resistance.

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ANATOMICAL
CLASSIFICATION OF TB
PULMONARY TUBERCULOSIS -
EXTRA PULMONARY TUBERCULOSIS
MILIARY -
Pulmonary TB
Miliary TB

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CLASSIFICATION – BASED ON HISTORY OF THE
PREVIOUS TREATMENT
1. New case – A TB patient who has never had treatment for TB or has taken ATD for <1 month.
2 Previously treated patients have received one month or more ATD in the past. This may be:
(a) Recurrent TB case – A TB patient previously declared as successfully treated
(cured/treatment completed) and who is subsequently found to be microbiologically confirmed
TB case is a recurrent TB case. (Previously called relapse.)
(b) Treatment after failure – Patients are those who have previously been treated for TB and
whose treatment failed at the end of their most recent course of treatment. (Previously, it was
called failure)
3. Treatment after loss to follow-up – A TB patient previously treated for TB for one month or
more and who was declared lost to follow-up in their most recent course of treatment and
subsequently found microbiologically confirmed TB cases. (Previously called treatment after
default)

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CLASSIFICATION ON THE BASIS OF DRUG RESISTANCE
1. Mono resistance (MR) – A TB patient whose biological specimen is resistant to one first-line anti-TB
drug only.
2. Poly resistance (PDR) – A TB patient whose biological specimen is resistant to more than one
first-line anti-TB drug, other than both INH and Rifampicin.
3. Multi-drug resistance (MDR) – A TB patient whose biological specimen is resistant to both INH and
Rifampicin with or without resistance other first-line ATD, based on results from a Quality Assured
Laboratory. (No changes.)
4. Rifampicin resistance (RR) – Resistance to Rifampicin detected by phenotypic or genotypic methods
with or without resistant to other ATD excluding INH. Patient with RR should be managed as if they
are in MDR TB case.
5. Extensive drug resistance (XDR) – MDR TB case whose biological specimen was resistant to a
Fluroquinolone (FQ) and a second-line injectable ATD from a Quality Assured Laboratory. (No
changes.)

NEW GUIDELINES
For new TB cases
• Treatment in IP will consist of 8 weeks of INH, Rifampicin, Pyrazinamide and Ethambutol in daily dosages as
per four weight bands categories
• There will be no need for extension of IP
• Only Pyrazinamide will be stopped in CP while the other three drugs will be continued for another 16 weeks
as daily dosages.
For previously treated cases:
• IP will be of 12 weeks, where injection Streptomycin will be stopped after 8 weeks and the remaining four
drugs in daily dosages as per weight band for another 4 weeks
• No need of extension of IP
• At the start of CP, Pyrazinamide will be stopped while rest of the drugs will be continued for another 20
weeks as daily dosages.

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NEW GUIDELINES
Management of extra-pulmonary TB (new guidelines) –
• The CP in both new and previously treated cases may be extended 3–6 months in certain TB such as
a) CNS
b) skeletal
c) disseminated TB
d) based on clinical decision of the treating physicians
Extension beyond 3 months will only be on recommendation of experts of concerned field.

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MDR/RR TB cases (without additional resistance)
Treatment regimen for MDR TB contains 6–9 months of IP with Kanamycin, Levofoxacin, Ethambutol,
Pyrazinamide, Ethionamide and Cycloserine and 18 months of CP with Levofoxacin, Ethambutol, Ethionamide
and Cycloserine (no change).

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But if INH resistance is not known or DST result shows sensitivity to INH, then addition of INH
in the regimen of ATD is to be done. (New addition)
Appropriate modification of the treatment regimen can be done in case of additional resistance.
If isoniazid resistance is found, the use of isoniazid depends on:
1. If high-level resistance detected by liquid culture – omit INH.
2. If low-level resistance detected by LC – add high dose INH.
3. If LPA reports INH resistance by Kat G mutation – omit INH.
4. If LPA reports INH resistance by INH A mutation – add high dose INH.
MDR/RR TB cases (without additional resistance)

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Tuberculosis In AIDS Patients
• When CD4 count is <150 cells/μL, extrapulmonary and dual TB is more commonly encountered.
• Adverse reactions to anti-TB drugs are more common in HIV patients.
• All HIV positive TB patients should also receive cotrimoxazole preventive therapy at least throughout the
anti-TB regimen - to reduce mortality, probably by preventing Pneumocystis jirovecii and other infections

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Isoniazid Preventive Therapy (IPT) for PLHIVs
(a) Adult and adolescents living with HIV should be screened for TB and those who are unlikely to
have active TB should be offered IPT
(b) Children with HIV who have no TB symptoms and who are unlikely to have active TB on
symptom-based
screening should be offered IPT regardless of their age
(c) All children with HIV who have successfully completed treatment for TB disease should
receive IPT.

