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TUBERCULOSIS
DR SHAHNAWAZ F SHAH
MD, FPM, FIAPM,FCPM (MUHS)
Interventional Spine & Pain Physician
Surat
TUBERCULOSIS
 Is the most prevalent communicable infectious
disease on earth and remains out of control in many
developing nations
 It is a chronic specific inflammatory infectious disease
caused by Mycobacterium tuberculosis in humans
 Usually attacks the lungs but it can also affect any
parts of the body
 Also Known as “ KOCH’s Disease”, “wasting disease”
and the “white plague.”
 Tuberculosis can produce atypical signs and
symptoms in
 Infants,
 Elderly, and
 Immunocompromised hosts
 It can progress rapidly in these patients
EPIDEMIOLOGY
EPIDEMIOLOGY
 Roughly one of every three people on earth is
infected by M. tuberculosis (WHO, 2008)
 The distribution is very uneven, with the highest
incidences found in southern Asia and sub-Saharan
Africa
 In the United States, about 13 million people have
LTBI, evidenced by a positive skin test [purified
protein derivative (PPD)] but no signs or symptoms of
disease
EPIDEMIOLOGY
 Every year approximately 1.7 million people
develop TB
 Tuberculosis (TB) kills about 2 million people
each year
 The emergence of drug resistant organism
threatens to make this disease once again
incurable
 India has the highest number of TB cases in the
world, accounting for around one in four cases
globally, according to the WHO.
ETIOLOGY
 MYCOBACTERIUM TUBERCULOSIS
 It presents either
 as latent TB infection (LTBI) or
 as progressive active disease.
 The latter typically causes progressive destruction
of the lungs, leading to death in most patients who
do not receive treatment
CHARACTERISTICS OF
M. TUBERCULOSIS
 Rod shaped,
 0.2-0.5 µ in D, 2-4 µ in L
 Mycolic acid present in its cell wall,
makes it acid fast
 It resists decolourization with acid &
alcohol
 Aerobic and non motile
 It multiplies slowly, can remain
dormant for decades
Main species of mycobacterium
causing tuberculosis:
TYPICAL MYCOBACTERIA
1. Mycobacterium tuberculosis
2. Mycobacterium hominis
3. Mycobacterium bovine
ATYPICAL MYCOBACTERIA
1. Saprophytic mycobacteria
2. Mycobacterium avium
RISK FACTORS OF TUBERCULOSIS
 Low socioeconomic status
 Crowded living conditions
 Diseases that weakens immune
system like HIV
 Person on immunosuppressant
like steroid
 Health care workers
 Migration from a country with a
high number of cases
 Alcoholism
 Recent Tubercular infection
(within last 2 years)
CO-INFECTION WITH
HUMAN IMMUNODEFICIENCY VIRUS (HIV)
 HIV is the most important risk factor for active TB,
because the immune deficit prevents patients from
containing the initial infection
 Coinfection with HIV
 Accelerates the progression of both diseases
 Requiring rapid diagnosis and treatment of both
diseases
Classification of TB
TB
Pulmonary (85-90%) Extra-pulmonary (10-15%)
Sputum
Positive TB
(Those who
have
bacteria in
sputum)
Sputum
Negative TB
(Those who
do not have
bacteria in
sputum)
Lymph Nodes
Bones & Joints
Genitourinary tract
Meninges
Intestines
Skin
How is TB Transmitted?
 Person-to-person through the
air by a person with active TB
disease of the lungs
 Less frequently transmitted
by: Ingestion of M. bovis
found in unpasteurized milk
 Inoculation (in skin
tuberculosis)
 Transplacental route (rare
route)
Type of tuberculosis infection
Pulmonary TB :
1. PRIMARY TUBERCULOSIS :
The infection of an individual who has not been previously infected or
sensitized is called Primary tuberculosis or Ghon’s complex or childhood
tuberculosis.
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.
PRIMARY TUBERCULOSIS
PRIMARY INFECTION
 The progression to clinical disease in a previously
unexposed, immunocompetent person depends on
three factors:
1. The number of M. tuberculosis organisms inhaled
2. Infecting dose and the virulence of these organisms
3. The development of anti-mycobacterial cell-mediated
immunity
 Immunity to M. tuberculosis is primarily mediated by
TH1 cells, which stimulate macrophages to kill the
bacteria
PRIMARY TUBERCULOSIS
 Disease that develops in a previously unexposed
person.
