Primary Tuberculosis 1

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LECTURE BY DR MUHAMMAD FAROOQUE
MB BS DTCD
CHEST SPECIALIST

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Primary Tuberculosis 1

  1. 1. PRIMARY TUBERCULOSIS DR.MUHAMMAD FAROOQUE M.B.,B.S. D.T.C.D. IN THE NAME OF ALLAH,THE MOST GRACIOUS,THE MOST MERCIFUL
  2. 2. PRIMARY TUBERCULOSIS DR. MUHAMMAD FAROOQUE MB BS DTCD
  3. 3. WHAT IS TUBERCULOSIS? <ul><li>Chronic, </li></ul><ul><li>granulomatous, </li></ul><ul><li>infectious, </li></ul><ul><li>communicable, </li></ul><ul><li>Multisystem, </li></ul><ul><li>curable disease. </li></ul>
  4. 4. Epidemiology: Global Threat <ul><li>One in three humans infected with TB (19-41%) </li></ul><ul><li>8 million new cases of active TB each year </li></ul><ul><li>3 million deaths/year (24 million/year all causes) </li></ul><ul><li>#1 cause of infection-related deaths worldwide </li></ul><ul><li>1993 WHO: global public health emergency </li></ul><ul><li>One death every 15 seconds. </li></ul>
  5. 5. 2 MILLION PEOPLE DIE EVERY YEAR EQUAL TO 20 SUCH STADIUMS
  6. 6. HISTORY OF TB <ul><li>A DISEASE OF GREAT ANTIQUITY. </li></ul><ul><li>EVIDENCE IN VERTEBRAE OF NEOLITHIC MAN IN EUROPE, </li></ul><ul><li>EGYPTIAN MUMMIES DATING POSSIBLY AS EARLY AS 3700BC. </li></ul><ul><li>IN 17 TH & 18 TH CENTURIES IN EUROPE 25% OF ADULTS DEATHS DUE TO TB NAMED AS WHITE PLAGUE. </li></ul><ul><li>CAUSE OF DEATH FOR MILLION OF MILLIONS OF PEOPLE INCLuDING MANY RENOWNED PERSONS. </li></ul>
  7. 7. KING TUTANKHAMEN EGYPTIAN PHARAOH                             
  8. 8. BARUCH SPINOSA DUTCH PHILOSOPHER                          
  9. 9. SIMON BOLIVER VENEZUELAN REVOLUTIONARY LEADER                             
  10. 10. JOHN KEATS ENGLISH POET                          
  11. 11. EDGAR ALLAN POE AMERICAN WRITER,POET                           
  12. 12. FREDERIC CHOPIN POLISH COMPOSER , PIANIST                        
  13. 13. ROBERT LOUIS STEVENSON SCOTISH WRITER                             
  14. 14. ANTON CHEKHOV RUSSIAN WRITER                       
  15. 15. FRANZ KAFKA CZECH NOVELIST                            
  16. 16. ELEANOR ROOSEVELT AMERICAN HUMANIYARIAN/FIRST LADY                            
  17. 17. EUGENE ONEILL AMERICAN PLAYWRIGHT                           
  18. 18. GEORGE ORWELL ENGLISH NOVELIST/ESSAYIST                         
  19. 19. REASONS FOR INCREASING INCIDENCE <ul><li>POVERTY. </li></ul><ul><li>POPULATION INCREASE. </li></ul><ul><li>LACK OF ACCESS TO HEALTH CARE. </li></ul><ul><li>LACK OF KNOWLEDGE. </li></ul><ul><li>CIVIL UNREST. </li></ul><ul><li>INEFFECTIVE TB CONTROL PROGRAMS. </li></ul><ul><li>SOCIAL DEPRIVATION (HOMELESS,IV DRUG ABUSER) </li></ul><ul><li>HIV. </li></ul><ul><li>DRUG RESISTANCE </li></ul><ul><li>IMMIGRATION FROM HIGH PREVALENCE AREAS. </li></ul>
  20. 20. TUBERCULOSIS WAS A KILLER AND IT REMAINS A KILLER DISEASE EVEN TODAY . <ul><li>Causative organism is just </li></ul><ul><li>2-4micrometer long & </li></ul><ul><li>0.2-0.5micrometer wide. </li></ul>
  21. 21. M.HAEMOPHILUM BCG M.GENAVENSAE M.FORTUITUM M.CHELONEI. . MAC(HIV-ASSOCIATED) DISSEMINATED(SEEN IN IMMUNODEFICENY STATES) M.TUBERCULOSIS M.MARINUM M.FORTUITUM M.CHELONEI. M.LEPRAE M.ULCERANS SOFT TISSUE/SKIN M.MALMOENSE M.BOVIS, M.FORTUITUM M.CHELONEI. M.TUBERCULOSIS MYCOBACTERIUM AVIUM COMPLEX (M.SCROFULACEUM,M.INTRACELLULARE & M.AVIUM) LYMPH NODE M.BOVIS M.XENOPI MAC M.KANSASII M.MALMOENSE M.TUBERCULOSIS PULMONARY LESS COMMON MAJOR SITE-SPECIFIC MYCOBACTERIAL DISEASE.
