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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
Human
Mycobacterium Bovis
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
Spread of Tuberculosis
Severe Symptoms
Persistentcough
Chest pain
Coughing with bloody sputum
Shortnessof breath
Urinediscoloration
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.
3) TB of Upper airways :-
Involvement of larynx, pharynx and epiglottis.
Symptoms :- Dysphagia, chronic productive cough
4) GenitourinaryTB :-
• 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 Hematogenousspead of 10 & 20 TB.
8) TB Pericardiatis :-
• 1- 8% of All Extra pulmonaryTB cases.
• Spreads mainly in mediastinal or hilar nodes
or from lungs.
9) Miliary ordisseminated TB :-
• Results from Hematogenous spread of Tubercle Bacilli.
•Spread isdue toentry of infection into pulmonaryvein
producing
lesions in different extrapulmonary sites.
10) Lesscommon Extra PulmonaryTB
uveitis, panophthalmitis, painfull Hypersensitivity
related phlyctenularconjuctivis.
Diagnosis
1.Bacteriological test:
a. Zeihl-Neelsenstain
b. Auraminestain(f luorescence microscopy)
2. Sputumculture 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(Pandyand 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.
⚫ Onlyvaccine available today forprotectionagainst tuberculosis.
⚫ It is mosteffective in protecting children from thedisease.
⚫ Given 0.1 ml intradermally.
⚫ Durationof Protection 15 to 20 years
⚫ Efficacy 0 to 80%.
⚫ Should begiven toall healthy infantsas soonas possibleafterbirth
unless thechild 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
 Intensivephase + 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 - Directlyobserved treatment, short-course
⚫ DOT means that a trained health care worker or other designated
individual provides the prescribed TB drugsand watches the patient
swalloweverydose.
Multi-Drug Resistance TB
TB caused by strains of Mycobacterium
tuberculosis that are resistant toat least isoniazid
and rifampicin, the mosteffectiveanti- TB drug.
Globally, 3.6% are estimated to have MDR-TB.
Almost 50% of MDR-TB cases worldwide are
estimated tooccur in China and India.
Extensively drug resistance TB
⚫Extensivelydrug-resistantTB (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 orcapreomycin).
Tuberculosis and HIV
⚫Worldwide the numberof people infected with both
HIV and TB is rising.
⚫The HIV virusdamages the body’s immunesystemand
accelerates the speed at which TB progresses from a
harmless infection toa life threatening condition.
⚫Theestimated 10% activationof dormantTB infection
overthe life span of an infected person, is increased to
10% activation in one year, if HIV infection is
superimposed.
⚫It is theopputunistic 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
peoplewith HIV can progress toactivediseasevery
quickly.
⚫Recurring infection- in peoplewhowerecured of
TB.
Diagnosis of TB in people with HIV
⚫HIV positive people with pulmonary TB may have a
higher frequencyof having sputum negativesmears.
⚫The tuberculin test often fails to work, because the
immunesystem has been damaged by HIV; It may not
even showa responseeven though the person is
infected with TB.
⚫ChestXraywill show lesscavitation.
⚫Casesof Extra pulmonaryTB are morecommon.
Thank you!

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tuberculosis-150808111627-lva1-app6891.pptx

  • 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”
  • 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 in 1882 by Robert Koch.
  • 6. 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
  • 7.
  • 9. Severe Symptoms Persistentcough Chest pain Coughing with bloody sputum Shortnessof breath Urinediscoloration Cloudy & reddish urine Fever with chills. Fatigue
  • 10. Based on types of TB
  • 12. 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.
  • 13. 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.
