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At least 109 records · Page 6Linked to original sources
PubMed1978

Development of inactivated vaccine for Akabane disease.

Virus inactivated by formalin or beta-propiolactone was superior to that inactivated by ether and heating in immunogenicity to mice. There were no significant differences in the antibody response of mice among such adjuvants as aluminum phosphate gel, aluminum hydroxide gel, and sodium arginate gel. When cattle were immunized with vaccine inactivated by formalin and adsorbed to aluminum phosphate gel, an excellent effect was obtained by injection with two doses of 3 ml each given at a 4-week interval. It was also suggested that mice and guinea pigs might be available for the potency test of vaccine. When calves and pregnant goats were injected with vaccine in the same manner as mentioned above, they were prevented from viremia and fetal infection caused by challenge virus. Even when stored at 4 degrees C for 12 months, vaccine was found to retain its stabilized immunogenicity. When pregnant cows were injected with vaccine in the field, the positive rate of neutralizing antibody was 88.5% in the 2 months after the first injection. When other pregnant cows were injected twice with vaccine, this rate was 34.6, 100, 65.4, and 45.8% in the 1, 2, 6, and 10 months, respectively, after the first injection. In another experiment, the antibody levels attained declined rather rapidly in several months. A single dose of vaccine given one year later provoked a rapid antibody response. The vaccination caused no clinical symptoms, abnormal birth, or decrease in milk yield in these cows.

Animals↗
PubMed2005

Changes in relative species compositions of biting midges (Diptera: Ceratopogonidae) and an outbreak of Oropouche virus in Iquitos, Peru.

Species compositions of Culicoides paraensis (Goeldi) (Diptera: Ceratopogonidae), the major vector of Oropouche virus to humans in Central and South American urban cycles, and Culicoides insinuatus Ortiz & Leon differed along a northeast-to-southwest transect across Iquitos, Department of Loreto, Peru. The relative distributions of the species were consistent with patterns of human outbreaks along the Amazon River. We resumed collection of biting midges between May 2000 and January 2004 at three sites previously sampled (1996 -1997) to determine whether the known vector was expanding its range relative to the earlier survey. C. paraensis did not replace C. insinuatus across the region surveyed. Instead, C. insinuatus dominated the more southern sites and significantly increased its relative proportion at all three sites. Apparently, microhabitat differences and not range expansion by C. paraensis were responsible for differences in species compositions across the sample sites.

Animals↗
PubMed1988

Myopathy and encephalopathy in chick embryos experimentally infected with Akabane virus.

Chick embryos infected with Akabane virus by the yolk sac route at 6 days of incubation developed polymyositis and encephalitis. At 3 to 7 days after inoculation, skeletal muscles had myotubule degeneration, clumping of muscle cell nuclei, and infiltration of heterophils; dysplasia and aplasia were evident at 9 to 15 days after inoculation. Changes in the cerebral neostriatum and optic lobes at 2 to 11 days after inoculation included necrosis of primordial nervous tissue, hemorrhages, and hyperplasia of the vascular endothelial cells. Cavities were in nervous tissue subsequent to encephalitis. Hydranencephaly and vascular wall thickening were found 13 and 15 days after inoculation. Embryos infected intravenously at 15 days incubation had foci of encephalitis 3 to 6 days after inoculation, including neuronal degeneration, neuroglial hyperplasia, vascular endothelial proliferation, and heterophil infiltration.

Anencephaly↗
PubMed1996

Hydranencephaly, cerebellar hypoplasia, and myopathy in chick embryos infected with aino virus.

Pathogenesis of Aino virus (AIV), a suspected causative agent of congenital abnormalities of calves, has not yet been established by experimental infection of dams. To investigate the pathogenesis, 10(3) median tissue culture infective doses per 0.2 ml of AIV strain JaNAr 28 was inoculated into the yolk sac of 8-day-old chick embryos. At 4, 7, 10, and 13 days post-inoculation (PI) 20 eggs were opened and macro- and microscopic studies combined with virus recovery and immunohistochemical detection of the virus antigen were performed. At 7 to 13 days PI chick embryos manifested marked hydranencephaly, cerebellar hypoplasia, arthrogryposis, and scoliosis, with the highest incidences of 86.7%, 73.3%, 80.0%, and 20.0%, respectively. At 4 days PI the viral antigen was found in nerve cells, gitter cells in mild necrotic foci of the central nervous system (CNS), degenerative myotubules, and macrophages in the interstitium, which was associated with the early phase of AIV-induced encephalitis and polymyositis, with occasional accompanying hemorrhage and clumping of myotubular fragments. From 7 to 10 days PI, AIV antigen increased markedly in the liquefactive necrosis and in both degenerative and normal-looking myotubules in conjunction with developing hydranencephaly and arthrogryposis. The encephalitis and myositis had a tendency to mitigate by 10 days PI, coincident with a slight decrease in amount of AIV antigen. At 13 days PI there was almost no detectable AIV antigen in CNS and skeletal muscles, probably due to depletion of cells having affinity to AIV.

