2. Infection Diseases and Parasitic Disease Tian Dong Ping Dept. of Pathology Shantou University Medical College

3. Routes of entry, dissemination, and release of microbes from the body(Pathogenesis of infection disease)

4. Section 2 Section 2Tuberculosis(TB)

6. 3. Basic pathological changes TB is a special type of inflammation. alteration exudation proliferation.

7. 3. Basic pathological changes TB is a special type of inflammation Exudationnecrosis proliferation

8. (1) Healing: Resolution and absorption fibrosis, fibrous encapsulation and calcification 2) deterioration: 1 ) enlargement and development 2) liquefaction and spread bronchial spread---lungs lymphatic spread-regional or distant LN hematogenous spread ------ - other organs Outcome

10. Microscopically: epithelioid cells, Macrophages Langhan’s giant cells lymphocytes, caseous necrosis, fibrosis Proliferation

13. (3)Alteration Caseous necrosis Grossly: yellowish homogenous greasy (dry and cheesy pale yellow) Liquefaction--- caused dissemination of TB in the body

14. Section 3 Section 3 Pulmonary tuberculosis

15. Pulmonary tuberculosis Pulmonary tuberculosis It is the most frequently encountered form of the disease Pulmonary TB is divided into primary and secondary types

16. 1. primary tuberculosis the first infection TB more frequent in children primary complex: 1) primary lung lesion (Ghon focus) 2) tuberculous lymphangitis 3) Hilar lymphadenitis x—ray : dumbbell likely

18. three routes (2%) bronchial dissemination----multiple foci pulmonary Infection even opposite lung lymphatic dissemination---hilar peribronchial cervical even distant lymph nodes hematogenous dissemination----miliary disease in lung or generalized military tuberculosis

19. Listeriosis of the liver

21. Section 4 Section 4 secondary tuberculosis

22. characteristic of secondary tuberculosis characteristic of secondary tuberculosis second time infection TB this form predominates in adults the lung infection is chiefly the result of bronchial dissemination infection from the apex downwards the course of the disease is usually protracted combination of old and fresh lesions proliferation is main lesions

23. there are six types of secondary tuberculosis focal pulmonary tuberculosis infiltrative pulmonary tuberculosis chronic fibrocaseous TB with cavitation caseous pneumonia tuberculoma tuberculous pleuritis

24. I focal pulmonary tuberculosis focal pulmonary tuberculosis

25. 1. focal pulmonary tuberculosis number: one or more small apical foci size: 0.5-1cm. shape: well circumscribed,grayish white to yellow in color nature: mostly proliferative with central caseous necrosis and peripheral fibrosis the foci may calicify or quiescent form of infection or change into other types

27. II infiltrative pulmonary tuberculosis infiltrative pulmonary tuberculosis

28. infiltrative pulmonary tuberculosis most common type of secondary TB. Sputum infection—open TB (1) (1)site: upper part of the lungs(subclsvicular infiltration) (2) (2)acute and exudative lesions with central caseous necrosis (3) (3)on chest x-ray many soft woolly infiltrates are seen (4) (4)clinically--------toxic symptom, easily cured and short clinical course

30. (5) (5) outcome: a: healing b: progressive enlargement, liquefaction, cavitation bronchogenic spread-- breaks through pleura- Pneumothorax pyopneumothorax transform into chronic fibrocaseous TB with cavitation

31. III chronic fibrocaseous TB with cavitation

32. chronic fibrocaseous TB with cavitation (1)thicked cavities (1)multiple thicked cavities of varying sizes can be seen (2) (2)thicked cavity wall consist of three components a. caseous necrosis b. granulation tissue of TB c. fibrous tissue (3) (3)old and new TB lesions are coexisting (4) (4)the upper lung has more lesions and older lesions than the lower lung

33. 5.marked fibrosis leads to small indurated lungs pleural adhesions----Cor Pulmonale 6. Significance: Sputum infective ---open TB Hemoptysis TB of larynx and intestine

35.  Caseous Pneumonia Caseous Pneumonia

36. 1) rapid serious condition of TB progression 2) one lobe or an entire lung affected and become consolidation 3) severe exudation and severe necrosis a large number of of mycobacterium tuberculosis can be seen 4) serous exudate in the alveoli contain monocytes and lymphocytes 5) Young patients are more frequently affected

37. Ⅴ Tuberculoma

38. 5. Tuberculoma 1) definition ； solitary globular caseous lesion surrounded by fibrosis 2)size: 2-5mm in diameter. 3)site:well delineated upper lobe 4) on chest x-ray: it is easily mistaken for tumor 5) Tuberculomas represent quiescent disease

40. Tuberculous pleuritis Ⅵ

41. 6. Tuberculous pleuritis two type : ① exudation ② proliferation

42. exudation type: early stege: early stege: serous exudation later stage: later stage: fibrineus→ organization →pleural thickening and adhesions

43. proliferation type: apical lesion location at mainly proliferation change, no hydrothorax

44. Section 5 Extrapulmonary tuberculosis

45. Extrapulmonary TB is the result of hematogenous spread from primary pulmonary TB, and can occur in the brain, liver, gut, spleen, kidney and genitourinary organs.

