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At least 19 recordsLinked to original sources
PubMed1994

Analysis of the hemagglutination activity domains of the Venezuelan equine encephalomyelitis and eastern equine encephalomyelitis viruses.

The hemagglutination (HA) domains of the Venezuelan equine encephalomyelitis (VEE) and the eastern equine encephalomyelitis (EEE) viruses providing the interaction of virions and red blood cells were studied with the use of a panel of 17 hemagglutination inhibition (HI) monoclonal antibodies (MAbs). A highly conserved domain (C domain) forming alphavirus-group-reactive MAbs was identified in the E2 protein of the VEE and EEE viruses. These MAbs inhibited HA of the western equine encephalomyelitis, Semliki Forest, Sindbis, Getah, Aura, Chikungunya and Pixuna viruses. The involvement of amino acid residues 59 and 232 in the formation of the C region was demonstrated by sequencing the gene encoding the E2 protein of three escape variants of the VEE virus.

Alphavirus↗
PubMed2001

Response to and efficacy of vaccination against eastern equine encephalomyelitis virus in emus.

OBJECTIVE: To evaluate humoral immune responses of emus vaccinated with commercially available equine polyvalent or experimental monovalent eastern equine encephalomyelitis (EEE) virus and western equine encephalomyelitis (WEE) virus vaccines and to determine whether vaccinated emus were protected against challenge with EEE virus. DESIGN: Cohort study. ANIMALS: 25 emus. PROCEDURE: Birds were randomly assigned to groups (n = 5/group) and vaccinated with 1 of 2 commercially available polyvalent equine vaccines, a monovalent EEE virus vaccine, or a monovalent WEE virus vaccine or were not vaccinated. Neutralizing antibody responses against EEE and WEE viruses were examined at regular intervals for up to 9 months. All emus vaccinated with the equine vaccines and 2 unvaccinated control birds were challenged with EEE virus. An additional unvaccinated bird was housed with the control birds to assess the possibility of contact transmission. RESULTS: All 4 vaccines induced detectable neutralizing antibody titers, and all birds vaccinated with the equine vaccines were fully protected against an otherwise lethal dose of EEE virus. Unvaccinated challenged birds developed viremia (> 10(9) plaque-forming units/ml of blood) and shed virus in feces, oral secretions, and regurgitated material. The unvaccinated pen-mate became infected in the absence of mosquito vectors, presumably as a result of direct virus transmission between birds. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that emus infected with EEE virus develop a high-titer viremia and suggest that they may serve as important virus reservoirs. Infected emus shed EEE virus in secretions and excretions, making them a direct hazard to pen-mates and attending humans. Commercially available polyvalent equine vaccines protect emus against EEE virus infection.

Animals↗
PubMed1993

A rapid diagnostic assay for eastern equine encephalomyelitis viral RNA.

Eastern equine encephalomyelitis virus (EEEV) has been a low-frequency, but serious human and veterinary health problem. Increased frequency of this mosquito-borne virus is anticipated as wetlands are maintained and re-established. Control of EEEV has depended on mosquito abatement in response to increasing frequency of EEEV in the environment. A coupled reverse transcription/polymerase chain reaction assay was designed to rapidly, sensitively, and specifically detect EEEV RNA. The assay successfully detected the viral RNA in a single-blind study of a set of field samples composed of either pooled mosquitoes or bird tissue. These results suggest that it would be practical to use this assay for deciding when and where to implement mosquito abatement.

Animals↗
PubMed1998

Effect of temperature on the development of Culiseta melanura (Diptera: Culicidae) and its impact on the amplification of eastern equine encephalomyelitis virus in birds.

