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Chapter18InfectivediseasesDepartmentofpathology病原微生物通过一定途径进入易感人群的机体所引起的疾病,并能在人群中传播,流行。第一节传染病概论一病原微生物的传播引起传染病的病原微生物：传染病流行过程：传染源传播途径:消化道,呼吸道,虫媒,接触,母婴易感人群二病原微生物致病机制病原微生物损害宿主细胞方式：1.进入细胞－细胞死亡；2.内、外毒素杀伤细胞，释放酶降解组织，损伤血管引起缺血性坏死；3.引起免疫反应，起防御作用，也可诱发超敏反应，引起组织损伤。（一）病毒致病机制只感染特定细胞:病毒损伤宿主细胞方式1抑制宿主细胞DNA，RNA及蛋白合成；2病毒蛋白插入宿主细胞质膜，损害其完整性；3病毒复制溶解宿主细胞；4在细胞表面表达的蛋白质，引起免疫反应—攻击被感染细胞(HBV)；5损伤宿主抗病原微生物能力(HIV-T4)-机会性感染；6杀死一种细胞—导致依赖此细胞的细胞死亡；7引起细胞增生，转化(HBV,HPV,EBV)-肿瘤。(二)细菌致病机制细菌黏附:细菌表面黏附素与靶细胞受体结合；细胞内细菌感染:感染上皮细胞;感染巨噬细胞;既感染上皮细胞又感染巨噬细胞；细菌毒素：endotoxin,exotoxin内毒素:革兰阴性菌细胞壁外层结构中的脂多糖；外毒素:革兰阳性菌产生，神经毒素、细胞毒素、肠毒素，由A和B两个亚单位构成；(三)宿主免疫反应第二节结核病（tuberculosis）1Conception•Chronicgranulomatousinflammationcausedbytuberclebacilli•typicallesion:formationoflocalizednoduleknownastuberclesEtiologicalfactor:bacillustuberculosis:人型,牛型抗酸染色阳性tuberclebacillituberclebacilli(immunofluorescence)routeoftransmission:呼吸道,消化道,皮肤等pathogenesy:1.Pathogenicmaterials:与结核杆菌菌体及细胞壁成分有关a.lipid:cordfactor-破坏线粒体膜;waxD-超敏反应;b.lipoarabinomannan:类似内毒素,抑制IFN-γ激活巨噬细胞,促进巨噬细胞分泌TNF-α,IL-10;c.complement:起调理素作用,利于细菌摄入但不能杀死;d.heat-shockprotein:高免疫源性蛋白质-自身免疫反应;e.tuberculinprotein:具有抗原性-超敏反应;f.caps:与巨噬细胞补体受体CR3结合-细菌识别摄入.巨噬细胞mechanisms上皮样细胞致敏T细胞淋巴细胞干酪样坏死初次感染,未免疫激活,巨噬细胞吞噬,无杀菌活性吞噬,杀菌活性增强细胞因子迟发超敏反应3~6周产生免疫反应组织破坏干酪样坏死肉芽肿ÌÌ类MHC杆菌抗原T细胞受体激活巨噬细胞Basicallylesionpathologicchages(1)Exudativechanges•decreasedresistance,largenumberofbacillus,hypersensitivity•Sero-fibrinousneutrophilcellsmarcrophages•Locationlung,pleurae,synovium,meningestuberclebacilli(2)Proliferativechanges•acquiredimmunity(resistance),smallnumberofbacillus•tubercle：caseousnecrosis，epithelioidcell，Langhansgiantcell，lymphocyte，fibroblast35#CaseousnecrosisepithelioidcelllymphocyteLanghansgiantcellfibroblastepithelioidcellLanghansgiantcellEpithelioidcellssizeoftubercle：0.1mmfusiontuberclenodulefusionwith3~4tuberclenodules(3)Necrosischanges•hugenumberofbacillusandstrongtoxin,vehementhypersensitivity,lowresistance•gross:gray-yellowish,massivecaseation,consolidatedCaseouspneumonianecrosisRelationshipbetweenimmunestatusofbodyandbasicallypathologicfeaturesPathologicStatusofBodyBacillusPathologicChangesImmuneSensitivityNO.ToxicityFeaturesExudativeSero-fibrinousChangeWeakStrongerLargeStrongorSerousProliferativeTubercleChangeStrongerWeakerLittleWeakernoduleNecrosisCaseousChangeWeakVehementLargeStrongnecrosisTransformatingregulationofbasicchangesofTB•healing(1)exudationisabsorbedx-ray：clinically:(2)fibrosis,fibrousencapsulationandcalcificationx-ray：clinically:TuberclenodulessurroundingfibrosisCaseousnecrosissurroundingfibrosiscalcification•Gettingdeteriorative(1)Infiltrativeprogression:producingexudationandcaseousnecrosissurroundingfocusx-ray:focalmarginisunclearclinically:Infiltrativeprogression(2)Solutionandwidespreaddissemination•liquefactionofcaseousnecrosis–formingcavity•Bronchialdissemination-formingnewfoci•Iymphaticdissemination•HematogeneousdisseminationTuberclecavityNewfocioftuberculosisOldfocioftuberculosis2pulmonarytuberculosisClassificationPrimaryandsecondary•Primarypulmonarytuberculosis•firstinfectionbybacilli•children•occasionalyouthprimarycomplex(Ghoncomplex)consistedof•primaryfocus(Ghonfocus):centralcaseousnecrosis•tubercularlymphangitis•tubercularlymphadenitisPrimaryfocustubercularlymphadenitistubercularlymphadeni-tisPrimaryfocustubercularlymphangitisprimarycomplexSwellingoflymphnodeswithcaseousnecrosisPrimaryfocuswithcaseousnecrosisprimarycomplex哑铃状阴影cliniccourse•fibrosisandcalcificationoffocusin95%ofpatients•tuberculosisofbronchiallymphnode•Dissemination:Spreadbybronchialsystem,bloodstreamandlymphvessels.Secondarypulmonarytuberculosis•reinfectionofbacilli•mainlyadult•mechanisms:primaryfocusreactivatingmorethan10yearslaterpresumablygettinglowerofresistanceofpatientDifferentcharacteristicsfromprimarytuberculosis•Constantlocalizationoflesionsintheupperpartoflung–apicalregion•Proliferativefeature–tuberclessurroundingcaseousnecrosis(lesionislocalized)•LongcourseandcomplexpathologicfeaturesPrimaryTBsecondTBBacillifirstre-infectionPatientschildrenadultimmunewithoutbeforewithPathologicprimarycomplexdiverse,freshwitholdFeaturelesionslocalizedInitialfocussubpleuralinaboveorbelowapicaloflungportionofupperorlowerPropertyofmainlyexudationmainlynecrosisLesionandnecrosisandgranulomaDissemi-mainlylymphchanneldevelopmentinlungnationandbloodstreambybronchiCourseshort,healinginmostcaseslong,labile,therapy1.Focalpulmonarytuberculosis•earlylesion•non-activativetuberculosisasymptomatic•locus:2~4cminthesubapicalportionofthelung•sizeofthefocus：0.5~1cmXray2.Infiltrativepulmonarytuberculosis•activatedlesion•mainlyexudationlesionwithcentercaseation•clinic:lowfever,nightsweats,coughing,hemoptysis,tiredness•x–ray:withcatkin-like,cloudingshadowatborderinsubapicalportionoflungInfiltrativeTBInfiltrativeTBInfiltrativeTBoutcome(1)therapeuticsintimeexudateabsorbed,necrosisandproliferationlesionfiberocalcified.(2)tocontinuedevelopmentexpandedcaseationfocus--liquefiction--drainedoffbybronchi–formingacutecavity——closurechroniccavitation——chronicfibro-cavitativepulmo