simple illustration of TB

1. By
Dr alaa metwally
Ass. Prof. of chest diseases

2. Know what is TB, historical overview
Define what bacteria can cause
tuberculosis.
Describe how someone can get TB .
Describe how TB is diagnosed.
Describe the treatment process for
someone diagnosed with TB.
.

3. TB disease has been found
in the mummies of ancient
Egyptians and Indians
Global problem for thousands
of years
Consumption, white plague,
Captain of the men of death!
Cause of TB identified 24
March 1882 by Dr. Robert
Koch

4. 1882 TB bacilli identified by Koch
1907 TST - tuberculin skin test (von Pirquet)
1919 BCG – Bacille Calmette & Guerin vaccine
1943 Schatz & Waksman discover streptomycin
1948 BMRC trial of streptomycin vs bed rest
1952 Development of isoniazid
1966 Development of rifampicin
1978 Short course chemotherapy (DOTS)

5. 5
From 1953 to 1984, reported cases
decreased by approximately 5.6% each
year
From 1985 to 1992, reported cases
increased by 20% (HIV resurgance)
25,313 cases reported in 1993
Since 1993, cases are steadily declining

6.  TB is a disease caused by a bacteria (single-
cell organism), the tubercle bacillus, TB.
 More specifically, it is a type of mycobacteria
• “myco” means waxy in latin and refers to TB’s waxy
cell wall
• There are 70 different types of mycobacteria
• Killed in the sun light
• Killed by temperature 60c
• Aerobic, gm+ve, acid fast, alchohol fast

7.  Five types of M.tuberculosis: human, bovine,
murine, avian, and reptilian. Only human and
bovine are important clinically.
 Direct sunlight kills the bacilli in 5 minutes.
 Bacilli may survive in dark for 5 months.
 In sputum, bacilli resist even 5% phenol for
several hours, but 1% sodium hypochlorate
liquefies the sputum and kills tuberculous bacilli
rapidly.
 Tuberculous bacilli are destroyed by heat of
60oC at 20 minutes and 70oC at 5 minutes.

8.  Size 0.3-0.6 micron x 2-4 micron
 Celll wall;A)Plasma membrane;
Peptidoglicans
Arabinogalactan
Micolik aside
B)Complex polymers
 Antigens; 38 kd, 88kd, Antigen 5, Antigen A6,
Lipoarabinomannan(LAM), Cord Factor

9. The scientific name for the TB microbe is
Tubercle bacillus or Mycobacterium
tuberculosis M.tb

10.  95% TB is an airborne disease, transmitted by
particles, or droplet nuclei that are expelled when
persons who have pulmonary or laryngeal TB
sneeze, cough, speak or sing
 1.4% By drinking infected milk
 1.4% Inoculation of bacilli by skin and mucosal
contusions
 Congenital TB

11. 11
 Transmission occurs when an infectious person
coughs, sneezes, laughs, or sings
 Spread person to person through airborne particles
that contain M. tuberculosis, called droplet nuclei
 Prolonged contact needed for transmission
10% of infected persons will develop TB disease at
some point in their lives

12. 12
Patients should be considered infectious if they:
•
•Are undergoing cough-inducing procedures
•Have sputum smears positive for acid-fast
bacilli
Are not receiving treatment
Have just started treatment, or
Have a poor clinical or bacterial response to
treatment
Have cavitary disease
Extra-pulmonary TB patients are not infectious

13. The lungs are the most
common place for TB.
This is known as
pulmonary TB.
TB of the voice box is
the second most
common and is usually
called laryngeal TB.

14. Not all TB infections lead to TB
disease
•Latent TB infection ( LTBI)
occurs when the immune system
has contains TB and prevents
disease.
• Active TB disease refers to the
time when TB breaks out and
causes disease.

15.  TB infection of the lungs fall into 2
categories of disease: Latent TB
or Active TB.
 Latent TB means a person is
infected by TB bacteria, but not
diseased, cannot infect others,
and is not coughing or appearing
sick.
 Latent TB means the body’s
immune system has contained
the infection.

16. Active pulmonary and laryngeal TB
means a person infected with the TB
bacteria is sick and can infect others
unless they are taking medicine
prescribed by their physician to treat TB.

