Tuberculosis (extra pulmonary)


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Tuberculosis (extra pulmonary)

  1. 2. TUBERCULOSIS (Extrapulmonary) Dr. Shahab Riaz Lecturer of Pathology PMC
  2. 3. Bacteriology <ul><li>Slender bacillus, 3 ųm long, non-motile, non-sporing </li></ul><ul><li>Acid fast, ZN staining or Auramine Rhodamine staining </li></ul><ul><li>Löwenstein Jensen medium (37ºC, aerobic atmosphere, several weeks, 6 weeks before discarding) </li></ul><ul><li>Faster growth in fluid media </li></ul><ul><li>14C-tagged substrate into medium (detection of free 14CO2 above liquid culture indicates growth of bacilli, growth + susceptibility to drugs) </li></ul><ul><li>Resistant to drying in dust for several months, susceptible to UV light, rapidly killed in sunlight </li></ul>
  3. 4. Common Agent <ul><li>Mycobacterium tuberculosis </li></ul><ul><li>(Mostly pulmonary focus, spreads by ingestion of infected sputum or blood-borne) </li></ul><ul><li>Mycobacterium bovis </li></ul><ul><li>(Tonsillar / intestinal TB in children, eradicated from developed countries, pasteurization of milk and removal of infected herds) </li></ul>
  4. 5. Gross Specimen <ul><li>Patient Name : Talha </li></ul><ul><li>Age : 25 years </li></ul><ul><li>SP No : 899/2008 </li></ul><ul><li>Specimen : Ileal Resection </li></ul>
  5. 8. Pathogenesis <ul><li>Transient acute inflammatory response  neutrophils  rapidly killed </li></ul><ul><li>Monocytes (blood)  macrophage infiltration  destruction of organisms </li></ul><ul><li>AFB  phagocytosed by macrophages  pale cytoplasm, eosinophilic nuclei, elongated and vesicular “Epitheloid Cells” </li></ul><ul><li>Some macrophages instead of Epitheloid cells fuse to form Langhans Giant cells </li></ul><ul><li>Surrounding altered macrophages, wide zone of small round cells, mostly lymphocytes and fibroblasts </li></ul><ul><li>10-14 days necrosis in centre (altered macrophages and cells of tissue) firm Coagulative necrosis  “Caseation” </li></ul><ul><li>High content of lipid (structureless and eosinophilic) T-cell mediated reaction  released cytokines TNF </li></ul><ul><li>Hypersensitivity to tuberculoprotein, Ischemia?? </li></ul><ul><li>“ Tubercle Follicle” central caseation, surrounded by epitheloid and Giant Cells, in turn closed in wide zone of small round cells </li></ul><ul><li>DDx deep-seated mycoses, for TB Dx, organism must be seen in ZN stain or LJ medium </li></ul>
  6. 10. Microscopy
  7. 14. Types of Microscopic Lesions <ul><li>Previously mentioned lesion “ Productive ” or “ Proliferative ” (cells primarily) </li></ul><ul><li>Variant </li></ul><ul><li>“ Exudative form of TB ”, </li></ul><ul><li>(inflammatory exudate rich in fibrin, considerable infiltration of lymphocytes and often polymorphs but epitheloid and Giant cells scanty, e.g., serous cavities like pericardium/peritoneum, epithelial surfaces also exhibit this character e.g., sterile pyuria in open renal TB) </li></ul><ul><li>Compact organs like liver, kidney  productive lesion </li></ul><ul><li>Lungs both types and latter is serious (extensive caseation and rapid spread of infection) </li></ul>
  8. 15. Types of TB <ul><li>1. Acute Caseous TB </li></ul><ul><li>2. Chronic TB </li></ul><ul><li>a. Caseous </li></ul><ul><li>b. Fibro-caseous </li></ul><ul><li>c. Fibroid </li></ul><ul><li>( immunity, bacilli destroyed, healing/fibrosis side by side with caseous destruction) </li></ul><ul><li>Non-Reactive TB </li></ul><ul><li>( most serious, extensive caseation, teeming with bacilli, no cellular reaction, leukemia complication and elderly people, tuberculin test – ve /over whelming infection) </li></ul>
  9. 16. Fate of Tuberculous Lesion <ul><li>Hallmark of Healing ≈ Fibrous tissue </li></ul><ul><li>a. Solid Fibrous nodule </li></ul><ul><li>b. Calcareous nodule </li></ul><ul><li>(rim of fibrous tissue, caseation  slow dystrophic calcification, organisms survive, years later become active again) </li></ul><ul><li>Hallmark of Activity ≈ Caseation and softening </li></ul><ul><li>(macrophages  bacilli  lymphatics/tissue spaces  satellite follicles) </li></ul><ul><li>(caseous material  phosphatides  inhibit autolytic enzymes) </li></ul><ul><li>(liquefaction serious, pyogenic secondary infection?? Delayed hypersensitivity reaction?) </li></ul><ul><li>(Cold Abscess  pus like material, tracks down to spread) </li></ul>