  22. 22. <ul><li>MYCOBACTERIA </li></ul><ul><li>FIRST DESCRIBED BY ROBERT KOCH IN 1882 </li></ul><ul><li>ACID ALCOHOL FAST </li></ul><ul><li>AEROBIC OR MICROAEROPHILIC </li></ul><ul><li>NON-SPORE FORMING </li></ul><ul><li>NON MOTILE </li></ul><ul><li>CAN REMAIN DORMANT IN TISSUES AND PERSIST FOR MANY YEARS </li></ul><ul><li>FACULTATIVE INTRACELLULAR PARASITE USUALLY OF MACROPHAGES </li></ul><ul><li>HAS SLOW GENERATION TIME 15-20HR </li></ul><ul><li>MICROSCOPICALLY LOOKS LIKE BENT RODS. </li></ul>
  23. 26. TRANSMISSION <ul><li>AIREBORNE </li></ul><ul><li>BY DROPLET NULEUS </li></ul><ul><li>1 DROPLET NUCLEUS CONTAINS AROUND 3AFB </li></ul><ul><li>MOST EFFECTIVELLY INFECTIVE D.N. HAS DIAMETER OF 5MICROMETER. </li></ul>
  24. 27. INFECTIVITY OF THE PATIENT. <ul><li>Smear positivity. </li></ul><ul><li>Frequency and duration of cough. </li></ul><ul><li>Physical and chemical characteristics of sputum,,,,tenaceous sp; more infectious than watery. </li></ul><ul><li>Pt; without ATT ,,,sputum more infectious. </li></ul><ul><li>1-2 weeks after effective ATT ,risk of transmission is minimal. </li></ul>
  25. 28. ROUTE OF TRANSMISSION AIRBORNE BY DROPLET NUCLEUS
  26. 29. HOW DROPLET NUCLEI ARE PRODUCED & SPREAD <ul><li>Any respiratory manoeuvres generate droplet nuclei due to evaporation of small respiratory droplets. </li></ul><ul><li>COUGHING….1bout =3000 D.N. </li></ul><ul><li>SINGING…….1minute =3000 D.N. </li></ul><ul><li>SPEAKING…..5minutes talk=3000 D.N. </li></ul><ul><li>SPITTING </li></ul><ul><li>SNEEZING=affects till 10 feet. </li></ul>
  27. 30. JOURNEY OF DROPLET NUCLEUS <ul><li>Once they are generated and released in air, the organism can remain viable for extended period of time. </li></ul><ul><li>If inhaled by other human being ,will produce infection. </li></ul><ul><li>May be eliminated by radiation from sun,infinite dilution. </li></ul>
  28. 31. WHO IS AT RISK? HIV, Silicosis, DM(IDDM), Immunocompromised, CRF, Malignancy(leukemia,) GIT Diseases associated with malnutition,.Gastectomy,Jejuno-ileal bypass,ca pancreas, malabsorption ASSOCIATED DISEASES <ul><li>Age. (children>young) </li></ul><ul><li>First-generation immigrants from high prevelnce countries </li></ul><ul><li>Close contacts of patients with smear positive pulmonary TB </li></ul><ul><li>CXR evidence of self-healed TB </li></ul><ul><li>Primary infection <1year </li></ul>PATIENT-RELATED
  29. 32. PREVENTION OF TRANSMISSION (especially in hospital setting) <ul><li>EARLY CASE FINDING </li></ul><ul><li>EARLY START OF TREATMENT </li></ul><ul><li>ISOLATION OF POSITIVE CASES </li></ul><ul><li>HIV POSITIVE STAFF SHOULD AVOID TO WORK IN TB WARDS </li></ul><ul><li>ISOLATION ROOMS ---WELL VENTILATED, + NEGATIVE SUCTION OF AIR EXHAUST FOLLOWED BY TREATMENT OF AIR </li></ul><ul><li>USE OF HIGH EFFICIENCY PARTICULATE AIR FILTER RESPIRATORS,MASKS LIKE N95 </li></ul>