17. 17
LTBI TB Disease
Tubercle bacilli in the body
TST or QFT-Gold® result usually positive
Chest x-ray usually normal Chest x-ray usually abnormal
Sputum smears and cultures
negative
Symptoms smears and cultures
positive
No symptoms Symptoms such as cough, fever,
weight, loss
Not infectious Often infectious before treatment
Not a case of TB A case of TB

18. 18
Persons more likely to progress from LTBI to
TB disease include;
 HIV infected persons
 Those with history of prior, untreated TB
 Underweight or malnourished persons
 Injection drug use
 Those receiving TNF-α antagonists for treatment
of rheumatoid arthritis or Crohn’s disease
 Certain medical conditions

19.  Lungs
 Pleura
 Central nervous
system
 Lymphatic system
 Genitourinary
systems
 Bones and joints
 Disseminated
(miliary TB)
 Pericardial disease
Source: CDC, 2001.

21. The first meeting of the TB bacillus
with immune system, is the
Primary TB
Other terms, childhood TB

22.  Droplet nuclei containing between one to 10 bacilli and
a diameter close to 10 μm are expelled with the cough,
suspended in the air and transported by air currents.
 Some of these droplet nuclei, usually larger than 10
μm, are inhaled and anchored in the upper respiratory
tract
 The mucus and the ciliary system of the respiratory
tract avoid further progression of mycobacteria.
Dannenberg, Jr AM Immunol Today 1991

23. Subsequently, alveolar macrophages
phagocytose the inhaled bacilli
These first macrophages are unable to kill
mycobacteria
The bacilli continue their replication inside
these cells
Logarithmic multiplication of the
mycobacteria takes place within the
macrophage at the primary infection site.

24.  Two or three weeks after the initial M. tuberculosis
infection, a cell-mediated immune response is fully
established
 While CD4+ T helper cells activate the macrophages
to kill the intracellular bacteria and finally cause
epithelioid granuloma formation,
 CD8+ suppressor T cells lyse the infected
macrophages, resulting in the formation of caseous
granulomas with central necrosis
 The only evidence of a real and effective infection is a
positive TST

25. The hallmark of active TB infection is tubercle:
• The predominant cells are non- lymphoid
mononuclear cells.
• Epithelioid cells.
• Langhan's giant cells.
• Central necrosis.
• The pathological hallmark of TB is the granuloma
formation

26. Granuloma
• The prepheral rim of lymphocytes and mononuclear
cells.
• Epithelioid cells (large activated macrophages)
• Langhan's giant cells. Fused actviated macrophages
with multiple nuclei
• Central necrosis.

27. Reactivation, liquefaction, cavitation
Bacilli begins to replicate Extra cellularly
Airborde spread is possible; Transmission

28. The combination of
Enlarged hilar L.node and
Pulmonary focous of caseastion and
The intervening lymph vessel
Is called the primary complex
When this pulmonary focus, and L N are
calcified
The complex is called Rank Triad

30.  Progression of the pulmonary parenchymal
component leads to enlargement of the caseous area
and may lead to pneumonia, atelectasis.
 This is more likely to occur in young children than in
adolescents
 The child usually appears ill with symptoms of fever,
cough, malaise and weight loss
 This form presents classic signs of pneumonia,
including tachypnea, dullness to percussion, nasal
flaring, grunting, egophony, decreased breath sounds,
and crackles

31.  95% of the primary complex is resolved spontaneously
 Only 5 % will progress to progressive primary TB
 Facors that may lead to progress of the primary
infection include;
 Immunosuppression by drugs or diseases
 Malnutrition
 Heavy load of bacilli, milliary TB

32. 32
TB Disease
• Occurs when immune system cannot
keep bacilli contained
• Bacilli begin to multiply rapidly
• Person develops TB symptoms

33.  50 % of pediatric patients may remain asymptomatic with subtle
abnormalities on the chest radiograph
 Primary TB in children has a low bacillary load and cavities are
also rarely present.
 The disease more often progresses from an initial or primary
infection.
 Children younger than five years old may develop disseminated
TB in the form of miliary disease or
Tuberculosis every where

34.  Lungs
 Pleura
 Central nervous
system
 Lymphatic system
 Genitourinary
systems
 Bones and joints
 Disseminated
(miliary TB)
 Pericardial disease
Source: CDC, 2001.