46. 1. Intestinal tuberculosis (1) primary intestinal TB——rare in children Intestinal primary complex: ① primary intestinal tuberculosis ② Intestinal tuberculous lymphangitis ③ Mesenteric tuberculous lymphadenitis

47. (2) Secondary intestinal tuberculosis—— ileocecal region ileocecal region ① most cases are due to swallowing of infectous sputum ② two morphological form of the disease Ulcerative type Ulcerative type­——belt-like ulcer Hyperplastic type Hyperplastic type (rare) thickening of wall--- multiple polyps

50. 2. Tuberculosis peritonitis Wet type- Ascitic fluid Dry type- Fibrinous exudate- Adhesions

52. 3 Tuberculosis of genito---urinary tract :

53. 1)TB of kidney 2) TB of genital organs

54. ** TB of kidney begins at the cortico-medullary junction. **Necrosis material is discharged through the ureter leaving multiple cavities. **The entire kideny,pelvic mucosa and urinary bladder via the urethra may occue.

55. Renal tuberculous

56. Genital tuberculosis Females are more frequently affected.--- TB of uterus,fallopian tubes and ovaries are most common.

57. 4.TB of bone joint : Example: (1)TB of Bone----Spine Caseous necrosis of vertebral bodies--- --------collapse---------kyphosis

59. (2) Joint : Tuberculous granulation tissue in synovial membrane. Sero-fibrinous exudated in joint cavity—fibrous ankylosis

60. 5.Tuberculous meningitis * The base of the brain is usually affected *Subarachnoid space is filled with yellowish gelatinous exudate *The brain surface is covered with small tubercles * Adhesions may obstruct CSF flow and lead to hydrocephalus

62. 6. Tuberculous lymphadenitis **The result of lymphatic dissemination **It Involves groups of nodes ---- enlarged and adherent, with central caseation necrosis

65. Mediastinal lymph nodes TB ---the miliary tubercle appear as subpleural spots

66. Typhoid Fever

67. Introduce acute of proliferation inflammation caused by typhoid bacilli The predominant pathological change is generalized proliferation of monocular phagocytes. This is most pronounced in the ileum.

68. Etiology: Typhoid bacilli (salmonellae type) Three antigens: flagellar (H) Somatic (O) Outer coat (Vi) Endotoxin

69. Pathogenesis Five “FS” most concerned with spread of this disease Food Fingers Flies Fomites Feces

70. 1.Typhoid bacilli enter into mouth Stomach HCI Lymphoid tissue (intestine mesenteric LN) Liver Thoracic ductBloodstream Bacterium

71. Ingestion of S. typhi (contaminated water or food) PHASE I Invasion of intestinal lymphoid tissue and proliferation of bacteria. This phase lasts for 2 weeks and is virtually asymptomatic. PHASE II Invasion of blood stream causing bacterium. General toxaemia is caused with rise of temperature. Immunological reaction occurs leading to the next phase in 10 days’ time. PHASE III Localisation of bacteria in intestinal lymphoid tissue, mesenteric nodes, gall bladder, liver, spleen and sometimes the bones. Local necrosis, probably due to antigenantibody hypersensitivity reactions, results in characteristic lesions.

72. 2. The bacilli are engulfed by moncyte- macrophage system →proliferate → release endotoxin→ toxemia 3.Hypersensitivity reaction lymphoid tissue second time of intestine (bacilli in gall-bladder) intestine

73. Pathological change Basic pathology: acute proliferative inflammation (1) typhoid cell: macrophage engulfed RBC lymph cell, bacilli and cellular debris transform into typhoid cell (2) typhoid nodules (granulomas)——collections of typhoid cell form typhoid granuloma. (3) Focal necrosis

76. Intestinal lesion Location: peyer’s patches and solitary lymph follicles of the distal ileum.

77. Four pathologic stages: (one week of every stage) 1.Medullary swelling 2.Necrosis 3.Ulceraztion 4.healing

78. 1) stage of medullary swelling: (the first week) Grossly: Grossly: swelling of the solitary lymphoid follicles and peyer’s patches convoluted like the surface of brain

80. Microscopely: marked proliferation of macrophages and formation of typhoid nodules —— (typhoid cell)

83. 2. stage of necrosis ( the second week ) necrosis is due to re-entry of large numbers of organisms from the gallbladder to the intestine. Cause: a. hypersensitive reaction b. endotoxin c. pressure of proliferative lesion on capillary

85. Gross: grayish-whit or grayish-green areas. Microscopely:

86. 3. stage of ulceration (in the third week) Grossly *necrotic mucosa sloughs off, leaving round or oval ulcers *margins is slightly elevated *Typhoid ulcer lie parallel to the long axis of small intestine,and healing will not cause strictures two serious complications easily cured: perforation hemorrhage.