  30. 33. TIME TABLE FOR TB. PRIMARY COMPLEX TST POSITIVE Meningeal,Miliary,Pleural dis. GIT,Bone & Joint,L/N disease Post prim;Dis due to reactivation or reinfection Genito-Urinary & Skin Lesion <ul><li>3-8 weeks </li></ul><ul><li>3-6 months (3-12M) </li></ul><ul><li>Upto 3 Years </li></ul><ul><li>From 3 year onward (1-5 Yr) </li></ul><ul><li>Around 8 years (average5-15) </li></ul>MANIFESTATION TIME FROM INFECTION
  31. 34. TST
  32. 35. Screening for TB “ppd” the Mantoux Tuberculin Skin Test <ul><li>Delayed-type hypersensitivity reaction </li></ul><ul><li>Induration not erythema </li></ul><ul><li>Most common TB test </li></ul><ul><ul><li>Best supportive data </li></ul></ul><ul><ul><li>Established thresholds </li></ul></ul><ul><li>Not ideal test </li></ul><ul><ul><li>False positive results </li></ul></ul><ul><ul><li>False negative results </li></ul></ul><ul><ul><li>Poor follow-up compliance </li></ul></ul>
  33. 36. Screening for TB Anergy <ul><li>Inability to react to TST </li></ul><ul><li>Impaired immune response to delayed-type hypersensitivity reaction (Type IV) </li></ul><ul><li>Most common with highest risk groups </li></ul><ul><ul><li>prolonged corticosteroids </li></ul></ul><ul><ul><li>recent immunomodulators </li></ul></ul><ul><ul><li>current chemotherapy </li></ul></ul><ul><ul><li>HIV infection </li></ul></ul>
  34. 37. Screening for TB Boost Phenomenon / Two-Step Testing <ul><li>Initial TST false negative </li></ul><ul><li>Occurs following long latency between infection and testing </li></ul><ul><ul><li>“ hibernating” immune response </li></ul></ul><ul><li>TST reactivates immune response </li></ul><ul><ul><li>subsequent tests positive </li></ul></ul><ul><li>Common, ~20% </li></ul><ul><li>2 step testing recommended for high risk </li></ul><ul><ul><li>TST repeated in 2 weeks </li></ul></ul>
  35. 38. Tuberculin Skin Test Positive Result <ul><li>≥ 5 mm induration </li></ul><ul><li>HIV infection </li></ul><ul><li>Recent contact active TB </li></ul><ul><li>CXR c/w prior TB (fibrotic changes) </li></ul><ul><li>Immunosuppressive therapy </li></ul><ul><ul><li>Organ transplant recipients </li></ul></ul><ul><ul><li>Corticosteroids (>15mg prednisone/day) </li></ul></ul><ul><ul><li>TNF- α antagonists </li></ul></ul>
  36. 39. Tuberculin Skin Test Positive Result <ul><li>≥ 10 mm induration </li></ul><ul><li>Converters (>10mm change within 2 years) </li></ul><ul><li>Recent immigrants from endemic region </li></ul><ul><li>High risk settings </li></ul><ul><li>Targeted chronic medical disorders </li></ul><ul><ul><li>Health care workers </li></ul></ul><ul><ul><li>Chronic care facility </li></ul></ul><ul><ul><li>Prisoners and prison workers </li></ul></ul><ul><ul><li>Homeless and homeless shelter workers </li></ul></ul><ul><ul><li>Diabetes Mellitus </li></ul></ul><ul><ul><li>ESRD </li></ul></ul><ul><ul><li>Leukemia/lymphoma </li></ul></ul><ul><ul><li>Head, neck, lung cancer </li></ul></ul><ul><ul><li>Silicosis </li></ul></ul><ul><ul><li>Gastrectomy </li></ul></ul><ul><ul><li>≤ 90% ideal body weight </li></ul></ul>
