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At least 19 recordsLinked to original sources
PubMed1975

Rapid diagnosis of Venezuelan equine encephalomyelitis by fluorescence microscopy.

Goat Venezuelan equine encephalomyelitis (VEE) antiserum and normal serum were conjugated and evaluated for staining sensitivity and specificity. Cross-staining with either eastern or western equine encephalomyelitis virus-infected cells did not occur. The baby hamster kidney (BHK-21) cell line when combined with highly specific VEE conjugate detected 100 medium suckling mouse intracerebral lethal doses (suckling mouse LD-50/IC) of the 1B subtype of VEE virus per milliliter of equine tissue suspension. Conjugated goat antiserum was assayed for sensitivity for detection of VEE virus-infected equine serums and tissue suspensions. The BHK-21 cell line was superior to either primary duck embryo fibroblast (DEF) cells or African green monkey kidney (Vero) cells for propagating the GJ9-1BJ subtype of VEE virus.

Animals↗
PubMedDate not supplied

Eastern equine encephalomyelitis outbreak in coturnix quail.

Eastern equine encephalomyelitis (EEE) was the cause of heavy mortality in coturnix quail (Coturnix coturnix) reared commercially in South Carolina. The birds showed depression, tremor, and partial paralysis that advanced into complete paralysis, torticollis, and death within a few hours. The only consistent lesion on necropsy was a catarrhal enteritis in the duodenal area. The disease spread rapidly to all pens throughout the two houses on the farm in all birds over 2 weeks old, and mortality ranged from 40 to 90% in the various pens within the house. Total mortality exceeded 90,000 birds. Age groups on the farm ranged from 1 day to 8 weeks, at which time the birds went for slaughter. It appears that the initial infection was spread by cannibalism. EEE was diagnosed by isolating the virus in fertile eggs and suckling mice, with subsequent identification by complement-fixation. This is the first documented case of EEE in coturnix quail.

Animals↗
PubMed1975

A field study of persistence of antibodies in California horses vaccinated against western, eastern, and Venezuelan equine encephalomyelitis.

As a result of the continuing threat of Venezuelan equine encephalomyelitis (VEE), a study was made to determine if revaccination against VEE (TC-83 vaccine) was feasible and if revaccination could be incorporated into other routine vaccination practices. Of the horses given annual vaccination with bivalent western equine encephalomyelitis (WEE) and eastern equine encephalomyelitis (EEE) vaccine, 57% retained detectable serum-neutralizing (SN) antiboyd titers for VEE 18 months after the initial VEE vaccination was given. Of horses with no record of WEE-EEE vacinnation, 100% retained detectable VEE SN antibody titers over the same period. The VEE geometric mean titer was 25 times greater for horses not previously vaccinated against WEE-EEE than for horses given annual WEE-EEE vaccination at the time of VEE vaccination. In horses vaccinated against VEE 18 months previously, the geometric mean titer increased from 4 to 70 at 48 days after the intitial WEE-EEE vaccination. This increase indicated that similar antigenic factors for VEE are possibly present in bivalent WEE-EEE vaccine. In horses previously vaccinated against WEE-EEE and VEE, the best SN antibody response to VEE revaccination occurred when VEE vaccine was given simultaneously with the bivalent WEE-EEE vaccine. Of 150 serum samples tested by both the SN and the hemagglutination-inhibiton tests, agreement between positive reactions at greater than or equal to 1:10 was 70% for VEE, 81% for EEE, and 87% for WEE.

Animals↗
PubMed1976

Preparation and testing of vaccines prepared from the envelopes of Venezuelan, eastern, and western equine encephalomyelitis viruses.

Envelope components were separated from Venezuelan, Eastern, and Western equine encephalomyelitis viruses after treatment of the virions with detergent. Vaccines prepared from the envelope component were capable of stimulating mice to produce humoral antibodies. Protective efficacy studies were performed using mono-, di-, and trivalent vaccine combinations. These elicited varying degrees of homologous protection, and Eastern and Venezuelan equine encephalomyelitis envelope products appeared to confer protection to mice challenged with Western equine encephalomyelitis virus.

