• Introduction.

• Method of staining.
• Mode of transmission.
• Classification of drugs.
• Description of individual drugs.
• Newer anti tubercular drugs.
• Drug Resistant Tuberculosis.
• Immunization against Tuberculosis.
• Diagnosis of T.B.
• Different kinds of T.B.
• Treatment of T.B (RNTCP-2017)
• TUBERCULOSIS is an infectious disease caused
by Mycobacteria; Mycobacterium tuberculosis
& Mycobacterium bovis.
• The name Mycobacterium is derived from its
"fungus-like" nature. Branching filamentous
forms are sometimes seen.
• First member of Mycobacteria discovered was
M. leprae by Hansen in 1868, hence called
Hansen's bacilli. M. tuberculosis was
discovered by Robert Koch in 1882.
• Mycobacteria are difficult to stain, but once
stained they are not readily decolorized even
by weak mineral acids. Hence they are termed
acid fast bacilli. Acid fastness is due to
presence of un-saponifiable wax (mycolic acid)
• It can not be stained by Gram stain, yet is
considered a gram positive bacilli based on
cell wall structure.

M.tuberculosis M.bovis
 Ziehl–Neelsen stain.
• The Ziehl–Neelsen stain, also known as the
acid-fast stain, was first described by two
German doctors: the bacteriologist
Franz Ziehl (1859–1926) and the pathologist
Friedrich Neelsen (1854–1898). It is a special
bacteriological stain used to identify acid-fast
organisms, mainly Mycobacteria.
MODE OF TRANSMISSION
Inhalation of droplets
Ingestion --self swallowing of infected
sputum/ or ingestion of un pasteurised milk of
infected cow
Inoculation – of organism in to skin may occur
rarely from infected postmortem tissue.
Transplacental – ie tuberculosis of foetus from
mother.
• Major portion of tubercle bacilli
become intracellular(i.e reside in
macrophage)so it is inaccessible for
majority of antibiotics as they cannot
penetrate easily in to the
macrophage.
• It was once considered to be an
Macrophage
incurable disease but now it is with tubercle
curable by a number of bacilli
chemotherapeutic agents.
 Classification of anti TB drugs

1st Line Essential 1st Line

drugs supplemental 2nd Line drugs
Eg- drugs Eg-
RIFAMPICIN Fluroquinolones
ISONIAZID Amikacin
PYRIZINAMIDE Eg-
Capreomycin
ETHAMBUTOL Rifabutin
Ethionamide
Rifapentin
p-Aminosalicylic
(RIPE) streptomycin
acid
Cycloserine
(FACEPaC)
• 1st line essential drugs– most effective & basic
components of anti tubercular treatment.
• 1st linesupplemental drugs– are quite effective &
posseses an acceptable limit of toxicity. These are
kept as reserved drugs & used in special settings.
• 2nd line drugs—these drugs are used if there is
resistance to 1st line drugs or if 1st line drugs are
contraindicated for some reason. These drugs are
less effective & slightly more toxic than Ist line
drugs(except Fluoroquinolones)
• NEWER DRUG UNDER INVESTIGATION--
LINEZOLID
 Drugs not FDA approved for TB.
• Other Aminoglycosides:
Amikacin
Kanamycin
• Fluoroquinolones:
Moxifloxacin
Levofloxacin
Drugs not FDA approved for TB contd..
• Amoxicillin - clavulanate
• ( role not established )
• Clofazimine ( role being re - evaluated )
Rifabutin ( used for TB and MAC )
• Linezolid , newer agents Sutezolid and AZD-
5847
• Outside US: prothionamide, thiacetazone,
viomycin
• A Standardized recording and reporting is maintained
by health worker or medical professional. This helps
to keep track of each individual patient and to
monitor overall programme performance.
• T.B therapy normally begins with 4 1st line
drugs: rifampicin + isoniazid + pyrizinamide +
ethambutol for 2months followed by a course
of isoniazid + rifampicin for next 4 months.
• Combination of drugs ensures prevention of
resistance by mycobacteria
 Individual drugs.
Isonicotinic acid hydrazide
• INH is a pro drug & is converted into active
form by bacterial enzyme catalase peroxidase.
• SITE OF ACTION– Both intracellular &
extracellular ; also in caseous lesions.
• It is bactericidal to actively growing tubercle
bacilli but not to dormant organisms which
are only inhibited.
• It is active against mycobacterium tuberculosis
& mycobacterium kansasii
MECHANISM OF ACTION
INH is converted to active form by catalase
peroxidase (produced by mycobacterium) .
The active form inhibits mycolic acid in outer layer
of cell wall.
Also inhibits DNA, RNA & various oxidative
enzymes.
It is equally active in acidic & alkaline medium
Mycobaterium cell wall has the following layers viz.
– mycosides, mycolic acid, arabinoglycan,
MYCOLIC
peptidoglycan.INH inhibits mycolic acid synthesis ACID
INHethambutol inhibit arabinoglycan layer SYNTHESIS
while
(PRODRUG) INHIBITED

