Presentation on theme: "Infectious Diseases 1. Infectious disease Infectious diseases are a group of diseases caused by pathogenic organisms and can be epidemic among certain."— Presentation transcript:
Infectious Diseases 1
Infectious disease Infectious diseases are a group of diseases caused by pathogenic organisms and can be epidemic among certain population. Necessary factors for transmission of infectious disease Source of transmission 传染源 Routes of transmission 传染途径 Susceptible host 宿主
Epidemiology: infectious disease is a public condition associated with the socioeconomic conditions. 发展中国家？ The organisms producing diseases in human are various. Major histologic patterns of tissue reaction in infections suppurative inflammation mononuclear and granulomatous inflammation necrotizing inflammation chronic inflammation and scarring
Tuberculosis 结核病 This is the chronic, communicable disease caused by mycobacterium tuberculosis. Tuberculosis is estimated to affect 1.7 billion individuals worldwide, with 8 to 10 million new cases and 1.7 million deaths each year. After HIV, tuberculosis is the leading infectious cause of death in the world. Infection with HIV makes people susceptible to rapidly progressive tuberculosis; over 50 million people are infected with both HIV and M. tuberculosis.
1.Etiology and pathogenesis: The common human strain infects only humans. Patients with pulmonary tuberculosis who cough up bacilli in the sputum are the source of transmitted infections. 痰 The bovine strain of M. tuberculosis infected dairy, causing human infection via contaminated milk. Bovine tuberculosis typically involved the oropharynx or intestine because the organism was ingested in milk.
Components of the M. tuberculosis cell wall (such as cold factor, wax D, complement, heat-shock protein, etc ) and host response(immune response and delayed hypersensitivity) contribute to its pathogenicity.454
2. Basic pathological changes Exudative changes dominate 渗出 — Early infections, numerous mycobecteria, high bacteria virulence, low host immunity and pronouned hypersensitivity. — Serous membrane, synovium, meninx and lung. — Serous or sero-fibrinous inflammation.
Proliferative changes dominate 增生 - 结核结节 — Few organisms, low virulence and high host immunity. —The tubercle-the most characteristic changes in tuberculosis. Typical tubercle (tuberculous granuloma) consists of caseous necrosis in the center,surrounding it by the epithelioid and some Langhan’s giant cells,with a peripheral aggregation of small Lymphocytes and fibroblasts. The tubercle can be isolated or fuse to a large one.
Necrotic changes dominate 干酪样坏死 —Numerous organisms, high bacteria virulence, low host immunity and strange hypersensitivity reaction. —Extensive caseous necrosis Gross : pale yellowish or creamy-white in color,soft and friable, similar to dry cheese. Microscopically: red strained homogeneous amorphic material with cell debris sometimes or slightly granular material Caseous necrosis is equal diagnostic importance in TB. Large areas of caseous necrosis are a sign of TB progression.
—The lesions of tuberculous infection depends on the interaction between the organism and the host(the infecting host, virulence of the organism, the degree of immunity or resistance, and hypersensitivity of the host). —These three basic pathological changes can also interchange according to host conditions. Hence the disease may be manifest different. 变质、渗出、增生 3. Conclusion :
4. Fate of the tuberculosis Healing of tuberculosis lesion 愈合 — Absorption and resolution. 吸收消散 — Fibrosis, fibrous encapsulation and calcification of lesions. 纤维化、纤维包裹及钙化 Exacerbation of tuberculous lesions 恶化 — Infiltration and progression. 浸润进展 —Dissolution and dissemination. 溶解消散
5. Pulmonary tuberculosis 肺结核 The lungs are the most commonly affected by tuber- culosis than any other organs. The pattern of host response depends on whether the infection represents a primary first exposure to the organism or secondary reaction in an already sensitized host. 原发、继发 456
Ⅰ.Primary pulmonary tuberculosis This form occurs when child who has not been previously exposed to tuberculous bacillus or immunised by BCG. So called the childhood type TB, but primary lesion may also occurs in adult at a low rate of the tuberculosis.