 Almost always begins in lungs
 Inhaled bacilli implant in the distal airspaces of lower
part of upper lobe or upper part of lower lobe
 1-1.5 cm area of grey white inflammation with
consoldation develops, called as Ghon focus which
often caseates
FATE OF PRIMARY TUBERCULOSIS
 No progression
 Healing by fibrosis and calcification
 Ghons complex after undergoing progressive fibrosis
produces radiologically detectable calcification called
as RANKE COMPLEX
 Progressive primary tuberculosis
 Primary miliary tuberculosis
 Dissemination to organs like liver, spleen, kidney,
..etc.
FATE OF SEC. PULMONARY TB
 The lesion may heal with fibrous scarring and
calcification
 The lesions may coalesce together to form large area
of tuberculous pneumonia and produce progressive
secondary pulmonary tuberculosis producing
pulmonary & extra pulmonary lesions:
 Tuberculous caseous pneumonia
 Fibrocaseous tuberculosis
 Miliary tuberculosis
MILIARY TUBERCULOSIS
Extensive infection via hematogenous spread
 In lung: lesions are either microscopic or small, visible
foci (2mm) of yellow white consolidation scattered
through out lung parenchyma
 Miliary pulmonary disease can cause pleural
effusion, tuberculous empyema or obliterative
fibrous pleuritis.
 Extra pulmonary miliary tuberculosis is most
prominent in the liver, spleen, bone marrow,
adrenals, meninges, kidneys, fallopian tubes and
epididymis but can involve any organ
MILIARY TUBERCULOSIS
Miliary tuberculosis of the spleen
The cut surface shows numerous gray-white granulomas
EXTRA PULMONARY TUBERCULOSIS
In tissues or organs seeded hematogenously
Commonly involved organs include:
 Intestinal tuberculosis (Primary, Secondary and
hyperplastic)
 Meninges (Tuberculous meningitis)
 Kidneys (Renal tuberculosis)
 Adrenals (Addison disease)
 Bones (Osteomyelitis)
 Vertebrae (Pott disease)
 Fallopian tubes (Salpingitis)
SYMPTOMS OF TB
Most common symptom of TB
•Cough for 2 weeks or more
Other symptoms of TB are:
• Fever, especially evening rise
• Pain in the chest
• Loss of weight
• Loss of appetite
• Coughing up blood-stained
sputum
• Shortness of breath,
• Tiredness
DIAGNOSTIC STEPS
HISTORYANDCLINICAL
EXAMINATION
RADIOGRAPHIC
FEATURES
BACTERIOLOGIC
EVALUATION
Tests may include:
 Chest CT scan
 Chest X-ray
 Tuberculin skin test (also called a PPD test)
 Sputum examination and cultures
 Interferon-gamma release blood test such as
the QFT-Gold test
 Bronchoscopy
 Thoracentesis
 Biopsy of the affected tissue (rare)
Chest X-ray
Tuberculosis creates cavities
visible in x-rays like this one in the
patient's right upper lobe.
Abnormalities on chest
radiographs may be suggestive, but
are never diagnostic of TB.
However, chest radiographs
may be used to rule out.
BACTERIOLOGIC
EVALUATION
SPUTUM EXAMINATION
 Are essential to confirm TB
 Best collected in morning before any meal
 Sputum examination on 3 days, increase chances of detection
 Sputum can be collected from laryngeal swab or bronchial
washing In small children, gastric lavage can be examined.
 Smear should be prepared from thick dirty part of sputum &
stained with Ziehl-Neelson technique
Acid Fast Bacilli “AFB”
Smear Test
Specimen examined for acid fast bacilli by staining:
Ziehl-neelson Acid Fast
Staining
Auramine-rhodamine
Staining
Tuberculin skin Test / Mantoux test / PPD test
Purified Protein Derivative (PPD) :
Is a concentrated filter of broth in which tubercle bacilli have
grown for 6 weeks(old).
 Standard method for screening & measuring of a person’s
cellular response.
 Measuring the size of induration 48-72 hours.
Tuberculin skin Test
1 2
Positive If ≥ 10 mm Induration Size.
Positive Reaction
 Person infected in the past or latent TB infection.
 After BCG vaccination, but this may last for only 3-7 years .
 Persons are retested 2 weeks later; their ppd skin test “boosted” by
the recent antigen injection. High risk of (endogenous infection)
Negative Reaction
 Persons who have NEVER been infected, they are not
subject to that risk, though they may become infected
from an external source (exogenous infection)
 A positive tuberculin test result signifies cell-
mediated hypersensitivity to tubercular antigens.
 It does not differentiate between infection and
disease
 False-negative reactions may be produced by certain
viral infections, sarcoidosis, malnutrition,
immunosuppression
 False-positive reactions may also result from
infection by atypical mycobacteria
γ-Interferon release assays (GIRA)
 Test rely on the fact that T-lymphocytes will release γ-
interferon when exposed to specific antigens.
