Dr. Nikhil Oza
Intern
BVDUMC
A presentation on-
Definition
 Tuberculosis (TB) is a potentially fatal
contagious disease that can affect almost any part
of the body but is mainly an infection of the
lungs.
Neo-latin word :
- Round nodule/Swelling
- Condition
“Tubercle”
“Osis”
Causative Organisms
Mycobacterium tuberculosis
Mycobacterium Bovis
Human
Animals
Other causative organisms
 Mycobacterium africanum
 Mycobacterium microti
Non-Mycobacterium Genus
 Mycobacterium leprae
 Mycobacterium avium
 Mycobacterium asiaticum
M.
africanum
M. Bovis
M. Canetti
M. microti
M. tuberculosis complex
 Discovered in 1882 by Robert Koch.
Classification
Pulmonary TB
- Primary Disease
- Secondary Disease
Extra pulmonary
i. Lymph node TB
ii. Pleural TB
iii. TB of upper airways
iv. Skeletal TB
v. Genitourinary TB
vi. Miliary TB
vii. Pericardial TB
viii. Gastrointestinal TB
ix. Tuberculous Meningitis
x. Less common forms
Epidemiology
 In 2011,there were an estimated 8.7million incidence cases
of TB globally.
 Its equivalent to 125 cases in 1,00,000 population.
Asian : 59%
African : 26%
Eastern Mediterranean Region: 7.7%
The European Region : 4.3%
Region of the America : 3%
Incidence of Tuberculosis
Spread of Tuberculosis
Severe Symptoms
Persistent cough
Chest pain
Coughing with bloody sputum
Shortness of breath
Urine discoloration
Cloudy & reddish urine
Fever with chills.
Fatigue
Based on types of TB
Pathogenesis
Types
A. Pulmonary TB :-
1. Primary Tuberculosis :-
 The infection of an individual who has not been previously
infected or immunised is called Primary tuberculosis or Ghon’s
complex or childhood tuberculosis.
 Lesions forming after infection is peripheral and accompanied by
hilar which may not be detectable on chest radiography.
2. Secondary Tuberculosis :
The infection that individual who has been previously infected or
sensitized is called secondary or post primary or reinfection or chronic
tuberculosis.
B} Extra Pulmonary TB :-
• 20% of patients of TB Patient
• Affected sites in body are :-
1) Lymph node TB ( tuberculuous lymphadenitis):-
• Seen frequently in HIV infected patients.
• Symptoms :- Painless swelling of lymph nodes most commonly at
cervical and Supraclavical (Scrofula)
• Systemic systems are limited to HIV infected patients.
•
2) Pleural TB :-
Involvement of pleura is common in Primary TB
and results from penetration of tubercle bacilli into pleural
space.
 Involvement of larynx, pharynx and epiglottis.
 Symptoms :- Dysphagia, chronic productive cough
3) TB of Upper airways :-
4) Genitourinary TB :-
• 15% of all Extra pulmonary cases.
• Any part of the genitourinary tract get infected.
• Symptoms :- Urinary frequency, Dysuria, Hematuria.
5) Skeletal TB :-
• Involvement of weight bearing parts like spine, hip,
knee.
• Symptoms :- Pain in hip joints n knees, swelling of
knees, trauma.
6) Gastrointestinal TB :-
• Involvement of any part of GI Tract.
• Symptoms :- Abdominal pain, diarrhea, weight loss
7) TB Meningitis & Tuberculoma :-
 5% of All Extra pulmonary TB
 Results from Hematogenous spead of 10 & 20 TB.
8) TB Pericardiatis :-
• 1- 8% of All Extra pulmonary TB cases.
• Spreads mainly in mediastinal or hilar nodes
or from lungs.
9) Miliary or disseminated TB :-
• Results from Hematogenous spread of Tubercle Bacilli.
• Spread is due to entry of infection into pulmonary vein
producing
lesions in different extra pulmonary sites.
10) Less common Extra Pulmonary TB
• uveitis, panophthalmitis, painfull Hypersensitivity
related phlyctenular conjuctivis.