  • 14. 3) TB of Upper airways :- Involvement of larynx, pharynx and epiglottis. Symptoms :- Dysphagia, chronic productive cough 4) GenitourinaryTB :- • 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
  • 15. 7) TB Meningitis & Tuberculoma :- 5% of All Extra pulmonary TB Results from Hematogenousspead of 10 & 20 TB. 8) TB Pericardiatis :- • 1- 8% of All Extra pulmonaryTB cases. • Spreads mainly in mediastinal or hilar nodes or from lungs. 9) Miliary ordisseminated TB :- • Results from Hematogenous spread of Tubercle Bacilli. •Spread isdue toentry of infection into pulmonaryvein producing lesions in different extrapulmonary sites. 10) Lesscommon Extra PulmonaryTB uveitis, panophthalmitis, painfull Hypersensitivity related phlyctenularconjuctivis.
  • 16. Diagnosis 1.Bacteriological test: a. Zeihl-Neelsenstain b. Auraminestain(f luorescence microscopy) 2. Sputumculture test: a. Lowenstein –Jensen(LJ) solid medium: 4-18 weeks b. Liquid medium : 8-14 days c. Agar medium : 7 to 14 days
  • 17. 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
  • 18. 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.
  • 21. 6. Other biological examinations  Cell count(lymphocytes)  Protein(Pandyand Rivalta tests) – Ascites, pleural effusion and meningitis.
  • 22. 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
  • 23.
  • 24. BCG vaccine ⚫ Bacille Calmette Guerin (BCG). ⚫ First used in 1921. ⚫ Onlyvaccine available today forprotectionagainst tuberculosis. ⚫ It is mosteffective in protecting children from thedisease. ⚫ Given 0.1 ml intradermally. ⚫ Durationof Protection 15 to 20 years ⚫ Efficacy 0 to 80%. ⚫ Should begiven toall healthy infantsas soonas possibleafterbirth unless thechild presented with symptomatic HIV infection.
  • 26. 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.
  • 27. Drugs MOA Diagram ETHAMBUTOL •Bacteriostatic •Inhibition of Arabinosyl Transferase STREPTOMYCIN •Inhibition of Protein synthesis by disruption of ribosomal function
  • 28. ADRs and its Management
  • 29. Dosage regimen  Intensivephase + continuation phase  HREZ (2 months) + HRE (4 months)
  • 30. Treatment regimen according to WHO ISONIAZID (H) RIFAMPICIN (R) PYRAZINAMIDE (Z) ETHAMBUTOL (E) STREPTOMYCIN (S)
  • 31. DOTS DOTS - Directlyobserved treatment, short-course ⚫ DOT means that a trained health care worker or other designated individual provides the prescribed TB drugsand watches the patient swalloweverydose.
  • 32. Multi-Drug Resistance TB TB caused by strains of Mycobacterium tuberculosis that are resistant toat least isoniazid and rifampicin, the mosteffectiveanti- TB drug. Globally, 3.6% are estimated to have MDR-TB. Almost 50% of MDR-TB cases worldwide are estimated tooccur in China and India.
  • 33. Extensively drug resistance TB ⚫Extensivelydrug-resistantTB (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 orcapreomycin).
  • 34. Tuberculosis and HIV ⚫Worldwide the numberof people infected with both HIV and TB is rising. ⚫The HIV virusdamages the body’s immunesystemand accelerates the speed at which TB progresses from a harmless infection toa life threatening condition. ⚫Theestimated 10% activationof dormantTB infection overthe life span of an infected person, is increased to 10% activation in one year, if HIV infection is superimposed. ⚫It is theopputunistic infection that most frequently kills HIV-positive people.
  • 35. 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 peoplewith HIV can progress toactivediseasevery quickly. ⚫Recurring infection- in peoplewhowerecured of TB.
  • 36. Diagnosis of TB in people with HIV ⚫HIV positive people with pulmonary TB may have a higher frequencyof having sputum negativesmears. ⚫The tuberculin test often fails to work, because the immunesystem has been damaged by HIV; It may not even showa responseeven though the person is infected with TB. ⚫ChestXraywill show lesscavitation. ⚫Casesof Extra pulmonaryTB are morecommon.