 QFT-gold test measures interferon-gamma in the testee's
blood after incubating the blood with specific antigens
from m. Tuberculosis proteins
FIRST LINE DRUG
1. Isoniazid(H)
2. Rifampin (R)
3. Pyrazinamide (Z)
4. Ethambutol (E)
5. Streptomycin (S)
SECOND LINE DRUG
1. Thiacetazone (Tzn)
2. Paraaminosalicylic acid (PAS)
3. Ethionamide (Etm)
4. Cycloserine (Cys)
5. Kanamycine (Am)
6. Capriomycine (Cpr)
NEWER DRUG
1. Ciprofloxacin
2. Ofloxacine
3. Clarithromycine
4. Azithromycine
5. Rifabutine
6. Bedaquiline(Recently)
ANTI-TUBERCULAR DRUG
ANTI-TUBERCULAR DRUGS
Medication Drug action Dose(Thrice a
week)***
Dose in
children(mg/kg)
Isoniazid Bactericidal 600 mg 10-15
Rifampicin Bactericidal 450 mg* 10
Pyrazinamide Bactericidal 1500 mg 30-35
Ethambutol Bacteriostatic 1200 mg 20-25
Streptomycin Bactericidal 0.75 g** 15
* Patients who weigh 60 kg or more at the start of treatment
are given an extra 150mg dose of Rifampicin
** Patients over 50 years of age are given 0.5g of streptomycin
*** Adult patients weighing <30kg receive drugs in patients-
wise from the weight band suggested for pediatric patients
ISONIAZIDE(H)-Pyridine hydrazide.
Action
 Bacteriostatic for resting mycobacteria, bactericidal for proliferating
mycobacteria.
Mechanism of Action
Inhibit cell wall synthesis
Adverse reaction
 Peripheral neuritis
 Liver damage.
 Optic neuritis, Convulsions, Hypersensitivity reactions
RIFAMPICIN (R)-Rifamycine
Action
 Bactericidal for mycobacteria; also effective against most Gram-positive
and many Gram-negative bacteria.
Mechanism of Action
Binds to the β subunit of DNA-dependent RNA polymerase (rpoB) .
Inhibit RNA synthesis
Dose
 10 mg/kg (600 mg),OD
 Oral
Adverse reaction
 Flu like symptoms.
 Thrombocytopenic purpura.
 GIT disturbances &
 Harmless orange tint to saliva, sweat &
tears
PYRAZINAMIDE (Z)-Nicotinamide analogue
Action
Bactericidal for actively dividing intracellular mycobacteria.
Main effect occur in first few months.
Mechanism of Action
PYRAZINAMIDE
Enter M.tuberculosis
Pyrazinoic acid (POA+)
Kill the mycobacteria
Pyrazinamidase/Nicotinamidase
Inhibit FAS
Inhibit growth mycobacteria
Go extra-
cellular
Adverse reaction
 SideroblasticAnemia.
 Hepatotoxic &
 Joint pains
STREPTOMYCIN (S)-aminoglycoside
Action
 Bactericidal for actively dividing intracellular mycobacteria.
Mechanism of Action
Bind 30S ribosomes.
False pair of
codon:anticodone
False reading of genetic
code
Inhibit protein synthesis
Adverse reaction
 Ototoxicity
 Nephrotoxicity
 Neuromuscular blockade- ↓release of Ach by inhibiting fusion
of vesicles with terminal membrane
ETHAMBUTOL(E)-Ethylenediamine derivative
Action
 Tuberculostatic drug.
Mechanism ofAction
Inhibit Arabinosyl transferase-Ш enzyme
Disrupt the transport of Arabinose sugar
Arbinogalactan biosynthesis impaired
Disruption in mycobacterial cell wall formation
Adverse reaction
 Optic neuritis
 Colour blindness
FLASH CARD OF ANTITUBERCULARDRUG
Revised National Tuberculosis Control
Programme
Goal
1. To decrease the mortality and morbidity
2. To cut down the chain of transmission of infection
until TB ceases to be a public health problem
Objectives
To achieve and maintain:
1. Cure rate of at least 90% among newly detected
smear positive (infectious) pulmonary TB cases
2. Case detection of at least 85% of the expected new smear
positive PTB cases in the community
Implementation
• Case finding- by passive surveillance on patient with
symptoms of
i) Persistent cough for 2weeks or more.
ii) Haemoptysis
iii) Night sweats
iv) Evening rise of temperature
v) Chest pain
In lab.-
i) Sputum collection for diagnosis
ii) Radiography
iii) Tuberculin test
Sputum examination is the best method to diagnose TB
 Pulmonary TB diagnosis can be confirmed by sputum
examination.
