First simultaneous isolation of influenza A virus and duck enteritis virus from commercial ducks in France.
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Biomedical subjects
Publications and source records attributed to D J Alexander.
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During the period July 1983 to June 1985, 76 submissions of material from feral pigeons were received. Five separate submissions resulted in the isolation of an avian paramyxovirus type 1 (A/PMV-1) variant indistinguishable from the virus responsible for the 1058 disease outbreaks confirmed in racing pigeons up to the end of 1984. In addition 11 separate submissions of pigeon sera had haemagglutination inhibition titres of log(2)4 or greater to A/PMV-1 antigen. Feral pigeons from six sites widely distributed throughout England had evidence of A/PMV-1 infection.
The neurotropic disease of pigeons caused by a variant avian paramyxovirus type 1 virus was confirmed in 866 lofts in Great Britain during 1984, in comparison with 192 lofts during July to December 1983. The 1984 outbreaks were spread over 48 counties in England and Wales and three regions in Scotland. The main methods of spread of disease in the 1984 outbreaks appeared to be similar to 1983 with 574 of 866 probably resulting from contact with infected birds at, or travelling to, races or shows. In 791 of 866 (92.5 per cent) outbreaks in 1984 disease was seen only in unvaccinated birds. A further 61 (7 per cent) occurred in inadequately vaccinated birds or birds vaccinated after clinical signs appeared.
The immune response and protection from challenge afforded to adult pigeons by four different vaccination schedules were assessed. Intravenous challenge with a field pigeon isolate was done four weeks after the second of two doses of vaccine given four weeks apart. Little difference in protection was seen between two 0.25 ml and two 0.5 ml doses of oil emulsion vaccine, although the latter produced a slightly higher immune response. In both cases one of 10 challenged pigeons became sick and died. One dose of Newcastle disease virus B1 live vaccine followed four weeks later by 0.5 ml oil emulsion vaccine gave a comparable immune response to two 0.25 ml doses of oil emulsion but only six birds survived challenge. Two doses of Newcastle disease virus B1 vaccine gave a poor immune response and little protection from challenge; all 10 birds became sick and eight died. Assessment of the onset of protection following one dose of either 0.5 ml oil emulsion vaccine or Newcastle disease virus B1 indicated some partial protection in the latter group as early as five days after vaccination. Both groups showed protection at 10 days but by 21 days, although protection was sustained in the oil emulsion group, birds receiving live vaccine were fully susceptible. Measurement of the duration of protection in pigeons given two 0.5 ml doses of oil emulsion vaccine indicated that protection had begun to wane by 40 weeks after the first dose.
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Thirteen viruses isolated from feral birds and one isolated from a domestic duck, obtained in 1979-1980 during a survey of birds in Western Australia, were shown to be Newcastle disease viruses of low virulence for chickens. The binding of mouse monoclonal antibodies, raised against NDV-Ulster 2C to MDBK cells infected with the isolates was assessed using an indirect immunoperoxidase test. Five viruses caused binding of all 9 monoclonal antibodies tested, whereas the other 9 isolates induced binding of only 4 monoclonal antibodies.
During February to July 1984, 23 outbreaks of Newcastle disease were confirmed in chickens in Great Britain. Use of available mouse monoclonal antibodies enabled unequivocal identification of the virus responsible for 22 of the outbreaks as similar to the avian paramyxovirus type 1 (A/PMV-1) virus causing neurotropic disease in pigeons during 1983 and 1984. Epidemiological investigations presented evidence that 19 of these outbreaks occurred either directly or indirectly as a result of spread from diseased pigeons infesting food stores at Liverpool docks. Virus was isolated from carcases of pigeons found among the food and samples of the food itself. The remaining outbreak was shown to involve a virus unrelated to the virus infecting pigeons.
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During July to December 1983 birds in 192 racing pigeon lofts were confirmed as infected with paramyxovirus type 1 virus on the basis of disease signs alone when contact with infected cases was known (10) or with supporting serology (130), virus isolation (eight) or both (44). These outbreaks were mainly concentrated in south Wales (89) and Dorset (40). In all, 29 counties of Great Britain were involved. In the majority of outbreaks (69 per cent) activities associated with racing were strongly implicated in the spread of the disease but trade in birds, stray bird contact, loft visits and contact at shows were also possible methods of spread. Although considerable variation was seen in the pathogenicity of the viruses isolated from affected birds there were no apparent epizootiological links between isolates of similar virulence.