35. •Symptoms vary according to the degree of airway irritation and
obstruction
•Frequently a persistent cough that may mimic pertussis and
Mild fever
•70 % of the primary foci are subpleural, 25% of cases have
multiple parenchymal foci
• A common radiographic sequence is adenopathy followed by
localized hyperinflation and then atelectasis of contiguous
parenchyma
•Adenopathies are more striking than parenchymal focus
• Adenopathies heal with calsification
Primary pulmonary Tuberculosis

36. •Affected regional lymph nodes attach to the bronchus
• In some children, particularly infants, the lymph nodes
continue to enlarge, resulting in lymphobronchial
involvement, in which the affected bronchus may become
partially or totally obstructed (epi-tuberculosis)
•The area of caseation may discharge into a bronchus,
resulting in the formation of a cavity with possible
endotracheal spread
•The most frequently affected lobes are the right upper, the
right middle, and the left upper lobe

37.  Primary infection in adolescent and adult occur
between the age of 16-30 years,
 The pulmonary component overshadows the
glandular component,
 Rigid structure and increase diameter of bronchi
make its occlusion and stenosis less common,
 Local progression more common.
 Primary pleural effusion more common.
 Haematogenous spread is more common in
those who developed pleural effusion.

39. •Pleural involvement may result from direct spread of caseous
material from a subpleural parenchymal or lymph node focus,
or from hematogenous spread
• The presence of caseous material in the pleural space may
trigger a hypersensitivity reaction, with the accumulation of
serous straw-colored fluid containing few tubercle bacilli
• This exudate has a high protein count and lymphocyte
predominance; the number of polymorphonuclear cells
depends on the acuteness of onset
• Although direct microscopy often is negative, culture yields
may be as high as 70 percent

40. 85 % acute onset of fever,
52 % chest pain on deep inspiration
28 % shortness of breath
•Pleural effusion due to TB usually occurs in older children
The pain accompanies the onset of the pleural effusion,
but after that the pleural involvement is painless.
• Fever usually persists for 14-21 days.
The signs of pleural effusion include tachypnea, respiratory
distress, decreased breath sounds, dullness to percussion,
and occasionally, features of mediastinalshift.

41. Any forms other than primary
pulmonary TB is termed ; post
primary TB, secondary TB,
reactivation TB, adulthood TB

42. Name Clinical form
 Phthisis Original Greek name for TB
 Lung Sickness TB
 Consumption TB
 Lupus vulgaris TB of the skin
 Mesenteric disease TB of the abdominal lymph nodes
 Pott’s disease TB of the spine
 Scrofula TB of the neck lymph nodes
 King's evil TB of the neck lymph nodes
 White Plague TB especially of the lungs
 White swelling TB of the bones
 Miliary TB Disseminated TB

43. “Any person who presents with symptoms or
signs suggestive of TB, in particular cough
of long duration (more than 2 weeks).”
Source: WHO, 2003

44. By
Dr alaa metwally
Ass. Prof. of chest diseases

45. Chiclls
FFeverTHINK TB!
Chills
Fatigue
Difficulty
in
Breathing
Anorexia
Loss
of Appetite
Night sweats
Coughing
up Blood

47. Priority is in diagnosing and curing infectious
cases
ALL persons with TB symptoms should also
be tested for HIV
• Routine HIV testing
• Rapid HIV testing available in all public health
facilities

48. Highest priority to find and cure infectious
cases: people with smear-positive PTB
Two ways of identifying TB cases:
• Passive case finding: illness diagnosed
when patient presents for medical care at
health facility
• Active case finding: health workers actively
search for patients with TB in the
community

49. Most common tools for case finding include:
History taking
Physical examination
Sputum examination
X-ray examination
Tuberculin skin testing

50. Contact investigation most common method
Other methods include special surveys based
on:
• Geography
• Targeted testing of defined populations
(e.g., schools, prisons)

51. Take a thorough history for each
patient
• Determine if signs and symptoms point
to pulmonary or extrapulmonary TB
• Also obtain medical and social history
Do a general physical examination
with additional care to detect signs of
tuberculosis

52.  Have you had close contact with someone with TB?
 Do you have a cough? How long, dry, productive, colour?
 Is blood present in your sputum?
 Do you have chest pain? When & where?
 Do you have shortness of breath? How long?
 Do you sweat profusely at night?
 Have you lost weight?
 When did you start losing weight?
 When did you lose your appetite?
 How long have you been feeling weak and tired?
 Do you smoke?
 Have you previously been tested for TB?
 Do you know your HIV status?
Source: Chiang C-V et al., 2007.

