幻灯片 1

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1 Infectious disease Wang Yishu Infectious disease of Department of Pathology gastrointestinal tract Basic Medical School

2 Typhoid fever 伤寒

3 玛丽是一名家庭厨师她看上去身体健康并无疾病,10 年中她先后为 8 户人家操厨, 造成伤寒杆菌污染食物, 导致 200 多人相继患了伤寒 10 年后才引起雇主和卫生部门的警觉 : 怎么玛丽到哪里操厨哪里就有伤寒病发生? 卫生部门给她检查后发现, 原来玛丽体内潜藏着伤寒杆菌, 但她本人却无任何症状, 她成了长期的 " 病原携带者 ", 一旦玛丽与别人密切接触, 就能将体内潜藏的伤寒杆菌传染给周围健康的人们, 让别人患病, 而她自己则安然无恙伤寒玛丽

4 Typhoid Fever Acute proliferation inflammation caused by typhoid bacilli. 急性增生性炎 The predominant pathological change is generalized proliferation of monocular phagocytes of mononuclear phagocyte system (MPS). 单核巨噬细胞系统增生 Lesion is most pronounced in the ileum lymphoid tissues. 回肠淋巴组织

endotoxin Typhoid Fever H antigen O antigen Vi antigen

5 Etiology and pathogenesis Pathogen typhoid bacilli (Salmonella typhi ), G - lesion was caused mainly by endotoxin Typhoid Fever H antigen O antigen Vi antigen Antibody Reservoir: typhoid fever patients bacteria-carrier Widal reaction

6 Salmonella typhi (G - ) H antigen Widal reaction O antigen

7 Typhoid Fever Pathway of spread : Salmonella typhi (dejecta, urine) fly (intermediary) polluted foods, water source mouth digestive tract

8 Pathogenesis bacteria lymphotissue of small intestine Becteremia MPS (10 days) Incubation period Septicemia (1st week) (the 2nd 3rd week) lymphotissue of small intestine form lesion healing (the 4th week)

10 Pathological changesand Clinical pathological connection Pathological changes Inflammation: Acute proliferative inflammation Locus: Mononuclear phagocyte system: ileac 回肠 lymphoid tissues, mesenteric lymphoid node, liver, spleen, marrow and so on. Feature:typhoid typhoid cell typhoid nodule (typhoid granuloma)

11 Pathological changes typhoid cell: large macrophages contain phagocytized erythrocytes, lymphocytes, bacteria, and necrotic cellular debris. typhoid cells aggregates and formed typhoid granuloma or typhoid nodule.

14 Intestinal tract lesions Four pathologic stages: 1. Medulloid swelling 2. Necrosis 3. Ulceration 4. Healing per stage lasts for one week, the total process lasts for about four weeks.

15 Stage of medullary swelling (first week) Swelling of Peyer s patches and the solitary lymphoid node of the ileum and show protrusion like cerebral convolution on the surface.

18 Stage of medullary swelling marked proliferation of macrophages and formation of typhoid nodules

19 marked proliferation of typhoid cell and form typhoid nodules

20 Stage of necrosis (second week) Gross: grayish-white or grayish-green areas

21 Stage of necrosis (second week) Necrosis of Peyer s patches and the solitary lymph follicles of the ileum

22 Stage of necrosis (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

long axis of the intestine, and healing will do not cause

23 Stage of ulceration(third week) The shape of ulcerations is round or oval, margins is slightly elevated elongated parallel to the long axis of the intestine, and healing will do not cause strictures. Hemorrhage and perforation may often occur during this stage.

25 Stage of ulceration(third week)

26 Complications 1) Perforation 穿孔 2) Haemorrhage 出血

27 Healing stage (fourth week) Ulceration is followed by granulation tissue formation, and ultimately epithelia regeneration takes place.