Eastern equine encephalomyelitis virus (EEE) is perpetuated in a maintenance cycle that involves Culiseta melanura (Coquillett) as the enzootic vector and passerine birds as the amplifying hosts. Amplification of virus in any given year requires an influx of nulliparous Cs. melanura in the presence of susceptible avian hosts. We conducted laboratory experiments at constant temperatures from 10 to 34 degrees C to develop thermal heat summation models to predict emergence in nature. Embryonic development progresses slowly at 10 degrees C, and the time to eclosion decreased significantly as temperatures increased to 28 degrees C. High temperature were lethal and eggs failed to hatch at 32 degrees C. The thermal minimum (t0) for embryonic development was 9.38 degrees C, and 38.46 degrees-days (DD) were required for egg hatch. The time for larval development decreased with increasing temperatures. Cs. melanura larvae develop in subterranean habitats (crypts) where water temperatures remain below 20 degrees C throughout the summer. Under controlled conditions, egg hatch to emergence took 8 mo at 10 degrees C, 3 mo at 16 degrees C, and 1 mo at 22 degrees C. The thermal minimum for larval development (t0) was 8.5 degrees C, and 467.29 DD were required from eclosion to adult emergence. Our findings indicate that Cs. melanura is well suited to develop in cold water crypts where the larvae are collected most frequently. The mosquito appears to be bivoltine in the northeast with an overwintering generation of larvae that emerges as a spring brood of adults and a summer generation of larvae that emerges in fall. Higher than normal water temperatures hasten development of the summer generation and increase the probability for amplification of EEE by bringing large numbers of nulliparous mosquitoes into contact with recrudescing virus for subsequent transfer to the growing population of susceptible juveniles. Water temperatures in the crypts also may regulate the northern limit for virus amplification each year.

Animals↗
PubMed2001

Clinical, pathologic, immunohistochemical, and virologic findings of eastern equine encephalomyelitis in two horses.

Natural eastern equine encephalitis alphavirus (EEEV) infection was diagnosed in two adult horses with anorexia and colic, changes in sensorium, hyperexcitability, and terminal severe depression. Myocardium, tunica muscularis of stomach, intestine, urinary bladder, and spleen capsule had coagulative necrosis and perivascular lymphocytic infiltrate. Central nervous system (CNS) lesions were diffuse polioencephalomyelitis with leptomeningitis characterized by perivascular T lymphocyte cuffing, marked gliosis, neuronophagia, and multifocal microabscesses. Lesions were more prominent within cerebral cortex, thalamus, hypothalamus, and mesencephalon. EEEV was identified in the cytoplasm of cardiac myocytes and smooth muscle cells of spleen, stomach, intestine, urinary bladder, blood vessels, and dendritic cells. In the CNS, EEEV-positive cells included neurons, astrocytes, oligodendrocytes, microglia, and neutrophils. EEEV was isolated from the CNS of both horses. The detailed description of the encephalic and spinal EEEV localization and the findings of EEEV in extraneural tissues contribute to the understanding of this important multisystemic zoonotic disease.

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↗
PubMed2001

Habitat preference of host-seeking Coquillettidia perturbans (Walker) in relation to birds and eastern equine encephalomyelitis virus in New Jersey.

Coquillettidia perturbans (Walker) has been implicated as a bridge vector of eastern equine encephalomyelitis virus in North America. Eastern equine encephalomyelitis virus epizootics occur regularly in wild birds in New Jersey with little or no involvement of susceptible dead end hosts even though high populations of Cq. perturbans are present. Several factors may limit eastern equine encephalomyelitis (EEE) virus transfer from birds to mosquito bridge vectors like Cq. perturbans (Walker), including bird/mosquito density, differences in bird/mosquito habitat preference, mosquito host preference, mosquito host-seeking behavior and mosquito avoidance behavior by birds. Our investigations focused on the host-seeking activities of Cq. perturbans at Colliers Mills Wildlife Management Area in Ocean County, New Jersey. We first examined the abundance of host-seeking Cq. perturbans at a height of 1.0 m in each of three habitats: forest, open field and marsh. We collected significantly more mosquitoes in the forest as compared to the marsh. Forest and field collections did not differ significantly from one another nor did field and marsh. Second, we examined the temporal and vertical distribution of host-seeking Cq. perturbans in a sylvan habitat at three heights (1.0, 2.5, and 6.0 m) from dusk to dawn. We found that Cq. perturbans did significantly more host-seeking during the night period than either the evening or morning. Host-seeking mosquitoes also tended to stay near the ground and at no time did they ascend into the forest canopy. Host-seeking Cq. perturbans and their apparent spatial disparity to roosting/nesting birds are discussed as a possible barrier to the transmission of EEE virus in New Jersey.

