Eastern Encephalitis Research Articles

Far Eastern encephalitis virus

This datasheet on Far Eastern encephalitis virus covers Identity, Distribution, Vectors & Intermediate Hosts.

The economic burden imposed by a residual case of eastern encephalitis.

To estimate the economic burden imposed by eastern encephalitis (EE), we identified a series of residents of eastern Massachusetts who had survived EE infection and enumerated any costs that could be attributed to their experience. The records of three people who suffered only a transient episode of disease were analyzed as well as those of three who suffered severe residual sequelae. Transiently affected subjects mainly required assistance for direct medical services; the average total cost per case was $21,000. Those who suffered persistent sequelae remained at home and seemed likely to live a normal span of years, but without gainful employment. Early in the course of their chronic illness, costs ranged as high as $0.4 million per year, but plateaued at about $0.1 million after three years. Hospital costs, which dominated early in the disease experience, approached $0.3 million per patient. Educational costs tended to replace hospital costs after two years as the dominant economic burden and totaled about $0.3 million per patient during the first six years. Total costs then averaged almost $0.8 million. By the time that these subjects will have reached 22 years of age, disease-related costs will have totaled about $1.5 million. Institutionalization will impose an additional lifetime cost of $1.0 million. Insecticidal interventions designed to avert outbreaks of human EE infection cost between $0.7 million and $1.4 million, depending on the extent of the treated region. The direct costs of an intervention are less than the $3 million imposed on one person suffering residual sequelae of EE.

Emergence of eastern encephalitis in Massachusetts.

The 20th century emergence in Massachusetts of zoonotic eastern encephalitis was interpreted in terms of recorded environmental change. The main mosquito vector of the infection, Cs. melanura, appears to have been scarce in eastern North America before the 1930s. Its relative scarcity resulted from destruction of the swamps that had been lumbered or drained for farming in the 18th and 19th centuries. When swamps matured once again early in the 1900s, the formation of subsurface pools of water beneath mature trees would have increased the availability of breeding sites for this mosquito. Transmission would have further been enhanced by the simultaneous proliferation of wetland-roosting robins and the extinction of such vagile birds as the passenger pigeon. Although numerous horses were maintained in Massachusetts at the time, no outbreaks of "equine sleeping sickness" came to public notice between the 1830s and the 1930s, when mature trees were scarce and the fauna was most disturbed. The severity of the first major outbreak in 1938 may have been potentiated by the absence of herd-immunity in a rapidly proliferating population of reservoir birds. These considerations suggest that recent landscape and faunal changes caused zoonotic EE to emerge in Massachusetts after waning for a century.

Most Alphaviruses Share a Conserved Epitopic Region on Their Nucleocapsid Protein

Fourteen hybridoma cell lines secreting antibodies against the Semliki Forest virus nucleocapsid protein were established and employed for identification of conserved epitopes among 27 alphavirus types and subtypes. Using an antibody capture test, the antibodies were found to cross-react to variable degree with alphaviruses belonging to the Semliki Forest, western encephalitis and eastern encephalitis complexes, as well as Middelburg and Ndumu. None of the antibodies reacted with either Venezuelan equine encephalitis or Barmah Forest virus. Due to their reactivity with Fort Morgan, Y62-33, Whataroa and chikungunya, the monoclonal antibodies were divided into six reactive types. Competition assays showed that the epitopes for all the types were either identical or clustered on a single domain of the nucleocapsid protein.

Arthropod vectors of human disease in the United States

Arthropod vectors of human disease in the United States

Pheasant Susceptibility at Different Ages to Eastern Encephalitis Virus from Various Sources in Massachusetts

Thirteen isolates of Eastern encephalitis (EE) virus recovered from various hosts in Massachusetts differed significantly in pathogenicity for pheasants, 21 days old or older, inoculated subcutaneously with graded doses of virus. Among the least pathogenic were two isolates from Culiseta melanura mosquitoes, and among the most pathogenic isolates was one of pheasant origin. Nine-day-old pheasant chicks were highly susceptible to EE virus. Mortality did not appear to be totally dose-related, for inocula larger than an infecting dose did not increase mortality substantially.

Immunization of Pheasants for Eastern Encephalitis

Pheasants vaccinated twice with as much as one-half horse dose of a commercial Eastern-Western encephalitis adjuvanted cell-culture vaccine did not develop significant hemagglutination-inhibition titers and were not protected against artificial challenge by an Eastern encephalitis virus.

