Bovine Leukemia Virus Involvement In Enzootic Bovine Leukosis
Arsène BurnyFrançoise BexH. ChantrenngY. CleuterD. DekegelJacques GhysdaelR. KettmannM LeclercqJ. LeunenM. MammerickxDaniel Portetelle
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Bovine leukemia virus
Enzootic
Complement fixation test
Diagnosis of enzootic bovine leucosis is based on detection of antibodies against bovine leukemia virus, BLV. Some ELISA modifications have proved sensitive enough for use in the examination of pooled blood samples from slaughterhouses, milk and pooled milk samples. Suggestions for the standardisation of different ELISA modifications using a common reference serum are presented.
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Enzootic
Bovine leukemia virus
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Complement fixation test
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Complement fixation test
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BLV detection by the syncytial test was performed in 27 heifers experimentally and naturally infected by the enzootic bovine leukosis virus (BLV). The presence of BLV was demonstrated in 94.7% of the animals. The bovine foetal spleen cells (FBS) were found to be suitable for the syncytial test. Positive animals not reacting to infection by the production of anti-BLV antibodies were identified during the syncytial-test investigation. The importance of this finding for the programme of controlling enzootic bovine leukosis on farms is discussed. As suggested by the results, temporary occurrence of anti-BLV antibodies followed by their disappearance can be observed together with a negative result of the syncytial test in some circumstances. The discussion deals with the problems of the determination of anti-BLV antibodies in milk, and/or milk secretion, by the ELISA method.
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Complement‐fixing antibody to Mycoplasma hyopneumoniae in the serums of pigs experimentally infected with enzootic pneumonia was demonstrated by comparing the haemolytic titre of guinea‐pig complement titrated in the presence of heated test serum, M. hyopneumoniae antigen and unheated normal pig serum with the titre obtained when the antigen was omitted. The haemolytic titres against sensitised sheep erythrocytes were determined after a fixation period of 16 to 18 hours at 5°C. When serums, collected at intervals of 3 to 7 days, from 43 pigs exposed to pigs experimentally infected with enzootic pneumonia were tested, 4.6 or more complement units were first fixed 14 to 44 (mean 23.4) days after contact began. Serums collected subsequently fixed from 4.6 to more than 31 complement units. This positive reaction usually persisted until the pigs were killed 4 to 35 weeks after contact began. Thirty‐three had gross enzootic pneumonia lesions and 9 had lung lesions detected microscopically. Serum antibody was not detected in 73 weaned pigs aged 7 weeks in a pneumonia‐free herd but serums from 9 of 15 unweaned piglets aged 9 to 14 days in the same herd, fixed between 3 and 7 complement units.
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The direct, the modified direct and the indirect complement-fixation tests were investigated as methods for the detection of antibodies for the enzootic pneumonia mycoplasma and for Mycoplasma hyorhinis in the serum of infected pigs and of immunized rabbits. Only the modified direct complement-fixation test in which the guinea-pig complement is supplemented with fresh, normal unheated calf serum was suitable for the detection of mycoplasma antibodies in sera of infected swine. Based on the close correlation between the production of typical lung lesions in experimentally infected pigs and the appearance of significant serum antibody titres, the modified direct complement-fixation test provides for the first time a sensitive, specific in vitro method for the detection of enzootic pneumonia in the live pig. This test also permitted the in vitro differentiation of the mycoplasma causing enzootic pneumonia from M. hyorhinis which causes polyserositis. Antibodies in the sera of rabbits were demonstrable by the ordinary direct complement-fixation test. However, in contast to the observation made with swine sera, only a slight quantitative antigenic difference between the enzootic pneumonia mycoplasma and M. hyorhinis was seen when the tests were performed with rabbit serum antibodiies.
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Abstract Conducted three series of infecting the rabbits with bovine leukemia virus (BLV) using milk and blood from cows having enzootic leukemia with different doses of infecting material and different mode of administration showed a high degree of repeatability of the experiment. The obtained results testify to the ability of BLV to successfully overcome the interspecific barrier when ingested by an alimentary pathway with milk, as well as by the direct injection of infected lymphocytes into the bloodstream.
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Abstract Dissemination of oral vaccine baits is a cost‐effective method to contain and control infectious wildlife diseases. The effectiveness of vaccine barriers in slowing or halting disease spread depends on host ecology and landscape variability. However, it is not clear the extent to which the success of vaccine barriers to manage disease may change from an epizootic to an enzootic phase of a disease invasion, nor is it apparent if this depends on the quality and configuration of host habitats. We explore these questions using the raccoon variant rabies virus ( RRV ) as a model system. This zoonotic disease of high concern has been enzootic in eastern North America for decades, pushing into new areas and re‐emerging in previously controlled zones. We use a spatially explicit individual‐based model to assess how levels of oral vaccination and habitat fragmentation affect RRV spread across vaccine barriers during epizootic and enzootic phases. We use space‐time characteristics of infection chains (individual‐to‐individual transmission of RRV ) to compare simulated outcomes. Results indicate that vaccine barriers have the strongest impact on the control of RRV during the epizootic phase. Counterproductively, mid‐levels of immunisation during an enzootic phase lead to more rabies‐induced mortalities than lower or higher vaccination levels. Infection chains spread faster during the epizootic phase. Landscape effects on chain characteristics were more subtle than effects of invasion phase and vaccination. Synthesis and applications . A spatially explicit individual‐based modelling approach to examine mechanisms of raccoon variant rabies virus spread during epizootic and enzootic phases provides insights into efficacy of wildlife disease vaccination efforts. Our results demonstrate the importance of detecting and controlling outbreaks before they become enzootic. We discuss the implications for moving vaccine barriers to push back and decrease the size of enzootic areas.
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Following a 19-year hiatus, Venezuelan equine encephalitis (VEE) reemerged in western Venezuela in December 1992. This outbreak is important in understanding VEE emergence because phylogenetic studies imply that sympatric, enzootic, subtype ID VEE viruses mutated to generate the epizootic/epidemic. Although the 1992-1993 strains belong to subtype IC, a serotype implicated in extensive outbreaks during the 1960s and in 1995, relatively small numbers of human and equine cases occurred in 1992-1993. We, therefore, evaluated the pathogenicity of these Venezuelan enzootic ID and epizootic IC viruses to determine 1) if they exhibit phenotypes like those described previously for more distantly related enzootic and epizootic strains, and 2) if the 1992-1993 outbreak was limited by the inability of these IC viruses to exploit equines as amplification hosts. All strains were virulent in mice and guinea pigs, but were benign for cotton rats, natural hosts of enzootic viruses. However, only the IC strains produced equine disease, with mean peak viremias of 10(5) suckling mouse 50% lethal doses per mL serum, and some titers exceeding 10(7). These viremias approximate those observed previously with VEE strains isolated during more extensive epizootics, suggesting that efficient equine amplification did not limit the scope and duration of the 1992-1993 outbreak. Enzootic ID virus infection protected all horses from challenge with epizootic strain P676, supporting the hypothesis that epizootics bypass regions of enzootic transmission due to natural immunization of equines by enzootic VEE viruses.
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