  37. 40. Tuberculin Skin Test Positive Result <ul><li>≥ 15 mm induration </li></ul><ul><li>All others </li></ul><ul><li>Avoid testing in this group </li></ul><ul><li>High false positive rate </li></ul>
  38. 41. Tuberculin Skin Test False Positive Results <ul><li>Nontuberculosis mycobacteria </li></ul><ul><ul><li>NTMB, MOTT </li></ul></ul><ul><ul><li>Typically < 10 mm </li></ul></ul><ul><li>BCG administration </li></ul><ul><ul><li>Positive ppd for 5-10 years </li></ul></ul><ul><li>Reading erythema instead of induration </li></ul>
  39. 42. Tuberculin Skin Test False Negative Results <ul><li>Reading erythema instead of induration </li></ul><ul><li>Immunocompromised / Anergy </li></ul><ul><li>Inappropriate test administration/reading </li></ul><ul><li>Recent infection (2-12 wks to convert TST) </li></ul><ul><li>Extremes of age </li></ul><ul><li>Boost phenomenon </li></ul><ul><li>Live viral immunization (measles, smallpox) </li></ul><ul><li>Overwhelming active TB infection </li></ul>A negative ppd DOES NOT rule-out active disease
  40. 43. SKIN TESTING IN TB SINGLE PRICK TEST. READ AT 2-4 DAYS. POSITIVE IF INDURATION 5-14 MM(=HEAF GRADE 2) >15 MM =HEAF GRADE 3-4 MULTIPUNCTURE METHOD. READ AT 3-7 DAYS. GRADE 1:4– 6 PAPULES. GRADE 2: CONFLUENT.FORMING RING. GRADE 3:CENTRAL INDURATION GRADE 4: > 10 MM INDURATION MANTOUX TEST HEAF METHOD
  41. 44. Bacillus Calmette-Guerin Vaccine “BCG” <ul><li>Live vaccine from M. bovis strain </li></ul><ul><li>Used in highly endemic regions </li></ul><ul><li>Limited efficacy in preventing TB </li></ul><ul><li>Reduces mortality a/w TB meningitis among children </li></ul><ul><li>Results in positive TST </li></ul><ul><li>ppd reaction and efficacy wane over time </li></ul>
  42. 45. Screening for TB Boost Phenomenon / Two-Step Testing <ul><li>Initial TST false negative </li></ul><ul><li>Occurs following long latency between infection and testing </li></ul><ul><ul><li>“ hibernating” immune response </li></ul></ul><ul><li>TST reactivates immune response </li></ul><ul><ul><li>subsequent tests positive </li></ul></ul><ul><li>Common, ~20% </li></ul><ul><li>2 step testing recommended for high risk </li></ul><ul><ul><li>TST repeated in 2 weeks </li></ul></ul>
  43. 46. PRIMARY PULMONARY TUBERCULOSIS. <ul><li>THE FIRST INFECTION WITH THE TUBERCLE BACILLUS IS KNOWN AS PRIMARY TUBERCULOSIS. </li></ul><ul><li>IT USUALLY INCLUDES INITIAL LESION AND DRAINING LYMPH NODES. </li></ul>
  44. 47. PRIMARY TB ORGANS INVOLVED <ul><li>LUNGS </li></ul><ul><li>TONSILS </li></ul><ul><li>INTESTINE </li></ul><ul><li>SKIN </li></ul>
  45. 48. ---
  46. 49. Prim;Pulm;TB. <ul><li>LUNGS ARE MOST COMMON SITE OF INFECTION. </li></ul><ul><li>ALL LOBAR SEGMENTS ARE AT EQUAL RISK OF BEING SEEDED BY INHALED INFECTED DROPLETS. </li></ul><ul><li>25% OF CASES MAY BE MORE THAN ONE PRIMARY FOCUS. </li></ul>
  47. 52. DIFFERENCE B/W INFECTION & DISEASE INFECTION MEANS THAT MTB IS IN THE BODY BUT IMMUNE SYSTEM IS KEEPING THE BACTERIA UNDER CONTROL.