28 Typhoid Fever Intestinal lesion 髓样肿胀期坏死期溃疡期穿孔

Swelling,typhoid granuloma formation and loci necrosis Non-MPS

29 Typhoid Fever Changes of other organs Other MPS: mesenteric lymph node, liver, spleen and bone marrow. Swelling,typhoid granuloma formation and loci necrosis Non-MPS organs a. myocardium b. kidney c. skin d. muscle e. change of gall bladder-chronic carriers

30 Typhoid Fever Diarrhea 腹泻 Clinical feature Continued fever 稽留热 Leukopenia 白细胞减少 The diagnosis can be established by blood and dejecta culture.

31 Typhoid Fever Outcome and Complication Healing Recurrence Complication Hemorrhage and perforation Bronchopneumonia Other

32 小结伤寒杆菌引起的急性传染病以全身单核 - 巨噬细胞系统的巨噬细胞增生为特点的急性增生性炎症, 以回肠末段淋巴组织病变为著 ( 四期 ) 临床表现 : 持续高热, 相对缓脉, 肝脾大, 皮肤玫瑰疹和血白细胞减少等

33 Bacillary dysentery 细菌性痢疾

34 记载, 慈禧 73 岁那年, 为了给这位老佛爷祝寿, 宫廷内忙得不亦乐乎寿诞那天, 请了京城数十名最好的厨师, 置办了 100 多道菜肴, 文武官员近千人欢聚一堂, 为慈禧太后祝寿慈禧那天特别高兴, 她先饮了几杯白酒, 然后吃了不少美味佳肴第二天, 慈禧即感腹痛, 大便次数明显增加, 每天达几十次, 并带有脓血一星期后, 慈禧变得骨瘦如柴, 虽然请了太医切脉诊治, 据说还服了加倍的鸦片, 但病情仍无好转, 鸦片止痛痛不止又过了一个星期, 慈禧陷于昏迷状态光绪三十四年 (1908 年 ) 十月二十二日, 西太后命归黄泉

35 Bacillary dysentery It is pseudomembranous inflammation cansed by dysentery bacilli. Easily occur in summer and autumn. Children or adult may affected. Patient present with high fever, bellyache 腹痛, diarrhoea 腹泻, blood and pus in the stools and tenesmus( 里急后重 ).

36 Bacillary dysentery Etiology and pathogenesis Pathogen: dysentery bacterium, G - S.Flexneri 福氏 S.Sonnei 宋内氏 S.Boydii 鲍氏 S.Dysenteriae 志贺氏 Lesion was mainly caused by endotoxin (exotoxin) and ability of attack Reservoir:patients and bacteria-carrier

37 Reservoir and mode of spread: dysentery bacterium intermediary Fly foods, drinking appliance and hand mouth

38 pathogenesis bacterium stomach large intestine lamina propria breed and release endotoxin Mucosal epithelium inflammatory reaction lesions of intestinal mucosa S.dysenteriae exotoxin absorb enter blood toxemia watery diarrhea

39 Bacillary dysentery Pathological changes Locus:large intestine (sigmoid colon, rectum) Clinical Types 乙状结肠直肠 acute bacillary dysentery acute catarrhal inflammation, pseudomembranous inflammation ulcer chronic bacillary dysentery toxic bacillary dysentery

40 Acute bacillary dysentery acute catarrhal inflammation 急性卡他性炎

41 Acute bacillary dysentery pseudomembranous inflammation Pseudomembrane formation: fibrin, necrotic tissue, neutrophil cells, erythrocyte and bacilli. Gross: gray-white, dirty greenish, overlay intestinal mucosa

43 Acute bacillary dysentery Ulceration formation The ulcers are usually irregular,superficial, different size and shape, like a map Granulation tissue, regeneration of the mucosal epithelium Scar

45 Acute bacillary dysentery Clinically features systemic toxic symptom symptom of digestive tract abdominal cramps --- bellyache 腹痛, diarrhea 腹泻 (stool contains blood, mucus, pus), tenesmus 里急后重 severe cases: vomiting, dehydration 脱水, electrolyte disturbance, shock

46 Chronic bacillary dysentery Usually from acute bacillary dysentery, most cases are infected by S. flexneri. Mixture of new and old lesions in the Intestine. Chronic ulceration formation, polypoid hyperplasia in mucosa, the wall irregular thicken and hard. Clinically: abdominal pain, diarrhea constipation ( 便秘 ), mucus or bloody purulent stool. Some cases become chronic carrier.

