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TUBERCULOSİS

TUBERCULOSİS. Prof.Dr.Yıldız Camcıoğlu. Tuberculosis(TB). Mycobacterium tuberculosis Mycobacterium bovis

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TUBERCULOSİS

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  1. TUBERCULOSİS Prof.Dr.Yıldız Camcıoğlu

  2. Tuberculosis(TB) • Mycobacteriumtuberculosis • Mycobacteriumbovis • Mycobacterium tuberculosis infects millions of children every year and yet exact rate of morbidity and mortality is not known in developing countries due to difficulties in diagnose of diseases in childhood. Poverty, overcrowding, inadequate tuberculous control programmes, MDR tuberculosis and HIV infection have all contributed to spread of Tuberculosis worldwide

  3. Childhood TB • It has beenestimatedthat 3.1 millionchildrenunder 15 years of ageareinfectedwith TB worldwide. • AccordingtotheWorldHealthOrganization (WHO), childrenwith TB represent 10 % to 20 % of all TB cases.

  4. M.tuberculosis and M.bovis 0,3-0,6 micron x 2-4 micron aerobic Celll wall;A)Plasma membrane; Peptidoglicans Arabinogalactan Micolik aside B)Complex polymers Antigens; 38 kd, 88kd, Antigen 5, Antigen A6, Lipoarabinomannan(LAM), Cord Factor

  5. Transmission 95% TB is an airbornedisease, transmittedbyparticles, ordropletnucleithatareexpelledwhenpersonswhohavepulmonaryorlaryngeal TB sneeze, cough, speakorsing 1.4% Bydrinkinginfectedmilk 1.4% Inoculation of bacilliby skin andmucosal contusions • Congenital TB

  6. Features of The TB in Childhood • Pulmonary TB in children has a lowbacillaryloadandcavitiesarealsorarelypresent. • Childrenalsolacktheforcefulcoughmechanismseen in adults • Adolescentsandolderchildrenareimportantexceptions since theirdiseasecloselyresemblesthat of adults • Thediseasemoreoftenprogressesfrom an initialorprimaryinfection. • 50 % of pediatricpatientsmayremainasymptomaticwithsubtleabnormalities on thechestradiograph • Childrenyoungerthanfiveyearsoldmaydevelopdisseminated TB in the form of miliarydiseaseortuberculousmeningoencephalitis

  7. Stage I • Droplet nuclei containing between one to 10 bacilli and a diameter close to 10 μm are expelled with the cough, suspended in the air and transported by air currents. • Some of these droplet nuclei, usually larger than 10 μm, are inhaled and anchored in the upper respiratory tract • The mucus and the ciliary system of the respiratory tract avoid further progression of mycobacteria. Dannenberg, Jr AM Immunol Today 1991

  8. Stage II:Symbiotic stage • Subsequently, alveolar macrophages phagocytose the inhaled bacilli • These first macrophages are unable to kill mycobacteria • The bacilli continue their replication inside these cells • Logarithmic multiplication of the mycobacteria takes place within the macrophage at the primary infection site.

  9. Stage III: CMI and DTH • Two or three weeks after the initial M. tuberculosis infection, a cell-mediated immune response is fully established • While CD4+ T helper cells activate the macrophages to kill the intracellular bacteria and finally cause epithelioid granuloma formation, • CD8+ suppressor T cells lyse the infected macrophages, resulting in the formation of caseous granulomas with central necrosis • The only evidence of a real and effective infection is a positive TST

  10. Primarypulmonary Tuberculosis • Symptomsvaryaccordingtothedegree of airwayirritationandobstruction • Frequently a persistentcoughthatmaymimicpertussisandMildfever • 70 % of theprimaryfociaresubpleural • 25% of caseshavemultipleparenchymalfoci • A commonradiographicsequence is adenopathyfollowedbylocalizedhyperinflationandthenatelectasis of contiguousparenchyma • Adenopathiesaremorestrikingthanparenchymalfocus • Adenopathieshealwithcalsification

  11. Pulmonary Infection • Affectedregionallymphnodesattachtothebronchus • Insomechildren, particularlyinfants, thelymphnodescontinuetoenlarge, resulting in lymphobronchialinvolvement, in whichtheaffectedbronchusmaybecomepartiallyortotallyobstructed • Thearea of caseationmaydischargeinto a bronchus, resulting in theformation of a cavitywithpossibleendotracheal spread • Similarly, regionallymphnodeinvolvementmayaccompanymarkedclinicalsymptoms • Themostfrequentlyaffectedlobesaretherightupper, therightmiddle, andtheleftupperlobe

