流行性乙型脑炎的教育课件ppt （1）

Epidemic Encephalitis B Epidemic Encephalitis B Case reportCase report n History taking： A boy,4 years old，born in the countryside. Fever last for 4 days，convulsion and confusion last about 6 hours. Physical examination：T 40.5，R 30bpm， P 120bpm，BP100/60mmHg. Unconsciousness, conjunctival edema, lungs can be heard wheezes. Muscle hypertonia, knee hyperreflexia, Babinski sign(+) Other history? Accessory examination? AbstractAbstract n Japanese encephalitis(JE), an acute infectious disease caused by the mosquito- borne Japanese encephalitis virus(JEV) and featured as inflammation in brain parenchyma. n Fever, confusion, coma, convulsion,pathological reflex and meningeal irritation . Respiratory failure in severe cases,high mortality,and10% result in permanent neuropsychiatric sequelea. EtiologyEtiology n A single stranded RNA, 40-50nm,11 kilobases genomes.RNA genome is packaged in the capsid protein forming the core of the virus. n The genomes also encodes several nonstructural proteins (NS1,NS2a,NS3,NS4a,NS4b,and NS5) n JEV can be killed by disinfectant,100 2 minutes or 56 30 minutes EtiologyEtiology n Antigenic stability, infection can produce complement-binding antibodies, neutralizing antibodies and hemagglutination inhibition antibodies, contribute to clinical diagnosis and epidemiological investigation EpidemiologyEpidemiology n Sources of infection: JE is a zoonosis, mosquitoes become infected by feeding domestic pigs and wild birds infected with the JEV. JEV is amplified in the blood systems of the domestic pigs and wild birds. Pigs are the improtant amplified and reservoirs. n Other reservior includes cow, sheep, horse,duck,goose and chicken. EpidemiologyEpidemiology n Route of transmission: the bite of an infected mosquito, primarily Culex species. Humans are a dead-end host in the JEV tramsmission cycle. JEV is not transmitted from person-to-person. Only domestic pigs and wild birds are carriers of the JEV. EpidemiologyEpidemiology . n Susceptible population: Generally susceptible, especially residents of rural areas in endemic location, mostly asymptomatic. The ratio of patients and latent infection was 1 :1000-2000 . Pre- existing antibodies. Countries that still have periodic epidemics include India ,Cambodia ,Nepal and so on. EpidemiologyEpidemiology . n Epidemic feature: most cases in temperate and subtropical areas occur from June to September, while in tropical areas occur throughout the year. n Five genotypes : genotypes I ,II ,III, IV,V. Genotypes I and III occur principally in temperate, epidemic areas,and genotype II and IV occur principally in tropical ,endemic regions. Pathogenesis and PathologyPathogenesis and Pathology JEV Mononuclear macrophages multiply viremia Invade the CNS Not invade the CNS Incidence Latent infection This section of brain was taken from a patient with Japanese This section of brain was taken from a patient with Japanese encephalitis, and shows the gross pathology found in all of the encephalitis, and shows the gross pathology found in all of the arbovirus encephalitides. The changes, which consist of perivascular arbovirus encephalitides. The changes, which consist of perivascular congestion and hemorrhage, may be diffuse or focal, but they are congestion and hemorrhage, may be diffuse or focal, but they are seen predominantly in cortical gray and deep gray matterseen predominantly in cortical gray and deep gray matter Pathogenesis and PathologyPathogenesis and Pathology JEV Direct invasion Antigen-antibody binding to the immune attack Nerve cell lesions Vascular sheath formation Thalamus, basal ganglia, brain stem, cerebellum,hippocampus, cerebral cortex Glialcell proliferatio n Show softening lesions, oval-shaped light pale Show softening lesions, oval-shaped light pale area, the structure was loose mesharea, the structure was loose mesh Clinical manifestationsClinical manifestations Incubation period of 5-15 days.the vast majority of infections are asymptomatic,only 1 in 250 infections develop into encephalitis. Typical manifestation:there are four stages The primary stage (1-3 days): onset was sudden with high fever, up to 39-41 in 1-2 days accompanied headache and malaise. Anorexia, nausea,or abdominal pain. Apathy and neck rigidity. Clinical manifestationsClinical manifestations n The proximity stage (fourth to tenth days) Hyperthermia Conscious disturbance Convulsion Respiratory failure Other nervous symptoms and signs Circulation failure Clinical manifestationsClinical manifestations n The proximity stage： Hyperthermia: acute onset; more than 40, lasts 7-10 days generally and some grave cases can last for 3 weeks. The higher temperature, the longer course, the more serious of JE. Clinical manifestationsClinical manifestations n The proximity stage Conscious disturbance： Lethargy, delirium, coma, and disorientation are main presentations Appears mostly at the 3-8 days,lasting for almost 1 week A positive corralation between the serious and the lasting time of coma and the gravity of JE and prognosis Clinical manifestationsClinical manifestations n The proximity stage Convulsion： Causes: high fever, cerebral edema, brain parenchymal inflammation One or more focal/asymmetric signs appearing in the first few days Light : the face, lips, local convulsions, severe cases of the body About 30% of survivors have frank persistent motor language impairment. Clinical manifestationsClinical manifestations Respiratory failure: caused by inflammatory of brain parenchyma, hypoxia, cerebral edema, acute intracranial hypertension and cerebral hernia Cerebral henia： Spitting vomiting, convulsions Coma increased Pupil changes. Anterior fontanel bulging, papilledema Clinical manifestationsClinical manifestations n The proximity stage： Circulation failure: rarely, tachycardia, hyper or hypotension and rarely ECG evidence of pericarditis. Other nervous symptoms and signs: superficial reflex disappears or weakens; deep reflex accentuations first and the disappears and there are symptoms and meningeal irritation. Clinical manifestationsClinical manifestations hyperthermia convulsion Respiratory failure Are critical presentations of JE and respiratory failure is the leading cause of death Clinical manifestationsClinical manifestations n The convalescence stage： Defervescence of fever and neurologic improvement It usually lasts for at least two weeks Clinical manifestationsClinical manifestations n The sequelae stage： the existence of neuropsychiatric symptoms after 6 months 。 