47 Toxic bacillary dysentery 中毒性菌痢 Sudden onset Mostly from S.flexneri and S.sonnei Severe systemic toxic symptoms--- toxic shock or respiratory failure Mild pathological changes in intestines, catarrhal or follicular enteritis Children at the age of 2-7 years old

48 中毒性细菌性痢疾 ( 滤泡性肠炎 )

49 小结由痢疾杆菌引起的一种常见肠道传染病病变多局限在末段结肠以大量纤维素渗出形成假膜性炎为特征假膜脱落伴有不规则浅表溃疡形成临床表现为发热, 腹痛, 腹泻, 粘液脓血便和里急后重

50 Parasitosis

51 Lumbricus ( 蛔虫 )

53 Parasitosis 寄生虫病 Three basic link of Infectious disease Reservoir host Pathways of spread Susceptible population The role of parasitosis Rob nutrition Mechanical injury Toxic effect Immunity injury

54 Amoebiasis Amoebiasis is the infection caused by Entamoeba histolytica protozoan ( 溶组织内阿米巴原虫 ). Mostly parasitize at colon or by hematogenous spread to other organs. Intestinal amobiasis (amoebic colitis) --- amoebic dysentery Extraintestinal amoebiasis

55 Intestinal Amoebiases Etiology and pathogenesis Pathogen: Entamoeba histolytica Cysts 包囊 spread Trophozoites 滋养体 lesion small large

56 传染阶段 Cysts 致病阶段 Trophozoites

57 Intestinal Amoebiases Etiology and pathogenesis Cysts stomach end piece of small intestine ileocecum small trophozoites Cysts ( 肠腔型 ) ileocecum colon lesion large trophozoites ( 组织型 ) out of body

59 Pathogenesis Mechanical lesion and phagocytosis Action of contact lysis Action of cellular toxin Bacterial action Susceptivity 易感性 Immuno depression and elusion

60 Intestinal Amoebiases Pathological changes Locus:blindgut 盲肠 ascending colon 升结肠 sigmoid colon 乙状结肠 rectum 直肠 Character: Necrotizing inflammation flask shaped ulcer Staging: acute, chronic

61 Acute phase The initial lesion is located in the surface of intestinal mucosa- crypts 隐窝 of colonic glands. Multiple elevated lesion with grayish- yellow color can be seen necrotic, superficial pinpoint sized ulceration.

62 Intestinal Amoebiases Acute phase The trophozoites penetrate the muscularis mucosa into the submucosa, producing large undermined 潜行性, narrow neck and broad base --- flask- shaped 烧瓶样 ulceration can be seen

63 Flask shaped ulcer --- microscopy

65 Intestinal Amoebiases Acute phase large trophozoites were found between viable tissue and necrotic tissue.

66 large trophozoites were found between viable tissue and necrotic tissue. necrotizing inflammation

68 Complication and clinical features intestinal perforation 肠穿孔 forming regional amoebic peritonitis hematorrhea narrow of intestinal lumen abdominal pain, diarrhoea, stools contain mucus, blood and necrotic tissue. Mostly patients can be heal, fewness transform to chronic phase.

69 Chronic phase The pathological changes are very complicated : new and old lesions, necrosis, ulceration, granulation tissue and scar formation may repeated alternate hyperplasia of epithelium or polyp formation and fibrosis. sometime amoeboma 阿米巴肿 formation can be seen.

70 Extraintestinal amoebiasis Amoebic liver abscess Amoebic pulmonary abscess Amoebic cerebral abscess

71 Amebic liver abscess Solitary or multiple Mostly occurs in the right lobe The abscess contains reddish hue pasty material ( liquefied necrotic tissue and old blood) likened to jam It has irregular shaggy wall, due to incompletely liquefied necrosis.