  12. Differential Diagnosis • Astma • Aspiration; • Chemicals; Drugs • Bacterial pneumonia S.Pneumoniae TWAR B.pertussis • Viral pneumonia Influenza A, B Adenovirüs 3, 4,7 RSV • Fungal pneumonia H.capsulatum C.immitis B.dermatitis

  13. Stage IV:Liquefaction Rapid replication of Bacilli • Reactivation, liquefaction, cavitation • BacillibeginstoreplicateExtracellularly • Airborde spread is possible; Transmission

  14. Progressive primary pulmonary tuberculosis Progression of the pulmonary parenchymal component leads to enlargement of the caseous area and may lead to pneumonia, atelectasis, and air trapping. This is more likely to occur in young children than in adolescents The child usually appears ill with symptoms of fever, cough, malaise and weight loss This form presents classic signs of pneumonia, including tachypnea, dullness to percussion, nasal flaring, grunting, egophony, decreased breath sounds, and crackles

  15. Pleural Involvement • Pleuralinvolvementmayresultfromdirect spread of caseousmaterialfrom a subpleuralparenchymalorlymphnodefocus, orfromhematogenous spread • The presence of caseousmaterial in thepleuralspacemaytrigger a hypersensitivityreaction, withtheaccumulation of serousstraw-coloredfluidcontainingfewtuberclebacilli • Thisexudate has a high protein countandlymphocytepredominance; thenumber of polymorphonuclearcellsdepends on theacuteness of onset • Althoughdirectmicroscopyoften is negative, cultureyieldsmay be as high as 70 percent

  16. Pleural involvement 85 % acute onset of fever, 52 % chest pain on deep inspiration 28 % shortness of breath Pleural effusion due to TB usually occurs in older children The pain accompanies the onset of the pleural effusion, but after that the pleural involvement is painless. Fever usually persists for 14-21 days. The signs of pleural effusion include tachypnea, respiratory distress, decreased breath sounds, dullness to percussion, and occasionally, features of mediastinalshift.

  17. TB Pericarditis • Directly dissemination or by lymphatic drainage from subcarinal lymph nodes • Fever, cough, weight loss, malaise, chest pain • Physical exam ; Dyspnea and ortopnea Edema at ankle Pericardial rubbing • Pericardial fluid; Serofibrinous or mildhemoragic 30-70 % bacilli yielded • Constrictive pericarditis

  18. Miliary Tuberculosis 100 % Fever 63 % Cough 25 % Dyspnea 24 % Malaise 23% Vomiting 16 % weight loss 13 % Abdominal pain 11 % Convulsions 11 % Diarrhea 8 % Wheezing 5 % Headache

  19. Lymph Node Involvement • 17 % of those all TB cases • 9 billionnew cases • Drinking of infected cow milk ; M.bovis or M.avium, M.intracellulare, M.scrofulaceum • M.tuberculosis • 30-70 %primary focus is at lung • Patients with scrofula may complain of enlarged nodes • Fever, weight loss, fatigue,and malaise are usually absent or minimal • Lymph node involvement typically occurs between six to nine months following the initial infection.

  20. TB Meningitis • Pathology: meningoencephalitis • Caseousfocusus(Richfocus) at Cerebralcortexorbasalmeninges • Dissemination of subarachnoidarea • Thickexudateenriched of lympocytesandplasmacellscoversinterpedincularandpontincisterna • Disseminateslateralsulcusandcisternaambiens, cisternamagnaandchiasmatikcisterna

  21. TB Meningitis • Cerebralvessel, nerves , choroidplexus in ventricullesarealllcoveredbythickexudate Cerebralvesseldamageandbraininfarcts Vasculitis,aneurisma, trombosisand Focalhemoragicinfarcts • Thickexudateresult in(earlystage); Impairment of CSF flow in latestage;Adhesionsandhydrocephaly • Hyponatremia • Inapproprite ADH release(%70)

  22. TB Meningitis I. Onset: insidious onset of the disease, 1-2 weeks, low-grade persistent fever, malaise, anorexia, weight loss,fatigue, hepatomegaly, splenomegaly and generalized lymphadenopathy II.Meninges irritation: vomiting,headache, nuchal rigidity, seizures,hypertonia, minor neurological changes;mild consciousness,anisochory,double vision, loss of abdominal reflexes, convulsion III.The final stage:Alteration in consciousness and sensorium, III, VI ,VII nerve involvement comprises major neurological defects, including coma, seizures,and abnormal movements (e.g. choreoathetosis, paresis, paralysis of one or more extremities) , decerebrated or decorticated posturing, opisthotonus

