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  1. 1. Presented By: Nasir Nazeer
  2. 2. Sequence of the Presentation • History of TB • TB Transmission • Drug-Resistant TB • TB Pathogenesis • Progression from LTBI to TB disease • Sites of TB disease • TB Classification System • Laboratory and Physical examination of TB
  3. 3. History of TB
  4. 4. History of Tubercluosis • TB has affected humans for millennia • Historically known by a variety of names, including: – Consumption – Wasting disease – White plague • TB was a death sentence for many
  5. 5. History of TB Scientific Discoveries in 1800s • Until mid 1800s, many believed TB was hereditary • 1865 Jean Antoine-Villemin proved TB was contagious • 1882 Robert Koch discovered M. tuberculosis, the bacterium that causes TB
  6. 6. Germany issued a Postal stamp to give tribute to Robert Koch
  7. 7. History of TB Sanatoriums • Before TB antibiotics, many patients were sent to sanatoriums • Patients followed a regimen of bed rest, open air, and sunshine • TB patients who could not afford sanatoriums often died at home Sanatorium patients resting outside
  8. 8. Famous personalities affected with TB
  9. 9. Breakthrough in the Fight Against TB • Drugs that could kill TB bacteria were discovered in 1940s and 1950s • Streptomycin (SM) discovered in 1943 • Isoniazid (INH) and paminosalicylic acid (PAS) discovered between 1943 and 1952 • TB death rates in U.S. began to drop dramatically • Each year, fewer people got TB • Most TB sanatoriums in U.S. had closed by mid 1970s
  10. 10. TB Resurgence • Increase in TB in mid 1980s • Contributing factors: – Inadequate funding for TB control programs – HIV epidemic – Increased immigration from countries where TB is common – Spread in homeless shelters and correctional facilities – Increase and spread of multi drug-resistant TB March 16, 1992 Newsweek Magazine Cover
  11. 11. TB History Timeline 1993: TB cases decline due to increased funding and enhanced TB control efforts 1865: JeanAntoine Villemin proved TB is contagious 1840 1860 1884: First TB sanatorium established in U.S. 1880 1900 1882: Robert Koch discovers M. tuberculosis 1943: Streptomycin (SM) a drug used to treat TB is discovered Mid-1970s: Most TB sanatoriums in U.S. closed 1920 1960 1940 1943-1952: Two more drugs are discovered to treat TB: INH and PAS 1980 2000 Mid-1980s: Unexpected rise in TB cases
  12. 12. TB Transmission
  13. 13. TB Transmission Transmission is defined as the spread of an organism, such as M. tuberculosis, from one person to another.
  14. 14. TB Transmission Types of Mycobacteria • • • There are different types of Mycobacterium M. tuberculosis causes most TB cases in the world Mycobacteria that can cause TB: – M. tuberculosis – M. bovis (the bovine tubercle bacillus) – M. africanum (isolated from • cases in West, Central, and East Africa) – M. microti (the "vole" bacillus, a less virulent and rarely encountered organism) – M. pinnipedii (a bacillus infecting seals and sea lions in the southern hemisphere and recently isolated from humans) Mycobacteria that do not cause TB – e.g., M. avium complex
  15. 15. TB Transmission • TB is spread person to person through the air via droplet nuclei • M. tuberculosis may be expelled when an infectious person: – Coughs – Sneezes – Speaks – Sings • Transmission occurs when another person inhales droplet nuclei
  16. 16. TB Transmission Dots in air represent droplet nuclei containing M. tuberculosis
  17. 17. TB Transmission • Probability that TB will transmitted depends on: be – Infectiousness of person with TB disease – Environment occurred in which exposure – Length of exposure – Virulence (strength) of the tubercle bacilli • The best way to stop transmission is to: – Isolate infectious persons – Provide effective treatment to infectious persons as soon as possible
  18. 18. Etiological Agent • M. tuberculosis is a rod-shaped, non-spore-forming, thin aerobic bacterium measuring 0.5 um to 3 um the bacilli cannot be decolorized by acid alcohol; this characteristic justifies their classification as acid-fast bacilli. • Acid fastness is due mainly to the organisms' high content of mycolic acids, long-chain crosslinked fatty acids, and other cellwall lipids • It grows slowly . • It can’t tolerate heat, but It can live in humid or dry or cold surroundings.
  19. 19. Symptoms associated with the TB • • • • • • • • • Cough (2-3 weeks or more) Coughing up blood Chest pains Fever Night sweats Feeling weak and tired Losing weight without trying Decreased or no appetite If you have TB outside the lungs, you may have other symptoms
  20. 20. Pathological changes of TB • • • • • Following are the different pathological changes associated with TB. – Infiltration – Hyperplasia – Calcification These changes happen in different stages of the tuberculosis When defense system is predominant, there are less number of bacteria and only hyperplasia and calcification would happen. When defense system is weak, there are large number of bacteria and only calcification would happen. As a result of infection, infected areas are enlarged and deteriorated.