ARABINOGLYCAN
PEPTIDOGLYCAN

CELL MEMBRANE

INH
Catalase peroxidase (ACTIVE)
 MECHANISM OF RESISTANCE
• Resistance to INH is due to mutation in
CATALASE – PEROXIDASE GENE which is
responsible for activation of INH.
• Another mechanism responsible for resistance
is mutation in PROMOTER GENE , which is
involved in mycolic acid biosynthesis
 Pharmacokinetics
• Absorption– well absorbed orally
• Distribution– readily distributed in pleural ,
peritoneal & synovial fluids.
CSF concentrations are reached up to 100% if
meninges are inflammed.
• Metabolism – metabolised in liver by N –
acetyl transferase
 INH N- acetyl transferase Acetyl INH Hepatotoxic

The rate of above reaction varies in different people

i.e the reaction may be rapid or slow.
Accordingly people are classified as RAPID
ACETYLATORS( rate of reaction is rapid forming
acetyl INH eg.- 30-40% Indians, Japanese) &
SLOW ACETYLATORS (rate of reaction is sloweg.-
60-70% Indians, egyptians, jews,swedes).
Plasma half life– a)in rapid acetylators– T ½ = 1h
b)in slow acetylators– T ½ = 3h
• The acetylator status of an individual may
influence nature of INH toxicity but not
the anti tubercular response(if INH is
given once daily) because its plasma
concentration normally remains above
inhibitory concentration.

Peripheral neuritis --- commonly in slow

acetylators because accumulated INH
inhibits pyridoxine kinase which converts
pyridoxine to its active form pyridoxyl
phosphate.
• Also INH increases excretion of pyridoxine in
urine.
• This side effect can be prevented by giving vit-
b6(pyridoxine) prohylactically in 10-40 mg /
day.
• Hepatotoxicity --- common in fast acetylators
because INH is metabolised in to acetyl INH
which is hepatotoxic.
• Hepatotoxicity is a common side effect by INH
in alcoholics, liver diseases & in people aged
50-65 years.
• The drug has to be discontinued at onset of
symptoms like nausea, loss of appetite,
abdominal pain, & on rise of aminotransferase
enzymes by 3 fold.
• Other side effects are allergic reactions like fever,
rashes, & xerostomia , haematological changes &
convulsions in seizure – prone patients, drug
induced lupus erythematous.
Drug interactions
 Aluminium hydroxide inhibits absorption of INH.
 Alcohol increases risk of hepatitis.
 INH inhibits metabolism of phenytoin &
carbamazepine
• DOSAGE
In adult– 300mg O.D or 5mg/kg/day
For serious infections or meningitis – 600mg O.D
Duration of treatment is related to drug
combination used.

RIFAMPICIN is a semi synthetic derivative of

macro cyclic antibiotic Rifamycin
Anti microbial activity- bactericidal against both
intracellular & extracellular tubercle bacilli. In
addition , it is active against M.leprae,
Staph.aureus, N meningitidis, H. influenza,
Brucella, Legionella.
Mechanism of action of Rifampicin
Rifampicin inhibits bacterial DNA DEPENDENT
RNA POLYMERASE.
Mammalian RNA polymerase is not inhibited , so
RNA synthesis of host cells is not affected.
MECHANISM OF RESISTANCE
Resistance develops mutation in rpo B gene which
prevents binding of rifampicin to RNA
polymerase.
Hence if used alone resistance develops rapidly. It is
a potent enzyme inducer
Pharmacokinetics
Absorption--well absorbed after oral administration
Distribution – it penetrates in all tissues , tubercular
cavities, placenta. Adequate CSF levels are
reached if meninges are inflammed.
It is significantly protein bound.
• Excretion – drug is excreted via bile &
undergoes entero hepatic circulation.
ADVERSE EFFECTS
• HEPATITIS is major side effect. It is dose
dependent & reversible. It is common in
patients with underlying liver disease. Risk
of hepatitis increses when used in
combination with INH.
• Occasional side effects include FLU-LIKE
SYNDROME characterised by fever chills ,
myalgias & thrombocytopenia,
• Rifampicin imparts RED ORANGE COLOR
TO URINE.
DOSAGE
For T.B- 600mg(10mg/kg/day) as a single dose
before breakfast.
For brucellosis – in combination with doxycycline
(first choice combination)
For leprosy – in combination with dapsone
For prophylxis of meningitis caused by
meningococcus—600mg B.D for 2 days.
For prophylxis of meningitis caused by H.influenza–
600mg/day for 4 days.
Rifampicin can also be used for prosthetic valve
endocarditis.
DRUG INTERACTIONS
Accelerates metabolism of oral contraceptives,
anticoagulants, protease inhibitors used in HIV
patients, which may result in therapeutic
failure.