Pathology Primary complex (the Ghon complex). The lesion consists of three components — Primary lesion (Ghon focus). — Tuberculous lymphangitis. — Tuberculous lymphadenitis (in the hilar lymph nodes).
Primary pulmonary tuberculosis is usually asymptomatic or manifested as a mild flu-like illness. Clinical features
—In 95% of cases, immunity stops disease progression and healing occurs. The lesions heal by fibrosis and may calcify. —In 5% of cases, rapidly progressive pulmonary disease causing extensive caseous consolidation of the lung, usually occurs only in malnourished or immunodeficient children. The fate of primary pulmonary TB
Caseous necrosis in the hilar lymphadenopathy escape into a systemic vein, either directly or by involvement of the thoracic duct, and via right heart, pulmonary artery, disseminating to the lung. Ⅱ. Acute pulmonary milliary tuberculosis
Large numbers of mycobacteria enter usually one of the pulmonary veins, via left heart, into the arterial systemic circulation and spreading to the general various organs. Gross: multiple,scattered, too small(approximate 1-2mm in diameter), fairly uniform size, round, gray white well demarcated nodules. Microscopically: proliferative changes dominate(formation tubercle, often without giant cells, but with central necrosis. Clinical symptoms: high fever, night sweats, loss of appetite, failure, hepatomegaly and splenomegaly. Ⅲ. Acute systemic miliary tuberculosis Hematogenous disseminated lesions of pulmonary TB
Secondary pulmonary TB is occurrence of the disease in a patient who has a prior primary infection. It usually occurs in an adult as a result either of reinfection or reactivation,with the latter more common. 内源性 Secondary tuberculosis,however,tends to produce more damage to the lungs than does primary tuberculosis. 肺部 The subsequent course of the secondary lesions is variable. Ⅳ、 Second pulmonary tuberculosis 继发性肺结核
① Focal pulmonary tuberculosis 局灶性肺结核 The earliest lesions. The most common site is the lung apex 肺尖, one or more small focus of consolidation. Small epithelioid cell granulemas characterized by caseous necrosis and fibrosis. Usually asymptomatic. They either may heal spontaneously or with therapy, resulting in a fibrocalcific nodule 钙化点.
② Infiltrative pulmonary tuberculosis 浸润型肺结核 This is a most common form in the second pulmonary tuberculosis and usually transformed from focal pulmonary TB. This is a activity pulmonary TB. The heavy exudation and caseous necrosis continue to appear at the periphery focal tuberculous lesion and to cause the lesion enlargement. Complication: irregular acute cavities. 空洞 spontaneous pneumothorax. 气胸 tuberculosis pyopneumothorax. 脓胸 Clinic features: tuberculous toxic symptoms and chronic cough, frequently with hemoptysis.
③ Chronic fibro-cavitative pulmonary TB 慢纤空 This is a most common form of chronic pulmonary TB in an adult. Pathological changes : It may affect one, many or all lobes of both lungs. The upper lobes of lung contains multiple variant sizes, thick-walled chronic cavities. The wall of cavity is lined by a yellow-green caseous material, tuberculous granulation tissue and fibrous tissue successively. There may be coexisting bronchial disseminated many tuberculous lesions and diffuse fibrosis in the pulmonary tissues. Later period, the lung becomes small, indurated,with pleural extensive adhesion, the function of the lung may be severely damaged.
May occur in debilitated immunodeficient or highly sensitized patients. Dissemination large numbers of organisms in the focus via the bronchial tree,and spreading rapidly throughout large areas of lung parenchyma and producing a diffuse bronchopneumonia or lobar exudative consolidation ④ Caseous pneumonia 干酪性肺炎
The caseous necrosis coalescence to form a large solid and spherical mass (usually 2-5cm in diameter), well- demarcated margin, surrounded by fibrous tissue. 与肺癌鉴别 ⑤ Tuberculoma 结核球
⑥ Tuberculosis pleuritis 结核性胸膜炎 According affected feature divide into: 湿性 Moist tuberculous pleuritis (exudative tuberculous pleuritis) This is a exudative inflammation dominate(serious or serofibrinous). Heave serious liquid→hydrothorax. 胸水 heavy fibrin formation→thoracalgia. 干性 Dry tuberculous pleuritis (proliferative tuberculous pleuritis) This is a proliferative lesion dominate. Localized tubercles may form in the visceral pleura, and this may be followed by an tuberculous focus beneath pleura.