Diagnosis
1.Bacteriological test:
a. Zeihl-Neelsen stain
b. Auramine stain(fluorescence microscopy)
2. Sputum culture test:
a. Lowenstein –Jensen(LJ) solid medium: 4-18 weeks
b. Liquid medium : 8-14 days
c. Agar medium : 7 to 14 days
3.Radiography:
Chest X-Ray(CXR)
4.Nucleic acid amplification:
 Species identification ; several hours
 Low sensitivity, high cost
 Most useful for the rapid confirmation of
tuberculosis in persons with AFB-positive sputa
 Utility
 AFB-negative pulmonary tuberculosis
 Extra pulmonary tuberculosis
5.Tuberculin skin test (PPD)
 Injection of fluid into
the skin of the lower
arm.
 48-72 hours later –
checked for a reaction.
 Diagnosis is based on
the size of the wheal.
1 dose = 0.1 ml contains 0.04µg
Tuberculin PPD.
Tuberculin test interpretation
Pathogenesis of tuberculin test
6. Other biological examinations
 Cell count(lymphocytes)
 Protein(Pandy and Rivalta tests) – Ascites, pleural
effusion and meningitis.
Preventive measures
1) Mask
2) BCG vaccine
3) Regular medical follow up
4) Isolation of Patient
5) Ventilation
6) Natural sunlight
7) UV germicidal irradiation
BCG vaccine
 Bacille Calmette Guerin (BCG).
 First used in 1921.
 Only vaccine available today for protection against tuberculosis.
 It is most effective in protecting children from the disease.
 Given 0.1 ml intradermally.
 Duration of Protection 15 to 20 years
 Efficacy 0 to 80%.
 Should be given to all healthy infants as soon as possible after birth
unless the child presented with symptomatic HIV infection.
Management
Drugs MOA Diagram
Isoniazid Inhibits mycolic acid synthesis.
RIFAMPICIN Blocks RNA synthesis by blocking
DNA dependent RNA polymerase
PYRAZINAMIDE •Bactericidal-slowly metabolizing
organism within acidic
environment of Phagocyte or
caseous granuloma.
Drugs MOA Diagram
ETHAMBUTOL •Bacteriostatic
•Inhibition of Arabinosyl
Transferase
STREPTOMYCIN •Inhibition of Protein
synthesis by disruption of
ribosomal function
ADRs and its Management
Dosage regimen
 Intensive phase + continuation phase
 HREZ (2 months) + HRE (4 months)
Treatment regimen according to WHO
ISONIAZID (H) RIFAMPICIN (R) PYRAZINAMIDE (Z)
ETHAMBUTOL (E) STREPTOMYCIN (S)
DOTS
DOTS - Directly observed treatment, short-course
 DOT means that a trained health care worker or other designated
individual provides the prescribed TB drugs and watches the patient
swallow every dose.
Multi-Drug Resistance TB
TB caused by strains of Mycobacterium
tuberculosis that are resistant to at least isoniazid
and rifampicin, the most effective anti- TB drug.
Globally, 3.6% are estimated to have MDR-TB.
Almost 50% of MDR-TB cases worldwide are
estimated to occur in China and India.
MDR-TB among new TB cases
MDR-TB in previously treated cases
Extensively drug resistance TB
 Extensively drug-resistant TB (XDR-TB) is a form of TB
caused by bacteria that are resistant to isoniazid and
rifampicin (i.e. MDR-TB) as well as any fluoroquinolone
and any of the second-line anti-TB injectable drugs
(amikacin, kanamycin or capreomycin).
Tuberculosis and HIV
 Worldwide the number of people infected with both
HIV and TB is rising.
 The HIV virus damages the body’s immune system and
accelerates the speed at which TB progresses from a
harmless infection to a life threatening condition.
 The estimated 10% activation of dormant TB infection
over the life span of an infected person, is increased to
10% activation in one year, if HIV infection is
superimposed.
 It is the opputunistic infection that most frequently
kills HIV-positive people.
Epidemiological Impact
 Reactivation of latent infection- People who are
infected with both HIV and TB are 25 to 30 times more
likely to develop TB again than people only infected
with TB.
 Primary Infection- New tubercular infection in
people with HIV can progress to active disease very
quickly.
 Recurring infection- in people who were cured of
TB.
Diagnosis of TB in people with HIV
 HIV positive people with pulmonary TB may have a
higher frequency of having sputum negative smears.
 The tuberculin test often fails to work, because the
immune system has been damaged by HIV; It may not
even show a response even though the person is
infected with TB.
 Chest Xray will show less cavitation.