  23. intestinal TB Drinking unpasteurised milk or milk infected with M.bovis mesenteric lymph nodes and peritoneum infection occurs by lymphatic drainage 60 % ulsers occurs Jejunum, ileum and appendices Sığ ülserler pain, tenesmus, diarrhea or constipationveya kabızlık, abdominal distension, weight loss , low set fever Diag; Biopsy Gastrointestinal TB At every site of GIS Rare at oral cavity lympadenopathies accompanies painless ulsers at the mucosa of month, gums, tonsils Eosophagal TB Trachea-eosophagal fistula at infants

  24. Gastrointestinal TB Mesenteric TB • Hematogenousdissemination • Lymphoma ? • Pain at exercise • Intestinalobstruction, peritonitis Peritonitis • Disseminatefromadjacenttissues • Palpablelymphnodes, omentumand periton klampseachotherandresemblesirregularabdominalmasses • Mildfever, abdominaldistension, loss of appetite,, weightlossandserouseffussion(asite) mayoccur

  25. Osteoarticular TB • Appear in 1 % to 6 % of untreated primary infections • Clinical and radiographic presentations vary widely and depend upon the stage of the disease at the time of diagnosis • Skeletal TB may remain unrecognized for months to years because of its lack of specific signs and symptoms and indolent nature • Bone or joint TB may present acutely or subacutely • Sites commonly involved are the large weight-bearing bones or joints including the vertebrae (50 %), hips (15 %), and knees (15 %) • Less common skeletal sites are the femur, tibia, and fibula. • Destruction of the bones with deformity is a late sign of TB • Manifestations may include angulation of the spine or “gibbus deformity” and/or the severe kyphosis with destruction of the vertebral bodies or “Pott’s disease” • Cervical spine involvement may result in atlantoaxial subluxation, which may lead to paraplegia or quadriplegia • TB of the skeletal system may also lead to involvement of the inguinal, epitrochlear, or axillary lymph nodes

  26. Osteoarticular TB TB Dactilitis (spina ventoza). Distal endarteritis No pain Cystic enlargement Rarely occurs abscess

  27. Cutaneous Tuberculosis Hypersensitvity or haematogenous dissemination Cutaneous papules 3-8 weeks later regional lymphadenopathies No systemic symptoms Papulonecrotic tuberculide Miliary lesions on skin On face, trunk, Upper extremities Verrucosa cutis Wart like lesion On extremities Dif.diag; Letterer-siwe diseases and urticary

  28. Congenital TB A very rare event in the whole spectrum of TB presentations. This infection is caused by lymphohematogenous spread during pregnancy from an infected placenta or aspiration of contaminated amniotic fluid. Symptoms typically develop during the second or third week of life Poor feeding, poor weight gain, cough, lethargy, and irritability Other symptoms include fever, ear discharge, and skin lesions, failure to thrive, icterus, hepatosplenomegaly,tachypnea, and lymphadenopathy.

  29. Congenital TB diagnosis Congenital TB diagnosis is based on clinical features and the infant should have at least one of the following proven TB Lesions • Skin lesions during the first week of life, including papular lesions or petechiae, necrotic or purpuric lesions • Choroidal tubercles in the retina • Documentation of TB infection of the placenta or the maternal genital tract • Presence of a primary hepatic complex (liver and regional lymph-node involvement) • Exclusion of the possibility of postnatal transmission

  30. Suspicion Of TB • Symptoms: persistent cough, fever, night sweats, weight loss • Risk factors for exposure to TB: close contact of case, residence/travel in high prevalence country, congregate living with other high risk individuals • Risk factors for development of active disease if infected: recent infection, HIV/AIDS, other underlying medical condition

  31. Blood Cells Mild anemia Monocytosis High ESR

  32. Radiological Studies(80-85% of TB Cases) • Chest x-ray • Standard PA and lateral films; apical lordotic views may be helpful • Infiltrates, nodular densities, cavities, +/- hilar adenopathy • Abnormalities may be subtle in immunocompromised patients • Previous x-rays for comparison may be useful • CT scans • Often obtained • Nice to have but rarely critical to diagnosis • Expensive

  33. Diagnosis of Pulmonary TB • TST • Positive supports but does not make diagnosis • Negative does not exclude TB as possible diagnosis • Quantiferon • Screening test only, not diagnostic

  34. TST > 5mm • Contact with infectious cases • Abnormal Chest X ray • HIV infection and other immunocompromise >10 mm • Age ≤ 4years of age • Certain medical risk factors: Hodgkin, diabetes Mellitus , renal diseases, malnutrion • Member of local high –risk group • Birth or previous residence in high prevalence • Occupation in health care field, exposure to patients with TB • Close contact with a high –risk adult • Residence in long term care or correction facilities >15mm No risk factor