Ethambutol is a synthetic tuberculostatic drug

active against M.tuberculosis, M.kansasi &
M.avium intracellulare.
MECHNISM OF ACTION
ETHAMBUTOL inhibits polymerisation of
arabinoglycans of cell wall by inhibiting
arabinosyl transferase

MYCOLIC ACIDS
ARABINOGLYCAN

PEPTIDOGLYCAN
CELL MEMBRANE
MECHANISM OF RESISTANCE
Resistance develops due to point mutations in
emb B gene that encodes arabinosyl
transferases enzyme involved in mycobacterial
cell wall synthesis.
Pharmacokinetics
Bioavailability– 80%
Distribution– widely distributed in all body fluids
including CSF
DOSAGE
Should not be used alone as resistance
develops rapidly.
Usual daily dose is 800-1000mg orally
(15mg/kg/day).
It can also be given in a dose of 1600mg/day
In the treatment of M.avium intracellulare
infection in AIDS patients– ethambutol is used
in combination with rifabutin + clarithromycin.
Higher doses are needed to treat tuberculous
meningitis.
ADVERSE EFFECTS
Ethambutol if used in a dose of
25mg/kg/day for more than 9
days can cause RETROBULBAR
NEURITIS IMPAIRING VISUAL
ACTIVITY & RED – GREEN COLOR
DISCRIMINATION.
This effect is dose related reverses
slowly after discontinuing the
drug.
Periodic visual activity testing is
desirable during is desirable
during treatment period.
• Ethambutol should be avoided
in in children below 5 years
where it is difficult to asses
visual activity & red – green
color discrimination.
• Ethambutol decreases renal
excretion of urates & may
precipitate gouty arthritis.
• Mild GIT intolerance , rashes,
fever & dizziness are also
possible.
 Pyrazinamide(PZA)
• It is pyrazine derivative of nicotinamide.
• Because of its hepatotoxicity its use had declined
earlier.
• But recently pyrizinamide in reduced doses & in
combination re -emerged as 3rd most important
anti tuberculosis agent.
o It is bactericidal to M.tuberculosis & is active only
at low pH only.
o It is highly effective only on intracellular
mycobacteria(due to acidic environment
intracellularly in macrophages)
MECHNISM OF ACTION
PZA is thought to enter M.tuberculosis by
passive diffusion & is converted to pyrizinoic
acid (its active metabolite) by bacterial
enzyme pyrizinamidase enzyme.
The active metabolite then inhibits
mycobacterial fatty acid synthase 1 enzyme &
disrupts mycolic acid synthesis needed for cell
wall synthesis.
 MYCOLIC
ACID
PZA SYNTHESIS
INHIBITED

ARABINOGLYCAN
PEPTIDOGLYCAN

CELL MEMBRANE

pyrizinoic
pyrizinamidase acid
• Mechanism of resistance
A mutation in the gene (pnc A) that encodes
pyrizinamidase is responsible for drug
resistance which can be minimised by drug
combination therapy.
Pharmacokinetics
Absorption– well absorbed orally
Distribution– widely diustributed in all tissues,
macrophages, tubercular cavities & in
meningitis.
Plasma half life– 9-10hrs.
 Streptomycin
• It is the first antitubercular drug.
• It is bactericidal but because of poor
penetration it acts only on extracellular
tubercular bacilli.
• It is also active against M.kansasii & M.avium
intracellulare.
• It is less effective than INH or Rifampicin
Pharmacokinetics
Route of administration– I.M , cant be given
orally as it is highly polar
• Distribution – poorly distributed , do not
penetrate most cellular compartments.
• Metabolism -- as they do not penetrate most
cellular compartments , they do not undergo
significant metabolism.
• Excretion- nearly all of the drug is cleared by
kidneys as they do not undergo significant
metabolism.
• Plasma half life– 1.5 – 3 hrs(24-48 hrs in renal
insufficiency)
Mechanism of action
The mechanism of action of streptomycin is
inhibition of protein synthesis of mycobacteria in
the ribosome
Mechanism of resistance
Spontaneous resistance to streptomycin is related
to point mutation of the genes –rpsl or rrs that
encode for ribosomal proteins & ribosomal tRNA
respectively.
Dosage
1000mg/day I.M (15mg/kg/day)
Should be reduced to 500-750mg in elderly & in
renal insufficiency.
• Even for thrice a week dose schedule the
dose structure remains the same.
Adverse effects– nephrotoxicity & ototoxicity.