The incidence of about 5% to 20%. Axial T2 weighted (TR/TE=2500/90) image. (A) Hyperintense Axial T2 weighted (TR/TE=2500/90) image. (A) Hyperintense lesions at bilateral thalami (arrows) were shown on the 14th days lesions at bilateral thalami (arrows) were shown on the 14th days after onset. (B) Small hyperintense lesions at bilateral thalami after onset. (B) Small hyperintense lesions at bilateral thalami (arrows) on the 60th day after onset(arrows) on the 60th day after onset Clinical manifestations Laboratory examinationsLaboratory examinations n White blood cell: grows up to 1020109/L,neutrophil occupied more than 80%. Some patients have normal WBC counts. n Cerebrospinal fluid (CSF)：lumbar puncture to obtain CSF samples. Laboratory examinationsLaboratory examinations n Cerebrospinal fluid (CSF)：The opening pressure is usually normal but may be raised. Mononuclear white blood cells may be 50500106/L; Glucose levels are normal; Protein levels are mildly elevated in most cases,often less than 900mg/dl Laboratory examinationsLaboratory examinations n Antiboby detection: Specific IgM antibodies is the standard diagnostic test for JE, nearly 100% sensitivity; IgM antibody levels may be found even within 7 days of symptoms. False- negative results may occur if the samples are testd too early. Some cross -reactivity may arise from other flaviviruses and from JE and yellow fever vaccinations Laboratory examinationsLaboratory examinations n Nucleic acid detection: detection of viral genome by RT-PCR is easier to perform and highly reliable with 100% sensitivity , JEV has been isolated up to even almost 4 months after clinical symptoms have begun n Inmaging studies: MRI and CT DiagnosisDiagnosis n Epidemiology data: rigorous seasonality :summer and autumn; less than 10 years old are more susceptible but more adult patients are seen now n Clinical features：acute onset headache, vomitting, hyperthermia, convulsion and positive pathologic reflex and meningeal irritation sign DiagnosisDiagnosis n Laboratory examinations：peripheral blood picture , CSF, serum antibodies,EEG,CT and MRI, brain biopsy n Virological investigation: JEV is difficult to be separated from blood and CSF. JEV antigen can be detected in such body fluid using PCR. Differential diagnosisDifferential diagnosis Toxic bacillary dysentery Tuberculous meningitis Purulent meningitisEncephalitis b OnsetAcute，24 hour peak Chronic,long course 1-2 peak1-2 peak SeasonSummer to autumn Non-seasonalwinter and springSummer to autumn CSFNormal Chloride and glucose are low, high protein, cell count 50*106/L Chloride and glucose are low, high protein, cell count 1000*106/L Chloride and glucose are normal, high protein, cell count 50500*106/L Pathog en Anus dry smear of pus cells, blood cultures of Shigella CSF film smear TB CSF smear staining bacteria CSF bacterial testing was negative. Specific IgM antibodies TreatmentTreatment n General treatment n Symptomatic treatment hyperthermia, convulsion , respiratory failure TreatmentTreatment n General treatment Coma patients should pay attention ： Oral cleaning Prevent secondary bacterial infection Prevent bed sores occur Protect the cornea Anti-falling bed prevent the tongue bitten Note that water, electrolytes, acid-base balance, but not too much infusion volume to prevent brain edema TreatmentTreatment n hyperthermia： Lower the room temperature Physical cooling:ice or alcohol cool saline With convulsions: hibernation therapy (chlorpromazine + promethazine) TreatmentTreatment n convulsion： Cerebral edema: dehydration, 20% mannitol 1-2g / Kg, intravenous infusion, 4-6h time, while combined with adrenal cortex hormones, furosemide, 50% GS, to reduce vascular permeability, Prevention of brain edema and dehydration agent rebound application Respiratory blockage: suction, oxygen, if necessary, tracheotomy TreatmentTreatment n Respriatory failure： Brain edema : dehydrating agent Central respiratory failure: available respiratory stimulants Improve microcirculation, reduce cerebral edema: vasodilators TreatmentTreatment n Respriatory failure： Respiratory secretions Infarct: suction, atomization inhalation of -chymotrypsin; with bronchospasm may be 0.25% -0.5% isoproterenol inhalation. And appropriate treatment with antibiotics such as bacterial infection. If necessary, endotracheal intubation or incision, artificial respiration ventilation TreatmentTreatment n Recovery and sequelae of treatment: acupuncture, physical therapy, hyperbaric oxygen therapy prognosisprognosis n Control the source of infection : Vaccine the pigs before the epidemic season n Cut off the transmission: anti- mosquito, mosquito control. n Protection of susceptible populations, vaccination injections prognosisprognosis n Vaccination injections: the current dosing schedule for patients aged 3 years or older is 1ml subcutaneously on days 0,7,and 30 (0.5ml in patients aged 1-2y). Administer the last dose of vaccine at least 10days prior to travel in an endemic area. n Adverse reactions include local pain and redness, fever, gastrointestinal symptoms, headache Case reportCase report n History taking： A boy,4 years old，born in the countryside. Fever last for 4 days，convulsion and confu