 Two sputum samples are collected over one/two consecutive
days
 If the health facility is a DMC, spot sample is collected
immediately and the patient is given a sputum container to
collect early morning sample & brought to the lab
Diagnosis of TB
 Alternatively the patient can be asked to collect a
morning sample and go to a DMC where a spot
sample can be taken
 In case the patient is not able to reach a DMC, both
samples - morning and spot, can be collected and
transported
 The sputum samples are subjected to microscopy
examination as early as possible
 A patient is diagnosed positive if one or both the
samples is positive for bacteria
 If the bacteria are not visible in any sputum sample,
the patient is negative and should be referred to a
medical officer for further evaluation
 TB of other organs is diagnosed by a medical officer
RNTCP revised diagnostic algorithm (2009)
Note: RNTCP has
separate diagnostic
algorithm for
pediatric pulmonary
TB and common
forms of extra-
pulmonary TB
DOTS
Directly Observed Treatment
Short Course
Tuberculosis control strategy recommended by the World Health Organization
as the strategy that ensures cure of TB
Directly
observed
treatment
(DOT) is one
element of
the DOTS
strategy
An observer
watches and
helps the
patient
swallow the
tablets
Direct observation
ensures treatment for the
entire course
• with the right
drugs
• in the right doses
• at the right
intervals
Directly Observed Treatment Short Course
Directly Observed Treatment Short Course
There are two phases in DOTS treatment
1 Intensive Phase(IP):-
 Intensive phase is of 2 to 3 months duration
Patient swallow medicine under the observation of a
health worker during IP
Medicines are taken 3 times a week on alternate
days
If the sputum is negative for bacteria after IP,
continuation phase is started
Directly Observed Treatment Short Course
2. Continuation Phase
• This phase is of 4 or 5 months duration
• The patient is provided with a weekly blister pack to
take home
• The medicines from the blister pack are taken on
alternate days, three times a week and in the
remaining days, Vitamin tablets are taken
• The first dose of the weekly blister pack is taken under
direct observation of the health worker
• Empty blister packs are collected to ensure that the
medicines are taken at home by the patient
H: Isoniazid (300 mg), R: Rifampicin (600 mg), Z: Pyrazinamide (1500 mg), E:
Ethambutol (1000 mg), S: Streptomycin (1000 mg)
1. Patients who weigh 60kg or more receive additional Rifampicin
150mg.
2.Patients who are more than 50 years old receive Streptomycin
500mg.
3. Patients who weigh less than 30kg receive drugs as per Paediatric
weight band boxes according to body weight.
Category Type of Patient Regimen Duration in months
Category I
Color of box:
RED
New Sputum Positive ,
Seriously ill sputum negative,
Seriously ill extra pulmonary,
2 (HRZE)3, 6
4 (HR)3
Category II
Color of box:
BLUE
Sputum Positive relapse,
Sputum Positive failure
Sputum Positive treatment after
default
2 (HRZES)3, 8
1 (HRZE)3
5 (HRE)3
ADVANTAGES
 The patient is supported to successfully complete the full
course of medication
 The patient is monitored closely for side effects of
medications and supported to work through the side
effects appropriately
 The patient is encouraged and support.
 Reduces the possibility of tuberculosis germs becoming
resistant to the medication.
DRUG RESISTANT TB
1. MULTIPLE DRUG RESISTANCE TB (MDR-TB)
 An MDR-TB suspect who is sputum culture positive and whose
TB is due to Mycobacterium tuberculosis that are resistant in-
vitro to at least ISONIAZID AND RIFAMPICIN.
2. EXTENSIVELY DRUG RESISTANT TB (XDR–TB)
 subset of MDR-TB where the bacilli, in addition to being
resistant to R and H, are also resistant to any
fluoroquinolones and any one of the second-line injectable
drugs (namely Kanamycin, Capreomycin, or Amikacin).
For the treatment of MDR-TB cases
STANDARDISED TREATMENT REGIMEN
6 drugs
- kanamycin
- ethionamide
- ethambutol
- ofloxacin
- pyrazinamide
- cycloserine
for 6-9 months of the INTENSIVE PHASE
CONTINUATION PHASE-
4 drugs
Ofloxacin
Ethionamide
Ethambutol
Cycloserine
for 18 months.
For the treatment of MDR-TB cases
BCG VACCINE
Protective effect against
meningitis and
disseminated TB in
children.
It does not prevent
primary infection and
does not prevent
reactivation of latent
pulmonary infection
ROLE OF PHYSIOTHERAPISTS
 PT's should be prepared to take a thorough history and a
proper examination in order to better identify TB.
 Recognize your patient's signs and symptoms
 Patients may present in clinic with musculoskeletal problems
with unknown causes or arthritic pain.