53. 53
Productive prolonged cough*
Chest pain*
Hemoptysis*
Fever and chills
Night sweats
Fatigue
Loss of appetite
Weight loss
*Commonly seen in cases of pulmonary TB

54. 54
Obtain chest x-ray for patients with positive
TST results or with symptoms suggestive
of TB
Abnormal chest x-ray, by itself, cannot
confirm the diagnosis of TB but can be
used in conjunction with other diagnostic
indicators

55. Chest X-Ray (CXR) can support a
diagnosis of PTB
• Not used routinely for follow-up
• PTB can exist with normal CXR
• Must be interpreted with other information
 History and exam
 Sputum smear results
Also useful in diagnosing other types of
TB, especially in bones, joints, and spine

56. Courtesy of: San Francisco City and
County Dept. of Public Health, TB
Division

58. LUL cavities and bilateral endobronchial spread
Ddx: TB, CA

59. LUL cavitary lung opacity; TB Ddx:
CA, abscess

60. Right lung from elderly
homeless man showing
cavitation and consolidation
Cavitation, consolidation of RUL
in a 25 y woman. Sputum
smear was positive for AFB.

61. Value of radiology in TB :
• Early detection of TB.
• The extent of lesions.
• Response to treatment.
• Follow up.

62. Bacterilogical tests

63. 63
Sputum specimens are essential to
confirm TB
• Specimens should be from lung secretions, not
saliva
Collect 3 specimens on 3 different days
Spontaneous morning sputum more
desirable than induced specimens
Collect sputum before treatment is
initiated

64. 64
Direct sputum smear examination is the
most simple, cheap tool in Dx of TB.
TB is considered in patients with smears
containing acid-fast bacilli (AFB)
Use subsequent smear examinations to
assess patient’s infectiousness and
response to treatment

65.  Ziehl Nielsen is a stain for TB Bacilli,
 First, smear is heated to dissolve lipids
in the cell wall to allow dye to penetrate
cell wall.
 after heating the primary stain,strong
carbol fucsin is applied.
 Decolorization of the smear by strong
alchohol 70%, or conc sulphuric acid.
 The counter stain, methelen blue is then
applied.


66. Direct Microscopy is the most reliable and cost effective way to
identify persons who are most likely to transmit TB to others
© ITECH, 2006 © University of Alabama at Birmingham, Department of Pathology

67. 67
Used to confirm diagnosis of TB
Culture all specimens, even if smear
is negative
Initial drug isolate should be used to
determine drug susceptibility

68.  Culture of mycobacteria is a much more
sensitive test than smear examination
and has been estimated to detect 10-100
viable mycobacteria per ml of sample
and in case of active disease they are
found to be 80% sensitive and 99%
specific.
Culture-based Methods

69. Media used for cultivation may either be;
Solid media (6-8 weeks):
• Lowenstein Jensen’s (L-J) media,an egg-
based medium
• Middlebrook 7H10 and 7H11 are agar-
based media.
Liquid media (few days to 2 weeks):
• Middlebrooks 7H9.
• Bactic 460, based on assesment of
radiolabelled CO2 consumption
better but expensive,

70. Immunological tests

71. TST is done by intradermal injection of 0.1 ml
of PPD into the volar aspect of the forearm.
 Result is red 72 hours later.
TST
• Positive supports but does not make diagnosis
• Negative does not exclude TB as possible
diagnosis

73.  Measure reaction in 48 to 72
hours
 Measure induration,
not erythema (redness)
 Record reaction in millimeters,
not “negative” or “positive”
 Ensure trained health care
professional measures and
interprets the TST (PPD)

74. > 5mm
 Contact with infectious cases
 Abnormal Chest X ray
 HIV infection and other immunocompromised
>10 mm
 Certain medical risk factors: Hodgkin, diabetes Mellitus
, renal diseases, malnutrion
 Birth or previous residence in high prevalence areas
 Occupation in health care field, exposure to patients
with TB
 Close contact with a high –risk adult
 Residence in long term care or correction facilities
>15mm
No risk factor

75. 75
 Nontuberculous mycobacteria
• Reactions are usually ≤10mm of induration
 BCG vaccination
• Reactivity in BCG vaccine recipients generally wanes
over time
• Positive TST results is likely due to TB infection if risk
factors are present
• BCG-vaccinated persons with positive TST result
should be evaluated for treatment of LTBI
• QFT is able to distinguish M.tb from other
mycobacteria and BCG vaccine

76. 76
Anergy, or inability to react to TST because
of weakened immune system
Recent TB infection (2-10 weeks after
exposure)
Very young age (newborns)
Recent live-virus vaccination can
temporarily suppress TST reactivity
Poor TST administration technique (too
shallow or too deep, or wheal is too small)