Resolving power in a practical application of preparative sodium dodecyl sulfate polyacrylamide gel electrophoresis: Preparation of Eastern encephalitis virus proteins

Preparative polyacrylamide gel electrophoresis (PAGE) was used to separate the three proteins of Eastern equine encephalitis virus. The effect of gel length and gel concentration on the separation of these proteins was examined systematically. A single trial of preparative PAGE and the relative mobilities from analytical gel electrophoresis of a protein mixture provided the parameters needed to predict the elution times and resolution of the mixture components at other gel concentrations and gel lengths. The practical use of two simple formulas to determine the elution times and resolution of protein mixture components was demonstrated.

Equine viral encephalitis.

The most important neurotropic viral infections of the horse are the arthropod-borne encephalitides. These include Venezuelan encephalitis (VE), eastern encephalitis (EE) and western encephalitis (WE), which are found in the Americas, and Japanese B encephalitis which occurs in the Far East. All the viruses cause encephalitis in man. Between 1969 and 1972 an epidemic of VE occurred in Central America. In 1971 the disease was reported in Texas, where it was brought under control by the vaccination of susceptible horses with an attenuated live virus vaccine and by the reduction of the mosquito population with insecticides sprayed from aircraft. A high titre viraemia occurs with VE virus in the horse and epidemics are maintained by a mosquito/horse cycle; infection of man and other species is incidental. EE and WE have been recognised as separate diseases since 1933 and in the U.S.A. horses are protected by routine vaccination. Epidemics of these diseases are routine vaccination. Epidemics of these diseases are now uncommon. In contrast with VE, both EE and WE viruses are maintained by a bird/mosquito cycle. The viraemia in the horse is generally considered insufficient to infect mosquito vectors; the horse is a "dead end host". Several species of mosquito can act as vectors of VE, WE and EE. The extension of other arthropod-borne diseases to areas originally outside their geographical distribution (e.g. bluetongue in sheep) serves to illustrate the potential of VE, WE and EE to cause disease on other continents.

An attenuated variant of Eastern encephalitis virus: biological properties and protection induced in mice.

Wild type Eastern equine encephalitis virus (E) was compared with a mutant (Em) derived from it. The latter was tested as an attenuated vaccine in mice. They differed in the following properties: Em formed smaller plaques on chick embryo (CE) cell monolayers and, unlike E, did not plaque on mouse embryo (ME) monolayers. Futher, Em had a longer latent period and attained a lower peak titer than E after infection of CE cells, was more senssitive than E to chick interferon, and was less virulent for mice (SC and IP routes) and hamsters (IP route) than E. Both viruses were similar in several other properties tested. The mutant was found to induce a gradient in the specificity of protection in mice against challenge by selected viruses after a single subcutaneous injection of living virus. The protection was best against autologous (Em) challenge, was next best against challenge by the virulent parent (E) virus, but was not demonstrable against cross challenge by Venezuelan encephalitis (V) virus. Conventional hemagglutination-inhibiting (HI), complement-fixing (F), and neutralizing (N) antibodies could not be detected in Em-immunized mice even when fresh monkey or guinea pig serum was included in Ntests to provide complement and/or accessory factor(s). However, N antibodies were detected in protected mice by an indirect antiglobulin test. Passive protection by serum or ascites fluids (a.f.) was characterized by a lower but otherwise similar protection gradient like that found after active immunization with virus as described above. Interferon was not detected in the a.f. used for passive protection, nor was heterologous interference evident in Em immunized mice challenged 18 days later with vaccinia or vesicular stomatitis virus. Immunized mice that survived autologous (Em) challenge showed broadened protection against a second challenge by parent E virus, and cross protection against V virus. This typical protection was associated with the presence of HI and conventional N antibodies, except for V which showed no detectable neutralizing antibodies by either a standard or antiglobulin technique.

Attenuation and immunogenicity of ts mutants of Eastern encephalitis virus for mice.