 A patient could also be seen in physical therapy if they have
had surgery on their back, in which case the normal
rehabilitation protocols would be followed
ROLE OF PHYSIOTHERAPISTS
 All physical therapists should be aware of the proper
personal protective equipment (PPE) that should be
worn.
 Therapists are able to provide percussion and postural
drainage to clear secretions out of the lung
For more updates:
thepainkillerMD

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Tuberculosis

  • 1. TUBERCULOSIS DR SHAHNAWAZ F SHAH MD, FPM, FIAPM,FCPM (MUHS) Interventional Spine & Pain Physician Surat
  • 2. TUBERCULOSIS  Is the most prevalent communicable infectious disease on earth and remains out of control in many developing nations  It is a chronic specific inflammatory infectious disease caused by Mycobacterium tuberculosis in humans  Usually attacks the lungs but it can also affect any parts of the body  Also Known as “ KOCH’s Disease”, “wasting disease” and the “white plague.”
  • 3.  Tuberculosis can produce atypical signs and symptoms in  Infants,  Elderly, and  Immunocompromised hosts  It can progress rapidly in these patients
  • 5. EPIDEMIOLOGY  Roughly one of every three people on earth is infected by M. tuberculosis (WHO, 2008)  The distribution is very uneven, with the highest incidences found in southern Asia and sub-Saharan Africa  In the United States, about 13 million people have LTBI, evidenced by a positive skin test [purified protein derivative (PPD)] but no signs or symptoms of disease
  • 6. EPIDEMIOLOGY  Every year approximately 1.7 million people develop TB  Tuberculosis (TB) kills about 2 million people each year  The emergence of drug resistant organism threatens to make this disease once again incurable  India has the highest number of TB cases in the world, accounting for around one in four cases globally, according to the WHO.
  • 7. ETIOLOGY  MYCOBACTERIUM TUBERCULOSIS  It presents either  as latent TB infection (LTBI) or  as progressive active disease.  The latter typically causes progressive destruction of the lungs, leading to death in most patients who do not receive treatment
  • 8. CHARACTERISTICS OF M. TUBERCULOSIS  Rod shaped,  0.2-0.5 µ in D, 2-4 µ in L  Mycolic acid present in its cell wall, makes it acid fast  It resists decolourization with acid & alcohol  Aerobic and non motile  It multiplies slowly, can remain dormant for decades
  • 9. Main species of mycobacterium causing tuberculosis: TYPICAL MYCOBACTERIA 1. Mycobacterium tuberculosis 2. Mycobacterium hominis 3. Mycobacterium bovine ATYPICAL MYCOBACTERIA 1. Saprophytic mycobacteria 2. Mycobacterium avium
  • 10. RISK FACTORS OF TUBERCULOSIS  Low socioeconomic status  Crowded living conditions  Diseases that weakens immune system like HIV  Person on immunosuppressant like steroid  Health care workers  Migration from a country with a high number of cases  Alcoholism  Recent Tubercular infection (within last 2 years)
  • 11. CO-INFECTION WITH HUMAN IMMUNODEFICIENCY VIRUS (HIV)  HIV is the most important risk factor for active TB, because the immune deficit prevents patients from containing the initial infection  Coinfection with HIV  Accelerates the progression of both diseases  Requiring rapid diagnosis and treatment of both diseases
  • 12. Classification of TB TB Pulmonary (85-90%) Extra-pulmonary (10-15%) Sputum Positive TB (Those who have bacteria in sputum) Sputum Negative TB (Those who do not have bacteria in sputum) Lymph Nodes Bones & Joints Genitourinary tract Meninges Intestines Skin
  • 13. How is TB Transmitted?  Person-to-person through the air by a person with active TB disease of the lungs  Less frequently transmitted by: Ingestion of M. bovis found in unpasteurized milk  Inoculation (in skin tuberculosis)  Transplacental route (rare route)
  • 14. Type of tuberculosis infection Pulmonary TB : 1. PRIMARY TUBERCULOSIS : The infection of an individual who has not been previously infected or sensitized is called Primary tuberculosis or Ghon’s complex or childhood tuberculosis. 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.
  • 15. PRIMARY TUBERCULOSIS PRIMARY INFECTION  The progression to clinical disease in a previously unexposed, immunocompetent person depends on three factors: 1. The number of M. tuberculosis organisms inhaled 2. Infecting dose and the virulence of these organisms 3. The development of anti-mycobacterial cell-mediated immunity  Immunity to M. tuberculosis is primarily mediated by TH1 cells, which stimulate macrophages to kill the bacteria
  • 16. PRIMARY TUBERCULOSIS  Disease that develops in a previously unexposed person.  Almost always begins in lungs  Inhaled bacilli implant in the distal airspaces of lower part of upper lobe or upper part of lower lobe  1-1.5 cm area of grey white inflammation with consoldation develops, called as Ghon focus which often caseates
  • 17. FATE OF PRIMARY TUBERCULOSIS  No progression  Healing by fibrosis and calcification  Ghons complex after undergoing progressive fibrosis produces radiologically detectable calcification called as RANKE COMPLEX  Progressive primary tuberculosis  Primary miliary tuberculosis  Dissemination to organs like liver, spleen, kidney, ..etc.
