[Experimental investigations in the problem of epidemic encephalitis].
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The neuropathology of 8 cases of S. Paulo south coast epidemic encephalitis (Rocio flavivirus), a new arbo B virus encephalitis, is described. The topographic pattern of the lesions appears to be almost specific. The gray matter is predominantly affected. Interstitial mononuclear infiltration, microglial proliferation and perivascular lymphocytic cuffing were seen. Neuronophagia was seldom seen except during the acute phases of the disease. Throughout the neuraxis, the gray matter was affected to a greater degree than white matter. The more damaged structures, in descending order, were as follows: thalamus, dentate nucleus, substantia inominata, brain stem, spinal cord and basal nuclei. Most of the cases exhibited thalamic inflammatory necrosis. Electron microscopy disclosed in one case virus-like particles, resembling those described in other arbo B viruses in the cytoplasm of thalamic neurons. In this case, virus was isolated from the brain and an immunofluorescence test also showed antigenic material in the thalamic neurons.
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Epidemic of Japanese Encephalitis has occurred in Andhra Pradesh during October-November, 1999 affecting 15 out of 23 districts. In total, 873 cases with 178 deaths have been recorded up to the day 29.11.99. The epidemiological investigation has been done in Anantapur district in western Andhra Pradesh, where the outbreak has started in the third week of October. In the district 47 PHC have been affected. On an average 4.5 per cent of 3175 villages have been affected. Average number of cases per affected village have been 1.5. Rural population has been primarily affected. Age groups 1-14 years including infants have been affected but nearly 86.8% of cases have been among 1-9 year age group. The overall case fatality rate has been 18.4 per cent. Clinical features have been high fever, headache, altered sensorium, convulsions and coma. A marked seasonal onset of a few cases per village and 93.75 per cent of human serum samples collected from hospitalised cases showed the evidence of J.E. virus infection indicating that the present outbreak was due to JE virus. High density of Culex vishnui complex mosquitoes has been observed in the area. All the environmental and ecological conditions, temperature, rainfall and relative humidity have been in favour of JE transmission. Analysis of the data for the last 10 years showed that the human JE cases occurred in Anantapur in September-October months, which shifted to October-November, 99. Prolonged draught conditions were observed till October. Possibly the delayed monsoon and congenial atmospheric conditions after monsoon were favourable to the vector species for extra-human cycle of transmission in 1999. Low level transmission leading to small number of cases continued during the succeeding years every September-October till the present epidemic. In all 24 PHCs and urban towns were identified with 212 cases and 39 deaths till 29.11.99.
There was extensive and exuberant breeding of waterbirds before and during an epidemic of arboviral encephalitis in the Murray Valley of south eastern Australia in 1974. As estimated by haemagglutination inhibition tests on 432 bird sera collected between 4th and 13th February, 1974, infection with Murray Valley encephalitis virus, Kunjin virus and possibly other flaviviruses was concentrated in species of the Order Ciconiiformes (55% positive) and Pelecaniformes (41%), compared with only 5% in Anseriformes. Although Sindbis virus infections were also highest in these 2 Orders (56% and 46%, respectively), the incidence of antibodies was spread more uniformly through other Orders than with the flaviviruses: e.g. Anseriformes, 33%, Podicipitiformes, 27%. As viruses were recovered virtually only from Culex annulirostris mosquitoes, the different patterns of infection seem unrelated to host preference by mosquito species or behavioural response to mosquito attack, and suggest a specific relationship between MVE/KUN and Ciconiiformes and Pelecaniformes. The highest infection rate was 22/25 in mature rufous night herons (formerly nankeen night herons) Nycticorax calendonicus, and here tolerance to mosquito attack was probably a contributing factor. Assays of sera from 13 horses indicated high infection rates both alphaviruses and flaviviruses.
Two major epidemics of viral encephalitis occurred in Asia in 1997 and 1998. The first was a re-emergence of neurovirulent strains of enterovirus 71, which caused severe encephalomyelitis in children in Malaysia, Taiwan and Japan, on a background of hand, foot and mouth disease. Necropsy studies of patients who died of enterovirus 71 infection showed severe perivascular cuffing, parenchymal inflammation and neuronophagia in the spinal cord, brainstem and diencephalon, and in focal areas in the cerebellum and cerebrum. Although no viral inclusions were detected, immunohistochemistry showed viral antigen in the neuronal cytoplasm. Inflammation was often more extensive than neuronal infection, suggesting that other factors, in addition to direct viral cytolysis, may be involved in tissue damage. The second epidemic of viral encephalitis was the result of a novel paramyxovirus called Nipah, which mainly involved pig handlers in Malaysia and Singapore. Pathological evidence suggested that the endothelium of small blood vessels in the central nervous system was particularly susceptible to infection. This led to disseminated endothelial damage and syncytium formation, vasculitis, thrombosis, ischaemia and microinfarction. However, there was also evidence of neuronal infection by the virus and this may also have contributed to the neurological dysfunction in Nipah encephalitis. Some patients who seemed to recover from the acute symptoms have been re-admitted with clinical findings suggestive of relapsing encephalitis. As these two epidemics indicate, the emergence and re-emergence of viral encephalitides continue to pose considerable challenges to the neuropathologist, in establishing the diagnosis and unravelling the pathogenesis of the neurological disease.
