TB diagnosis

1. Mycobacterioum tuberculosis:
Etiology, Pathology and Laboratory
Diagnosis.
ANSAR AHMAD PARAY
Programme: Ph.D. Medical Microbiology
Centre for Interdisciplinary Biomedical Research(CIBR)
Adesh University Bathinda
Credit seminar (CBR.799)

2. Contents.
• Mycobacterium tuberculosis Introduction.
• History
• Classification
• Etiological agent
• Morphology of Mycobacterium tuberculosis.
• Antigenic structure
• Pathogenesis
• Clinical manifestations
• Laboratory diagnosis.
• Treatment
• Prophylaxis

3. Introduction

4. History
• Identified by Robert Koch in 1882 Robert Koch

5. Classification .
Kingdom: Bacteria
Phylum: Actinomycetota
Class: Actinomycetia
Order: Mycobacteriales
Family: Mycobacteriaceae
Genus: Mycobacterium
Species: tuberculosis

6. Antigenic structures
• Cell wall associated antigens
• Cytoplasmic Antigens

7. Cell wall (Insoluble)associated antigens
Peptidoglycan layer:
• This layer maintains the shape and rigidity of
cell wall.
Arabinogalactan Layer:
• It facilitates the survival of bacteria inside
macrophages.

8. Cell wall associated antigens continue…
Mycolic acid layer:
• This is made up of long chains of fatty acids
attached with arabinogalactan and is main
constituent of cell wall.
• This is responsible for Acid fastness of MTb
• This decreases permeability of cell wall.

9. Cell wall associated antigens continue…
Outermost layer:
• It is composed of Lipids, Glycolipids and
Mycosides.
Porins and Transport Proteins :
• These are found throughout the layer.

10. Cell wall associated antigens continue…
Plasma membrane:
• This layer consists of various proteins,
Lipoarabinomannan (LAM) and other
constituents .
LAM helps in attachment with host cell.
LAM is also a target antigen for diagnosis.

11. Cytoplasmic (Soluble )Antigens
• Antigen 5,
• Antigen 6,
• Antigen 60
They are used in serodiagnosis

12. Source of Infection
• Humans: Cases of Pulmonary tuberculosis .
• Other Sources: Infected milk

13. Mode of transmission.
• Inhalation of droplet Nuclei
• Ingestion: Swallowing of Sputum in infants or
consumption of Infected milk
Potential transmitters: Tb patients who
• cough
• Have smear positive TB
• Not on Tb Treatment or have shown poor
response to treatment.
• Who smoke

14. RISK FACTORS
• Overcrowding
• HIV
• Organ transplantation
• IV drug abuse
• Climatic conditions such as the cold climate
(as doors and windows are kept closed)

15. Risk factors continue…
• TB incidence is generally higher in older age
groups
• Higher in males compared to females.

16. • Patients infected with TB who have no active
signs or symptoms of disease were previously
deemed to have latent TB, Which more
recently changed to TB infection
• Whereas patients with active disease are
termed to have TB disease.

17. • Patients with TB infection have a 5–10%
lifetime risk of developing TB disease, which
increases in varying states of
immunodeficiency up to a 16% annual risk of
activation of TB infection into TB disease in
HIV patients

18. EPIDEMOLOGY
• Globally in, 6.4 million people with a new
episode of TB (new and relapse cases) were
diagnosed and notified in 2021 (WHO)
• India has the world’s highest tuberculosis (TB)
burden, with an estimated 26 lakh people
contracting the disease and approximately 4
lakh people dying from the disease every year

19. PATHOGENESIS
• Droplet nuclei which are generated by coughing
etc are inhaled by person nearby.
• These droplet contains MTB
• Majority of the bacilli are trapped in upper
airways and by Ciliary action they are expelled
out .
• Small amount of these droplets (<5 microns in
diameter) they are able to gain entry into the
deeper alveoli and establish themselves as
infection.