Animals↗
PubMed1976

Host immune responses after administration of inactivated Venezuelan equine encephalomyelitis virus vaccines. I. Description and characterization of adoptive transfer by immune spleen cells.

Cellular immune responses after immunization with a number of inactivated Venezuelan equine encephalomyelitis (VEE) virus vaccines were evaluated in mice by means of an adoptive transfer system. Formalin-inactivated, TC-83 strain VEE virus vaccine was immunogenic and highly effective in protecting recipient mice against challenge with virulent VEE virus. In contrast to immunization with live TC-83 VEE virus vaccine, however, immunization with inactivated VEE vaccine did not provide donor mice with the capacity to transfer adoptive immunity readily. Only when mice were immunized with inactivated VEE vaccine combined with specific adjuvants (particularly complete Freund's adjuvant or Bordetella pertussis) were donors capable of consistently transferring adoptive immunity. The total dose of inactivated VEE vaccine did not appear to influence the capacity to transfer adoptive immunity. On the other hand, weekly boosters of VEE vaccine and/or administration of vaccine with specific adjuvants did markedly influence donor immune responses.

Animals↗
PubMed1976

Host immune responses after administration of inactivated Venezuelan equine encephalomyelitis virus vaccines. II. Kinetics of neutralizing antibody responses in donors and adoptively immunized recipients.

Lymphoid cell responses to immunization with various formalin-inactivated Venezuelan equine encephalomyelitis (VEE) virus vaccines were monitored in mice by assessment of the development of both the neutralizing antibody response in sera of spleen cell donors and the adoptive neutralizing antibody response induced by spleen cell transfer in recipients. Donors immunized intraperitoneally with formalin-inactivated VEE vaccine (a single dose or a dose on three consecutive days) developed early serum neutralizing antibody responses (larger than or equal to 1:88-1:100) by seven days after immunization. Recipients of spleen cells from such mice were, however, incapable of eliciting a neutralizing antibody response (less than or equal to 1:10). Only spleen cells from donors immunized with inactivated VEE vaccine plus adjuvants (particularly complete Freund's adjuvant and Bordetella pertussis) were consistently capable of producing early, high-titer serum neutralizing antibody responses in adoptively immunized recipients (larger than or equal to 1:50-1:120 on day 4). The magnitude of neutralizing antibody responses of donors to inactivated VEE vaccines did not serve as a useful indicator of whether spleen cells from such mice could adoptively induce antibody responses in recipients. Finally, treatment of immune spleen cells with rabbit antiserum to mouse thymocytes, but not with rabbit antiserum to mouse gamma-globulin or normal rabbit serum, abolished the capacity of such cells to transfer an antibody response adoptively.

Adjuvants, Immunologic↗
PubMed1977

Modification of Venezuelan equine encephalomyelitis virus infection in mice by X radiation.

A highly virulent strain of Venezuelan equine encephalomyelitis (VEE) virus produced less severe histopathologic changes in brain tissues of mice previously exposed to sublethal total-body x-irradiation than it caused in nonirradiated mice. Prior exposure to 600 R of x-irradiation virtually eliminated the lesions of vasculitis and encephalitis that were found in the infected nonirradiated control mice. Mean peak brain lesion scores generally decreased as radiation exposure dose was increased. Irradiation of mice before inoculation often decreased median time to death, whereas the severity of pathologic changes in brain tissues from inoculated irradiated mice was often reduced, without significantly altering ultimate host survival. The inflammatory response did not appear to have a significant role in clearance of this virus from the brain. There was no evidence that participation of the immune response contributed to total mortality from VEE virus encephalitis, as indicated by the failure of radiation immunosuppression to reduce mortality. Death apparently was caused by the direct cytocidal effects of VEE virus replication.