  10. 17. <ul><li>Bones, joints, lymph nodes, epididymis  no immediately available passages </li></ul><ul><li>Large cold abscesses accumulate e.g., collar stud abscess of neck  cervical LN TB </li></ul><ul><li>In other cases pus tracks through tissues  advancing tuberculous lesion destroys tissue (sinuses formed  lined by tuberculous granulation tissue formed of systems of tubercle follicles irregularly disposed in a mass of newly formed fibrous tissue heavily infiltrated with lymphocytes and macrophages) </li></ul><ul><li>Sometimes pus tracks for long distances e.g., infected vertebrae  psoas sheath  psoas abscess and finally points below inguinal ligament </li></ul><ul><li>Open TB abscesses  serious bcz open and infectious character & aerobic organism exposed to atmosphere </li></ul>
  11. 18. Spread of Tuberculosis in Body <ul><li>1. Local Spread (macrophages or pus tracking) </li></ul><ul><li>2. Lymphatic Spread (tuberculous lymphadenitis, primary focus + attending lymphangitis + lymphadenitis = Primary Complex) </li></ul><ul><li>3. Blood Spread (as an extension of lymphatic involvement) </li></ul><ul><li>Miliary TB (lungs, spleen, liver, kidneys) </li></ul><ul><li>Caseous LN  adjacent pulmonary vein (fever, wasting, hepato-splenomegaly, leucopenia, thrombocytopenia) </li></ul><ul><li>Tuberculous meningitis  miliary TB  direct involvement of choroid plexus or small sub-cortical lesion (Rich’s Focus) rupturing into subarachnoid space </li></ul><ul><li>Miliary TB  large number of organisms via blood stream or pulmonary vein </li></ul><ul><li>Sometimes in older children and adults  small pulmonary vein branch  few bacilli  destroyed by mononuclear phagocyte system or lodged as metastatic disease  (a) progresses immediately to produce clinical effects or (b) remain dormant, reactivation years later (local metastatic TB) e.g., kidney, adrenals, uterine tubes, epididymis, bones, joints, tendon sheaths </li></ul><ul><li>(thyroid, pancreas, heart and voluntary msls?? Spleen… </li></ul>
  12. 19. Spread (cont…..) <ul><li>4. Spread in Serous Cavities (pleurisy of lung lesions, localized peritonitis found around tuberculous salpingitis, TB meningitis) </li></ul><ul><li>5. Spread along epithelial lined surface </li></ul><ul><li>e.g., intra bronchial spread of TB when sputum inhaled into adjacent lung segments </li></ul><ul><li>when coughed up can produce tuberculous laryngitis </li></ul><ul><li>when swallowed, ileo-cecal region of bowel (tuberculous enteritis) </li></ul><ul><li>Rectal involvement  ischio-rectal abscess </li></ul><ul><li>TB kidney  ureter  trigone of bladder </li></ul><ul><li>TB salpingitis  endometrial disease </li></ul>
  13. 20. Why ileo-cecal area is common site of infection? <ul><li>Gastrointestinal tract tuberculosis usually involves the ileo-cecal region , because of abundant lymphoid tissue and relative stasis. </li></ul>
  14. 21. Tissue Response Factors <ul><li>1. Dose and Virulence of Organism </li></ul><ul><li>2. Innate and Acquired resistance of body </li></ul><ul><li>a. Innate Immunity : </li></ul><ul><li>Black Africans, American Indians, Australian Aborigines are susceptible </li></ul><ul><li>b. Age and Sex: </li></ul><ul><li>1 st 5 years ---- resistance poor, high mortality </li></ul><ul><li>5-15 years ----- resistance at peak </li></ul><ul><li>15-30 years ---- resistance breaks down esp. in women </li></ul><ul><li>After 30 years --- resistance quite high </li></ul><ul><li>Old age ---- again breaks down esp. in men </li></ul><ul><li>c. General Health of Individual: </li></ul><ul><li>Malnutrition & over crowding  prison camps/ slums  TB predisposed </li></ul><ul><li>Psychological stress, chronic debilitating diseases  lower resistance </li></ul><ul><li>DM esp. notorious  rapidly spreading type of infection </li></ul><ul><li>Like wise glucocorticoid therapy  can reactivate previously quiescent TB foci (use with caution in TB) </li></ul>