20. Pathogenesis continue…
• Once bacilli reach the alveoli they bind there
with complement receptors and mannose
receptors present on surfaces of macrophages
with the help of LAM , leading internalization
of bacilli.
• As LAM impairs fusion of Phagosome and
lysosome (by increase in Intracellular Ca2+ and
phosphatydilylinisotol-3-phophate, the
enabling bacilli to survive inside macrophage.

21. Pathogenesis continue…
• If the impairment of fusion of Phagosome and
lysosome is successful, the bacilli replicate
inside the macrophage .
• The macrophage then rupture and release
bacilli and its metabolites , infecting other
phagocytes and by this cycles continues

22. Pathogenesis continue…

23. HOST IMMUNE RESPONSE
1. Cell mediated Immune response
2. Humoral Immune response

24. Cell mediated Immune response
• Here antigens of bacilli are presented by
macrophages to T-helper (T h) cells .
• The Th cells differentiate into subtypes T h 1
and T h 2 .
• T h 1 cells secrete Cytokines (such as IL-2 &
IFN- Ɣ) activating monocytes and
macrophages.

25. Cell mediated Immune response
• Activated Th 1 cells lead development of two
host responses.
1. Macrophage activating response
2. Tissue damaging response

26. Macrophage activating response
• Major portion of the population shows resistance
and are able to contain bacilli.
• Resting alveolar macrophages are activated by
IFN- Ɣ into activated macrophages, capable of
digesting and killing the bacilli.
• These macrophages which are activated
aggregate around centre of lession and lead
granuloma formation called Tubercles.

27. Tubercles
• Essential pathological findings in TB
Hard Tubercle:
• Initially tubcules are hard
• Central zone contains activated macrophages
• Peripheral zone of lymphocytes and
fibroblasts.

28. Tubercles continue…
• Soft Tubercle:
• Later central part of tubercles undergo
Caseous necrosis.
• Here Growth of bacilli is inhibited within
necrotic environment (due to low oxygen and
pH)
• Now the lession heals and calcifies
• Here the bacilli can remain viable in dormant
form for years.

29. Tissue damaging response
• In some cases where macrophage activating
response is weak and bacilli are more virulent.
• Infection can be limited only by extensive
delayed Hypersensitive reaction leading
damage to tissue of lungs.

30. Tissue damaging response continue…
The caseous necrosis becomes liquefied and
contains large number of bacilli which spread
via:
1. While coughing and taking: As they drain into
airways,
2. Lymphatic spread to other lung and organs
3.Haematogenous spread.

31. Humoral Immune response
• The interleukins such as IL4, IL5 secreted by
T h 2 cells activate B cells to produce
antibodies.
• As M. tuberculosis is Obligate Intracellular
organism, Humoral Immune response plays
minor role.
• But anti –LAM antibodies plays role in
preventing disseminated TB in childrens.

32. Reactivation of TB Common causes
• Diabetes,
• Malnutrition,
• Smoking,
• Alcohol Consumption,
• Treatment With Glucocorticoids
• Silicosis Hematological
• Malignancies Uremia And
• Indoor air pollution are some.

33. REACTIVATION OF TB
• The commonest mechanism that underlies
reactivation of TB is the quantitative and
qualitative T cell defects that occur in people
with HIV infection
• Therapeutic neutralization of TNF alpha
especially by monoclonal antibodies, can also
cause reactivation

34. Reactivation Of Tb Continue…
• The effects of TNF alpha blockade that
account for reactivation TB include
 Decreased macrophage mediated
antimicrobial micro bacterial activity and
 Subsequent death of macrophages,
 induction of a higher frequency of
regulatory T cells, depletion of a subset
of effector memory T cells that contain
granulysin etc.

35. HIV and TB Co-infection
• HIV one in fact, CD 4 T cells as well as
macrophages
• M. TB primarily infects macrophages which
require CD 4 positive T cells, to augment the
clearance of microbial pathogens
• The definition of CD 4 positive T cells that is
associated with HIV infection is thought to
have a major role in the increased risk of TB in
individuals with HIV

36. HIV and TB Co-infection continue…
• HIV disease and TB are characterized by
chronic inflammation driven by the failure to
clear pathogen .

