1. 1 Typhoid fever You Chengcheng Dept. of pathology China Three Gorges University

2. 2 Contents  Introduction  Pathogenesis  Pathological changes  Symptoms  Complication

3. 3 First, let me tell a story of typhoid Mary ……

4. 4 Prevalent in the third world country Outbreaks are rare,but in some areas such as in Indonesia and New Guinea,it ranks among the 5 most common causes of death Bacterial infection of the intestinal tract and occasionally the bloodstream The ileum is most affected

5. 5 Mononuclear Phagocytic System(MPS): Monocytes and its derivations mononuclear cells (blood) macrophages (connective tissue) kupffer cells (liver) ……….. Typhoid fever is characterized by macrophages Proliferation of MPS, which are particularly predominant in ileum.

6. 6 The germ that causes typhoid is a unique human strain of salmonella called Salmonella typhi Gram negative bacillus. O-Ag, H-Ag, vi-Ag (Widal reaction) Pathogenesis

7. 7 Infection source ： typhoid fever patient and carrier route of transmission ： fecal-oral route susceptible population:children and young people Food, fly, finger, water

8. 8 Salmonella typhi Contaminanted food Proliferate in ileum tissue bacteremia First contactWhole body Gall bladder second contact Lymph tissue in ileum Septicaemia Hyperplasia stage (1w) Toxemia Excretion Necrosis and ulceration (2w) Healing (1w) Incubation period(10 d)

9. 9

10. 10 Pathological changes Hallmark histologic finding:the infiltration of tissue by typhoid cells typhoid cells:large macrophages contain Phagocytized erythrocytes, lymphocytes, bacteria and necrotic cellular debris Typhoid nodule (typhoid granuloma) : the aggregates of typhoid cells

11. 11 Typhoid nodule can present in the lymph tissue of small intestine, mesenteric lymph node, the liver, spleen and marrow, its typical changes often occur in the lower part of ileum, especially in the Peyer‘s patches and Isolated lymphonodulus.

12. 12 typhoid cell

13. 13 typhoid cell

14. 14 typhoid cell

15. 15 typhoid cell

16. 16 Typhoid granuloma

17. 17 Intestinal pathological changes The principal lesions are those of lymphoid tissue of terminal small intestine. (1) Hyperplasia Stage ( Peyer’s patches) (2) Necrosis Stage; (3) Ulceration Stage; (4) Healing Stage.

18. 18 Hyperplasia stage ： the 1st w after onset lymphoid tissue swelling protrude out the mucosa, looks like lymphoid tissue swelling protrude out the mucosa, looks like cerebral convolution

19. 19 Showing the hyperplasia of Peyer’s patches of ileum, which is button-like elevation Hyperplasia stage

20. 20 Hyperplasia stage looks like cerebral convolution

21. 21 Hyperplasia stage looks like cerebral convolution

22. 22 Hyperplasia stage

23. 23 Microscopy:

24. 24

25. 25 the 2nd w after onset multi-focal necrosis in lymphoid tissueNecrosis stage ： the 2nd w after onset multi-focal necrosis in lymphoid tissue

26. 26 Ulceration stage ： the 3rd w after onset ， necrosis tissue fall off and ulcer formation, longitudinal ulceris parallel with the axis of longitudinal ulcer is parallel with the axis of intestinal canal, deep to the muscularis layer and involve the artery,which will result in bleeding

27. 27 Key features ： Round or oval Elevated margins Uneven bottom Parallel to the axis of intestine ulceration stage

28. 28 ulceration stage Key features ： Round or oval Elevated margins Uneven bottom Parallel to the axis of intestine

29. 29 ulcer ulceration stage

30. 30 Difference Typhoid fever Tuberculosis

31. 31 Healing stage ： the 4th w after onset the 4th w after onset Granulation tissue proliferation, Granulation tissue proliferation, scar formation scar formation

32. 32 Changes in other MPS Typhoid nodule formation and ulceration in mesenteric lymph node, the liver, spleen and marrow.