  48. 53. YES NO Defined as TB case +ve -ve Infectivity +ve -ve S/S +ve -ve Sputum C/S +ve -ve Sputum D/S +ve -ve CXR +ve +ve TST +ve +ve MTB DISEASE TB infection DIFF;B/W
  49. 54. FATE OF INFECTION <ul><li>Most prim;infection heals with or without calcification of primary complex. </li></ul><ul><li>Hematogenous spread …via lymphatic.. seeding of tubercle bacilli to other parts of lungs as well as other organs. </li></ul><ul><li>Infection usually contained at pulm. & extra pulm;sites. </li></ul><ul><li>Potential for reactivation of infection at all sites is present </li></ul>
  50. 55. RISK OF PROGRESSION OF INFECTION TO DISEASE . <ul><li>Once infected, stays infected for many years,probably for life. </li></ul><ul><li>Approx.90% Do Not develop TUBERCULOSIS (asymptomatic,but INFECTED POSITIVE TST. </li></ul><ul><li>Infected individuals can develop TB disease at any time. </li></ul><ul><li>Chance of dvlping dis;is greatest shortly after infection and then steadily lessens as time goes by. </li></ul><ul><li>The most important trigger is weakening of immune resistance . </li></ul>
  51. 56. NATURAL HISTORY OF UNTREATED TB . <ul><li>Without treatment,after 5 years::::50% of pulm. TB pts;will be dead. </li></ul><ul><li>25% self-cured by there strong immune response. </li></ul><ul><li>25% will remain ill with chronic,infectious TB. </li></ul>
  52. 57. 50% Dead 25% CURED 25% chronic
  53. 58. STAGES OF DISEASE PATHOLOGY STAGE 1 DROPLET NUCLEI INHALED… REACH ALVEOLI.---VASODILATION—INFLUX OF PMN & MACROPHAGES
  54. 59. STAGES OF DISEASE PATHOLOGY Stage 2 <ul><li>7-21 days..MTB multiplies within a group of phagocytic cells”macrophages”which are not activated to kill AFB. </li></ul><ul><li>Macrophages from blood travel to alveoli. These new macrophages engulf MTB. </li></ul><ul><li>These macrophages remains unable to destroy these MTB as they are not activated….RESULT.. Macrophages burst. </li></ul>
  55. 61. Stages of disease PATHOLOGY STAGE 3 <ul><li>Lymphocytes begins to infiltrate. </li></ul><ul><li>T-cells recognise MTB. </li></ul><ul><li>These T-LYMPHOCYTES liberate cytokines including gamma –interferon. </li></ul><ul><li>IFN can activate the macrophages to become capable of destroying MTB. </li></ul><ul><li>TST becomes POSITIVE. </li></ul><ul><li>Activated macrophages release IL-1,TNF. </li></ul>
  56. 62. Stages of disease PATHOLOGY STAGE 3 CONTD; <ul><li>Tubercle Formation Begins. Macrophages develop pale foamy cytoplasm & crowd togather as epitheliod cells to form the tubercle. </li></ul><ul><li>Some mono nuclear cells fuse to form MULINUCLEATED OR LANGHANS GIANT CELL. </li></ul><ul><li>Centre of tubercle is characterized by Caseation Necrosis . </li></ul><ul><li>MTB can not multiply with in these tubercle because of low PH & ANOXIC environment. </li></ul><ul><li>MTB can persist for long time. </li></ul>