37. MALNUTRATION AND TB
• It cause impairment of cellular immunity
• Malnutrition is also associated with
diminished production of protective cytokines,
and increased production of regulatory
cytokines, both of which might
• Contribute to the promotion of the
development of active disease.

38. SMOKING AND TB
• It is associated with a compromised function
of alveolar macrophages,
• it is associated with inhibition of Th1
activation and enhancement of regulatory T
cell activation
• It is associated with the polarization of
recruited macrophages to an
immunosuppressive phenotype

39. Clinical manifestations of Tuberculosis
Tuberculosis is classified as:
• Pulmonary tuberculosis
• Extrapulmonary tuberculosis

40. General symptoms of TB
• Unexplained Fever Of Long Duration,
• Loss Of Weight,
• Loss Of Appetite,
• Night Sweats,
• Fatigue Or Tiredness,
• In Children A Failure to thrive can be the only
symptom

41. Pulmonary tuberculosis
• TB primarily effects the lung which constitutes
85 percent of total cases of TB, which is
referred as pulmonary TB

42. Clinical manifestations of pulmonary
TB
• Chronic cough which may be either productive
or dry, it may usually lasting for more than 2
weeks,
• Blood in the sputum (Haemoptysis)
• Chest pain,
• Difficulty in breathing dyspnoea and
• Other symptoms such as fever, weight loss,
anorexia and lassitude

43. Extra pulmonary TB
• TB can effect any other organ system in our
body other than the lung, which is referred as
extra pulmonary TB.
• It can occur either in isolation or along with
the primary TB with the pulmonary focus
• Clinical manifestation can be either general or
it can be organ specific.

44. Types of Extra pulmonary Tuberculosis
(EPTB)
• lymph node TB
• Pulmonary effusion
• Tuberculosis of CNS: Meningitis, Tuberculoma
• Gastrointestinal TB
• TB involving bone and joints
• TB of Spine
• Miliary TB

45. Extra pulmonary TB Continues…
TB can also involve
• Musculoskeletal system involving the bones and joints
of the upper and lower limbs,
• The pericardium
• Kidneys and genitourinary system,
• The skin,
• Eyes,
• Breast,
• Larynx,
• Ear nose and
• Throat

46. lymph node TB
• It is also known as Tuberculous lymphadenitis
• It is the most common form EPTB accounting
for 35 percent of all EPTB cases.
• It primarily affects the children and the young
adults,
• It is more common among common in women
unlike the pulmonary TB which is common in
men.

47. lymph node TB continue…
• It affects both the superficial and deep lymph
nodes
Features:
• May be associated with systemic symptoms, such
as fever, weight loss, loss of appetite
• Physical presentation depends on the stage of the
lymph node TB.
• Most common presentation in clinical practice
includes painless, single or multiple, unilateral or
bilateral enlarged peripheral nodes

48. Pulmonary effusion
• It is also known as pleural tuberculosis
• It is the second commonest form of extra
pulmonary TB
• It usually present with cough, chest pain or
shortness of breath, with or without fever and
weight loss.
• There is pleural collection of pus in the pleural
space

49. Pulmonary effusion continues…
• Pleural effusion usually present as an acute
illness, unless symptoms usually last for few
days to few weeks, with the symptoms of
pleuritic chest pain, breathlessness, non
productive cough and fever.
• Occasionally, the onset may be less acute,
with mild chest pain, low grade fever, cough,
weight loss and anorexia

50. TB meningitis
• It is most severe manifestation of extra pulmonary
TB, of all the cases of neurological TB.
• It accounts for 70 to 80 percent of the cases.
• In industrialized nation people leaving on HIV
account for more than 50 percent of cases of TB
meningitis.
• Most common clinical features include fever,
headache, seizures and or neck stiffness.
• The pathological features include inflammatory
meningeal exudates,
• vasculitis, encephalitis, disturbance of the CSF
circulation and absorption