77. 77
Some people with history of LTBI lose their
ability to react to tuberculin (immune
system “forgets” how to react to TB-like
substance, i.e., PPD)
Initial TST may stimulate (boost) the ability
to react to tuberculin
Positive reactions to subsequent tests may
be misinterpreted as new infections rather
than “boosted” reactions

78. 78
A strategy for differentiating between
boosted reactions and reactions caused by
recent TB infection
Use two-step testing for initial (baseline)
skin testing of adults who will be re-tested
periodically
2nd skin test given 1-3 weeks after baseline

79. 79
If the 1st TST is positive, consider the
person infected
If the 1st TST is negative, administer 2nd
TST in 1-3 weeks
If the 2nd TST is positive, consider the
person infected
If the 2nd TST is negative, consider the
person uninfected at baseline

80.  Was approved by the FDA in 2001 as an aid for
detecting latent TB infection.
 QFT is a blood test that measures interferon-gamma
released from sensitized lymphocytes in whole
blood incubated overnight with purified protein
derivative (PPD) from M. tuberculosis and control
antigens.
 The TST and QFT do not measure the same
components of the immunologic response and are not
interchangeable. Due to lack of specificity of this test,
it has not been used widely.

81. QuantiFERON gold (G) test; using more
specific antigenic protiens which are mixtures
of synthetic peptides simulating two proteins
present in M. tuberculosis: early secretory
antigenic target-6 (ESAT-6) and culture
filtrate protein-10 (CFP-10).

82.  ESAT-6 and CFP-10 are secreted by all M.
tuberculosis and pathogenic M. bovis strains.
 Because these proteins are absent from all Bacille
Calmette-Guérin (BCG) vaccine strains and from
commonly encountered nontuberculous
mycobacteria (NTM) except M. kansasii, M. szulgai,
and M. marinum,
 QFT-G is expected to be more specific for M.
tuberculosis than tests that use tuberculin purified
protein derivative (PPD) as the antigen.

83.  On May, 2005, this new in vitro test,
QuantiFERON®-TB Gold, received final approval
from the (FDA) as an aid in diagnosing
Mycobacterium tuberculosis infection, including
both latent tuberculosis infection (LTBI) and
tuberculosis (TB) disease.
 This enzyme-linked immunosorbent assay test
detects the release of interferon-gamma (IFN-g) in
fresh heparinized whole blood from sensitized
persons when it is incubated with mixtures of
synthetic peptides simulating two proteins present
in M. tuberculosis:

84. QFT-G is not affected by prior BCG
vaccination and is expected to be less
influenced by previous infection with
nontuberculous mycobacteria, while TSTs
are variably affected by these factors.
 However, there is still little data in children
and immunosuppressed (HIV) individuals.

85. QFT-G does not trigger boosting response
because it does not expose persons to antigen.
Injection of PPD for the TST can boost
subsequent TST responses, primarily in persons
who have been infected with NTM or vaccinated
with BCG.

86.  After incubation, the concentration of IFN-g in the
plasma is determined by ELISA by using the
reagents included in the test kit.
 The amount of IFN-g released is determined by
subtracting the amount in the nil from the amount
in the ESAT-6, CFP-10, or mitogen-stimulated
plasma. QFT-G test results can be calculated by
using software provided by the manufacturer.

87. Biochemichal tests

88.  Niacin accumulation test
 p- nitrobenzoic acid
 Nitrate reduction test
 Catalase test
 Pyrazinamidase test
 thiophen-2-carboxylic acid hydrazide
 Tuberculostearic acid
 Radioactive Bromide Partition Test
 A basic indolic compound
 Glutaraldehyde test

89.  A non-specific product of activated host T-
lymphocytes. Its normal serum level is 8-20 IU/L
 Is an enzyme involved in the metabolism of
purines. Its presence is needed for the breakdown
of adenosine from food and for the turnover of
nucleic acids in tissues.
 The utility of ADA determination in body fluids
(spinal, pleural, ascitic, pericardial)

90. The specificity is very high in fluids with a
lymphocyte-to-neutrophil ratio higher than
0.75.
The suggested laboratory cut-off of ADA
activity is 40 U/L for pleural, peritoneal
and pericardial fluids and 10 U/L for
cerebrospinal fluid.