  • 18.
  • 19. FATE OF SEC. PULMONARY TB  The lesion may heal with fibrous scarring and calcification  The lesions may coalesce together to form large area of tuberculous pneumonia and produce progressive secondary pulmonary tuberculosis producing pulmonary & extra pulmonary lesions:  Tuberculous caseous pneumonia  Fibrocaseous tuberculosis  Miliary tuberculosis
  • 20. MILIARY TUBERCULOSIS Extensive infection via hematogenous spread  In lung: lesions are either microscopic or small, visible foci (2mm) of yellow white consolidation scattered through out lung parenchyma  Miliary pulmonary disease can cause pleural effusion, tuberculous empyema or obliterative fibrous pleuritis.  Extra pulmonary miliary tuberculosis is most prominent in the liver, spleen, bone marrow, adrenals, meninges, kidneys, fallopian tubes and epididymis but can involve any organ
  • 21. MILIARY TUBERCULOSIS Miliary tuberculosis of the spleen The cut surface shows numerous gray-white granulomas
  • 22. EXTRA PULMONARY TUBERCULOSIS In tissues or organs seeded hematogenously Commonly involved organs include:  Intestinal tuberculosis (Primary, Secondary and hyperplastic)  Meninges (Tuberculous meningitis)  Kidneys (Renal tuberculosis)  Adrenals (Addison disease)  Bones (Osteomyelitis)  Vertebrae (Pott disease)  Fallopian tubes (Salpingitis)
  • 23. SYMPTOMS OF TB Most common symptom of TB •Cough for 2 weeks or more Other symptoms of TB are: • Fever, especially evening rise • Pain in the chest • Loss of weight • Loss of appetite • Coughing up blood-stained sputum • Shortness of breath, • Tiredness
  • 24.
  • 26. Tests may include:  Chest CT scan  Chest X-ray  Tuberculin skin test (also called a PPD test)  Sputum examination and cultures  Interferon-gamma release blood test such as the QFT-Gold test  Bronchoscopy  Thoracentesis  Biopsy of the affected tissue (rare)
  • 27. Chest X-ray Tuberculosis creates cavities visible in x-rays like this one in the patient's right upper lobe. Abnormalities on chest radiographs may be suggestive, but are never diagnostic of TB. However, chest radiographs may be used to rule out.
  • 29. SPUTUM EXAMINATION  Are essential to confirm TB  Best collected in morning before any meal  Sputum examination on 3 days, increase chances of detection  Sputum can be collected from laryngeal swab or bronchial washing In small children, gastric lavage can be examined.  Smear should be prepared from thick dirty part of sputum & stained with Ziehl-Neelson technique
  • 30. Acid Fast Bacilli “AFB” Smear Test Specimen examined for acid fast bacilli by staining: Ziehl-neelson Acid Fast Staining Auramine-rhodamine Staining
  • 31. Tuberculin skin Test / Mantoux test / PPD test Purified Protein Derivative (PPD) : Is a concentrated filter of broth in which tubercle bacilli have grown for 6 weeks(old).  Standard method for screening & measuring of a person’s cellular response.  Measuring the size of induration 48-72 hours.
  • 32. Tuberculin skin Test 1 2 Positive If ≥ 10 mm Induration Size.
  • 33.