Preliminary experiments were intiated to test the attenuation for mice of chemically induced temperature-sensitive (Ets) mutants of a virulents strain of Eastern encephalitis (E) virus, and the potential of such mutants as live virus vaccines for mice. The reversion frequencies of eight mutants to temperature insensitivity were measured and the defects in their biosynthesis at the non-permissive temperature were studied. All eight mutants were less virulent for mice, but the extent of avirulence varied with the mutant and route of injection. The mutants selected as potential vaccines protected mice against subsequent challenge at 10 to 21 days by the virulent virus of strain E. Neutralizing antibody activity was detected in almost all the mutant-infected mice after 10 days, and was found in all infected mice at 21 days. Immunization by two doses of virus induced a very high protection against intracerebral challenge by virus strain E.

Density gradient characterization of disrupted and untreated eastern encephalitis virus.

Preparations of eastern encephalitis virus were disrupted by treatment with sodium deoxycholate. Tween 80 and ether, and sodium lauryl sulfate. The effect of these treatments on the viral specific activities of eastern encephalitis virus were studied. Untreated and disrupted preparations of eastern encephalitis virus were physically characterized by buoyant density centrifugation in cesium chloride density gradients and by rate zonal sedimentation in sucrose density gradients. Disruption by both sodium deoxycholate and Tween 80-ether resulted in the release of hemagglutinating subunits of higher density than the hemagglutinin associated with the intact virion. The hemagglutinating subunits released by both treatments were similar in density and size. A dense complement-fixing component, believed to represent released viral nucleoprotein core, was detected in cesium chloride gradients after sodium deoxycholate treatment of the virus. It was not detected in untreated preparations or in preparations treated with Tween 80-ether. Even at low concentrations, sodium lauryl sulfate was destructive of all viral activities save complement-fixation activity. The hemolytic activity of eastern encephalitis virus was physically closely associated with infectivity and hemagglutinating activity of the virus and was apparently dependent on the structural integrity of the virion.

Serologic evidence of Venezuelan equine encephalitis virus infections in raccoons of south central Florida.

A presumed second human case of Venezuelan equine encephalitis (VEE) approximately 175 miles north of the Everglades National Park, prompted an epizootiological survey to document the presence and distribution of VEE virus in small mammals throughout the state. Sera from 339 small mammals from 25 counties in Florida were tested for hemagglutination-inhibiting antibodies against VEE, eastern encephalitis (EE) and St. Louis encephalitis (SLE) viruses. Sera reactive to VEE in HI tests were also examined for neutralizing antibody to VEE and EE. Significant HI and neutralizing antibody to VEE virus was detected in raccoons (Procyon lotor), cotton rats (Sigmodon hispidus), cotton mice (Peromyscus gossypinus) and an opossum (Didelphis marsupialis) in various habitats along the Gulf and Atlantic Coasts of Florida. These data indicated that (1) VEE virus may be widespread in south central Florida; perhaps endemic in Indian River County (2) Raccoons may be excellent indicators of VEE activity in a statewide arbovir...

Latex agglutination test for the detection of arbovirus antibodies.

Polyvinyl latex particles have been successfully used for the detection of eastern encephalitis, St. Louis encephalitis, dengue II and Cache Valley antibodies in human and animal sera. Antibodies detected by latex agglutination are in agreement with the results of haemagglutination inhibition tests. It is claimed that latex agglutination could be used for the detection of some arbovirus antibodies as an easier test.

Serologic study of some infectious diseases of Canada geese.

A serologic study was conducted to investigate the exposure of captive and free-flying Canada geese (Branta canadensis) to five arboviruses, chlamydiae and Mycoplasma gallisepticum. Of more than 1200 serums screened in the metabolic-inhibition test (MIT), no serums neutralized eastern encephalitis virus (EEV), less than 1% neutralized western (WEV) or Venezuelan (VEV) encephalitis viruses, 2% neutralized St. Louis encephalitis virus (SLEV), and 29% neutralized California encephalitis virus (CEV). Supplementary serologic procedures indicated that a nonspecific inhibitor probably caused inhibition of CEV in the MIT. Fifty-six per cent of 197 serums had hemagglutination-inhibition titers of 1:80 or higher against M. gallisepticum and were considered “positive”. Two hundred and eight serums were negative for complement-fixing antibody against chlamydiae.