 Cases of Extra pulmonary TB are more common.
Thank you!

Tuberculosis

  • 1.
  • 2.
    Definition  Tuberculosis (TB)is a potentially fatal contagious disease that can affect almost any part of the body but is mainly an infection of the lungs. Neo-latin word : - Round nodule/Swelling - Condition “Tubercle” “Osis”
  • 3.
  • 4.
    Other causative organisms Mycobacterium africanum  Mycobacterium microti Non-Mycobacterium Genus  Mycobacterium leprae  Mycobacterium avium  Mycobacterium asiaticum M. africanum M. Bovis M. Canetti M. microti M. tuberculosis complex
  • 5.
     Discovered in1882 by Robert Koch.
  • 6.
    Classification Pulmonary TB - PrimaryDisease - Secondary Disease Extra pulmonary i. Lymph node TB ii. Pleural TB iii. TB of upper airways iv. Skeletal TB v. Genitourinary TB vi. Miliary TB vii. Pericardial TB viii. Gastrointestinal TB ix. Tuberculous Meningitis x. Less common forms
  • 7.
  • 8.
     In 2011,therewere an estimated 8.7million incidence cases of TB globally.  Its equivalent to 125 cases in 1,00,000 population. Asian : 59% African : 26% Eastern Mediterranean Region: 7.7% The European Region : 4.3% Region of the America : 3%
  • 11.
  • 12.
  • 13.
    Severe Symptoms Persistent cough Chestpain Coughing with bloody sputum Shortness of breath Urine discoloration Cloudy & reddish urine Fever with chills. Fatigue
  • 14.
  • 15.
  • 16.
    Types A. Pulmonary TB:- 1. Primary Tuberculosis :-  The infection of an individual who has not been previously infected or immunised is called Primary tuberculosis or Ghon’s complex or childhood tuberculosis.  Lesions forming after infection is peripheral and accompanied by hilar which may not be detectable on chest radiography. 2. Secondary Tuberculosis : The infection that individual who has been previously infected or sensitized is called secondary or post primary or reinfection or chronic tuberculosis.
  • 17.
    B} Extra PulmonaryTB :- • 20% of patients of TB Patient • Affected sites in body are :- 1) Lymph node TB ( tuberculuous lymphadenitis):- • Seen frequently in HIV infected patients. • Symptoms :- Painless swelling of lymph nodes most commonly at cervical and Supraclavical (Scrofula) • Systemic systems are limited to HIV infected patients. • 2) Pleural TB :- Involvement of pleura is common in Primary TB and results from penetration of tubercle bacilli into pleural space.
  • 18.
     Involvement oflarynx, pharynx and epiglottis.  Symptoms :- Dysphagia, chronic productive cough 3) TB of Upper airways :- 4) Genitourinary TB :- • 15% of all Extra pulmonary cases. • Any part of the genitourinary tract get infected. • Symptoms :- Urinary frequency, Dysuria, Hematuria. 5) Skeletal TB :- • Involvement of weight bearing parts like spine, hip, knee. • Symptoms :- Pain in hip joints n knees, swelling of knees, trauma. 6) Gastrointestinal TB :- • Involvement of any part of GI Tract. • Symptoms :- Abdominal pain, diarrhea, weight loss
  • 19.
    7) TB Meningitis& Tuberculoma :-  5% of All Extra pulmonary TB  Results from Hematogenous spead of 10 & 20 TB. 8) TB Pericardiatis :- • 1- 8% of All Extra pulmonary TB cases. • Spreads mainly in mediastinal or hilar nodes or from lungs. 9) Miliary or disseminated TB :- • Results from Hematogenous spread of Tubercle Bacilli. • Spread is due to entry of infection into pulmonary vein producing lesions in different extra pulmonary sites. 10) Less common Extra Pulmonary TB • uveitis, panophthalmitis, painfull Hypersensitivity related phlyctenular conjuctivis.
  • 20.
    Diagnosis 1.Bacteriological test: a. Zeihl-Neelsenstain b. Auramine stain(fluorescence microscopy) 2. Sputum culture test: a. Lowenstein –Jensen(LJ) solid medium: 4-18 weeks b. Liquid medium : 8-14 days c. Agar medium : 7 to 14 days
  • 21.