Animals↗
PubMed1975

Extension of the mean time to death of mice with a lethal infection of Venezuelan equine encephalomyelitis virus by antithymocyte serum treatment.

The mean time to death of mice infected with Venezuelan equine encephalomyelitis (VEE) virus was increased 2 days by antithymocyte serum (ATS) treatment given 1 day before and 1 day after virus inoculation. Virus assays of blood, brain, and spleen indicated that VEE virus replication was delayed by ATS. Additionally, mice treated with ATS exhibited neurological signs later than untreated mice. During the infection, the percentage of splenic B lymphocytes as determined by surface immunoglobulin staining increased. ATS treatment caused a further elevation of the percentage of splenic B lymphocytes. These results show a selective depletion of the non-immunoglobulin-bearing lymphocyte population during VEE virus infection and support the hypothesis that ATS destroys or alters an important population of cells associated with the normal course of pathogenesis and the replication of VEE virus to high titers in the mouse.

Animals↗
PubMed1976

Virological and serological studies of Venezuelan equine encephalomyelitis in humans.

During the 1971 epidemic of Venezuelan equine encephalomyelitis (VEE) in south Texas, 203 suspect VEE cases were evaluated by the Center for Disease Control. Sixty-seven were confirmed as cases of VEE. Laboratory confirmation was accomplished by isolation of VEE virus from a serum specimen taken during the acute illness in 50 (75%) of the confirmed cases. Serological confirmation was obtained in 17 cases (25%). Virus isolations were most often obtained from sera collected during the first 3 days of illness. Peak serum virus titers (algebraic mean, 10(5-7) suckling mouse intracranial 50% lethal doses [SMICLD50] per ml) occurred on day 2 of illness. One-half of the sera from which virus was isolated contained at least 10(5) SMICLD50/ml, which has been shown to be sufficient to infect some vector mosquitoes. Blood from 13 virus-positive VEE cases was obtained 1 and 11 months after illness. Hemagglutination-inhibiting, complement-fixing, and neutralizing antibodies were formed by all 13 patients 1 month after illness. Hemagglutination-inhibiting antibody titers were essentially unchanged 11 months after illness. Complement-fixing antibody was undetectable 11 months after illness in 23% of cases and was detectable at dilutions of 1:8 or 1:6 in 77%. Neutralizing antibody (measured by log neutralization index) was not detectable 1 year after illness in one person (8%); titers had declined from 1.0 to 2.0 in 46%, were unchanged in 39%, and were not tested in one person (8%). No evidence of intrafamilial spread of VEE virus was obtained in either of two illness and antibody surveys. A randomized household illness and antibody survey of 681 Port Isabel residents revealed an inapparent infection ratio of 1:11 and an overall antibody prevalence of 3.2%.

Adolescent↗
PubMed1978

Intranasal exposure of the Richardson's ground squirrel to Western equine encephalomyelitis virus.

Adult Richardson's ground squirrels were infected with western equine encephalomyelitis virus by intranasal instillation. Mortality followed the instillation of a minimum threshold of 4.7 logs of virus while infection was produced by a dosage of 2.3 logs. The incubation period was from four to seven days, being preceded by a viremic phase. Signs were depression, ataxia and paralysis of the limbs. Highest titres of virus were recovered from the brain and histopathological changes involving the central nervous system included meningitis, vasculitis, perivascular cuffing, gliosis, neuronophagia and neuronal degeneration. The virus was also found in a variety of extraneural tissues. Lesions in extraneural tissues included necrosis of brown fat and an apparent increase in number of Kupffer's cells in the liver. The lymphoid tissue was involved indicating a possible source for viremia. The duration and magnitude of viremia were ample enough to provide virus source for arthropods. The potential for transmission of the virus independent of arthropods was discussed in view of the pathogenesis demonstrated in the experimental infections.

Animals↗
PubMed1976

Kinetics of heat inactivation of Venezuelan equine encephalomyelitis virus.