  • 34. Positive Reaction  Person infected in the past or latent TB infection.  After BCG vaccination, but this may last for only 3-7 years .  Persons are retested 2 weeks later; their ppd skin test “boosted” by the recent antigen injection. High risk of (endogenous infection)
  • 35. Negative Reaction  Persons who have NEVER been infected, they are not subject to that risk, though they may become infected from an external source (exogenous infection)
  • 36.  A positive tuberculin test result signifies cell- mediated hypersensitivity to tubercular antigens.  It does not differentiate between infection and disease  False-negative reactions may be produced by certain viral infections, sarcoidosis, malnutrition, immunosuppression  False-positive reactions may also result from infection by atypical mycobacteria
  • 37. γ-Interferon release assays (GIRA)  Test rely on the fact that T-lymphocytes will release γ- interferon when exposed to specific antigens.  QFT-gold test measures interferon-gamma in the testee's blood after incubating the blood with specific antigens from m. Tuberculosis proteins
  • 38. FIRST LINE DRUG 1. Isoniazid(H) 2. Rifampin (R) 3. Pyrazinamide (Z) 4. Ethambutol (E) 5. Streptomycin (S) SECOND LINE DRUG 1. Thiacetazone (Tzn) 2. Paraaminosalicylic acid (PAS) 3. Ethionamide (Etm) 4. Cycloserine (Cys) 5. Kanamycine (Am) 6. Capriomycine (Cpr) NEWER DRUG 1. Ciprofloxacin 2. Ofloxacine 3. Clarithromycine 4. Azithromycine 5. Rifabutine 6. Bedaquiline(Recently) ANTI-TUBERCULAR DRUG
  • 39. ANTI-TUBERCULAR DRUGS Medication Drug action Dose(Thrice a week)*** Dose in children(mg/kg) Isoniazid Bactericidal 600 mg 10-15 Rifampicin Bactericidal 450 mg* 10 Pyrazinamide Bactericidal 1500 mg 30-35 Ethambutol Bacteriostatic 1200 mg 20-25 Streptomycin Bactericidal 0.75 g** 15 * Patients who weigh 60 kg or more at the start of treatment are given an extra 150mg dose of Rifampicin ** Patients over 50 years of age are given 0.5g of streptomycin *** Adult patients weighing <30kg receive drugs in patients- wise from the weight band suggested for pediatric patients
  • 40. ISONIAZIDE(H)-Pyridine hydrazide. Action  Bacteriostatic for resting mycobacteria, bactericidal for proliferating mycobacteria. Mechanism of Action Inhibit cell wall synthesis
  • 41. Adverse reaction  Peripheral neuritis  Liver damage.  Optic neuritis, Convulsions, Hypersensitivity reactions
  • 42. RIFAMPICIN (R)-Rifamycine Action  Bactericidal for mycobacteria; also effective against most Gram-positive and many Gram-negative bacteria. Mechanism of Action Binds to the β subunit of DNA-dependent RNA polymerase (rpoB) . Inhibit RNA synthesis Dose  10 mg/kg (600 mg),OD  Oral
  • 43. Adverse reaction  Flu like symptoms.  Thrombocytopenic purpura.  GIT disturbances &  Harmless orange tint to saliva, sweat & tears
  • 44. PYRAZINAMIDE (Z)-Nicotinamide analogue Action Bactericidal for actively dividing intracellular mycobacteria. Main effect occur in first few months. Mechanism of Action PYRAZINAMIDE Enter M.tuberculosis Pyrazinoic acid (POA+) Kill the mycobacteria Pyrazinamidase/Nicotinamidase Inhibit FAS Inhibit growth mycobacteria Go extra- cellular
  • 45. Adverse reaction  SideroblasticAnemia.  Hepatotoxic &  Joint pains
  • 46. STREPTOMYCIN (S)-aminoglycoside Action  Bactericidal for actively dividing intracellular mycobacteria. Mechanism of Action Bind 30S ribosomes. False pair of codon:anticodone False reading of genetic code Inhibit protein synthesis
  • 47. Adverse reaction  Ototoxicity  Nephrotoxicity  Neuromuscular blockade- ↓release of Ach by inhibiting fusion of vesicles with terminal membrane
  • 48. ETHAMBUTOL(E)-Ethylenediamine derivative Action  Tuberculostatic drug. Mechanism ofAction Inhibit Arabinosyl transferase-Ш enzyme Disrupt the transport of Arabinose sugar Arbinogalactan biosynthesis impaired Disruption in mycobacterial cell wall formation
  • 49. Adverse reaction  Optic neuritis  Colour blindness
  • 50. FLASH CARD OF ANTITUBERCULARDRUG
  • 51. Revised National Tuberculosis Control Programme
  • 52. Goal 1. To decrease the mortality and morbidity 2. To cut down the chain of transmission of infection until TB ceases to be a public health problem Objectives To achieve and maintain: 1. Cure rate of at least 90% among newly detected smear positive (infectious) pulmonary TB cases 2. Case detection of at least 85% of the expected new smear positive PTB cases in the community
  • 53. Implementation • Case finding- by passive surveillance on patient with symptoms of i) Persistent cough for 2weeks or more. ii) Haemoptysis iii) Night sweats iv) Evening rise of temperature v) Chest pain In lab.- i) Sputum collection for diagnosis ii) Radiography iii) Tuberculin test
  • 54. Sputum examination is the best method to diagnose TB  Pulmonary TB diagnosis can be confirmed by sputum examination.  Two sputum samples are collected over one/two consecutive days  If the health facility is a DMC, spot sample is collected immediately and the patient is given a sputum container to collect early morning sample & brought to the lab Diagnosis of TB