  35. Biochemicalresults CSF, synovial Fluid; High Protein level Lymphocytes 500/ mm3 Pleural ve peritoneal fluid ; Exudate Dansity >1016 Protein level >3 gr/dl Lymphocytes 500/mm3 Glycose LOW Lactic dehidrogenase HİGH Adenosine deaminase HİGH

  36. SCAN and US • *CT SCAN; • TB meningitis;Tuberculomaand • hydrosefaly • Ultrasonography; • Peritonitis, mesentericadenitis

  37. Laboratory Tests for M.tb • Culture and Identification of Isolate • “Gold standard” for TB diagnosis • Usually complete in 2-4 weeks • Not signed out as negative until 8 weeks • Traditional identification based on growth characteristics, biochemical tests • ID by “probe” now standard • Requires isolate (2-4 weeks) • Tests DNA – can ID M.tb complex, M.avium, +/- others • More rapid than chemicals, just as accurate • Cannot distinguish among M.tb complex species (M.tb vs. M.bovis)

  38. Laboratory Tests for M.tb • Antimicrobial susceptibility testing • Requires isolate • 2-4 weeks after isolate available • IREZ +/- S testing standard • Second line drug testing only on request • 3-10% of VA TB isolates resistant to > 1 first line TB drug • Continue IREZ until susceptibility results available

  39. Biopsy Skin Lymphnodes Bone Pleura Granulomaformation

  40. Treatment of TB Disease • The first rules of TB treatment are: • Enough drugs (4 to start) • The right drugs (antimicrobial sensitivities) • Enough milligrams of each drug (patient weight) • Enough doses (count doses) • Enough attention to detail (monitoring of laboratory studies and clinical course)

  41. First-line Drugs Isoniazid Rifampin Rifapentine Rifabutin Ethambutol Pyrazinamide Second-line Drugs Cycloserine Ethionamide Levofloxacin Moxifloxacin Gatifloxacin P-Aminosalicylic acid Streptomycin Amikacin/kanamycin Capreomycin Linezolid Antituberculosis Drugs Currently in Use

  42. Preventive therapy Preventive therapy may be given to persons who have a negative skin test reaction • High-risk contacts • Children younger than 6 months of age who have been exposed to TB Persons receiving preventive therapy are those who have a positive skin test, and those who are: • more likely to be exposed to or infected with M. tuberculosis • more likely to develop TB disease once infected All persons receiving preventive therapy should receive a medical evaluation to: • Exclude the possibility of TB disease • Determine whether they have ever been treated for TB infection or disease • Identify any medical problems that may complicate therapy or require more careful monitoring

  43. Features of Childhood TB • Farmacokinetic effects of drugs vary • Few bacilli found in caseous lesion • Development of secondary resistance ratio is low • Extrapulmonary diseases are frequent • Drug tolerance is better than adults • Low side effects against drugs • Drugs are for adults • For that reason children have problems to swallow the tablets, taste are not good

  44. Treatment Asymptomaticinfection TTS(+) INH 6-9 m NO Disease Pulmonary TB INH+RIF 9-12 m or INH+RIF+SM or INH+RIF+PZA orINH+RIF+ETB (DOT) INH+RIF2 monthsdaily + 7 months 2 daysweekly HilaradenopathySame as Pulmonary Extratorasic TB Same as Pulmonary (ExceptMiliary, meningitis, osteoarticular) Miliary, meningitis, INH+RIF+PZA+SM2 monthsdaily+ osteoarticular+ INH+RIF 10 monthsdaily +or INH+RIF 10 months2 daysweekly

  45. Risk of Drug Resistance • Treated patients with Active TB • Contact with patients who have drug resistant TB • Contact with immigrants • Living in the population with INH resistance higher than 4% • The patients with bacilli(+) sputum after 2 months of antituberculous treatment and contact with those patients

  46. STEROİD • Meningitis • Pleural involvement • Pericarditis • Peritonitis • Severe Miliary TB • Atelectasis or obstruction 2 mg/kg/day for 15 days. than in decreased doses, Stop 4-6 weeks after

  47. Pulmonary Sputum for AFB smear and culture Chest x-ray helpful Follow-up sputum smears and cultures useful to monitor treatment Extra-pulmonary More variability in presentation; may be more difficult to diagnose AFB smear and culture done on tissue or fluid Follow-up smears/cultures may not be possible Must evaluate for pulmonary disease Chest x-ray may be normal; x-rays/scans may be helpful Diagnosis/Follow-up of Pulmonary vs. Extra-Pulmonary TB

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