51. CNS Tuberculoma
• It is a less common than meningitis.
• Its clinical features depends on the anatomical
location.
• Seizure is a most common presenting feature
and it may present with headache, fever or
focal neurological deficits

52. Gastrointestinal TB
• The most commonest site of a TB of abdomen
occurs in the ileocaecal region
• It is usually manifested as enteritis or peritonitis.
• TB enteritis is more common in the adolescents
and it is due to swallowing the infected sputum
• Peritoneal TB results from the reactivation of a
latent, peritoneal focus, or as a part of military
spread

53. Gastrointestinal TB continues…
• Symptom will be abdomen pain, which can be
colicky due to the luminal compromise, if
there is involvement of the mesenteric lymph
nodes, the abdomen pain will be dull and
continuous.
• TB abdomen also can present with
constitutional symptoms, such as fever, weight
loss and fatigue

54. Bone and joint TB
• It accounts 10 percent of all the extra
pulmonary TB.
• Spinal TB is the commonest form, it occurs in
both in adults and children
• Usually the patient complaints of localized
back pain with tenderness of this spinous
process, fever and weight loss.

55. Milinary TB
• It is also known as disseminated tuberculosis
• It is most common in immunocompromised
individuals such as HIV patients.
• Usually there is multi organ involvement, the
visceral sites with rich vascular supply such as
liver, spleen, bone marrow and brain, are
usually affected

56. Diagnosis of Tuberculosis
• Diagnosis of TB can be done based on clinical findings
or
• Radiological findings or
• Bacteriological findings through
•Direct demonstration of the causative agent as a
whole or
•Its component for example, the smear, culture or
nucleic acid or
•By means of growth characteristics
•By means of demonstration of a metabolic product

57. Laboratory Diagnosis of Tuberculosis
SPECIMEN
The good diagnosis is dependent on a good quality
specimen
• Sputum is the most suitable specimen in pulmonary
tuberculosis.
• In case of children's children who are not able to
expectorate sputum gastric aspirate can be collected.
• Two sputum specimens are collected one on spot and
one early morning.
In EPTB specimens collection depends on the anatomical
site involved.

58. L/D of Tuberculosis continue…
• sample is collected in leak proof containers with
proper labeling and sent to the laboratory at the
earliest time
• A cold chain of 4 to 8 degree C is required a
whenever a delay of more than 72 hours is
expected.
• A triple packaging system is mandatory for
samples if they have to be sent by post or by
courier
• Tissues or biopsy is sent either in saline or in
buffer and never in formaline solution

59. Direct Smear Microscopy
• Old technique, but still used as a basic
diagnostic tool.
• Ziehl-Neelsen staining of Smear is done and
then visualized under light microscope.
• Bacilli appears as a bright pink slender beaded
road against a blue background

60. Fluorescence microscope
• Here the smear is stained with fluorescent
dyes such as auramine phenol.
• After staining smear is visualized under the
fluorescence microscope.
• Bacilli appears as a bright yellow rod against
black background.

61. Grading of Smear

62. limitations of smear microscopy
• low sensitivity about 55 %
• The limit of detection ranges between 5000 to
10000 organisms per ml of sputum
• This cannot differentiate between M
tuberculosis and other non-tuberculous
mycobacteria, nor between dead and live
bacilli.

63. Light Emitting Diode (LEd)microscopy
• WHO in 2011 came out the recommendation
that conventional fluorescence microscopy be
replaced by LED microscopy and LED.

64. Culture
• As culture provides definitive diagnosis ,it is
still considered as the gold standards
• It is suitable for all samples, but requires
decontamination of the specimens to
eliminate the common contaminants
• More sensitive and requires 10-100 bacilli per
ml of sputum.
• Susceptibility of drug can be performed
• Growth indicates viability of bacteria.