Thermal inactivation of Venezuelan Equine Encephalomyelitis Virus (VEEV) was studied at temperatures from 26 degrees to 55 degrees C. Inactivation of infectivity took place by two thermodynamically different reactions, one of which predominated at temperatures below 44 degrees C and the other at higher temperatures. The presence of 1 or 2 M NaCl stabilized the VEE virus at low temperatures but enhanced the inactivation at high temperatures. This latter effect at temperatures higher than 50 degrees C, is associated with the occurrence of two-component survival curves. The different effects of hypertonic NaCl concentrations at the two ranges of temperature, are related to different mechanisms of inactivation operating at each range (protein denaturation and nucleic acid-RNA breakdown). Different kinetics of thermal inactivation at 55 degrees C were observed between virus strains with different virulence. However, no significant correlations was found between the virulence of the eleven VEE virus strains studied and their thermostability at 37 degres and 55 degrees C.

Cell Line↗
PubMed1978

Study of homologous and heterologous antibody response in California horses vaccinated with attenuated Venezuelan equine encephalomyelitis vaccine (strain TC-83).

Of 359 horses vaccinated with attenuated Venezuelan equine encephalomyelitis (VEE) vaccine (strain TC-83), 87% developed hemagglutination-inhibition (HI) antibodies to VEE virus within 1 month. Blood from a subsample of 101 of the 359 horses was obtained over a 1-year period. Within 1 month after vaccination, 84% of the 101 horses had developed VEE HI antibodies, 87% had developed VEE-neutralizing (Nt) antibodies, and 78% had developed VEE complement-fixing (CF) antibodies. One year after vaccination, 58% of the horses had VEE HI antibodies and 73% had VEE Nt antibodies. The percentage of horses with VEE CF antibody titers dropped to a low level (46%) within 6 months after vaccination, and most horses were seronegative for VEE CF antibodies 1 year after vaccination. The presence of antibodies to heterologous (western equine or eastern equine encephalomyelitis, or both) alphaviruses suppressed VEE antibody formation in horses vaccinated with TC-83 vaccine. However, the proportion of horses that developed VEE antibodies exceeded levels that generally were believed adequate to suppress a VEE epizootic in a population. There was an 88% correlation between the HI and Nt tests for VEE antibodies.

Animals↗
PubMed1977

Persistence in humans of antibody to subtypes of Venezuelan equine encephalomyelitis (VEE) virus after immunization with attenuated (TC-83) VEE virus vaccine.

We studied the persistence of antibody to Venezuelan equine encephalomyelitis (VEE) virus subtypes in sera of 20 volunteers inoculated seven or nine years previously with attenuated TC-83 VEE virus vaccine. Serological patterns were compared with those of 10 other persons from whom samples of serum were obtained 28 days after vaccination with TC-83 virus. Vaccines had no other known exposure to a group A arbovirus. Titers of neutralizing antibody of greater than or equal to 1:10 were measured against the homologous TC-83 strain of virus in all long- and short-term vaccinees. In both groups of vaccinees the percentage of antibody-positive persons and their geometric mean titers of antibody to the epizootic subtypes I-A, I-B, and I-C were higher than titers to the enzootic subtypes I-D, I-E, II, III, and IV. However, proportionally fewer long-term vaccinees than short-term vaccinees had detectable neutralizing antibody reactive with enzootic strains. These results reveal long-lasting circulation of neutralizing antibody to TC-83 virus and closely related epizootic variants in 95%-100% of vaccinees. The relatively lower rate of antibody conversion and the loss of antibody to more antigenically remote enzootic subtypes of VEE virus suggest that vaccinees may be less well protected against infection by these strains.

Antibodies, Viral↗
PubMed1977

Antibody studies in ponies vaccinated with Venezuelan equine encephalomyelitis (strain TC-83) and other alphavirus vaccines.

