Tuberculosis presentation by Sohel MemonPresentation Transcript
Topics to be discussed Definition Classification Causative agents Spread of disease Epidemiology Pathophysiology Signs and Symptoms Precautions Diagnosis Treatment or Management
Definition Tuberculosis (TB) is a potentiallyfatal contagious disease that canaffect almost any part of the body butis mainly an infection of the lungs.Neo-latin word :- Round nodule/Swelling- Condition“Tubercle”“Osis”
Anatomy of M.tuberculosis Discovered in 1882 by Robert Koch.
ClassificationTuberculosisPulmonary TB- Primary Disease- Secondary DiseaseExtra pulmonaryi. Lymph node TBii. Pleural TBiii. TB of upper airwaysiv. Skeletal TBv. Genitourinary TBvi. Miliary TBvii. Pericardial TBviii. Gastrointestinal TBix. Tuberculous Meningitisx. Less common forms
In 2011,there were an estimated 8.7millionincidence 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• Airborne
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
Three important consideration for pathogenesis oftuberculosis:i. The basis of virulence of organism.ii. The relationship of HSN to immunity againstinfection.iii. Pathogenesis of tissue destruction and caseousnecrosis.
1. Virulence of organism. No endo-toxin,exo-toxins or histolytic enzymes. Capability to escape killing by macrophages anddelayed type HSN reaction.M.Tuberculosis contains several important components:1) Cord Factor2) Sulfatides3) LAM4) Heat shock Protein5) Complement on the surface
a. Cord Factor: Surface glycolipids, allows to grow organism in-vitro and in vivo.b. Sulfatides: Surface glycolipids containing sulfur. Prevent fusion of macrophage containing tuberculosis withlysosomes.c. LAM Major hetero-polysaccharide inhibits the activation of macrophageby IF-Ý. Also induces macrophages to secrete TNF-þ which causesfever,weight loss and tissue damage and secretes IL-10,whichsuppresses mycobacteria-induces T-cell proliferation.
d. Heat shock Protein Similar to human heat shock proteins. Responsible to carryout auto immune reactions.e. Complement on the surface Opsonization and responsible for its uptake bymacrophage.
2.The relationship of HSN to immunity againstinfection. The development of delayed type IVhypersensitivity reaction to the tubercules bacillusprobably explains the organism’s destructivenessin tissues and also the emergence of resistance tothe organism , the inflammatory response is notspecific.
3. Pathogenesis of tissue destruction and caseousnecrosis. Within in 2 or 3 seeks coincident with theappearance of the positive skin reaction,thereaction becomes granulomatus and the centers ofthe granulomas become caseous, forming typical“soft tubercles”.
A. Pulmonary TB :-1. Primary Tuberculosis :- The infection of an individual who has not been previouslyinfected or immunised is called Primary tuberculosis or Ghon’scomplex or childhood tuberculosis. Lesions forming after infection is peripheral and accompanied byhilar which may not be detectable on chest radiography.Types2. Secondary Tuberculosis :The infection that individual who has been previously infected orsensitized is called secondary or post primary or reinfection orchronic 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 atcervical and Supraclavical (Scrofula)• Systemic systems are limited to HIV infected patients.•2) Pleural TB :-Involvement of pleura is common in Primary TBand results from penetration of tubercle bacilli into pleuralspace.Contd…
Involvement of larynx, pharynx and epiglottis. Symptoms :- Dysphagia, chronic productive cough3) 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 ofknees, trauma.6) Gastrointestinal TB :-• Involvement of any part of GI Tract.• Symptoms :- Abdominal pain, diarrhea, weight loss
5% of All Extra pulmonary TB Results from Hematogenous spead of 10 & 20 TB.7) TB Meningitis & Tuberculoma :-8) TB Pericardiatis :-• 1- 8% of All Extra pulmonary TB cases.• Spreads mainly in mediastinal or hilar nodesor from lungs.9) Miliary or disseminated TB :-• Results from Hematogenous spread of Tubercle Bacilli.• Spread is due to entry of infection into pulmonary veinproducinglesions in different extra pulmonary sites.10) Less common Extra Pulmonary TB• uveitis, panophthalmitis, painfull Hypersensitivityrelated phlyctenular conjuctivis.
Diagnosis1.Bacteriological test:a. Zeihl-Neelsen stainb. Auramine stain(fluorescence microscopy)2. Sputum culture test:a. Lowenstein –Jensen(LJ) solid medium: 4-18weeksb. Liquid medium : 8-14 daysc. Agar medium : 7 to 14 days
3.Radiography:Chest X-Ray(CXR)20% error by physician4.Nucleic acid amplification: Species identification ; several hours Low sensitivity, high cost Most useful for the rapid confirmation oftuberculosis in persons with AFB-positive sputa Utility◦ AFB-negative pulmonary tuberculosis◦ Extra pulmonary tuberculosis
5.Tuberculin skin test(PPD) Injection of fluid intothe skin of the lowerarm. 48-72 hours later –checked for areaction. Diagnosis is basedon height of the skin.1 dose = 0.1 ml contains 0.04µgTuberculin PPD.
Tuberculin test interpretation
Pathogenesis of tuberculintest
6. Other biological examinations Cell count(lymphocytes) Protein(Pandy and Rivalta tests) – Ascites, pleuraleffusion and meningitis.
Preventive measures1) Mask2) BCG vaccine3) Regular medical follow up4) Isolation of Patient5) Ventilation6) Natural sunlight7) UV germicidal irradiation
BCG vaccine Bacille Calmette Guerin (BCG). First used in 1921. Only vaccine available today for protection againsttuberculosis. It is most effective in protecting children from the disease.
Drugs MOA DiagramIsoniazid Inhibits mycolic acid synthesis.RIFAMPICIN Blocks RNA synthesis by blockingDNA dependent RNA polymerasePYRAZINAMIDE •Bactericidal-slowly metabolizingorganism within acidicenvironment of Phagocyte orcaseous granuloma.
Drugs MOA DiagramETHAMBUTOL •Bacteriostatic•Inhibition of ArabinosylTransferaseSTREPTOMYCIN •Inhibition of Proteinsynthesis by disruption ofribosomal function
Treatment regimen according to WHOISONIAZID (H) RIFAMPICIN (R) PYRAZINAMIDE (Z)ETHAMBUTOL (E) STREPTOMYCIN (S)
DOTSDOTS - Directly observed treatment, short-course DOT means that a trained health care worker or otherdesignated individual provides the prescribed TB drugs andwatches the patient swallow every dose.
Multi-Drug Resistance TB TB caused by strains of Mycobacteriumtuberculosis that are resistant to at leastisoniazid and rifampicin, the most effectiveanti- TB drug. Globally, 3.6% are estimated to have MDR-TB. Almost 50% of MDR-TB cases worldwideare estimated to occur in China and India.
MDR-TB among new TB cases
MDR-TB in previously treated cases
Treating Drug Resistant TB
Extensively drug resistanceTB Extensively drug-resistant TB (XDR-TB) is a formof TB caused by bacteria that are resistant toisoniazid and rifampicin (i.e. MDR-TB) as well asany fluoroquinolone and any of the second-lineanti-TB injectable drugs (amikacin, kanamycin orcapreomycin).