RIFABUTIN

IT IS a structural analogue of rifampicin.

It shares with rifampicin a common mechanism
of action , common spectrum of activity ,
aginst gram positive & negative organisms,
common molecular basis for development of
resistance.
• Hence there is cross resistance between
rifabutin & rifampicin.
• But rifampicin has better activity against
M.avium complex(MAC) .it is active against
rifampicin resistant strains such as M.leprae &
M.fortuitum. It has longer plasma half
life.(45hrs)
• It is used either alone or in combination with
pyrizinamide in the treatment of latent
tubercular infection.
• It can be used in place of rifampicin for the
treatmen of tuberculosis in HIV infected
patients.
• Most important use of rifabutin is in HIV
infected population for prevention &
treatment of disseminated MAC.
Dosage
300mg/day(5mg/kg/day)
Adverse effects– red orange color urine, skin
rash, hepatitis, neutropenia,
Drug interactions—
• May decrease plasma conc. Of theophylline,
oarl anti coagulants, protease inhibitors & non
nucleoside reverse transcriptase inhibitors
(but less than rifampicin).
• Fluconazole increases plasma concentration of
rifabutin resulting in pseudojaundice &
polymyalgia syndrome.
 RIFAPENTINE
• Longer acting analogue of rifampicin(T ½ =13-
15hrs ).
• Its mechanism of action , cross resistance,
enzyme inducion, toxic profile & clinical use is
identical to rifampicin.
• It is not used alone but in 3-4 drug
combination regimen.
• Drug interactions are lower than rifampicin
but greater than rifabutin
• Dosage– 600mg once or twice weekly
 Fluoroquinolones
• Specially used in multidrug resistant strains.
• Very effective when used as a part of
combined regimen in HIV infected patients.
• Ciprofloxacin, ofloxacin, levofloxacin &
moxifloxacin inhibit 90 – 95% of strains of
tubercle bacilli including MAC & M.fortuitum.
• They kill intracellular pathogens because of
good penetration.
• These can be substitued in drug combinations
if any Ist line drugs are contraindicated.
Dosage-
Ciprofloxacin– 750mg BD or 500mg TDS
Ofloxacin– 400mg BD
Levofloxacin500mg OD (preferred over ofloxacin
because of once daily dose schedule)
Moxifloxacin—400mg OD recent studies suggest
use of moxifloxacin with other drugs reduces
duration of therapy for drug susceptible
tuberculosis.
M.O.A