65. Culture Continue…
Conventional medias:
Solid:
• Lowenstein-Jensen (LJ)media.
Liquid:
• Kirchner’s media
• Middlebrool media

66. Lowenstein-Jensen (LJ)media
• It is a solid media.
• Incubated for 6-8 weeks
• Colonies appear as rough, tuff and buff
coloured.
GRADING OF CULTURE ON LJ MEDIA
COL 1-9 Colonies
1+ 10-100 Colonies
2+ 100-200 individual
countable Colonies
3+ Conflicted growth

67. Limitations of solid culture
• Time consuming
• Require biosaftey Level II laboratory
• Cross contamination.

68. Automated Liquid media
BACTEC MGIT960 from Becton and Dickinson
• Manual version
• Automated version which is the actually the
MGIT960 system.

69. MGIT960 system Features
• Fully automated system
• It uses modified 7H9 medium.
• It holds about 960 tubes at any time point
• Measurement of every tube is done every one
hour.
• Software based detection.

70. MGIT960 system continues…
• The protocol length is 42 days for diagnosis of
tuberculosis;
• This system is useful for TB diagnosis as well
as for drug. susceptibility testing
• Once flag is positive culture bottles are
subjected to acid fast stain.
• If AFB is positive specific antigen detection
(MPT 64) and Biochemical tests are done for
identification.

71. DST using MGIT960
• It is a qualitative test with a turnaround time
of between 4 to 13 days.

72. Advantages and Disadvantage of
MGIT960 system
Advantages Disadvantage:
•Used for diagnosis
•DST is done
•Shorter timer and high
recovery
•Growth supplements
can be added to the
medium to enhance
growth.
•This system is useful for all samples
except blood and urine.
•Time consuming
•Require Biosaftey Level III laboratory
•Requires continuous power supply and
temperature controlled environment.
•Growth needs to be confirmed by
means of confirmatory test like AFB
staining and
•immunochromatography test

73. Phenotypic Drug Susceptibility Test
(DST) in TB.
• DST compares growth in the presence and
absence of the drug.
• They are available only in the reference
laboratories.
• The time to result may be up to 42 days for
solid media using DST or up to 14 days for
liquid DST.

74. Importance of DST
• It enables detection of emerging acquired drug
resistance.
• it provides information on the level of resistance
to the drug and level of cross resistance among
the same class of drugs and prevalence of
resistance in any geographical setting
• It enables recalculation of the epidemiological cut
off values that may necessitate the need to alter
the drug concentrations used in the in vitro tests

75. Proportion Sensitivity Testing (PST)
• This is currently the method of choice
employed in National Tuberculosis Programs
(NTPs)
• Estimate the proportion of resistant mutants.
• Resistance observed may be reported on day
28, and the reading has to be repeated on day
42 in the case of drug susceptible strains

76. Serological tests in TB
Not recommended because of;
• Low sensitivity
• Cross reactivity

77. Nine protein biosignature
• This has recently been discovered .
• Using fibrinogen, α2-macroglobulin, C-reactive protein,
matrix metalloproteinase-9, transthyretin, complement
factor H, interferon-γ, interferon-γ inducible protein-10
and tumour necrosis factor-α as a host biosignature
demonstrated 92% sensitivity and 72% specificity for
determining TB from other diseases .
• Most of these biomarkers are markers of
inflammation, and as such are widely variable
amongst patients and their differing metabolic and
disease states

78. Molecular methods
• Advantages:
• Less time consuming
• More sensitive
• Even genes coding for resistance can be
detected by these methods.

79. Various molecular methods
• GeneXpert
• line probe assay
• Expert Ultra,
• The OMNI,
• Trunats devices.
• Polymerase chain reaction (PCR) .

80. GeneXpert
• It is Cartridge based nucleic acid amplification
test (CBNAAT )system
• This technology is based on a semi nested real
time PCR and molecular beacon technology to
detect MTB as well as Rifampicin resistance.
• Test has been approved by the US FDA as a
diagnostic test for TB since 2013 and is used in
India since 2014.