A relatively small number of mycobacteria gain entrance the bloodstream (capillary vessel of primary focus) and may be formed latent lesion in the extrapulmonary organs, causing extrapulmonary tuberculosis such as meningitis and tuberculomas of brain, vertebral tuberculosis, renal tuberculosis, intestinal tuberculosis. 脑、骨、肾、肠 6. The extrapulmonary tuberculosis 肺外结核
Typhoid fever 伤寒 464 Typhoid fever is an acute infectious disease caused by salmonella typhi 伤寒沙门菌 with hyperplasia of mononuclear-macrophages in the reticuloendothelium of all over the body 全身单核巨噬细胞系统 (intestinal and the mesenteric lymph nodes, liver, spleen and bone marrow, etc) and corresponding clinic features.
1.Etiology and pathogenesis Pathogen S typhi is a facultative intracellular organism and infects only humans. endotoxin(strong pathogenicity). without exotoxin. Somatic antigen(“o”antigen). Flagellar antigen(“H” antigen)→serum agglutination. Surface antigen (“V1“ antigen) test(wildal’s test). 肥达反应
Source of infection — patients and healthful carriers. 健康携带者 Routes of infection — fecal-oral transmission. 粪口传染 The infection results from contamination of food and water with feces from a symptomatic case or a symptomatic carrier of typhoid. The files are important vectors. 苍蝇
Pathogenesis 1. The ingested bacillus invades the small intestinal mucosa, where it is taken up by macrophages and transported to regional lymph nodes and multiplies in the intestinal lymphoid tissue during the ten days incubation period. 2. At the end of the incubation period, the bacilli enter the bloodstream (endotoxaemia and bacteremic phase, in the first week), resulting in fever headache and muscle aches 肌肉痛. Many tissues may be infested during this phase, blood culture is positive in 95% of case.
3. S typhi reenters the intestinal lumen by way of biliary excretion. The organism reinfects lymphoid tissue in the small intestine causing acute inflammation, necrosis and ulceration (organism direct invasion, endotoxin released by the bacillus, together with delayed hypersensitivity). Stool and urine culture is positive at this stage blood culture is still positive in about 60% of pationts widal’s test is positive. 4. Healing usually begins’ about the end of the third week and is complete by the fifth week in uncomplicated cases.
2.Pathology and clinical features Acute hyperplastic inflammation(hyperplasia of the mononuclear-macrophages). 增生性炎症 The hyperplastic mactophages ingest bacteria, red cells and nuclear debris tend to form a small nodule in lymphoid tissue, such nodule is caused typhoid granuloma and the macrophage is called typhoid cells. 伤寒肉芽肿 、伤寒细胞
Ⅰ. Intestinal lesion 肠伤寒 *Location—terminal ileum and caecum. 回肠末端 *Lymphoid tissue in intestine tract—usually most marked in the Peyer’s patches of the distal ileum and solitary lymphoid follicles of the caecum.
Ⅰ.Intestinal lesion —The stage of medullary swelling (the first week) 髓样肿胀期 Gross: the lymphoid patches initially show an inflammatory swelling and enlargement correspond I shape and extent to the lymphoid patches. Microscopically: the lymphoid patches show congestion, edema, marked proliferation of macrophage and typhoid granuloma formation. Clinic: becteraemia is accompanied by progressive fever, sometimes with a staircase-like rise.
—The stage of necrosis (the second week) 坏死期 The necrosis extends deeply to involve the muscular propria and even the serosal coat. The development of focal necrosis can lead to softening and rupture of the lymphoid patches. Clinic: 5/6 persistent high fever. bradycardia. hepatosplenomegaly. rose—coloured spots in the skin. leukocytopenia. diarrhea.