Animals↗
PubMed1988

Akabane disease in sheep.

Perinatal lamb mortality, associated with malformations of the CNS due to Akabane viral infection, occurred in 4 of 9 flocks of ewes lambing on 3 farms between 26 May and 14 November, 1976. Cases were restricted to ewes conceiving prior to the second week of March and lambing between 26 May and 19 July. As judged by seroconversion in sentinel flocks on 2 of the farms, field infection with Akabane virus occurred mainly between mid-February and mid-April. Malformations of the CNS occurred in 42.5%, 51.2%, 100% and 31.0% of the dead lambs examined in the affected flocks respectively. Prevalence in the 4 affected flocks, expressed as the proportion of ewes lambing which delivered at least one malformed foetus, was 6.1%, 8.4%, 88.9% and 5.7% respectively. Lamb mortality due to malformations of the CNS was 7.1%, 5.5%, 92.3% and 5.7% of lambs born. Age-specific prevalence was calculated for 3 of the 4 flocks and 2-year-old ewes accounted for 71.4% and 76.9% of total cases respectively in 2 flocks, whereas in one flock malformations occurred at equivalent frequencies throughout several older age groups. Birthweights of affected lambs were usually significantly lighter than those of unaffected lambs of similar sex and birth-type, and their mean duration of gestation was slightly, and significantly, prolonged. Micrencephaly (88.1% of cases) and hydrocephalus (68.7% of cases) were the outstanding pathological features of the malformations with hydranencephaly, microgyria, porencephaly and attenuation of the spinal cord occurring at much lower frequencies.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The etiology of arthrogryposis (multiple congenital contracture).

In laboratory animals, prenatal contractures have been induced by viruses, neuromuscular blocking agents, toxins, insecticides, hyperthermia, and limb immobilization. In agricultural animals, prenatal contractures are related to pregnant animals foraging on plants containing toxic alkaloids. Epizootics of prenatal contractures in cattle have been related to Akabane viral infections, which can now be prevented by vaccination. Human arthrogryposis (multiple congenital contracture) may occur in any synovial joint in a large variety of combinations. Several lethal syndromes commonly associated with prenatal contractures (Pena Shokeir 1 and 11, Potter's) provide supportive evidence for the following concept of prenatal contracture etiology. Evidence is provided that indicates that the following multiple etiologic factors are related to production of human arthrogryposis: mutagenic agents, mitotic abnormalities, toxic chemicals or drugs, hyperthermia, neuromuscular blocking agents, and mechanical immobilization. These multiple factors mediate their effect via the central nervous system (craniospinal motor neuraxis), motor end-plates, or by primary degeneration of muscle. The resultant effect is loss of muscle mass with imbalance of muscle power at the joints, which provokes a collagenic response (Law of the Connective Tissue). The collagenic response consists of partial replacement of muscle volume and collagenous thickening of the joint capsules. The latter process leads to joint fixation.

Abnormalities, Drug-Induced↗
PubMed1987

Akabane epizootics in New South Wales: evidence for long-distance dispersal of the biting midge Culicoides brevitarsis.

In 1983 an outbreak of Akabane disease occurred in calves in New South Wales between Coolah and Dunedoo at the foothills of the Liverpool Range, from Molong to Oberon in the Blue Mountains and in the Bylong Valley. These areas, at the time of infection of the dams, were in a drought and conditions were unsuitable for the multiplication of C. brevitarsis. In late March meteorological phenomena developed producing air movements favourable for transporting infected midges from the Hunter Valley. A re-examination of the data from the epizootics of 1974 and 1955 showed that similar weather systems had developed. It is possible that the source of infected midges in these epizootics was also the Hunter Valley.

Animals↗
PubMedDate not supplied

[Outbreak of oropouche virus fever in Serra Pelada, municipality of Curionópolis, Pará, 1994].

In the final of November 1994, an outbreak of a febrile disease was observed in the Serra Pelada gold mine (5 degrees 35'S: 49 degrees 30'W) in the Southeast region of Pará State. Twenty samples were collected and sent to the laboratory of Arbovirus of Instituto Evandro Chagas. The tests showed that the disease was caused by Oropouche virus (Bunyaviridae, Bunyavirus, Simbu serological group). Between 8-22 December 296 serum samples were taken (54 from febrile patients, 16 paired samples and 242 from contacts and convalescent patients) of the 73 familiar groups. From febrile patients, ten Oropouche virus strains were obtained. From paired serum, six seroconversions were obtained and 242 other Oropouche infections were diagnosed by HI and MAC ELISA. The clinical-picture of febrile disease accompanied by severe bedache, chills, myalgia, photophobia retrobulbar pain and malaise was observed. Involvement of central nervous system was not observed. Based on the serological data, we estimated that in the outbreak of Serra Pelada around 5,000 cases occurred corresponding to a prevalence of 83%.