87. Ulcerative intestinal tuberculosis

89. Complications 1)Perforation 2)haemorrhage

90. 4. stage of healing healing by granulation and re-epithelialization

92. Changes of other organs: (1) Change in other organs : monocyte- macrophage system-liver, spleen, bone marrow. (2)Change in other organs(no monocyte macrophage system organs) a. myocardium b. central nervous system (3)change of gall balder——chronic carriers

94. Bacillary dysentery

95. Summary 1. It is a common intestinal infection cansed by shigellae organisms 2. Easily occur in summer. 3. male or female,children or adult may affected. 4. patient present with head,high fever, blood and pus in the stools and tenesmus

96. I.Etiology and route of infection Shagellae-four species. Sh shiga Sh flexmeri Sh boydii Sh gone bacilli.

97. Organisms are ingested orally through fecally- contaminated food, water, or utensils, flies serve as important vectors in transmission. Infectious sources: carriers and patients, via oral enter the intestine.

98. Ⅱ. Pathogenesis three steps are involved: three steps are involved: Bacilli reproduce in the epithelial cell of colon organisms penetrate the basement membrane or mucosa in to the lamina propria and replicated organisms produce endotoxin and both cause inflammation Two points are very important: Two points are very important: (1)dose of bacilli (2)the invasiveness of the organisms against to the epithelium.

99. Ⅲ. Pathologic changes There are three types: 1) Acute bacillary dysentery 2) Chronic bacillary dysentery 3) Toxic bacillary dysentery

100. 1.Acute bacillary dysentery

101. 1) Early stage------- acute catarrhal inflammation. (2) Pseudomembranous inflammation Gross: Greyish white, dirty greenish Microscopically: fibrin, neutrophils Necrotic mucous membrane (3) Ulcer formation—map shaped Clinically: abdominal cramps, diarrhea (stool contains blood, mucus, pus) severe cases; fever, vomiting, dehydration

104. 2. Toxic bacillary dysentery

105. Characteristic features: (1)Abrupt onset (2)Mild pathological changes in intestines: secretion of mucus, congestion, edema, infiltration of small amount of polys-a catarrhal inflammation. (3)Severe systemic toxic symptoms-shock, respiratory failure, etc. (4)Occurs mostly in children.

106. 3. Chronic bacillary dysentery

107. 3. Chronic bacillary dysentery: (1)From acute bacillary dysentery, more than two months to many years (2)Intestinal lesion- mixture of old and new lesion chronic ulceration- granulation tissue and scar polypoid growth at margin of muous membrane thickening of wall. (3)Clinically-abdominal pain, diarrhea constipation and mucus or bloody stool.

108. Leprosy

109. Leprosy A chronic inflammatory disease of low infectivity caused by mycobacterium leprae.

110. Leprosy ---------------- * This chronic inflammation mainly involving the skin and peripheral nerves. *It induce loss of sensation of skin. *In severe cases skin and muscle atrophy occur and autoamputation of fingers or toes.

111. Route of infection 1. By inhalation of droplet infection 2. Through intact skin by direct contact When infection develops in the skin, the initial lesion is the indeterminate macule. Thereafter two major clinical forms may develop.

112. Pathologic change: There are four types There are four types (two groups and two types) 1. Tuberculoid leprosy- 70% Tuberculoid granulomas lesion. This type is less infectious, and slowly progressive. The result of treatment and prognosis are better. The lepromin skin test is positive.

117. 2. Lepromatous leprosy—20% It is an infectious source. Characteristic change: (1)lepromatous lesion- diffuse aggregates of foamy macrophages, macrophage contain lepra bacilli, it is called lepra cell’s. A distinctive deformity of the face known as leonine facies. (2) Lepromatous leprosy invade nose, lymph node, liver, spleen and testes. Lesion in nose cause collapse of the bridge of the nose or perforation of the septum. (3) The lepromin test is negative.

119. 3. Borderline loprosy 4. Indeterminate leprosy- rarely occur

127. good bye! students