—The stage of ulceration (the third week) 溃疡期 The mucosal ulcers tend to take the shape and extent of the underlying lymphoid patches (round or oval), and typically occur as longitudinal ulcers overlying the peyer patches in the ileum. Clinic: the general symptoms remission of patients. 症状缓解但 小心穿孔
—The stage of healing (the fourth week) 愈合期 Healing of these ulcerated lesions leaves a smooth scar which never shows any tendency towards stricture formation. 无狭窄 Clinic: the temperature shows a staircase-like descend to recover normal.
Ⅱ.Chages in other organ Typhoid fever is associated with a great variety of lesions which are widely distributed and may arise during the course of the disease or later: they are due to endotoxaemia and bacteraemia.
3.complications 并发症 Severe hemorrhage may occur from the intestinal ulcers. A more serious complication resulting from extensive necrosis is perforation of the small vowel with usually fatal generalized peritonitis. 肠穿孔、腹膜炎 Development of laryngitis, bronchitis and bronchopneumonia may be due to invasion by other bacteria. 支气管性肺炎
Bacillary dysentery 细菌性痢疾 Bacillary dysentery — an acute pseudomembranous inflammation caused by shigella species and a common intestinal infectous disease. 1.Etiology and pathogenesis Pathogen — Shigella species, gram-negative bacilli. The four species of Shigella are pathogenic for humans *Shifella sonnei *Shigella flexneri *Shigella boydii—uncommon *Shigella dysenteriae—produces a severe illness the common species and cause a relatively mild illness
Source of infection —patients and healthful carriers. Routes of infection — atypical fecal — oral transmission. transmitted by food and water contaminated by shigella. flies serve as an important vectors in transmission. Pathogenesis— the organisms invade directly the intestinal mucosa. multiplication in the lamina propria and teleasing the toxin Toxaemia Producing an acute inflammation and tissues injury
2.Pathology and clinical features Location—sigmoid colon, rectum are the most commonly affected area and in severe conclitions all the colon and the terminal ileum can be affected 乙状结肠、直肠 ① Acute bacillary dysentery 急性细菌性痢疾 Initial, acute catarrh inflammation—producing an acute inflam- mation with diffuse hyperemia, edema, punctuate hemorrhage, infiltrating of inflammatory cells (neutrophils), excess mucus secretion and formation superficial erosion in the mucosa
*Pseudomembane is fibrinsuppurative exudate in nature *Just on the surface of the mucosa of affected colon firstly the pseudomembrane patchily distributed and then diffusely cover the mucosa and produce a dirty membranous matter *Under microscope, the pseudomembrane is composed of fibrins, numerous neutrophils admixed with red cells, cell debtis and bacteria 粘液脓血便 *When the seudomembrane sheds, the irregular superficial ulcer appears(maplike ulcers) Follow, pseudomembranous inflammation— Later, the ulcers heal and the patients recover
① Acute bacillary dysentery Clinic appearance Toxaemia—fever, peripheral blood leukocutosis. Inflammatory— abdominal cramping. irritation diarrhea with mucus, blood and pus in the stool. Complication: hemorrhage. perforation(less commonly). dehydration. electrolytic disturbance(in serious cases). Fate: healing (most cases). in some cases, protracted and pass into a chronic condition.
②.Chronic bacillary dysentery Course of disease has been exceeded more than 2 months. Such chronic cases are characterized by repeated injury and repair, ulceration and healing, and can lead to new and old lesions coexist, chronic ulcer formation, polypoid mucosal irregularity with fibrous scarring and subsequent stenosis of the bowel. Clinic appearance: Abdominal pain, chronic diarrhea intestinal obstruction.
③. Toxic bacillary dysentery 中毒型 The most common in children. Often from organism of lower virulence. the onset of disease is sudden. Intestinal lesion is child, showing catarrh enteritis or follicular enteritis. There are severe general toxic symptoms (high fever, convulsion). After onset some hours, toxic shock and coma or brain edema and respiratory failure appear rapidly. 注意并发症