  57. 65. Stages of disease PATHOLOGY Stage 4 <ul><li>Surrounding the Tubercle many macrophages are present in different states. ACTIVATED,POORLY ACTIVATED,& UNACTIVATED. </li></ul><ul><li>MTB uses these unactivated & poorly activated macrophages to replicate and hence TUBERCLE grows. </li></ul><ul><li>Growing tubercle invade surrounding structure Artery, Bronchus </li></ul>
  58. 66. STAGES OF DISEASE PATHOLOGY STAGE 5 <ul><li>Casseous centres of tubercle liquify. </li></ul><ul><li>It is conducive to MTB growth. </li></ul><ul><li>Now org; rapidly multiply extracellularly. </li></ul><ul><li>After some time----walls of nearby bronchi become Necrotic & Rupture…Cavity formation takes place. </li></ul><ul><li>MTB spill into other airways …spread to other parts of lung. </li></ul>
  59. 67. Pathology of TB. <ul><li>PRIMARY INFECTION IS USUALLY EVIDENT AS A SUBPLEURAL TUBERCLE CALLED AS GHON FOCUS </li></ul><ul><li>IT MAY BE IN ANY LUNG ZONE </li></ul><ul><li>GHON FOCUS + DRAINING HILAR L/N </li></ul>PRIMARY OR GHON FOCUS PRIMARY OR GHON COMPLEX
  60. 68. OUTCOME OF PRIMARY INFECTION <ul><li>NO CLINICAL DISEASE ; POSITIVE TST; USUAL OUT COME =90% OF CASES. </li></ul><ul><li>2. HYPERSENSITIVITY REACTIONS </li></ul><ul><li>ERYTHEMA NODOSUM </li></ul><ul><li>PHLYCTENULAR CONJUNCTIVITIS DACTYLITIS </li></ul><ul><li>3. PULM. AND PLEURAL COMPLICATIONS </li></ul><ul><li>TB PNEUMONIA, LOBAR COLLAPSE, PL EFFUSION </li></ul><ul><li>DISSEMINATED DISEASE . </li></ul><ul><li>LYMPHADENOPATHY (USUALLY CERVICAL) . MENINGITIS, </li></ul><ul><li>PERICARDITIS, MILIARY DISEASE . </li></ul>
  61. 69. Clinical Features of Prim; Pulm:TB <ul><li>Asymptomatic ….A great majority especially adults. </li></ul><ul><li>Brief febrile illness. At the time of tuberculin conversion. </li></ul><ul><li>Occasionally,typical prim;Tb may occur in elderly people who have lost their tuberculin sensitivity. </li></ul>
  62. 70. Clinical Features of Primary Pulmonary TB. <ul><li>In few cases with more severe infection or low host resistance,the child may be unwell,with anorexia,failure to gain weight. </li></ul><ul><li>Cough(if L/N or Granulation tissue impinge on Bronchial wall.) </li></ul><ul><li>Wheeze_+ </li></ul><ul><li>Sputum….rare in children. </li></ul><ul><li>Crepts. </li></ul><ul><li>Other signs according to complications. </li></ul>
  63. 71. ERYTHEMA NODOSUM PHLECTENULAR CONJUNCTIVITIS DACTILITIS HYPERSENSITIVITY LYMPHADENOPATHY COLLAPSE CONSOLIDATION OBSTRUCTIVE EMPHYSEMA CAVITATION PL EFFUSION ENDOBRONCHIAL LESION MILIARY MENINGITIS PERICARDITIS DISEASE INFLUENZA LIKE ILLNESS TST CONVERSION PRIMARY COMPLEX INFECTION (4-8 WEEKS) FEATURES OF PRIMARY TB
  64. 72. Radiological features <ul><li>In adults CXR changes(lung component of prim complex) + at time of TST conversion (7-30%) </li></ul><ul><li>In children –CXR---- Hilar >Paratracheal or Both OR B/L Hilar Lymphadenopathy & Parenchymal lesion. </li></ul><ul><li>Segmental or lobar consolidation or obstructive emphysema on CXR. </li></ul><ul><li>Radiological abnormality may persist upto 6 months ater diagnosis.But complete resolution after 2 year. </li></ul><ul><li>Calcification may occur </li></ul>