Pathogenicity index tests on 40 paramyxovirus type 1 viruses isolated from field cases of disease in racing pigeons produced a close grouping of the values obtained in intracerebral pathogenicity index ( ICPI ) tests in day-old chicks (mean 1.48, range 1.28 to 1.76) but a much greater variation in intravenous pathogenicity indices ( IVPI ) in six-week-old chickens (mean 0.38, range 0 to 1.81), although 25 out of 40 isolates had an IVPI in the range 0 to 0.3. Isolates with low IVPIs in chickens gave much higher values in intravenously infected adult pigeons. Virulence for chickens was increased by passage through chickens and, regardless of initial IVPI , indices of about 2 were recorded for isolates passaged three to four times. Passage through chickens also increased the virulence for pigeons in the one isolate tested. Pigeons inoculated with isolate 561/83 by intranasal route or by placing birds in contact with infected birds were shown to excrete virus and respond immunologically but no clinical signs were recorded. Isolate 561/83 was shown to readily infect chickens placed in contact with infected pigeons but no disease signs were seen. The clinical signs associated with field disease in racing pigeons could be reproduced in experimental pigeons by intravenous inoculation of virus. Similar clinical signs were seen in chickens infected by the intravenous route.
Viruses isolated from field outbreaks of disease in racing pigeons in continental Europe and Great Britain were shown to be identical by serological tests using conventional chicken antisera and mouse monoclonal antibodies. The pigeon viruses showed high levels of cross-reaction to Newcastle disease virus (NDV) in haemagglutination inhibition tests and Madin-Darby bovine kidney cells infected with pigeon virus isolates bound three out of nine mouse monoclonal antibodies prepared against NDV Ulster 2C. These results confirm their classification in the paramyxovirus type 1 serotype of avian paramyxoviruses. However, the pigeon viruses could be distinguished from more classical paramyxovirus type 1 viruses by the significantly different titres obtained in haemagglutination inhibition tests, the failure of mouse monoclonal antibodies directed against the HN1 epitope of NDV Ulster 2C to inhibit their haemagglutinating activity and a unique binding pattern seen with the nine mouse monoclonal antibodies.
The objective of this international collaborative study was to compare recent swine isolates of influenza viruses and determine whether significant antigenic differences among isolates from different areas of the world could be detected. H1N1 viruses isolated from pigs, birds and humans in 12 different countries were compared in haemagglutination-inhibition assays with post-infection ferret sera and monoclonal antibodies to H1N1 strains. Using A/NJ/8/76 as the reference strain, we found that recent swine isolates from Hong Kong, Italy, Japan, and the USA possess a haemagglutinin virtually indistinguishable from that of viruses typically associated with pigs, i.e., A/NJ/8/76. In contrast, recent swine isolates from several European countries (Belgium, Denmark, France, Federal Republic of Germany, and Spain) were distinguishable from A/NJ/8/76, as demonstrated by tests in the various laboratories. These studies suggest that the H1N1 viruses in pigs are antigenically heterogeneous and that the circulation of particular variants is associated with the geographical location of the animals. These results raise the question of whether these viruses originated from the same source, i.e., pigs, and have undergone antigenic drift or, alternatively, were introduced from other hosts, such as birds.
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Representatives of paramyxoviruses isolated from waterfowl in the U.S.A., goose/Delaware/1053/76, and Japan, pintail/Wakuya/20/78, were shown to be serologically closely related but distinct from other avian paramyxoviruses. Another isolate, from domestic ducks in the U.S.A., was shown to be representative of a further distinct serotype of avian paramyxoviruses. We propose that, in the current system of nomenclature these serotypes be designated PMV-8, for which the prototype strain would be PMV-8/goose/Delaware/1053/76 and PMV-9, for which the prototype strain would be PMV-9/domestic duck/New York/22/78.
Forty Newcastle disease virus strains and isolates could be placed in eight distinct antigenic groups on their ability to induce binding of nine mouse monoclonal antibodies, raised against strain NDV-Ulster 2C, to infected MDBK cells as assessed by an indirect immuno-peroxidase test. Viruses placed in each group appeared to share both biological and epizootiological properties.