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Chemoprophylaxis
Purpose - to prevent progression of latent tubercular infection to active disease. This is indicated only in :
(a) Contacts of open cases who show recent Mantoux conversion.
(b) Children with positive Mantoux and a TB patient in the family.
(c) Neonate of tubercular mother.
(d) Patients of leukaemia, diabetes, silicosis, or those who are HIV positive but are not anergic, or are on
corticosteroid therapy who show a positive Mantoux.
(e) Patients with old inactive disease who are assessed to have received inadequate therapy.
The standard drug for chemoprophylaxis of TB is H 300 mg (10 mg/kg in children) daily for 6 months. This is
as effective in HIV patients as in those with normal immune function. The CDC (USA) recommends 4 months R
prophylaxis in case H cannot be used.
The RNTCP recommend that MDRTB contacts should be watched without giving any prophylactic medication,
and treated promptly if they develop active disease.

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Tuberculosis In Pregnant Women
WHO and British Thoracic Society consider H, R, E and Z to be safe to the foetus and recommend the
standard 6 month (2HRZE + 4HR) regimen for pregnant women with TB.
S is contraindicated because it is ototoxic to the foetus.
Z is not recommended in the USA (due to lack of adequate teratogenicity data).
RNTCP 2016 Guidelines: consider Z to be safe & recommend full course TB therapy
Treatment of TB should not be withheld or delayed because of pregnancy.
All pregnant women being treated with INH should receive pyridoxine 10–25 mg/day.
All 1st line drug are compatible with breastfeeding – full course should be given- breastfeeding should be
continued.
Infant receive 6 month INH preventive therapy – rule out active TB followed by BCG vaccination.

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MANAGEMENT OF MDR TB(Pregnancy)

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Role of corticosteroids
Corticosteroids should not be ordinarily used in tubercular patients.
They may be used under adequate chemotherapeutic cover:
(a) In seriously ill patients (miliary or severe pulmonary TB) to buy time for drugs to act.
(b) When hypersensitivity reactions occur to anti tubercular drugs.
(c) In meningeal/renal/pericardial TB or pleural effusion—to reduce exudation, prevent its organisation and
strictures, etc.
(d) In AIDS patients with severe manifestations of tuberculosis.
Corticosteroids are contraindicated in intestinal tuberculosis because silent perforation can occur.(MCQ)
Corticosteroids, if given, should be gradually withdrawn when the general condition of the patient improves.

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Mycobacterium avium
complex (MAC) infection
MAC is an opportunistic pathogen which causes disseminated and
multifocal disease in immunocompromized(HIV-AIDS) patients.
Develops when - CD4 count drops to <50 cells/μL, HIV-RNA load is
high , presence of other opportunistic infections (P. jirovecii, etc.)
Duration of therapy:
Intensive phase - dependent on the response-till CD4 count rises
> 100 cells/μL and symptomatic relief -may take 2–6 months.
Maintenance therapy is continued till a and CD4 count stays > 100
cell/μL for at least 6 months.
All patients must simultaneously receive HAART for the HIV
infection.
Prophylaxis of MAC infection: Protect the AIDS patient from
developing active MAC disease during the period CD4 count
remains below 50 cell/μL.
Prophylaxis of MAC infection- A single drug is used.
azithromycin 1200 mg/week / clarithromycin 500 mg
twice a day-preferred drugs.
Rifabutin 300 mg/day – can also be used.
Duration - continued till the simultaneously instituted
HAART achieves complete suppression of HIV
replication, CD4 count rises above 100 cell/μL and
stays there for at least 3 months.

DIFFERENCE IN ACCEPTABILITY OF 99 DOTS

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Take Home Message

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• Face mask might serve dual purpose if it becomes a mandatory part of our lives post
COVID 19 pandemic.
• It not only curbs the spread of COVID 19, but also has been reported to reduce the
spread of TB & achieve the goal of END TB by 2025
COVID 19 ERA LEGACY

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