encephalitis bdept of infectious disease流行性乙型脑炎bdept传染病（ppt41）课件

Epidemic Encephalitis B Dept. Of Infectious Disease Shengjing Hospital CMU Definition vEpidemic encephalitis B is acute infectious disease caused by encephalitis B virus,usually occurs in summer &fall.The virus is transmitted by mosquito. vPathologic lesions: cerebral parenchyma vClinical feature: high fever altered consciousness convulsion meningeal irritation respiratory failure Etiology vCausative agent: encephalitis B virus genus flavivirus of flaviviridae single strain of positive-sense RNA, virion is spheric, diameter: 15 22nm, vResistance: unstable in environment, Sensitive to heat, disinfectants, ultraviolet rays Etiology vantigenicity: stable hemagglutination inhibiting Ab complement fixing Ab neutralizing Ab Epidemiology vSource of infection domestic animals: pig, horse, dog poultry: chicken, duck, goose. patients: Epidemiology vRoute of transmission insect borne: mosquito biting , vector: mosquito, culex tritaeniorhynchus. Survived winter mosquitoes pigs mosquitoes mosquitoes person pigs Epidemiology vSusceptibility of population: universal susceptible lifelong immunity subclinical infection : overt infection 10002000:1 Epidemiology vEpidemiologic features sporadic from July to Sep. children under 10yrs (26yrs) hypersporadic property Pathogenesis virus mosquito biting replication in mononuclear-phagocyte system (MPS) onset of illness CNS blood stream blood-brain barrier brief viremia subclinical inf. clearance No. of virus of invasion cellular immunity blood brain barrier Pathology vPlace of lesion: all of CNS cerebral cortex, midbrain and thalamus . vPathologic features gross examination: congestion hemorrhage cerebral edema soften focuses Pathology microscopic examination: vascular lesion: endothelial cells swelling, necrosis neuron degeneration & necrosis neurogliocyte hyperplasia & inflammatory cells infiltration, perivascular cuffing , neuronophagia. Clinical manifestation v incubation period:1014 days (421days ) v typical encephalitis B Initial period crisis period convalescent period sequela period Clinical manifestation vInitial period : on the 1st to 3rd days abrupt onset fever with headache , nausea, vomiting lethargy, abdominal pain , diarrhea, Clinical manifestation vCrisis period- on the 4th 10th days high fever: 40, sustained for 710 days. altered consciousness: lethargy, confusion, delirium, stupor, semicoma, coma. convulsion or twitch:(4060%) respiratory failure: 1540% Clinical manifestation central RF: reason of central RF: lesion of cerebral parenchyma (respiratory center injury in oblongata medulla) cerebral edema brain hernia intracranial hypertension hyponatremic encephalopathy Clinical manifestation manifestation of central RF: cacorhythmic breathing (cheyne-stokes breathing, apnea) brain hernia peripheral RF: dyspnea, regular breathing Clinical manifestation Other symptoms & signs of CNS meningeal irritations (neck stiffness Kernigs & Brudzinskis signs positive) Deep tendon reflexes from hyperactive to disappear pathologic reflexes positive limbs paralysis Clinical manifestation vConvalescent period T drop to normal in 25 days neurologic function regain gradually(2W) remain some behavioral & psychologic abnormalities, aphasia, dementia, rigidity paralysis. 6month - sequela Clinical manifestation vSequela period aphasia dementia persistent paralysis Clinical manifestation vClinical type: mild type common type severe type fulminant type Clinical manifestation TAC CV RFDCSQ mild2W + fulminant41deep coma + +death + Laboratory Findings vBlood picture: WBC 1020109 /L neutrophil 80% v Cerebrospinal fluid - aseptic meningitis transparent or slightly cloudy, pressure may be elevated pleocytosis: 50500106/L protein may be elevated mildly glucose and chloride are normal Laboratory Findings vSerological test: specific IgM Ab: blood or CSF, 34d after onset, peak on 2 week ELISA or indirect immunofluorescence complement fixing Ab: 2 week after onset, peak on 56 week, anamnestic diagnosis epidemiologic investigation Laboratory Findings hemagglutination inhibition Ab: 5d after onset, peak on 2 week diagnosis: 4 fold increase in titer epidemiologic investigation neutralized Ab epidemiologic investigation Laboratory Findings vpathogenic test virus isolation: blood, CSF, brain tissue RT-PCR : RNA Diagnosis vEpidemiological data: 79 month 10yrs vClinical manifestation: fever, headache, vomiting, altered consciousness, convulsion, meningeal irritation, pathologic reflexes positive. vLaboratory findings:WBC, CSF, IgM Differential Diagnosis vtoxic bacillary dysentery high fever,convulsion,coma. 24h circulatory failure: early stool examination: WBC, RBC CSF: normal meningeal irritation: negative Differential Diagnosis vtuberculous meningitis CSF, meningeal irritation vpurulent meningitis vother viral encephalitis Treatment vGeneral therapy: Isolation: preventing mosquito biting, T30 nursing: mouth, skin, eye, turn over clapping back sputum aspiration Treatment fluid & electrolyte supplementation adult: 15002000ml/d children: 5080ml/kg/d vSymptomatic therapy high fever: T38 Treatment physical cooling (ice bag, alcohol bathing, cold saline enema) drug cooling antipyretic subhibernation: chlorpromazine 0.51mg/kg/time phenergan 0.51mg/kg/time 46h, 35day Treatment convulsion: fever: cooling brain edema: 20% mannitol 12g/kg/time 50% glucose dexamethason Treatment sedative: valium: adult:1020mg/time children: 0.10.3mg/ kg/ time 10% chloral hydrate: adult:12g/time children: 6080mg/kg/time subhibernation: Treatment respiratory failure: keep airway clear sputum aspiration turn over , clapping back, postural drainage aerosolization inhalation of oxygen Treatment reducing cerebral edema & hernia dehydrate : 20% mannitol :12g/kg/time 50% glucose , vasodilator: 654-2: adult: 20mg/time children: 0.51mg/kg/time 10