81. GeneXpert continue…
• It has TAT of 2 hours
• It also detects rifampicin resistance.
• Note: Blood could not be an ideal specimen
for diagnosis using GeneXpert

82. line probe assay
• This is based based on a reverse hybridization
DNA strip technology
• WHO for use as rapid diagnostic test for the
detection of rifampicin as well as isoniazid
resistance
• TAT 72 hours
• The test is not useful in direct testing with smear
negative sputum,, in the extra pulmonary TB as
well as in samples with blood.

83. Second line probe assay MTBDRSL
• WHO issued recommendations to use the
second line LPA in May 2016
• This identifies genetic mutations in the
fluoroquinolone; the injectable second line TB
drug namely with, aminoglycosides and cyclic
peptides and also for ethambutol in MDR and
XDR patients

84. Expert ultra.
• launched in 2017

85. PCR method
• Nested PCR targeting genes IS6110 and the
16S RNA
• Other genes targeted by PCR include MPT64
gene, 65KDa and 35KDa gene.

86. whole genome sequencing for the
diagnosis of drug resistance
• Currently for patient management diagnosis it
is not used in country.
• In this method complete genome of the micro
bacteria is sequenced and the non genetic
mutations associated with drug resistance for
the clinical isolates are identified in one
stretch and this reduces the time, when
compared to culture based of susceptibility
testing.

87. Current medications in use for TB treatment and
their notable side-effects
Drug Notable side-effects
Rifampicin (RIF)
Hepatotoxicity, nausea, dyspepsia,
abdominal pain, rash, CYP450 interactions
Isoniazid (INH)
Hepatotoxicity, peripheral neuropathy,
optic neuritis, CYP450 interactions
Pyrazinamide (PZA) GI disturbance, hepatotoxicity, gout
Ethambutol (EMB) Optic neuropathy
Levofloxacin (LFX)/Moxifloxacin
(MFX)
QT prolongation, tendonitis,
hypoglycaemia, psychiatric disturbance
Bedaquiline (BDQ) QT prolongation, CYP450 interactions
Linezolid (LZD)
Myelosuppression, dysglycaemia,
peripheral neuropathy# optic neuropathy

88. Current medications in use for TB treatment and
their notable side-effects
Drug Notable side-effects
Clofazimine (CFZ)
Hepatotoxicity, GI disturbance,
neurological disturbance, QT
prolongation, altered skin pigmentation
Cycloserine (CYS)
Psychiatric disturbance, peripheral
neuropathy
Delamanid (DLM) QT prolongation, CYP450 interactions
Aminoglycosides (AMK,CAP, STR) Nephrotoxicity, Ototoxicity
Ethionamide (ETH)/Prothionamide
(Pro)
Psychiatric disturbance, peripheral
neuropathy, hepatotoxicity,
hypothyroidism, dysglycaemia
p-Aminosalicylic acid (PAS)
Hepatotoxicity, dysglycaemia,
hypothyroidism
Amoxicillin–Clavulanate¶ with
Meropenem or Imipenem–Cilastatin
Diarrhoea, candidiasis

89. Vaccines for tuberculosis
• BCG (bacillus Calmette–Guérin) is the only
licensed vaccine against TB
• BCG was discovered by Albert Calmette and
Camille Guerin, two French physicians. by
attenuating microbacterial bovis over 230
cycles over 13 (1908-1919) years.
• The first human immunization was done in
1921

90. • In India, BCG was first introduced in 1948
• 1949, BCG vaccination was extended to
schools in most all the states of India
• BCG became part of the national TB Control
Programme in 1962 when the TB Control
Programme was introduced
• In 1968 ICMR conducted a study to find out
whether BCG works or not (world’s largest
BCG vaccine study).

91. New vaccines for TB
• There are 3 vaccines in phase 1, 5 vaccines in
phase 2 a, 2 vaccines in phase 2 b and 2
vaccines in phase 3.