The Significance of Age of the Chick in Establishing the ICP Index

One of the markers is the intracerebral pathogenicity index (ICPI) for day-old chicks (1). The response of the inoculated chick is scored daily and a numerical value given, such as: dead, 2; sign of disease, 1; and normal, 0. The sum of these values is divided by the number of observations made within a period of 8 days. The reported ICP indices in day-old chicks is 0-0.5 for lentogenic strains, 0.5-1.5 for mesogenic strains, and 1-2 for velogenic strains. These index values depend on many variables-for example, the use of immune or nonimmune chicks. However, with a standard protocol this test has been valuable and reproducible with one reported exception (2). In characterization of lentogenic strains of NDV (3) we observed that ICP indices varied considerably if the chicks used were less than or more than a day old. Chicks 0-8 hours old were more susceptible to the virus than chicks 24-32 hours old. Chamberlain et al. (4) reported that 42-day-old, or wet, chicks were extremely sensitive to strains of western and eastern encephalitis viruses. This report seeks to define the effect of age on the ICP index.

The 1959 outbreak of Eastern encephalitis in New Jersey. 5. The inapparent infection:disease ratio.

Journal Article THE 1959 OUTBREAK OF EASTERN ENCEPHALITIS IN NEW JERSEY: 5. THE INAPPARENT INFECTION: DISEASE RATIO Get access MARTIN GOLDFIELD, MARTIN GOLDFIELD Search for other works by this author on: Oxford Academic PubMed Google Scholar JAMES N. WELSH, JAMES N. WELSH Search for other works by this author on: Oxford Academic PubMed Google Scholar BERNARD F. TAYLOR BERNARD F. TAYLOR Search for other works by this author on: Oxford Academic PubMed Google Scholar American Journal of Epidemiology, Volume 87, Issue 1, January 1968, Pages 32–38, https://doi.org/10.1093/oxfordjournals.aje.a120807 Published: 01 January 1968 Article history Received: 01 March 1966 Published: 01 January 1968

The 1959 outbreak of Eastern encephalitis in New Jersey. I. Introduction and description of outbreak.

THE 1959 OUTBREAK OF EASTERN ENCEPHALITIS IN NEW JERSEY: I. INTRODUCTION AND DESCRIPTION OF OUTBREAK12 MARTIN GOLDFIELD, MARTIN GOLDFIELD Search for other works by this author on: Oxford Academic PubMed Google Scholar OSCAR SUSSMAN OSCAR SUSSMAN Search for other works by this author on: Oxford Academic PubMed Google Scholar 1From the New Jersey State Department of Health, Box 1540, Trenton, New Jersey 08625. 2This work was supported in part by Grants E-2852 and AI-04397 from the United States Public Health Service, Bethesda, Maryland. 3The authors express their appreciation for the support and contributions to these investigations by other members of the New Jersey State Departments of Health and Agriculture, and by all physicians, veterinarians and local health officials in the areas studied. 4Portions of the work reported in this series of papers were presented at the Annual Meeting of the American Public Health Association in San Francisco, California, November, 1960, and received the first Annual Scientific Award of the Laboratory Section. Author Notes American Journal of Epidemiology, Volume 87, Issue 1, January 1968, Pages 1–10, https://doi.org/10.1093/oxfordjournals.aje.a120789 Published: 01 January 1968 Article history Received: 01 March 1966 Published: 01 January 1968

Research Note: Comparative Titration of Eastern Encephalitis Virus in Cell Suspension and in Cultures of Duck Embryo Fibroblasts

Research Note: Comparative Titration of Eastern Encephalitis Virus in Cell Suspension and in Cultures of Duck Embryo Fibroblasts

Antigenic Variants of Arboviruses

Summary A method for monitoring variations in antigenic constitution of arbovirus strains has been developed. The technique is based upon the magnitude of cross neutralization of virus strains by antisera prepared against virus fractions obtained from gradient sedimentation of a single strain. At a specific point in time, antigenically distinct Western encephalitis viral populations were found to coexist within various tissues of an infected mouse. The antigenic nature of such populations was found to be unstable and in a continuous state of flux. Eastern encephalitis virus strains had distinct antigenic properties when stocks were examined directly. The antigenic properties also varied when strains were carried from one passage to another in mice or in tissue culture, or when passaged in parallel in mice and tissue culture. The phenomenon of antigenic variation of strains was explained in part by the differential selection and ultimate accumulation of certain antigen subpopulations over others during virus replication in various tissue or cell types.