72 Amoebic liver abscess

74 Clinical manifestation Right upper quadrant abdominal pain, fever, liver enlarged and tenderness 触痛, weight loss, and night sweats. May rupture into other organs and tissue form amoebic abscess and amoebic inflammation. e.g. amoebic lung abscess, pleural and peritoneal cavity, and so on.

78 第二节血吸虫病 schistosomiasis

80 日本血吸虫病晚期病人腹壁静脉曲张脐周静脉曲张, 有海蛇头现象骨瘦如柴腹大如鼓

81 基本病理变化尾蚴性皮炎 : 一般在尾蚴钻入皮肤后数小时至 2~3 日内发生, 表现为局部瘙痒的小丘疹, 数日后可自然消退镜下见真皮充血出血及水肿, 起初有嗜中性及嗜酸性粒细胞浸润, 以后主要为单核细胞浸润目前认为主要与 I 及 IV 型变态反应有关童虫在体内移行到肺引起充血水肿点状出血及白细胞浸润成虫引起的损害 : 死亡虫体周围组织坏死, 大量嗜酸性粒细胞浸润, 形成嗜酸性脓肿

82 虫卵引起的损害 : 虫卵沉着所引起的损害是最主要的病变虫卵主要沉着于乙状结肠壁直肠壁和肝 1 急性虫卵结节 : 是由成熟虫卵引起的一种急性坏死渗出性病灶肉眼观为灰黄色粟粒至绿豆大的小结节镜下见结节中央常有 1~2 个成熟虫卵其周围是一片无结构的颗粒状坏死物质及大量嗜酸性粒细胞浸润, 状似脓肿, 故也称为嗜酸性脓肿随后虫卵周围产生肉芽组织层, 其中有以嗜酸性粒细胞为主的炎症细胞浸润随着病程的发展, 肉芽组织层逐渐向虫卵结节中央生长, 并出现围绕结节呈放射状排列的类上皮细胞层, 嗜酸性粒细胞显著减少, 构成晚期急性虫卵结节, 这是向慢性虫卵结节发展的过渡阶段

83 (2) 慢性虫卵结节 : 急性虫卵结节经 10 余天后, 卵内毛蚴死亡, 由它分泌的抗原物质消失, 病灶内坏死物质逐渐被巨噬细胞清除, 虫卵崩解破裂随后病灶内巨噬细胞变为类上皮细胞和少量异物巨细胞, 病灶周围有淋巴细胞浸润和肉芽组织增生, 形态上似结核样肉芽肿, 故称为假结核结节, 即慢性虫卵结节最后, 结节纤维化玻璃样变, 中央的卵壳碎片及钙化的死卵可长期存留

84 肝脏肝虫卵随门静脉血流到达肝汇管区, 形成急慢性虫卵结节, 导致血吸虫肝硬化, 但不形成明显假小叶是其特点肉眼, 肝表面不平滑, 可见粗大的结节状隆起显著的门静脉高压临床上常出现腹水巨脾食管静脉曲张等后果

85 小结掌握伤寒的基本病变肠道病变特点及其并发症掌握急性细菌性痢疾肠阿米巴病及阿米巴肝脓肿的病变特点理解伤寒菌痢及肠阿米巴病的病因和发病机制引起肠道溃疡的疾病有哪些? 其主要病变特点是什么你学过的疾病中, 有哪些能够形成感染性肉芽肿? 分别描述肉芽肿的病理变化

86 绪论第一章细胞组织的适应和损伤第二章损伤的修复第三章局部血液循环障碍第四章炎症第五章免疫性疾病第六章肿瘤第八章心血管系统疾病第九章呼吸系统疾病第十章消化道疾病第十一章肝胆胆道及胰腺疾病第十二章淋巴造血系统疾病第十三章泌尿系统疾病第十四章生殖系统和乳腺疾病第十五章内分泌系统疾病第十六章神经系统疾病第十八章传染病及真菌病第十九章寄生虫病

Microsoft PowerPoint - Diseases of gastrointestinal system (教材審查) [相容模式]

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