    3.Radiography: Chest X-Ray(CXR) 4.Nucleic acidamplification:  Species identification ; several hours  Low sensitivity, high cost  Most useful for the rapid confirmation of tuberculosis in persons with AFB-positive sputa  Utility  AFB-negative pulmonary tuberculosis  Extra pulmonary tuberculosis
  • 22.
    5.Tuberculin skin test(PPD)  Injection of fluid into the skin of the lower arm.  48-72 hours later – checked for a reaction.  Diagnosis is based on the size of the wheal. 1 dose = 0.1 ml contains 0.04µg Tuberculin PPD.
  • 23.
  • 24.
  • 25.
    6. Other biologicalexaminations  Cell count(lymphocytes)  Protein(Pandy and Rivalta tests) – Ascites, pleural effusion and meningitis.
  • 26.
    Preventive measures 1) Mask 2)BCG vaccine 3) Regular medical follow up 4) Isolation of Patient 5) Ventilation 6) Natural sunlight 7) UV germicidal irradiation
  • 28.
    BCG vaccine  BacilleCalmette Guerin (BCG).  First used in 1921.  Only vaccine available today for protection against tuberculosis.  It is most effective in protecting children from the disease.  Given 0.1 ml intradermally.  Duration of Protection 15 to 20 years  Efficacy 0 to 80%.  Should be given to all healthy infants as soon as possible after birth unless the child presented with symptomatic HIV infection.
  • 29.
  • 30.
    Drugs MOA Diagram IsoniazidInhibits mycolic acid synthesis. RIFAMPICIN Blocks RNA synthesis by blocking DNA dependent RNA polymerase PYRAZINAMIDE •Bactericidal-slowly metabolizing organism within acidic environment of Phagocyte or caseous granuloma.
  • 31.
    Drugs MOA Diagram ETHAMBUTOL•Bacteriostatic •Inhibition of Arabinosyl Transferase STREPTOMYCIN •Inhibition of Protein synthesis by disruption of ribosomal function
  • 32.
    ADRs and itsManagement
  • 33.
    Dosage regimen  Intensivephase + continuation phase  HREZ (2 months) + HRE (4 months)
  • 34.
    Treatment regimen accordingto WHO ISONIAZID (H) RIFAMPICIN (R) PYRAZINAMIDE (Z) ETHAMBUTOL (E) STREPTOMYCIN (S)
  • 35.
    DOTS DOTS - Directlyobserved treatment, short-course  DOT means that a trained health care worker or other designated individual provides the prescribed TB drugs and watches the patient swallow every dose.
  • 36.
    Multi-Drug Resistance TB TBcaused by strains of Mycobacterium tuberculosis that are resistant to at least isoniazid and rifampicin, the most effective anti- TB drug. Globally, 3.6% are estimated to have MDR-TB. Almost 50% of MDR-TB cases worldwide are estimated to occur in China and India.
  • 37.
  • 38.
    MDR-TB in previouslytreated cases
  • 39.
    Extensively drug resistanceTB  Extensively drug-resistant TB (XDR-TB) is a form of TB caused by bacteria that are resistant to isoniazid and rifampicin (i.e. MDR-TB) as well as any fluoroquinolone and any of the second-line anti-TB injectable drugs (amikacin, kanamycin or capreomycin).
  • 40.
    Tuberculosis and HIV Worldwide the number of people infected with both HIV and TB is rising.  The HIV virus damages the body’s immune system and accelerates the speed at which TB progresses from a harmless infection to a life threatening condition.  The estimated 10% activation of dormant TB infection over the life span of an infected person, is increased to 10% activation in one year, if HIV infection is superimposed.  It is the opputunistic infection that most frequently kills HIV-positive people.
  • 41.
    Epidemiological Impact  Reactivationof latent infection- People who are infected with both HIV and TB are 25 to 30 times more likely to develop TB again than people only infected with TB.  Primary Infection- New tubercular infection in people with HIV can progress to active disease very quickly.  Recurring infection- in people who were cured of TB.
  • 42.
    Diagnosis of TBin people with HIV  HIV positive people with pulmonary TB may have a higher frequency of having sputum negative smears.  The tuberculin test often fails to work, because the immune system has been damaged by HIV; It may not even show a response even though the person is infected with TB.  Chest Xray will show less cavitation.  Cases of Extra pulmonary TB are more common.
  • 43.