33. 33 Lesions in other organ Gall bladder: carrier Heart: slower pulse Kidney: Albuminuria Skin: rose rashes

34. 34 SYMPTOMS Fever (some as high as 40 Degrees) Weakness Headache Loss of Appetite Stomach pains Rose Rashes

35. 35

36. 36 Complications: intestinal bleeding intestinal perforation lobular pneumonia

37. 37

38. 38 Bacillary Dysentery Chengcheng You Dept. of pathology China Three Gorges University

39. 39 Bacillary dysentery is an acute bacterial infection caused by the genus Shigella resulting in colitis affecting predominantly the rectosigmoid colon. The disease is characterized by diarrhea, dysentery, fever, abdominal pain, and tenesmus. It is usually limited to a few days. Mainly occur in infants and young children Mainly occur in infants and young children

40. 40 Pathogen Shigellae are nonmotile gram-negative bacilli belonging to the family Enterobacteriaceae Four species: S. dysenteriae (group A), S. flexneri (group B), S. boydii (group C), S. sonnei (group D).

41. 41 Incidence most cases of shigellosis occur in children of developing countries S. flexneri is the predominant species Children between 1 and 4 years old

42. 42 Infection source ： patient and carrier route of transmission ： fecal-oral route Susceptible population:children and young people seasonal patterns: autumn and summer

43. 43 PATHOGENESIS organisms traverse the small bowel, penetrate colonic epithelial cells and multiply intracellularly acute inflammatory response pseudomembranous type of colitis Epithelial cells containing bacteria are lysed, resulting in superficial ulcerations and shedding of shigella organisms into stools Diarrhea results because of impaired absorption of water and electrolytes by the inflamed colon

44. 44 Feature  Location: predominantly the rectosigmoid colon  Clinical type : l Acute bacillary dysentery l Chronic bacillary dysentery l Toxic bacillary dysentery

45. 45 Acute bacillary dysentery Fibrinous inflammation Serous inflammation Mucus secretion increase diffuse hyperemia erosion Map-like ulcer healing bloody mucoid diarrhea

46. 46 Gross: Affect the colon, producing an acute inflammation with diffuse hyperemia 、 edema and multiple superficial ulcers. Pseudomembrane formation: exudate fibrin, neutrophils, necrotic debris, bacteria MI: epithelial cell necrosis, fibrin exudation monocytes and neutrophils infiltration abscess formation The lesions are often self-limited and can recover completely Acute bacillary dysentery

47. 47 Pseudomembrane

48. 48 pseudomembranous inflammation Gross: showing the pseudomembrane and irregular ulcers

49. 49 bacillary dysentery

50. 50

51. 51 Microscopy: Bacillary dysentery

52. 52

53. 53

54. 54 Complications Intestinal Bleeding Intestinal Perforation(seldom)

55. 55 Clinic Feature  Symptoms begin with sudden onset of high grade fever, abdominal cramps and watery diarrhoea.  Subsequently diarrhea become mucoid, of small volume and mixed with blood. This is accompanied by abdominal pain and tenesmus.  Physical signs are those of dehydration beside fever, lower abdominal tenderness and normal or increased bowel sounds.

56. 56 Chronic bacillary dysentery lasting more than 2 months, infected by S.flexneri( 福氏菌 ). Clinical features ： Mild symptom of abdominal pain,diarrhea Infectious source pathological changes ： ① chronic ulcers; ② forming polypi ; ③ intestinal wall are fibrosis.

57. 57 Toxic bacillary dysentery Children at the age of 2-7 years old are sensible most are result from S.sonnei and S.flexneri. clinical features ： ① toxic symptom all over the body: Toxic shock 、 respiratory or circulation failure. ② intestinal symptom: mild

58. 58 Questions for the class bacillary dysentery 1.What kind of inflammation is involved in bacillary dysentery? typhoid granuloma 2.The definition of typhoid granuloma