Adolescent↗
PubMed1988

Arboviruses recovered from sentinel cattle using several virus isolation methods.

A group of 20 sentinel steers was bled weekly for 5 months in 1986 and the blood samples were examined for arboviruses by inoculation firstly into embryonated chicken eggs (ECE), baby mice, Aedes albopictus cells and BHK21 monolayers. A second group of cattle was similarly examined for virus in 1987, except that baby mice were not used. Viruses were recovered from 26% of the 878 weekly bleeds. The viruses identified consisted of 14 types belonging to the bluetongue, epizootic haemorrhagic disease (EHD), Palyam and Simbu groups with a single isolation of bovine ephemeral fever virus. The ECE system was found to be the best for isolating bluetongue and Simbu viruses, though the eggs were not usually killed by the inoculum. The ECE and A. albopictus systems were equally sensitive for recovering EHD viruses, while Palyam group viruses were most efficiently isolated in BHK21 monolayers.

Animals↗
PubMed2001

Phylogeny of the Simbu serogroup of the genus Bunyavirus.

The Simbu serogroup of the genus Bunyavirus, family Bunyaviridae contains 25 viruses. Previous serological studies provided important information regarding some but not all of the relationships among Simbu serogroup viruses. This report describes the nucleotide sequence determination of the nucleocapsid (N) gene of the small genomic segment of 14 Simbu serogroup viruses and partial nucleotide sequence determination of the G2 glycoprotein-coding region (encoded by the medium RNA segment) of 19 viruses. The overall phylogeny of the Simbu serogroup inferred from analyses of the N gene was similar to that inferred from analyses of the G2 protein-coding region. Both analyses revealed that the Simbu serogroup viruses have evolved into at least five major phylogenetic lineages. In general, these phylogenetic lineages were consistent with the previous serological data, but provided a more detailed understanding of the relatedness amongst many viruses. In comparison to previous phylogenetic studies on the California and Bunyamwera serogroups of the Bunyavirus genus, the Simbu serogroup displays much larger genetic variation in the N gene (up to 40% amino acid sequence divergence).

Nucleocapsid↗
PubMed1982

Transmission of Oropouche virus from man to hamster by the midge Culicoides paraensis.

Oropouche virus (arbovirus family Bunyaviridae, Simbu serological group) was experimentally transmitted from man to hamster by the bite of the midge Culicoides paraensis. Infection rates and transmission rates were determined after the midge had engorged on patients with viremia. The threshold titer necessary to enable infection or transmission by the midges was approximately 5.3 log10 of the median lethal dose of the virus in suckling mice per milliliter of blood. Transmission was achieved 6 to 12 days after C. paraensis had taken the infective blood meal. This represents conclusive evidence of transmission of an arbovirus of public health importance to man by a member of the Ceratopogonidae family.

Animals↗
PubMed1998

Rapid detection of antigenic diversity of Akabane virus isolates by dot immunobinding assay using neutralizing monoclonal antibodies.

Akabane (AKA) virus is an arthropod-borne virus belonging to the Simbu group of the genus Bunyavirus. Neutralizing monoclonal antibodies (MAbs) against AKA virus were prepared, and the neutralizing epitopes of the virus were defined by competitive binding assay. Five distinct antigenic domains were identified and were designated A, B, C, D, and E. Domains A and C consisted of two epitopes each. It was demonstrated that seven neutralizing epitopes exist on the G1 glycoprotein of AKA virus. Dot immunobinding assays (DIAs) were performed with MAbs which recognize these seven neutralizing epitopes. The results were similar to those obtained by enzyme-linked immunosorbent assay. DIAs were performed using two Australian strains, one isolate from Taiwan, and isolates from Japan collected between the years 1959 and 1994, for a total of 63 isolates. The MAb response patterns were divided into five groups: the OBE-1 strain, the JaGAr39 strain, the Iriki strain, a group which consisted of features between those of the JaGAr39 strain and Iriki strain groups, and a group which did not belong to any of these patterns. The isolates which showed patterns similar to that of the JaGAr39 strain were found mostly among the isolates collected in 1974 and 1990, and isolates with patterns of MAb responses similar to the pattern of the Iriki strain were found mostly in the 1985 isolates. Those showing patterns in between were found mostly around 1977, 1987, and 1994. The results show that DIA can be used to effectively compare the antigenicities of AKA virus isolates within a few hours, even with lesser amounts of virus culture than is required for other assays.

Antibodies, Monoclonal↗