Circumstantial evidence implicates the influenza virus as the cause of epidemic encephalitis. Arguments used to refute influenza as the causative agent are examined and a challenge is made to naysayers to implicate a viral agent other than influenza.
To study the morbidity and mortality of inpatients with epidemic encephalitis B (EEB) admitted to No. 1 hospital of Lian Yungang city from 1988-1996, 107 inpatients with EEB in the pediatrics department the hospital were analyzed epidemiologically. Results showed that 107 children with EEB had a proportion of 0.65% to all children admitted in the pediatrics department during that 9 years including 98 cases from the countryside and 9 cases from cities. The ratio was 10.8/1.0 when comparing countryside to city. 87 inpatients (81.3%) of EEB children were below 4 year of age consisting. Most patients were infected in late July or early August in 1990 and 1992 with number of 55 out of 107 (51.4%) that consisted 1.56% and 1.53% of the inpatients in pediatrics those years. It was concluded that EEB had a strict seasonal feature. By comparing data from the first 4 years with the latter 5 years, we noticed that the incidence of the latter had a considerable decrease with more milder cases. The morbidity and mortality of the whole city also appeared a decreasing tendency.
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A St. Louis encephalitis (SLE) epidemic in Florida during 25 weeks in 1990-1, resulted in 222 laboratory-diagnosed cases, an attack rate in the 28 affected counties of 2.25/100,000. Disease risk rose with advanced age, to 17.14/100,000 in persons over 80 years, and all 14 fatal cases were in persons over 55 years (median, 70 years). Community serosurveys in Indian River County, the epicenter of the outbreak (attack rate 21/100,000), showed acute asymptomatic infections in 3.6% of the persons surveyed, with higher rates in persons with outdoor occupational exposure (7.4%) and in clients of a shelter for the indigent (13.3%). A matched case-control study found that evening outdoor exposure for more than 2 h was associated with an increased risk for acquiring illness (odds ratio [OR] 4.33, 95% CI 1.23-15.21) while a number of recommended personal protective measures were protective. Four SLE patients were dually infected with Highlands J virus, the first reported cases of acute infection with this alphavirus. The case-control study provided the first evidence that a public education campaign to reduce exposure had a protective effect against acquiring the disease.
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In 1991, the first epidemic of St. Louis encephalitis (SLE) ever reported in Arkansas resulted in 25 cases in Pine Bluff (attack rate: 44 per 100,000; 95% confidence interval [CI] 28-65). To identify risk factors for SLE viral infection and risk factors for neuroinvasive illness, we conducted a community-based, cross-sectional study of noninfected and asymptomatically infected persons and a case-control study of asymptomatically and symptomatically infected persons. The SLE viral infection rate was similar in all age groups and in all studied census tracts. Risk factors for asymptomatic infection included: living in a low income household (relative risk [RR] = 2.6, 95% CI 1.1-6.0), sitting outside in the evening (RR = 2.1, 95% CI 1.0-4.8), and living in homes with porches (RR = 2.9, 95% CI 0.9-9.3) or near open storm drains (RR = 2.2, 95% CI 1.0-4.9). Compared with asymptomatically infected persons, symptomatic persons were older (odds ratio [OR] for age > or = 55 years = 13.0, 95% CI 1.2-334) and more likely to have a previous history of hypertension (OR = 8.5, 95% CI 1.1-72). Our results indicate that advanced age is the most important risk factor for developing encephalitis after infection with SLE virus. Hypertension and vascular disease may predispose to neuroinvasive disease, but this epidemiologic study has not ruled out the confounding effects of age.
Cases of western equine encephalitis in horses in 1987 in western USA and Manitoba, Canada were examined by backward trajectory analysis of winds. Culex tarsalis mosquitoes infected with western equine encephalitis virus could have been carried on southerly winds from Texas and Oklahoma to northern USA and from there to Manitoba. The presence of the Polar front over North Dakota and Minnesota at the end of July would have led to the landing of Cx. tarsalis in Montana and Wisconsin and prevented further carriage into Manitoba. Temperatures in southern Texas during the winter months (average daily maximum temperatures 19.7 degrees C and higher) would have permitted continuous transmission of western equine encephalitis virus by Cx. tarsalis in this area. Weather factors involved in outbreaks from 1975-88 were analysed to see if epidemics in Manitoba (23 or more cases in horses) could be predicted. The conditions for epidemics could be defined as follows: (a) the number of cases in horses in USA was 98 or more, (b) winds were southerly with speeds 45 kmh-1 or higher, and (c) counts of Cx. tarsalis females/light trap per day were 3.2 or higher. There were 3 or fewer cases in Manitoba, when the number of cases in USA was 27 or less, even when Cx. tarsalis counts were higher than 3.2. With Cx. tarsalis counts below 3 and/or unsuitable winds, or the Polar front further south, the number of cases in Manitoba was between 0 and 17, even when the number of cases in USA was from 38-172. Without information on the extent of infection further south, the weather variables would probably be more useful in excluding the possibility of an epidemic in Manitoba than in predicting one.
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