Inhibition of DNA gyrase. Fluoroquinolones act

by inhibiting the activity of both the DNA gyrase
and the topoisomerase IV enzymes.
 Amikacin
• It is an aminoglycoside antibiotic.
• It is 2nd choice after streptomycin &
capreomycin for multi drug resistant
tuberculosis.
• Most M.tuberculosis strains are that are
resistant to streptomycin are sensitive to
amikacin.
• It is also used in disseminated MAC
• Dose– 15mg/kg/day IM or IV for 5 days a
week for 2 months. Then 1g/day thrice weekly
for another 4 months.
 Capreomycin
• It is tuberculocidal polypeptiode antibiotic.
• Effective against M.tuberculosis, M. kansassi,
M.avium .
• It is poorly absorbed from GIT , so should be
given parenterally( 1g/day IM).
• Side effects- ototoxicity & nephrotoxicity
• Rarely used tuberculostatic drug.
• It is hepatotoxic, neurotoxic & produces intense
gastric irritation.
• It blocks mycolic acid synthesis.
PARA-AMINO SALICYLIC ACID
It is a structural analogue of PABA.
Acts by inhibiting folate synthesis of bacteria.
Disadvantages – poor compliance due to GIT
intolerance, hypersensitivity reactions like skin rash,
lupus like reactions, drug fever , joint pain, hepatitis
Dose- 8-12g/ day in 2 or 3 divided doses
 Cycloserine
• It is tuberculostatic drug.
• It is excreted unchanged in urine so it is used
for renal tuberculosis.
• Also Used in multi drug resistant tuberculosis
• Dose- 500 mg BD
• Side effects- psychotic behavioural changes ,
dizziness, peripheral neuropathy
NEWER ANTI TUBERCULAR DRUGS
Linezolid is a synthetic antibacterial agent of the
oxazolidinone Very effective against resistant
strains.It has 100% oral bioavailability.
Linezolid disrupts bacterial growth by inhibiting
the initiation process of protein synthesis
Adverse effects on prolonged use (which
becomes necessary for treatment of tuberculosis)
may limit its usefulness.
Adverse events were managed by combinations,
temporary suspension of linezolid , dose
adjustments and symptomatic management
 Linezolid
Linezolid may have efficacy in the treatment of
MDR-TB, although treatment was complicated
by adverse events including
Myelosuppression, Neurotoxicity and
Gastrointestinal adverse events.
Dose- 600mg OD
 R-207910(Bedaquiline)
• Approved by the FDA on the 28th December 2012,
• It is di aryl quinoline derivative developed in year 2004
& completed phase II trials.
• It inhibits proton pump for ATP synthase of M.
tuberculosis.
• It remarkably shortens duration of treatment to 2
months or less.
• Nausea, joint and chest pain, and headache are the
adverse effects. it may induce long QT syndrome.
• It is manufactured by Johnson & Johnson (J&J).
• Use :(MDR-TB).
 Immunization against T.B
• B.C.G :The vaccine was developed over a period
of 13 years, from 1908 to 1921, by French
bacteriologists Albert Calmette and Camille
Guérin, who named the product Bacillus
Calmette-Guérin, or BCG.
• The BCG vaccine contains a live but weakened
form of a type of bacteria called Mycobacterium
bovis. The vaccine is known as BCG because a
strain of the bacterium known as Bacillus
Calmette-Guerin is used. ... Vaccines contain
extracts or inactivated forms of bacteria or
viruses that cause disease.
• Neonates should receive the BCG vaccine
before they leave hospital, or as soon as
possible following discharge from hospital.
• If the baby or child missed vaccination at
birth, they can be vaccinated anytime up to
five years of age.
• BCG (Bacille Calmette-Guérin) is a vaccine
given to babies to protect them from serious
forms of Tuberculosis (TB) such as TB
Meningitis (an infection of the brain)
and Miliary TB (wide spread infection).But it is
not protective for pulmonary T.B.
• The main use of BCG is for vaccination against
tuberculosis. BCG vaccine can be administered
after birth intradermally. BCG vaccination is
recommended to begiven intradermally. A
previous BCG vaccination can cause a false
positive Mantoux test, although a very high-grade
reading is usually due to active disease.

BCG vaccination is only recommended on the

NHS for babies, children and adults under the age
of 35 who are considered at risk of catching
tuberculosis (TB). The BCG vaccine isn't given to
anyone over the age of 35, as there's no evidence
that it works for people in this age.
 Mantoux test
• The Mantoux test or Mendel-Mantoux
test (also known as
the Mantoux screening test, tuberculinsensitiv
ity test, Pirquet test, or PPD test for purified
protein derivative) is a tool for screening for
tuberculosis (TB) and for tuberculosis diagnosis
• Skin tests should be read 48-72 hours after
the injection. The basis of the readingof
the skin test is the presence or absence and
the amount of induration (localized swelling).
A negative test does not always mean that a
person is free of tuberculosis.
• The reaction should be measured in result a
6-10 millimeters of the induration. The test is
done by putting a small amount of TB protein
(antigens) under the top layer of skin on inner
forearm.
 Ghon focus
• A Ghon focus is a primary lesion usually subpleural,
often in the mid to lower zones, caused
by Mycobacterium bacilli.
• It is a small area of granulomatous-inflammation,
only detectable by chest X-ray if it calcifies or grows
substantially.
• Typically these will heal, but in some cases,
especially in immunosuppressed patients, it will
progress to miliary tuberculosis.
• Classical location for primary infection is
surrounding the lobar fissures, either in the upper
part of the lower lobe or lower part of the upper
lobe.
• Ghon focus also involves infection of adjacent
lymphatics and hilar lymph nodes, it is known
as the Ghon's complex or primary complex.