92. MTBVAC,
• pre-exposure live attenuated vaccine
• Results from preclinical trials shows higher
protection against TB than BCG

93. VPM1002
• This is another live recombinant BCG vaccine.
• This is undergoing phase III studies at present
to evaluate its efficacy at not only preventing
infection, but in preventing active disease in
those already affected .
• This vaccine can modify T-cell immune
response and enhance Th1 immunity,
important in TB disease pathogenesis.

94. M72/AS01E
• This also is subunit vaccine, that prevents
pulmonary TB in adults already infected
with Mtb in 54% of patients, and thus could
be a potentially life-saving intervention for
one quarter of the world's population
• Also known as Mtb72F this vaccine comprises
two immunogenic proteins that promote T-
cell proliferation and interferon-γ release

95. National Tuberculosis Elimination
Programme (NTEP),
• NTEP was previously known as Revised
National Tuberculosis Control Programme
(RNTCP).
• It Aims to strategically reduce TB burden in
India by 2025, five years ahead of the
Sustainable Development Goals.
• RNTCP was renamed as NTEP in 2020

96. Pradhan Mantri TB Mukt Bharat Abhiyaan
• AIM: To eliminate TB by 2025, five years ahead
of global target

97. NI-KSHAY
• NI-KSHAY-(Ni=End, Kshay=TB) is the web
enabled patient management system for TB
control under the National Tuberculosis
Elimination Programme (NTEP).
• It is developed and maintained by the Central
TB Division (CTD),MOHFW, GOI, in
collaboration with the National Informatics
Centre (NIC), and the WHO Country office for
India.

98. Tuberculosis as Global Concern and
challenge
• The infection is reported from all over the
world.
• This affects all ages, classes and races of
society.
• Development and poverty are factors closely
related to infection.
• Infection causes serious economical burden.
• Serious concern is that TB is becoming drug
resistant.

99. • Transmission via airway routes.
• Less treatment response and more
vulnerability in population with extreme ages
and with lack of access to medical facility.
• Challenging diagnosis.
• No preventable vaccine yet.

100. • Cases estimated in 2016: Approximately 10.4
million
• Cases notified : Only 6.3 million
• 10% HIV co infected.
• 9Th leading cause of death.

101. Impact of Tb on social life
• Social rejection
• Mental health especially of women have more
effect
• Anxiety and depression
• Reduced productivity
•

102. End TB strategy.
• Launched by WHO in 2016
• AIM: To reduce incidence, morbidity and mortality of
by improving diagnostic and therapeutic practices, as
well as developing preventative strategies, through
innovative research and education
Target: Upto 2035 ( IN comparison to 2015)
• 95% reduction in deaths because of TB
• 90 % reduction in incidence rate of TB
• No affected family should face catastrophic costs
because of TB.

103. Elimination of TB in India.
• GOI has set target of 2025 for TB elimination.
• Reducing expenditure and nutrition support to
patients are key features of Strategy plan
(2017-25).
• Expansion of diagnosis and treatment services
with new technology and strategy to private
sector will be key drivers to end TB in India.

104. Causative agents of TB
• Mycobacterium Tuberculosis, a acid fast bacilli
is causative agents Tuberculsosis.
• Acid fastness is due the presence of Mycolic
acid in its cell wall.

105. LATEST
• At present, there are 16 new drugs under
evaluation for TB treatment in phase I or II
clinical trials, with an additional 22 drugs in
preclinical stages.

106. • Gill, C. M., Dolan, L., Piggott, L. M., and McLaughlin, A. M. (2022). New
developments in tuberculosis diagnosis and treatment. Breathe, 18(1).
• PRADHAN MANTRI TB MUKT BHARAT ABHIYAAN. GUIDANCE DOCUMENT.
Central TB Division.MoHFW. New Delhi
• Hon’ble President Smt. Droupadi Murmu ‘Pradhan Mantri TB Mukt Bharat
Abhiyaan’ to eliminate TB by 2025. Posted On: 09 SEP 2022 2:48PM by PIB
Delhi. Available at https://pib.gov.in/PressRelease.