pulmonary tuberculosis


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pulmonary tuberculosis

  1. 1. Al-Balqa Applied University Department of Allied Medical Science Pulmonary Supervised By :tuberculosi Dr. Waleed Al-Momani s Presented By : Ala’a Al-Dlahmeh
  2. 2. PulmonaryTuberculosis
  3. 3. DefinitionsTuberculosis or TB (tubercles bacillus) is : a contagious bacterial infection that attacks the lungs can also transmitted to other parts of the body.A Global public health Emergency : is the number one single infectious disease killer, taking nearly 3 million lives per year . Ref(4)
  4. 4. Causes Mycobacterium tuberculosis Mycobacterium africanum Mycobacterium microti Mycobacterium Bovisall cause tuberculosis (TB) and aremembers of the tuberculosis speciescomplex but the main cause isMycobacterium tuberculosis . Ref(4)
  5. 5. Sings & Symptoms Cough (that lasts 3 weeks or longer, and can bring up with blood) . Chest pain . Fever . Fatigue . Loss of appetite .  weight loss . Chills and night sweats . Ref(4)
  6. 6. TransmissionRespiratory routeM.TuberculosisInhalation of air dropletthat contain tuberclebacillusIntestinal routeM. bovis drinking oreatingcontaminated, unpasteurized (raw) milk or milkproducts.(uncommon) Ref(4)
  7. 7. Respiratory Rout•Infection requires of inhalation particles smallenough to traverse the upper respiratory defensesand deposit deep in the lung (alveoli).• Large droplets tend to lodge in the moreproximal airways and typically do not result ininfection.•when a person who is sick with active diseasecoughs, sneezes, or laughs.•To become infected with TB, a person usuallyneeds to share air space with someone sick withTB disease.Ref(1)
  8. 8. Risk factors A healthy immune system can often successfullyfight TB bacteria, but your body cant mount aneffective defense if your resistance is low. diseasesand medications can weaken your immunesystem, including : •HIV/AIDS •Diabetes •Chemotherapy •Malnutrition •Advanced age •Immunosuppressive medications •for people who live in or travel to countries that have high rates of tuberculosis such as (Sub-Saharan Africa, India, China, Mexico, Southeast Asia) Ref(1)
  9. 9. Tb Infection 90% 50%of those 10% death rate forinfected with chance that aM. tuberculosis these active TB latent infection caseshave will progress to if untreated.asymptomatic,latent TB TB disease.infection (LTBI)
  10. 10. Stage 1TB infection begins when the mycobacteriareach the pulmonary alveoli, where they invadeand replicate within the endosomes of alveolarmacrophages. tubercle bacilli Ref(1)
  11. 11. Stage2Lymphocytes and fibroblasts are among the cellsthat aggregate to form granulomas surroundingthe infected macrophages To preventsdissemination of the mycobacteria & provides alocal environment for interaction of cells of theimmune system. Ref(1)granulomas
  12. 12. Stage 3Bacteria inside the granuloma can becomedormant, resulting in a latent infection. Anotherfeature of the granulomas of human tuberculosis isthe development of abnormal cell death (necrosis)in the center of tubercles. To the naked eye this hasthe texture of soft white cheese and is termedcaseous necrosis. Ref(1)
  13. 13. The caseous centers of the tuberclesliquefy, and the organism begins to rapidlymultiply extracellularly. After time, the largeantigen load causes the walls of nearbybronchi to become necrotic and rupture.This results in cavity formation. Ghoncomplex. Typically, the Ghon complex isreadily visible upon chest X-ray.caseousnecrosis.Ref(1)
  14. 14. Stage 4Milliary or extrapulmonary stage : is the hematogenous spread of MTB .“Milliary" is derived from the fact thatmetastasizing tubercles are about the same size“millet seed”.Two types of lesions caused by milliary TB: I. Exudative lesions result from the accumulation of PMNs around MTB. Here the bacteria replicate with virtually no resistance. formation of a "soft tubercle". II. Productive “granulomatous” lesions occur when the host becomes hypersensitive to tuberculoprotein. formation of a "hard tubercle". Ref(4)
  15. 15. Reactivation Of TuberculosisOnly persons with latent infection have highrisk of Tuberculosis Reactivation.cased by tubercle bacilli that have survivedin the primary lesion.Reactivation infection characterized bychronic tissue lesions, formation of tuberclecaseation and fibrosis.The reactivation type almost always begins atthe apex of the lung, where the oxygentension (PO2) is highest. Ref(1)
  16. 16. Tubercle bacilli Characteristics Gram resistance (acid fast bacilli) Obligate aerobe & Mesophile Non-spore-forming & Non-motile rod Slow generation time:15-18 hours Lipid rich cell wall contains:Mycolic acids 50% of cell wall dry weight.Cord Factor responsible for the serpentinecording, toxic to mammalian cells ,an inhibitor of PMNmigration & resistance to detergents, antibacterial. Ref(1)
  17. 17. Diagnostic steps History and clinical examination Radiographic features Bacteriologic evaluation
  18. 18. 1 History and clinical examination“The first rule of TB diagnosis: is to think of TB….”The physician Include TB in his differentialdiagnosis when history & symptoms areconsistent with TB diagnosis THEN he willrecomendrd appropriate diagnostic tests toprove the infection.