Miliary Tuberculosis
• Miliary tuberculosis (TB) is the widespread
dissemination of Mycobacterium tuberculosis.
• Disseminated tuberculosis is a contagious
bacterial infection in which TB bacteria has
spread from the lungs to other parts of the
body through the blood or lymph system.
• The infection can spread via blood from the
lungs to all organs in the body. This
means tuberculosis in the pleura (the
covering of the lungs), in the bones, the
urinary tract and sexual organs, the intestines
and even in the skin.
 Pott’s disease
• Pott disease or Pott's disease is a form
of tuberculosis that occurs outside the lungs
whereby disease is seen in the vertebrae. ...
The infection then spreads from two adjacent
vertebrae into the adjoining intervertebral
disc space.
 Treatment of tuberculosis
• One of the main reason for threrapeutic failure
has been patients poor compliancen after having
symptomatic relief.
• WHO , therefore has recommended
DOTS(Directly Observed Therapy for Short
course) wherein the anti-TB drugs are given
under direct supervision of medical professional
(3 days a week.) Now it is to be given Daily.
• This helps to ensure the right drugs are taken at
the right time for the full duration of treatment
CATEGORY PATIENT TYPE DURATION OF DRUG REGIMEN
TREATMENT
CATEGORY 1 All New Cases Intensive phase( RIPE FOR 2
4FDC) MONTHS , THEN R I
Continuous Phase( E FOR 4 MONTHS-
3FDC) Another 3 to 6
Skeltal,CNS T.B Months
CATEGORY 2 SMEAR +VE Intensive phase( RIPE +
RETREATMENT 4FDC) + S ; 4FDC STREPTOMYCIN FOR
GROUP(RELAPSE 2MONTHS;THEN
OR TREATMENT Continuous phase ( RIPE FOR 1 MONTH;
FAILURE) 3FDC) THEN RIE FOR 5
MONTHS
Multiple choice questions

Mycobacterium tuberculosis
The scientist who discovered M. tuberculosis
was:
A: Louis Pasteur
B: Robert Koch
C: Jean-Antoine Villemin
D: Calmette and Guerin

Correct answer: B
MDR TB: is defined as resistance to
A: more than three anti tubercular drugs
B: isoniazid and rifampin irrespective of resistance
to any other drug
C: INH, PZA and Rifampicin
D: fluoroquinolones and at least one of the three
injectable second-line drugs used to treat TB

Correct answer: B
XDR TB is defined as
A: MDR TB that also is resistant to fluoroquinolones and at least
one of the three injectable second-line drugs used to treat TB
(amikacin, kanamycin, or capreomycin)
B: resistant to two most effective first-line therapeutic drugs,
isoniazid and rifampin irrespective of resistance to any other
drug
C: MDR TB that is resistant to either one of the injectable second
line drugs or second-line therapeutic fluoroquinolones
D: Strain resistant to more than one drug (excluding co resistance
to INH and rif)

– Correct answer: A
Tuberculosis is transmitted through:
A: Infected water
B: Infected hands
C: Infected blood
D: Infected air

Correct answer: D
Which of the following statements is incorrect:
A: People who are exposed to TB may or may not
develop TB infection
B: People with TB infection may or may not develop TB
disease
C: risk of developing TB disease is highest in first 2 years
after infection
D: Every individual exposed to TB develops disease

Correct answer: D
• Tubercular Granulomas are made up of:
A: organized aggregates of immune cells that
surround foci of infected tissues
B: Damaged tissue cells and bacilli only
C: Fibrous and damaged tissue and bacilli only
D: Necrotic tissue and damaged tissue and bacilli
only

Correct answer: A
• Cord growth seen on mycobacterial culture is
characteristic of:
A. Avirulent strains
B. Virulent strains
C. Saprophytic strains
D. Atypical mycobacteria

Correct answer: B
• Which one of the following are constituent of
Lowenstein Jensen media except:
A. Agarose
B.Malachite green
C. Mineral salts
D. Asparagine

Correct answer: A
• Following are the first line antitubercular
drugs except:
A. isoniazid
B. rifampin
C. PAS
D. streptomycin

Correct answer: C
• Which one of the following anti-tubercular
drugs acts best in acidic pH:
A. INH
B. Pyrazinamide
C. Streptomycin
D. Rifampicin

Correct answer: B
• Mutations in katG gene of Mycobacterium
tuberculosis are responsible for resistance to:
A. INH
B. Rifampicin
C. Pyrazinamide
D. Streptomycin

Correct Answer: A
• Which of the following tests are banned for
diagnosis of tuberculosis:
A. Culture
B. ELISA
C. PCR
D. LPA

Correct result: B
• Which of the following statements is incorrect:
A. Mycobacteria are obligate aerobes
B. Increased CO2 tension enhances growth
C. Can not grow in cell free media
D. Doubling time of tubercle bacilli is about 18
hours.