  21. 21. Common Clinical patterns of TB 1. Primary pulmonary tuberculosis (Primary Complex and Bronchial Lymphnod-Tuberculosis) 2. Milliary Tuberculosis (acute, subacute and chronic hematogenous pulmonary tuberculosis) 3. Secondary pulmonary tuberculosis Infiltrative pulmonary tuberculosis Chronic fibrocavenous pulmonary tuberculosis 4. Tuberculous pleuritis 5. Extrapulmonary tuberculosis
  22. 22. Clinical Manifestations of TB • Systemic signs: Most patients present as cases of pulmonary tuberculosis with fever, weight loss, anorexia, fatigue, night sweats wasting. • Respiratory signs: Cough may vary from mild to severe, and sputum may be scant and mucoid or copious and purulent. Hemoptysis may be due to cough of a caseous lesion or bronchial ulceration chest pain, tachypenea ect. • Physical signs: nonspecific.
  23. 23. Drug-Resistant TB
  24. 24. Drug-Resistant TB • Caused by M. tuberculosis organisms resistant to at least one TB treatment drug – – – – Isoniazid (INH) Rifampin (RIF) Pyrazinamide (PZA) Ethambutol (EMB) • Resistant means drugs can no longer kill the bacteria
  25. 25. Drug-Resistant TB Primary Resistance Caused by person-to-person transmission of drug-resistant organisms Secondary Resistance Develops during TB treatment: • Patient was not given appropriate treatment regimen OR • Patient did not follow treatment regimen as prescribed
  26. 26. Drug-Resistant TB Mono-resistant Resistant to any one TB treatment drug Poly-resistant Resistant to at least any 2 TB drugs (but not both isoniazid and rifampin) Multidrug resistant (MDR TB) Resistant to at least isoniazid and rifampin, the 2 best first-line TB treatment drugs Extensively drug resistant (XDR TB) Resistant to isoniazid and rifampin, PLUS resistant to any fluoroquinolone AND at least 1 of the 3 injectable second-line drugs (e.g., amikacin, kanamycin, or capreomycin)
  27. 27. TB infection and the World
  28. 28. TB Pathogenesis Pathogenesis is defined as how an infection or disease develops in the body.
  29. 29. TB Pathogenesis • Occurs when tubercle bacilli are in the body, but the immune system is keeping them under control • Develops when immune system cannot keep tubercle bacilli under control – May develop very soon after infection or many years after infection • About 10% of all people with normal immune systems who have LTBI will develop TB disease at some point in their lives • People with TB disease are often infectious
  30. 30. TB Pathogenesis Droplet nuclei containing tubercle bacilli are inhaled, enter the lungs, and travel to small air sacs (alveoli)
  31. 31. TB Pathogenesis 2 b r o n c h io le b lo o d v e s s e l t u b e r c le b a c illi a lv e o li Tubercle bacilli multiply in alveoli, where infection begins
  32. 32. TB Pathogenesis 3 b r a in bone lu n g k id n e y A small number of tubercle bacilli enter bloodstream and spread throughout body
  33. 33. TB Pathogenesis LTBI 4 s p e c ia l im m u n e c e lls fo r m a b a r r ie r s h e ll (in th is e x a m p le , b a c illi a r e in th e lu n g s ) • Within 2 to 8 weeks the immune system produces special immune cells called macrophages that surround the tubercle bacilli • These cells form a barrier shell that keeps the bacilli contained and under control (LTBI)
  34. 34. TB Pathogenesis 5 s h e ll b r e a k s dow n and tu b e r c le b a c illi e s c a p e a n d m u lt ip ly (in th is e x a m p le , T B d is e a s e d e v e lo p s in th e lu n g s ) • If the immune system CANNOT keep tubercle bacilli under control, bacilli begin to multiply rapidly and cause TB disease • This process can occur in different places in the body
  35. 35. TB Pathogenesis
  36. 36. LTBI vs. TB Disease Latent TB Infection (LTBI) TB Disease (in the lungs) Inactive, contained tubercle bacilli in Active, multiplying tubercle bacilli in the body the body TST or blood test results usually positive TST or blood test results usually positive Chest x-ray usually normal Chest x-ray usually abnormal Sputum smears and cultures negative Sputum smears and cultures may be positive No symptoms Symptoms such as cough, fever, weight loss Not infectious Often infectious before treatment Not a case of TB A case of TB
  37. 37. TB Pathogenesis Progression from LTBI to TB Disease
  38. 38. Progression to TB Disease • Risk of developing TB disease is highest the first 2 years after infection • People with LTBI can be given treatment to prevent them from developing TB disease • Detecting TB infection early and providing treatment helps prevent new cases of TB disease
  39. 39. Progression to TB Disease Some conditions increase probability of LTBI progressing to TB disease • Infection with HIV • Organ transplant • Chest x-ray findings suggestive of previous TB • Silicosis • Diabetes mellitus • Severe kidney disease • Certain types of cancer • Certain intestinal conditions • Low body weight • • • Substance abuse Recent TB infection Prolonged therapy with corticosteroids and other immunosuppressive therapy, such as prednisone and tumor necrosis factor-alpha [TNF-α] antagonists
  40. 40. Progression to TB Disease People Exposed to TB Not TB Infected Latent TB Infection (LTBI) Not Infectious Not Infectious Negative TST or QFT-G test result Positive TST or QFT-G test result No TB Infection Latent TB Infection May go on to develop TB disease