  19. 19. 2 Radiographic features Chest X-rayTuberculosis creates cavities visible in x-rays likethis one in the patients right upper lobe.Abnormalities on chest radiographs may besuggestive of, but are never diagnostic of TB.However, chest radiographs may be used to ruleout the possibility of pulmonary TB in a personwho has a positive reaction to the tuberculin skintest and no symptoms of disease.Ref(2) Chest X-ray
  20. 20. 3 Bacteriologic evaluation Conventional diagnostic methods {smear, culture} New diagnostic methods {NNA, BACTEC, MGIT}
  21. 21. Specimens :Fresh sputum ,gastric washing , urin,pleural fluid , cerebrospinal fluid , biopsymaterial , blood. Decontamination & concentration of specimens :sputum Specimens (nonsteril) should be :•Liquefied with N-acetyl-L-cysteine•Decontaminated with NaOH•Neutralized with buffer• concentrated by centrifugation.Specimens processed in this way can be used foracid fast stains and for culture.Ref(4)
  22. 22. Acid Fast Bacilli “AFB” SmearSpecimen examined for acid fast bacilli by staining: Ziehl-neelson Acid Fast Auramine-rhodamine Staining Staining Ref(4)
  23. 23. Acid Fast Bacilli “AFB”I. Solid media culture1. Löwenstein-Jensen (egg and also containhigh concentrations of malachite green toovercome contamination with other bacteria).2. Middlebrook 7H10 & 7H11 are ( containedefined vitamins, salts, catalase, glycerol, olicasid and albumin to neutrelize toxic effect of fattyacids).II. liquid media*1. BACTEC TB-460 *(new diagnostic methods)2. MGIT960 systems
  24. 24. Acid fast bacilli (AFB) smear microscopyand culture are still the “gold standards”for the diagnosis of active TB but thisconventional methods for culture required(6-8) weeks for isolation from media. Ref(4)
  25. 25. Immunologic diagnosisγ-Interferon release assays (GIRA)Tuberculin Skin Test
  26. 26. γ-Interferon release assays (GIRA)Test rely on the fact that T-lymphocytes willrelease γ-interferon when exposed tospecific antigens. These tests are mostlydeveloped for the field of tuberculosisdiagnosis, but in theory, may be used in thediagnosis of other diseases which rely oncell-mediated immunity. Ref(2)
  27. 27. Tuberculin kin TestPurified Protein Derivative (PPD) : is a concentrated filter of broth in whichtubercle bacilli have grown for 6 weeks(old).•A dose of 0.1 ml of 5-TU PPD injected.• measuring the size of induration 48-72 hours.• positive if ≥ 10 mm induration size.•Standard method for screening & measuring of aperson’s cellular response.1 2
  28. 28. Positive Reactionperson infected in the past or latent TBinfectionAfter BCG vaccination, but this may lastfor only 3-7 years .Persons are retested 2 weeks later; theirPPD skin test “boosted” by the recentantigen injection. High risk of (endogenous infection) Ref(4)
  29. 29. Negative Reaction persons who have NEVER beeninfected, they are not subject to thatrisk, though they may become infected froman external source (exogenous infection)
  30. 30. New Diagnostic MethodsMycobacteria Growth Indicator Tube(MGIT).BACTEC TB-460.Nucleic Acid Amplification Method(NAA).