91. Granuloma formation

92. When a person with active TB is diagnosed,
they should be;
1. Isolated from other people until the
medication begins to kill the bacteria- usually
2 weeks.
2. Notification of the local health authorities.
3. HIV screening
4. Contact monitoring
5. Medical treatment initiation

93. 93
Daily Isoniazid therapy for 9 months
• Monitor patients for signs and symptoms of
hepatitis and peripheral neuropathy
Alternate regimen – Rifampin for 4
months

94. TB is curable, IF it is
diagnosed early and
appropriate treatment is started
promptly.
Active TB can be spread to
other people if the person is
not taking medication to kill the
bacteria!

95. The CDC recommends that infections due
to Mycobacterium tuberculosis be treated
with several drugs in addition to INH:
Rifampin, Ethambutol, Streptomycin, and
Pyrazinamide.

96. The Aims of anti-TB Treatment
a. To cure the patient of TB
b. To prevent death from active TB
or its late effects
c. To prevent TB relapse or
recurrent disease
d. To prevent the development of
drug resistance
e. To decrease TB transmission to
others.

97.  First-line Drugs
• Isoniazid
• Rifampin
• Rifapentine
• Rifabutin
• Ethambutol
• Pyrazinamide
 Second-line Drugs
• Cycloserine
• Ethionamide
• Levofloxacin
• Moxifloxacin
• Gatifloxacin
• P-Aminosalicylic acid
• Streptomycin
• Amikacin/kanamycin
• Capreomycin
• Linezolid

98. Drug
Daily dose
mg/kg (max)
Weekly
2 times a week
mg/kg
(max)
Side effect
Isoniazid
5–10
(300 mg)
20–40
(900 mg)
hepatitis , neuritis
hypersensitivity
Rifampin
10–20
(600 mg)
10–20
(600 mg)
Orange coulor of urine, vomiting,
hepatitis, influenza like syndrome,
trhombocytopenia,
Pyrazinamide
2540
(2000 mg)
50–70
(4000 mg)
Hepatotoxick hiperürisemi,artralgia,
GİS symptoms
Ethambutol
15-25
(2500mg)
50
(2500mg)
Optic neuritis, GİS symptoms
after 7 years of age
Streptomycin
20- 40
(1000 mg)
Ototoxidity , nefrotoxic
Ethionamide
10–20
(1000mg)
-
GİS symptoms, hepatotoxic,,
hypothroidy

99. Divided into two phases:
Intensive phase (all 4 drugs) for 2-3 months depending
on if the patient has been treated before.
Continuation phase (rifampicin and isoniazid) for 4-7
months, depending on whether you have been treated
before.
7months continuation phase , for; cavitary lesions, twice
weekly regimen, retreatment, relapse.

100. 10
0
 Include four 1st-line drugs in initial regimen
• Isoniazid (INH)
• Rifampin (RIF)
• Pyrazinamide (PZA)
• Ethambutol (EMB)
 Adjust regimen when drug susceptibility
results become available or if patient has
difficulty with any of the medications
 Never add a single drug to a failing regimen
 Promote adherence and ensure treatment
completion

101.  Meningitis
 Pleural involvement
 Pericarditis
 Peritonitis
 Severe Miliary TB
 Atelectasis or obstruction
2 mg/kg/day for 15 days. than in decreased
doses,
Stop 4-6 weeks after

102. 10
2
Adherence is the responsibility of the
provider, not the patient and can be
ensured by:
• Patient education
• Directly observed therapy (DOT)
• Case management
• Incentives/enablers

103. 10
3
Health care worker watches patient
swallow each dose of medication
DOT is the best way to ensure adherence
Should be used with all intermittent
regimens
Reduces relapse of TB disease and
acquired drug resistance

104.  Large cavity with high bacillary load not responding
to medical ttt
 Massive hemoptysis
 Destroyed lobe or lung causing V/Q mismatch.
 Extensive pleural fibrosis causing restriction of
ventilation.
 Localized post TB bronchiactasis.
 Persistent broncho-pleural fistula.

105. 10
5
Instruct patients taking TB medications to
immediately report the following:
• Rash
• Nausea, loss of appetite, vomiting, abdominal pain
• Persistently dark urine
• Fatigue or weakness
• Persistent numbness in hands or feet

106. Complete cure; persistent sputum –ve
Treatment failure; persistent sputum +ve 5
months during ttt.
Relapse; conversion to sputum –ve on
starting ttt, then recurrence to +ve after ttt
completion.
Death; during treatment or after ttt
completion by TB complication.