Animals↗
PubMed1985

Immunological response of chickens to eastern equine encephalomyelitis virus.

The dominant immunoglobulin against eastern equine encephalomyelitis (EEE) virus and its duration and the longevity of the EEE virus haemagglutination inhibition (HI) antibodies were determined in sentinel and 125 immunised and hyperimmunised domestic chickens by enzyme-linked immunosorbent assay and the HI test respectively. The chickens ranged in age from 10 weeks to 18 months, were of varied pedigrees and from different countries. Results show that the HI antibody (IgG) is short-lived. It peaks and disappears within 30 days. The secondary response is dominated by the IgM immunoglobulin which is relatively long-lasting. These results are contrary to classical expectations and were observed in all the chickens studied. If these observations are found to be characteristic of birds generally, the present standard method of EEE virus seroepidemiological surveillance must be modified to be effective.

Alphavirus↗
PubMed1998

Intestinal lesions in a horse associated with eastern equine encephalomyelitis virus infection.

The primary lesions of eastern equine encephalomyelitis (EEE) virus infection in the horse are limited to the brain and spinal cord. Intestinal lesions in addition to the changes in the central nervous system were found in a 6-month-old male Tennessee Walking Horse. One week prior to death, this colt was vaccinated for EEE virus, western equine encephalomyelitis virus, influenza virus, equine rhinopneumonitis virus, and tetanus. The clinical signs consisted of ataxia and rear-end weakness, with a body temperature of 102.8 F. Gross lesions consisted of yellowish discoloration, swelling, edema, and hemorrhage of the brain stem and dark discoloration of the gray matter of the spinal cord. Microscopic lesions in the small intestine were mainly in the muscular layer and consisted of multifocal areas of myonecrosis and lymphomonocytic infiltration with a few focal areas of mild fibrous connective tissue proliferation. Occasional focal mild perivascular lymphocytic infiltration was observed in the submucosa. Lesions in the brain and spinal cord consisted of widespread areas of perivascular lymphomonocytic cuffing, focal areas of necrosis, neutrophilic infiltration, hemorrhage, neuronal degeneration, and gliosis. Hepatic changes consisted of periportal lymphocytic infiltration and mild vacuolar degeneration of hepatocytes. EEE virus was isolated from the intestine and detected by DNA in situ hybridization.

Animals↗
PubMed1994

Evolution of alphaviruses in the eastern equine encephalomyelitis complex.

Evolution of viruses in the eastern equine encephalomyelitis (EEE) complex was studied by analyzing RNA sequences and oligonucleotide fingerprints from isolates representing the North and South American antigenic varieties. By using homologous sequences of Venezuelan equine encephalomyelitis virus as an outgroup, phylogenetic trees revealed three main EEE virus monophyletic groups. A North American variety group included all isolates from North America and the Caribbean. One South American variety group included isolates from the Amazon basin in Brazil and Peru, while the other included strains from Argentina, Guyana, Ecuador, Panama, Trinidad, and Venezuela. No evidence of heterologous recombination was obtained when three separate regions of the EEE virus genome were analyzed independently. Estimates of the overall rate of EEE virus evolution (nucleotide substitution) were 1.6 x 10(-4) substitution per nucleotide per year for the North American group and 4.3 x 10(-4) for the Argentina-Panama South American group. Evolutionary rate estimates for the North American group increased over 10-fold (from about 2 x 10(-5) to 4 x 10(-4)) concurrent with divergence of two monophyletic groups during the early 1970s. The North and South American antigenic varieties diverged roughly 1,000 years ago, while the two main South American groups diverged about 450 years ago. Analysis of multiple strains isolated from an upstate New York transmission focus during the same years suggested that, in certain locations, EEE virus may be relatively isolated for short time periods.

Antigens, Viral↗