  31. 31. Mycobacteria Growth Indicator Tube (MGIT) Is an automated system that exploits thefluorescence of an oxygen sensor to detectgrowth of mycobacteria in culture.The instrument scans the MGIT every 60 minutesfor increased fluorescence. Analysis of thefluorescence is used to determine if the tube isPositive contains approximately 105 to 106(CFU/mL).Negative tubes remain for a minimum of 42 days(up to 56 days) Ref(2)
  32. 32. The BACTEC TB-460 Is an automated radiometric culturemethod used for the rapid growth ofmycobacteria.The methodology uses a liquid Middlebrook7H12 medium that contains radiometricpalmitic acid labeled with radioactive (14 C). Production of 14 CO2 by the metabolizingorganisms provides a growth index for themycobacteria. Growth is generally detectedwithin 9-16 days Ref(2)
  33. 33. Nucleic Acid Amplification Methodpolymerase chain reaction [PCR] allowsthe direct identification of M.tuberculosisin clinical specimens.Contamination of samples by products ofprevious amplification and the presence ofinhibitors in the sample may lead to false-positive or false-negative results
  34. 34. Treatment Latent infectionA person with a positive skin test, a normalchest X-ray, no symptoms and is notcontagious. treatment with an antibiotic may berecommended for this person to prevent the TBfrom turning into an active infection. Theantibiotic used for this purpose is calledisoniazid (INH). If taken for six to 12months, it will prevent the TB from becomingactive in the future. Ref(4)
  35. 35. Treatment Active infectionActive TB is treated with a combination ofisoniazid along with Rifampin, ethambutoland pyrazinamide are the drugs commonlyused to treat active TB. Four drugs are oftentaken for the first two months of therapy tohelp kill any potentially resistant strains ofbacteria. Then the number is usually reduced totwo drugs for the remainder of the treatmentbased on drug-sensitivity testing. Ref(4)
  36. 36. Multi Drug Resistance Tuberculosis (MDR –TB)between one in 10^6 and one in 10^8 tuberclebacilli are spontaneous mutants resistance to first-line antituberculosis drugs. When the drugs are usedsingly, the resistant tubercle bacilli emerge rapidlyand multiply. Treatment of MDR-TB must be doneon the basis of sensitivity testing. It is impossibleto treat such patients without this information.patient should be started on SHREZ(Streptomycin+isonicotinyl Hydrazine +Rifampicin+Ethambutol+pyraZinamide) Ref(4)
  37. 37. Prevention & Control prompt and effective treatment of patients withactive tuberculosis and carefully follow-up of theircontacts with tuberculin tests and x-rays .Drug treatment of asymptomatic tuberculin-positive persons .Immunization: BCG (bacillus calmette-guerin)used to induce a certain amount of resistance inthose heavily exposed to infectionThe eradication of tuberculosis in cattles and thepasteurization of milk have greatly reducedM.bovis infections. Ref(3)
  38. 38. Precaution TipsPrevent latent TB from becoming activeprevent TB by TB vaccine (BCG)Prevent inject illegal drugs.Do not spend long periods of time instuffy, enclosed rooms with anyone who hasactive TB until that person has been treated for atleast 2 weeks.Use protective measures, such as face masks, ifyou work in a facility that cares for people whohave untreated TB. Ref(3)
  39. 39. TB control in Jordan Jordanian Anti TB Association is providing supportto the national TB programme through financial aidto TB patients & health education. Jordan also madegood progress in the TB Elimination Initiative bylowering the incidence rate of smear positive newcases to 6 per 100,000 populations.At 2010 theres 336 case of TB in Jordan Ref(4)
  40. 40. DOTSThe WHO-recommended Directly ObservedTreatment, Short Course (DOTS) strategy waslaunched formally as Revised National TB Controlprogramme in India in 1997. Since then DOTS hasbeen widely advocated and successfully applied.DOTS is the most effective strategy available forcontrolling TB. Ref(3)
  41. 41. Ref(1)Tuberculosis, NICE Clinical Guideline (March 2011);Clinical diagnosis and management of tuberculosis, andmeasures for its prevention and control.Ref(2) Landau, Elaine. Tuberculosis. New York: F. Watts, 1995http://www.healthofchildren.com/T/Tuberculosis.Ref(3) TheStop TB Strategy: building on and enhancing DOTSto meet the TB-related Millennium Development GoalsWHO. Geneva, World Health Organization, 2006b(WHO/HTM/STB/2006.37).Ref(4) G.Brooks , K.Carrroll , J.Butel , S.Melnicks (MedicalMicrobiology 24th Edition ) Jawetz , Melnicks Dahlbergs .
  42. 42. Thank You For YourAttention !