Correct answer: C
One word answer
• Identify the stain
– ZN stain
• Identify the organism
– M. tuberculosis
• Describe the
morphology
– Acid fast, Long slender,
curved, bunch, beaded
 True/ False
• For people with TB infection and no risk factors, the
risk is about 5% in the first two years
–T
• For people with TB infection and no risk factors, the
risk is about 10% over a lifetime
–T
• For people with TB infection and diabetes, the risk is
about 30% over a lifetime
–T
• For people with TB infection and HIV infection , the
risk is about 7% to 10% over a lifetime
–F
• Which one of the following is a non cultivable
mycobacteria:
A. M. tuberculosis
B. M. Bovis
C. M. leprae
D. M. avium intracellulare

Correct Answer: C
• Which one of the following is a rapid grower
mycobacteria:
A. M. scrofulaceum
B. M. kansasii
C. M. fortuitum
D. M. avium intracellulare

Correct Answer: C
• Buruli ulcer is caused by:
– A. M. tuberculosis
– B. M. ulcerance
– C. M. marinum
– D. M. chelonei

• Correct answer: B
• Swimming pool granuloma is caused by:
– A. M. tuberculosis
– B. M. ulcerance
– C. M. marinum
– D. M. chelonei

• Correct answer: c
• Most common cause of disseminated
opportunistic infection in AIDS patients in
western world is:
– A. M. avium intracellulare complex
– B. Pneumocystis carinii
– C. Cryptosporidium
– D. Zygomycetes

• Correct answer: A
• Gerhard Henrik Armauer Hansen,s contribution
to Microbiology was;
A. First identified M. leprae as the cause of leprosy in
1873
B. First identified M. tuberculosis as a cause of TB in
1895
C. First identified B. anthracis as a cause of Anthrax in
1872
D. First identified that small pox is a contagious disease

• Correct Answer: A
• Which of the following description suits lepra bacilli best:
– A. acid-fast rod-shaped organism with parallel sides and
rounded ends, mostly extracellular, often grouped together like
bundles of cigars
– B. acid-fast rod-shaped organism with parallel sides and
rounded ends, chiefly in masses within the lepra cells (globi),
often grouped together like bundles of cigars or arranged in a
palisade
– C. acid-fast rod-shaped organism with parallel sides and
rounded ends, chiefly intracellular in Chinese letter form
– D. acid-fast rod-shaped organism, extracellular, Chinese letter
form

– Correct answer: B
• An adult male is presenting with hypo-pigmented
patches on forearm, partial loss of cutaneous
sensations in affected areas, presence of
thickened ulnar nerve and presence of AFB in
nasal smears. Your diagnosis is:
– A. Cutaneous Tuberculosis
– B. Leprosy
– C. Atypical mycobacteriosis
– D. Actinomycosis

– Correct answer: B
• A case of leprosy with good Cell mediated
immunity usually presents as following form
of disease:
– A. Lepromatous
– B. Tuberculoid
– C. indeterminate
– D. Borderline

– Correct answer: B
• Erythma nodosum leprosum as seen in
patients of leprosy on treatment, is due to:
– A. Type I hypersensitivity reaction
– B. Type II hypersensitivity reaction
– C. Type III hypersensitivity reaction
– D. Type IV hypersensitivity reaction

Correct answer: C
• Presence of sulfur granules in pus is
pathognomonic of:
– A. Subcutaneous mycosis
– B. Leprosy
– C. Actinomycosis
– D. Cutaneous Tuberculosis

– Correct Answer: C
• There is a 30 year old male presenting with lumpy
jaw, suppurative inflammation and formation of
multiple abscesses and sinus tracts with
discharge of pus containing sulfur granules. Most
probable clinical diagnosis is;
– A. Leprosy
– B. Actinomycosis
– C. Subcutaneous mycosis
– D. Cutaneous TB

– Correct Answer: B
• There is a 30 year old male presenting with lumpy jaw,
suppurative inflammation and formation of multiple
abscesses and sinus tracts with discharge of pus
containing sulfur granules. Following types of
microscpic examinations can be ordered to confirm the
diagnosis, except;
– A. Smear examination for Gram positive bacteria
– B. Microscopic examination of Crush smear of granule
– C. Smear examination for acid fast bacilli
– D. KOH mount

– Correct answer: D
• There is a 30 year old male presenting with lumpy
jaw, suppurative inflammation and formation of
multiple abscesses and sinus tracts with
discharge of pus containing sulfur granules. Best
therapy in this case will be:
– A. Antitubercular drugs
– B. Aminoglycosides
– C. Penicillin
– D. Co trimoxazole

• Correct Answer: C
• Which one of them is non acid fast:
– A. Mycobacterium tuberculosis
– B. Nocardia
– C. Actinomyces
– D. Mycobacterium leprosy