  • 55.  Alternatively the patient can be asked to collect a morning sample and go to a DMC where a spot sample can be taken  In case the patient is not able to reach a DMC, both samples - morning and spot, can be collected and transported
  • 56.  The sputum samples are subjected to microscopy examination as early as possible  A patient is diagnosed positive if one or both the samples is positive for bacteria  If the bacteria are not visible in any sputum sample, the patient is negative and should be referred to a medical officer for further evaluation  TB of other organs is diagnosed by a medical officer
  • 57. RNTCP revised diagnostic algorithm (2009) Note: RNTCP has separate diagnostic algorithm for pediatric pulmonary TB and common forms of extra- pulmonary TB
  • 58. DOTS Directly Observed Treatment Short Course Tuberculosis control strategy recommended by the World Health Organization as the strategy that ensures cure of TB
  • 59. Directly observed treatment (DOT) is one element of the DOTS strategy An observer watches and helps the patient swallow the tablets Direct observation ensures treatment for the entire course • with the right drugs • in the right doses • at the right intervals Directly Observed Treatment Short Course
  • 60. Directly Observed Treatment Short Course There are two phases in DOTS treatment 1 Intensive Phase(IP):-  Intensive phase is of 2 to 3 months duration Patient swallow medicine under the observation of a health worker during IP Medicines are taken 3 times a week on alternate days If the sputum is negative for bacteria after IP, continuation phase is started
  • 61. Directly Observed Treatment Short Course 2. Continuation Phase • This phase is of 4 or 5 months duration • The patient is provided with a weekly blister pack to take home • The medicines from the blister pack are taken on alternate days, three times a week and in the remaining days, Vitamin tablets are taken • The first dose of the weekly blister pack is taken under direct observation of the health worker • Empty blister packs are collected to ensure that the medicines are taken at home by the patient
  • 62. H: Isoniazid (300 mg), R: Rifampicin (600 mg), Z: Pyrazinamide (1500 mg), E: Ethambutol (1000 mg), S: Streptomycin (1000 mg) 1. Patients who weigh 60kg or more receive additional Rifampicin 150mg. 2.Patients who are more than 50 years old receive Streptomycin 500mg. 3. Patients who weigh less than 30kg receive drugs as per Paediatric weight band boxes according to body weight. Category Type of Patient Regimen Duration in months Category I Color of box: RED New Sputum Positive , Seriously ill sputum negative, Seriously ill extra pulmonary, 2 (HRZE)3, 6 4 (HR)3 Category II Color of box: BLUE Sputum Positive relapse, Sputum Positive failure Sputum Positive treatment after default 2 (HRZES)3, 8 1 (HRZE)3 5 (HRE)3
  • 63. ADVANTAGES  The patient is supported to successfully complete the full course of medication  The patient is monitored closely for side effects of medications and supported to work through the side effects appropriately  The patient is encouraged and support.  Reduces the possibility of tuberculosis germs becoming resistant to the medication.
  • 64. DRUG RESISTANT TB 1. MULTIPLE DRUG RESISTANCE TB (MDR-TB)  An MDR-TB suspect who is sputum culture positive and whose TB is due to Mycobacterium tuberculosis that are resistant in- vitro to at least ISONIAZID AND RIFAMPICIN. 2. EXTENSIVELY DRUG RESISTANT TB (XDR–TB)  subset of MDR-TB where the bacilli, in addition to being resistant to R and H, are also resistant to any fluoroquinolones and any one of the second-line injectable drugs (namely Kanamycin, Capreomycin, or Amikacin).
  • 65. For the treatment of MDR-TB cases STANDARDISED TREATMENT REGIMEN 6 drugs - kanamycin - ethionamide - ethambutol - ofloxacin - pyrazinamide - cycloserine for 6-9 months of the INTENSIVE PHASE
  • 67. BCG VACCINE Protective effect against meningitis and disseminated TB in children. It does not prevent primary infection and does not prevent reactivation of latent pulmonary infection
  • 68. ROLE OF PHYSIOTHERAPISTS  PT's should be prepared to take a thorough history and a proper examination in order to better identify TB.  Recognize your patient's signs and symptoms  Patients may present in clinic with musculoskeletal problems with unknown causes or arthritic pain.  A patient could also be seen in physical therapy if they have had surgery on their back, in which case the normal rehabilitation protocols would be followed
  • 69. ROLE OF PHYSIOTHERAPISTS  All physical therapists should be aware of the proper personal protective equipment (PPE) that should be worn.  Therapists are able to provide percussion and postural drainage to clear secretions out of the lung
  • 70.