  15. 22. <ul><li>d. Occupational Factors: </li></ul><ul><li>Silicosis risk works  tunnellers, miners and quarrymen </li></ul><ul><li>asbestosis strangely doesn’t increase the risk </li></ul><ul><li>e. Effects of previous infection: (Koch’s Phenomenon): </li></ul><ul><li>2 nd infection different from primary one  Robert Koch in Guinea pigs </li></ul><ul><li>TB bacilli  skin  10-14 days, nodule, ulcerates and persists until death </li></ul><ul><li>Organisms  RLN  blood  MTB  death </li></ul><ul><li>TB bacilli  injected into 4-6 weeks previously infected  different response bcz of T cell mediated response </li></ul><ul><li>Site of injection indurated 1-2 days  ulcerates/heals  no RLN </li></ul><ul><li>This 2 nd response is called Koch’s Phenomenon, due to immunity and hypersensitivity (tuberculin) </li></ul><ul><li>Tuberculin hypersensitivity  develops month to 6 weeks  T cell mediated </li></ul><ul><li>Partial degree acquired immunity  no effect on primary infection </li></ul>
  16. 23. Morphology of Tuberculous Infection <ul><li>Extra-pulmonary: </li></ul><ul><li>In Children: </li></ul><ul><li>Developed countries rare, Pakistan common </li></ul><ul><li>Alimentary tract mostly children (bovine bacilli in milk) </li></ul><ul><li>Abdominal disease  primary focus in bowel so small  rarely identifiable </li></ul><ul><li>First manifestation usually mesenteric lymphadenopathy, Tabes mesenterica </li></ul><ul><li>Ruptured MLN may cause Acute TB peritonitis </li></ul><ul><li>Usually calcification and recovery, sometimes progressive lymphatic spread to thoracic duct  Miliary TB </li></ul><ul><li>Rarely primary focus is tonsillar  unnoticed until CLN  softening and discharge through skin (scrofula) </li></ul><ul><li>In children mostly  primary focus small  extensive LN involvement </li></ul>
  17. 24. <ul><li>In Adults: </li></ul><ul><li>Enteric TB: </li></ul><ul><li>Same features of pathogenesis as lungs, </li></ul><ul><li>Depends on resistance of pt.  fibrosis or extensive cavitation </li></ul><ul><li>Severe cases  tissue destruction </li></ul><ul><li>Blood spread and LN involvement lesser than in children </li></ul><ul><li>Swallowing infected sputum of pulm. TB </li></ul><ul><li>Ileal wall ulceration, localized peritonitis, strictures/fistulae </li></ul><ul><li>Renal TB: </li></ul><ul><li>Cortical focus  spreads to destroy surrounding renal parenchyma </li></ul><ul><li>Other lesions in medulla  bacilli passage renal tubules  pelvis cavitation </li></ul><ul><li>Destructive lesion of tuberculous pyelonephritis  kidney converted to ragged cavity lined by tuberculous granulation tissue  down the ureter </li></ul><ul><li>If ureter occluded  large tuberculous pyonephrosis </li></ul><ul><li>Skeletal TB: </li></ul><ul><li>Metaphysial area of bone  great local destruction </li></ul><ul><li>Unlike pyogenic osteomyelitis, it destroys epiphyseal cartilage easily </li></ul><ul><li>Soon the neighboring joint is affected </li></ul><ul><li>“ Hence feature common in adult lesions is tendency to extensive local destruction with little lymphatic involvement” </li></ul>
  18. 25. Koch’s Phenomenon Application <ul><li>Adult lesion almost always secondary to primary lesion of childhood (difference in response of the 2 infections) </li></ul><ul><li>As in Koch’s Phenomenon  2 nd infection localized  so in adults no LNs </li></ul><ul><li>Exception: </li></ul><ul><li>Previously Mantoux – ve young adult  TB  even then adult type lesion rather than juvenile type  LN –ve  tissue maturation?? </li></ul><ul><li>Or may be avirulent atypical  in childhood as primary  possibility?? </li></ul><ul><li>But even then all the adult lesions should not be called as Secondary </li></ul><ul><li>So older the patient, lesser the LN involvement </li></ul><ul><li>Hence Childhood and Adult TB is more accurate terminology than Primary and Secondary TB. </li></ul><ul><li>In lungs of adults either Reactivation of quiescent primary lesion (Post-primary TB) </li></ul><ul><li>OR development of new lesion produced by re-infection from some external source </li></ul><ul><li>Other organs like kidneys and bones  TB mostly of reactivation of small lesions produced during bacteremia phase of earlier primary infection </li></ul>
  19. 26. Thank You
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