– Correct Answer: C
• 1. AntiTB drug that has bacteriociddal and sterilizing effect
on tissue is:
• A) Rifampicin
• B) INH
• C) Ethambutol
• D) Pyrazinamide.
• Answer:Answer: 1-A
• Rifampicin is a bacteriocidal antiTB drug that kills both
multiplying and dormant bacteria hence it sterilizes the
tissue. INH is effective against multiplying bacilli.
Ethambutol in low dose is bacteriostatic and in high
dosages, is bacteriocidal. Pirazinamide is a mild
bacteriocidal drug but has a property of killing bacilli in
acidic environment such as, in macrophages and areas of
acute inflammation. It can cross blood brain barrier in good
concentration
• 2. Following type of pulmonary TB is most likely to be
associated with AFB sputum positivity:
• A) Primary complex
• B) Fifronodular
• C) Cavitary
• D) Pleural effusion
• Answer: 2-C
• Cavities represent necrosis of tissue resulting in
communication of the infected material with the airways.
The bacteria are thus discharged in the bronchial tree from
where they can be coughed out with sputum. The infected
material can cause tubercular bronchopneumonia in host
by spread to other parts of lungs or gastro-intestinal
tuberculosis by means of swallowed secretions. The risk of
spread to other individual is very high with cavitary
tuberculosis.
• 3. Following antiTB drug is associated with major visual
side effects:
• A) INH
• B) Rifampicin
• C) Ethambutol
• D) Pyrazinamide
• Answer: 3-C
• Hepatotoxicity is the most common side effect of
antiTB treatment. INH, rifampicin and pyrazinamide
are hepatotoxic. INH may cause sensory neuropathy.
Rifampicin may cause itching in first two weeks and
may cause thrombocytopenia. Ethambutol can cause
retrobulbar neuritis which, in some cases, may be
irreversible.
• 4. Empyema necessitans is:
• A) Common manifestation of post primary
TB:
• B) Extension of empyema to the thoracic
cage
• C) Empyema associated with pneumonia
• D) Part of Primary complex
• Answer: 4-B
• Empyema necessitance is an uncommon
manifestation of TB when TB empyema
extends to the thoracic cage.
• 5. Fibro-cavitary lung lesion on x-ray is a feature
of:
• A) Primary TB
• B) Post primary TB
• C) Metastatic lung disease
• D) Lung abscess
• Answer: 5-B
• Primary complex is a small area of consolidation
in subpleural parenchyma. Post primary TB
occurs in immunocompetent hosts and causes
caseating granulomas. The caseous material gets
drained out through bronchi resulting in small
cavities surrounded by fibrosis. Lung abscess is a
thick walled cavity on X-ray
• 6. Miliary TB on CT scan has:
• A) Peribronchial distribution of lesions
• B) Lesions randomly distributed measuring
1-2 mm
• C) Small granulomas with satellite lesions
• D) Small nodules with caseation
• Answer: 6-B
• Miliary TB is caused by hematogenous spread
of TB bacilli and has characteristic appearance
on CT scan of chest with randomly distributed
lesions measuring 1-2 mm.
• 7. Gohn’s focus is usually:
• A) Subpleural
• B) Peribronchial
• C) Apical
• D) In lyphnode
• Answer: 7-A.
• 8. Mantoux test :
• A) Is carried out by intradermal inoculation of live
attenuated bacilli.
• B) Positivity indicates prior exposure of the
individual to M. Tuberculosis.
• C) Positivity indicates good immunity against TB
• D) Is a measure of individuals humoral immunity
• Answer: 8-B
• Mantoux test is carried out by intradernmal injection of
purified protein derivative extracted from tubercular
bacilli culture. It is a sterile solution and does not
contain live bacteria. Positive mantoux test indicates
prior exposure to TB. It is a measure of cell mediated
immunity and not of humoral immunity. Positive test
does not necessarily mean good immunity.
• Anti TB drugs with maximum CNS penetration
are:
• A) INH and Rifampicin
• B) INH and Streptomicin
• C) INH and Ethambutol
• D) INH and Pyrazinamide
• Answer: 9-D
• INH and pyrazinamide have 100% CNS
penetration and are important in treatment of
TB meningitis.
• 10. When TB is associated with AIDS:
• A) Mantoux reading is affected
• B) CSF parameters are affected
• C) First line management is affected
• D) TB is caused by atypical mycobacteria
• Answer: 10- A
• In an immunodeficient person such as, a case of
AIDS, cell mediated immunity is deficient.
Mantaox test detects cell mediated response of
an individual to tuberculin antigen. Hence the
test will show lower induration or less positivity.
Rest of the parameters are not affected