  65. 74. Diagnosis of primary pulmonary Tuberculosis <ul><li>HISTORY: contact +,vague ill health,brief febrile illness,cough,anorexia,wheeze, crepts, </li></ul><ul><li>TST +ve </li></ul><ul><li>CXR changes unilateral or bilateral Hilar, Paratracheal L/N, parenchymal lesion,consolidation,collapse, </li></ul><ul><li>SPUTUM rarely produced in children </li></ul><ul><li>GASTRIC WASHING for AFB Staining (rarely positive) </li></ul><ul><li>Gastric washing for AFB C/S (POSITIVE IN 20-25% CASES) </li></ul><ul><li>PCR. (Mycobacterial DNA amplification techniques) </li></ul>
  66. 75. COMPLICATIONS OF PRIMARY TB <ul><li>COLLAPSE/CONSOLIDATION </li></ul><ul><li>BRONCHIECTASIS </li></ul><ul><li>OBSTRUCTIVE EMPHYSEMA </li></ul><ul><li>BRONCHOLITH </li></ul><ul><li>ERYTHEMA NODOSUM </li></ul><ul><li>PHLYCTENULAR CONJUNCTIVITIS </li></ul><ul><li>PLEURAL EFFUSION </li></ul><ul><li>MILIARY TUBERCULOSIS </li></ul>
  67. 76. COLLAPSE/CONSOLIDATION <ul><li>Ass e enlarged tuberculous L/N.at hilum. </li></ul><ul><li>Middle lobe is most often affected. </li></ul><ul><li>Radiological appearances are due to: </li></ul><ul><li>1 collapse.. </li></ul><ul><li>2 inflammatory exudation.. </li></ul><ul><li>3 caseous pneumonia </li></ul>
  68. 78. COLLAPSE/CONSOLIDATION clinical presentation <ul><li>Wheeze </li></ul><ul><li>Cough </li></ul><ul><li>Dullness </li></ul><ul><li>Diminished air entry </li></ul><ul><li>Bronchial breathing </li></ul><ul><li>Crepts </li></ul><ul><li>Asphyxia in children +-resulting in death </li></ul>
  69. 79. Bronchiectasis <ul><li>Abnormal and permanently dilated airways. </li></ul><ul><li>Cause in prim TB—distension of airways by mucus,caseous tissue or sec;infection beyond a bronchial stenosis. </li></ul>
  70. 80. Obstructive emphysema <ul><li>Commoner in children </li></ul><ul><li>A valve action results due to bronchus compression,with air being admitted to a portion of lung on inspiration but unable to escape on expiration </li></ul><ul><li>This results in distention of a segment or a lobe. </li></ul>
  71. 81. Broncholith <ul><li>Calcification in a primary focus or L/N may be extruded into a bronchus as broncholith. </li></ul>
  72. 82. Erythema nodosum <ul><li>A manifestation of hypersensitivity reaction.due to vasculitis in deep dermis & skin fat. </li></ul><ul><li>Tender,dusky-red nodular lesions on anterior surface of legs>ant surface of thighs,>extensor surface of forearms>face.breast. </li></ul><ul><li>5-20 mm diameter nodule </li></ul><ul><li>Illdefined margin </li></ul><ul><li>Resolve over a week or two. </li></ul><ul><li>Red>purple>brown </li></ul><ul><li>Recurrent crops </li></ul><ul><li>Ass with fever positive TST recurrent crops of lesions may occur. </li></ul>
  73. 84. Phlyctenular conjunctivitis <ul><li>Reflects hypersensitivity to the tubercle bacilli. </li></ul><ul><li>Usually seen in first year of infection. </li></ul><ul><li>Common in children. </li></ul><ul><li>Usually in one eye. </li></ul><ul><li>Begin with LACRIMATION,IRRITATION,or PHOTOPHOBIA. </li></ul><ul><li>1-3 mm shiny yellowish or grey bleb @ the limbus,with a sheaf of dilated vessels running out toward it from edge of conjunctival sac. </li></ul>