  41. 41. Progression to TB Disease TB and HIV In an HIV-infected person, TB can develop in one of two ways: • Person with LTBI becomes infected with HIV and then develops TB disease as the immune system is weakened • Person with HIV infection becomes infected with M. tuberculosis and then rapidly develops TB disease Image credit: Mississippi State Department of Health
  42. 42. TB Pathogenesis Sites of TB Disease
  43. 43. Sites of TB Disease Bacilli may reach any part of the body, but common sites include: B r a in L a ry n x Bone Lym ph node P le u r a Lung K id n e y S p in e
  44. 44. TB Pathogenesis TB Classification System
  45. 45. TB Classification System Based on pathogenesis of TB Class Type Description 0 No TB exposure Not infected No history of TB exposure Negative result to a TST or IGRA 1 TB exposure No evidence of infection History of TB exposure Negative result to a TST (given at least 810 weeks after exposure) or IGRA 2 TB infection No TB disease Positive result to a TST or IGRA Negative smears and cultures (if done) No clinical or x-ray evidence of active TB disease
  46. 46. TB Classification System Based on pathogenesis of TB Class Type Description 3 TB, clinically active Positive culture (if done) for M. tuberculosis Positive result to a TST or IGRA, and clinical, bacteriological, or x-ray evidence of TB disease 4 Previous TB disease (not clinically active) Medical history of TB disease Abnormal but stable x-ray findings Positive result to a TST or IGRA Negative smears and cultures (if done) No clinical or x-ray evidence of active TB disease 5 TB suspected Signs and symptoms of TB disease, but evaluation not complete
  47. 47. Laboratory and Physical examination of TB
  48. 48. Laboratory and Physical Examination • Following methods are used for laboratory and physical examination of TB – Chest radiography – Sputum examination – Tuberculin testing – PCR test to detect TB – TB antibody testing – Bronchoscopy
  49. 49. Radiology
  50. 50. Radiology • Chest radiography is the most important method to detect TB • TB’s characteristics of a chest radiograph favor the diagnosis of tuberculosis as following • shadows mainly in the upper zone • patchy or nodular shadows • the presence of a cavity or cavities, although these, of course, can also occur in lung abscess, carcinoma, etc • the presence of calcification, although a carcinoma or pneumonia may occur in an areas of the lung where there is calcification due to tuberculosis • bilateral shadows, especially if these are in the upper zones • the persistence of the abnormal shadows without alteration in an x-ray repeated after several weeks • this helps to exclude a diagnosis of pneumonia or other acute infection
  51. 51. Primary Complex
  52. 52. Milliary Tuberculosis
  53. 53. Secondary Pulmonary TB infiltrate
  54. 54. Sputum examination • There are direct smear and culture methods. • Direct smear examination is only positive when a large no of bacilli begin to excrete
  55. 55. Tuberculin testing • A tuberculin skin test is done to see if you have ever had tuberculosis (TB). The test is done by putting a small amount of TB protein (antigens) under the top layer of skin on your inner forearm. If you have ever been exposed to the TB bacteria (Mycobacterium tuberculosis), your skin will react to the antigens by developing a firm red bump at the site within 2 days. • The TB antigens used in a tuberculin skin test are called purified protein derivative (PPD). A measured amount of PPD in a shot is put under the top layer of skin on your forearm. This is a good test for finding a TB infection. It is often used when symptoms, screening, or testing, such as a chest Xray, show that a person may have TB. • A tuberculin skin test cannot tell how long you have been infected with TB. It also cannot tell if the infection is latent (inactive) or is active and can be passed to others.
  56. 56. Tuberculin testing • A reaction of less then 05nm is considered as negative. • 5-9mm is considered positive (+) • 10-19mm is considered positive (++) • More then 20mm is considered positive (+++) • A positive tuberculin test indicates TB infection with or without disease.
  57. 57. PCR to detect Tuberculosis
  58. 58. Bronchoscopy • Bronchoscopy is a technique of visualizing the inside of the airways for diagnostic and therapeutic purposes. An instrument (bronchoscope) is inserted into the airways, usually through the nose or mouth. This allows the practitioner to examine the patient's airways for abnormalities such as foreign bodies, bleeding, tumors, or inflammation. Specimens may be taken from inside the lungs. The construction of bronchoscopes ranges from rigid metal tubes with attached lighting devices to flexible optical fiber instruments with real time video equipment.
  59. 59. White blood cells and ESR • The white blood count is usually normal. • In practice the white blood count is only useful in a minority of cases, When the patient is less ill and the radiological shadowing less extensive the count is often normal or high normal • ESR is often elevate