Serologic studies in 24 ponies indicated that prevaccination antibodies to Venezuelan equine encephalomyelitis (VEE) virus (strain TC-83) had no influence on hemagglutination-inhibition (HI) antibody stimulation by western equine encephalomyelitis (WEE) or eastern equine encephalomyelits (EEE)-WEE vaccines. However, studies of the effects of VEE neutralizing antibodies on neutralizing antibody stimulation by the heterologous alphavirus vaccines were inconclusive. The VEE, WEE, and EEE antibody responses were studied in 18 VEE-vaccinated (strain TC-83) animals (13 ponies and 5 horses) at 9 to 14 months after challenge of immunity with virulent VEE virus. The VEE HI, and neutralizing antibodies in combination were associated with greater suppression of VEE antibody stimulation than were VEE neutralizing antibodies alone. The VEE geometric mean antibody titers (GMT) increased 26- and 64-fold for HI antibodies and for neutralizing antibodies, respectively, in 5 animals that had prechallenge exposure titers of VEE neutralizing antibodies only. In contrast, the GMT increased only threefold and eightfold for VEE HI antibodies and for neutralizing antibodies, respectively, in 8 animals that had prechallenge exposure titers of both VEE HI and neutralizing antibodies. Five animals which were seronegative for prechallenge VEE antibodies and had survived challenge exposure gave primary VEE-immune response. Protection in these animals may have resulted from high-titer cross-reacting antibodies to WEE or EEE viruses, or both. Changes in the GMT for WEE HI, neutralizing, and complement-fixation antibodies after challenge exposure were statistically insignificant. However, a statistically significant increase in the EEE HI-GMT occurred in ponies that had low (or no) prechallenge exposure titers of VEE antibodies.

Animals↗
PubMed1975

Venezuelan equine encephalomyelitis viral infection of newly hatched chickens and embryonating eggs.

Fewer than 25% of 12-hour-old chicks died after subcutaneous inoculation of 5 strains or intracranial inoculation of 3 strains of Venezuelan equine encephalomyelitis virus. Mortality of embryonating chicken eggs inoculated by the allantoic route decreased from approximately 75% to 35% between 9 and 18 days of incubation, although all 18-day-old embryos died after intraembryonic inoculation. Thus, neither newly hatched chicks nor chicken embryos (unless inoculated intraembryonically) would be of value in safety testing inactivated Venezuelan equine encephalomyelitis viral vaccines.

Animals↗
PubMed1975

Natural infections of Richardson's ground squirrels with western equine encephalomyelitis virus, Saskatchewan, Canada, 1964-1973.

A survey (1964-1973) was conducted on naturally occurring western equine encephalomyelitis (WEE) virus infections of Richardson's ground squirrels (RGS) in agricultural areas of Saskatchewan. The survey included both serology and virus isolation attempts on live-trapped wild squirrels. Throughout the study, seropostive squirrels were found in the known enzootic regions of the province each summer. The infections rate was high (11.6% of 250) in the epidemic year of 1965 and low (less than 2% of 681) in the subsequent non-epidemic years. The maximal seasonal prevalence of seropositive RGS coincided with the time when the squirrel population and aedine mosquito abundance reached their seasonal peaks. Five virus isolations were obtained from the blood and brains of naturally infected squirrels. All isolations were from squirrels collected in June. The early seasonal infections in squirrels could provide a source of virus for Culex tarsalis, the epidemic vector. In view of their abundance in the enzootic agricultural areas and the high annual population turnover, the RGS may play an important role in the natural history of WEE virus in the Canadian prairies.

Animals↗
PubMed1978

Occurrence and distribution of western equine encephalomyelitis in Florida.

Research and surveillance programs relating to the occurrence and distribution of western equine encephalomyelitis virus in Florida, conducted between 1955 and 1976, suggest that the virus is (1) an endemic arbordae, (2) transmitted in a continuous cycle throughout the year by Culiseta melanura mosquitoes, and (3) restricted to fresh water swamps and waterways in central, north, and northwest Florida.

Animals↗