  74. 85. Pleural effusion <ul><li>MAY BE SEEN IN CHILDREN,5-12 YEARS. </li></ul><ul><li>SMALL </li></ul><ul><li>TRANSIENT </li></ul><ul><li>USUALLY OCCURS 3-6 MONTHS AFTER INFECTION. </li></ul><ul><li>SYMPTOMS MALAISE,FEVER,PLEURIYIC PAIN </li></ul>
  75. 87. Miliary TB <ul><li>Result of acute diffuse dissemination of tubercle bacilli via blood-stream. </li></ul><ul><li>Form of severe infection </li></ul><ul><li>Symptoms—fever, night sweats, anorexia, wt;loss, dry cough, </li></ul><ul><li>Signs-------hepatosplenomegaly, chest normal to crepts, </li></ul><ul><li>Fundoscopy –choroidal tbercles (5-10%) </li></ul><ul><li>CXR—1-2 mm millet seeds shadow through lung feild </li></ul>
  76. 90. CRYPTIC MILIARY TB <ul><li>AGE > 60 YEARS </li></ul><ul><li>INTERMITTENT LOW GRADE FEVER (PUO) </li></ul><ul><li>UNEXPLAINED WEIGHT LOSS </li></ul><ul><li>GENERAL DEBILITY </li></ul><ul><li>HEPATOSPLENOMEGALY (25-50 % ) </li></ul><ul><li>NORMAL CXR </li></ul><ul><li>BLOOD DYSCRASIAS; LEUKAMOID REACTION, PANCYTOPENIA </li></ul><ul><li>NEGATIVE TST </li></ul><ul><li>CONFIRMATION BY BIOPSY OF LIVER OR BONE MARROW. </li></ul>
  77. 91. TB MENINGITIS <ul><li>OCCURS SHORTLY AFTER A PRIM; INFECTION IN CHILDHOOD OR AS PART OF MILIARY TB </li></ul><ul><li>USUAL LOCAL SOURCE OF INFECTION IS A CASEOUS FOCUS IN THE MENINGES OR BRAIN ADJ; TO CSF PATHWAY. </li></ul><ul><li>BRAIN COVERED BY A GREENISH ,GELATINOUS EXUDATE, ESPECIALLY AROUND THE BASE </li></ul><ul><li>NUMEROUS SCATTERED TUBERCLES + ON MENINGES. </li></ul>
  78. 92. SYMPTOMS OF TBM <ul><li>HEADACHE </li></ul><ul><li>VOMITING </li></ul><ul><li>LOW-GRADE FEVER </li></ul><ul><li>LASSITUDE </li></ul><ul><li>DEPRESSION </li></ul><ul><li>CONFUSION </li></ul><ul><li>BEHAVIORAL CHANGES </li></ul>
  79. 93. SIGNS OF TBM <ul><li>MENINGISM + - </li></ul><ul><li>OCULOMOTOR PALSIES </li></ul><ul><li>PAPILLOEDEMA </li></ul><ul><li>DEPRESSION OF CONSCIOUS LEVEL </li></ul><ul><li>FOCAL HEMISPHERE SIGNS </li></ul>
  80. 94. INVESTIGATIONS FOR TBM. <ul><li>ROUTINE INCLUDING CXR </li></ul><ul><li>CSF RE (INCREASED PRESSURE,USUALLY CLEAR BUT WHEN ALLOWED TO STAND A FINE CLOT “SPIDER WEB” MAY FORM) </li></ul><ul><li>CSF CHEMISTRY ( INC PROTEINS & DEC.GLUCOSE. </li></ul><ul><li>CSF SMEAR AFB -+ </li></ul><ul><li>CT BRAIN ( HYDROENCEPHALUS,MENINGEAL ENHANCEMENT, TUBERCULOMA ) </li></ul>
  81. 95. TB IN HIV <ul><li>MORE LIKELY INFECTION AFTER EXPOSURE. </li></ul><ul><li>USUALLY PROGRESSIVE PRIMARY DISEASE AFTER INFECTION. </li></ul><ul><li>REACTIVATION OF LATENT INFECTION. </li></ul><ul><li>REINFECTION WITH NEW STRAIN. </li></ul><ul><li>REDUCED SMEAR-POS RATES IN PTB. </li></ul>
  82. 96. TB IN HIV <ul><li>LESS CAVITATION. </li></ul><ul><li>ATYPICAL CXR APPEARANCES. </li></ul><ul><li>MORE DISSEMINATED DISEASE. </li></ul><ul><li>MORE EXTRA PULM; INFECTION. </li></ul><ul><li>MORE RISK OF ADVERSE DRUG REACTIONS. </li></ul>
  83. 97. THANK YOU

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