Avian paramyxovirus type 1 infection of racing pigeons: 5. Continued spread in 1984

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.     

Evidence for the presence of avian paramyxovirus type 1 in feral pigeons in England and Wales

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.     

Newcastle disease virus isolated from recent outbreaks in Taiwan phylogenetically related to viruses (genotype VII) from recent outbreaks in western Europe

Three major outbreaks of Newcastle disease (ND) occurred in Taiwan in the last three decades (in 1969, 1984, and 1995). Newcastle disease viruses (NDVs) isolated in the three outbreaks, together with those isolated in 1998, were sequenced between nucleotides 47 and 435 of the fusion gene. A phylogenetic tree based on sequences obtained showed that the NDV isolated in 1969 was similar to the genotype III viruses. In contrast, all isolates in 1984 and seven of the eight isolates in 1995, together with all isolates in 1998, fell into the genotype VII. These results suggest that the 1969 outbreak of ND in Taiwan was caused by the genotype III virus, whereas the 1984 and 1995 outbreaks were caused by the genotype VII viruses. To date, the genotype VII viruses have caused many outbreaks in east Asia and western Europe. We suspect that these outbreaks have constituted the fourth panzootic of ND, which is distinct from the third panzootic caused by the "pigeon PMV-1 viruses." NDV isolated in Taiwan in 1984 was the earliest isolation of the genotype VII virus.     

Influenza in swine in Belgium (1969–1986) Epizootiologic aspects

From 1984 until 1986, influenza isolates were obtained from 59 outbreaks of respiratory tract disease in Belgium. In 21 of the outbreaks, H₃N₂-influenza virus isolates, related to the human A/Port Chalmers/1/73 strain were obtained. All other isolates were H₁N₁-influenza virus strains. The prevalence of variants of the human H₃N₂-influenza virus in the Belgium swine population was determined by examining sow sera which had been collected between 1969 and 1984. The results of this serological study showed that, although a Port Chalmers-like strain was associated with outbreaks of respiratory tract disease in swine only since 1984, such strain was already present in the swine population in 1974, when a low percentage of sow sera (7%) reacted with A/Port Chalmers/1/73. Between 1975 and 1984, antibody against this strain were present in 28–61% of the sera. Furthermore, 3–6% of the sera collected between 1971 and 1980 reacted with the A/Hong Kong/1/68 strain. There were no indications that more recent human H₃N₂-strains (A/Texas/1/77, A/Bangkok/1/79 and A/Belgium/2/81) circulated in the Belgian swine population.     

Review of the literature on avian influenza A viruses in pigeons and experimental studies on the susceptibility of domestic pigeons to influenza A viruses of the haemagglutinin subtype H7

The scientific literature of the past century is reviewed on fowl plague (presently termed highly pathogenic avian influenza, HPAI) in pigeons. HPAI viruses cause epidemic disease outbreaks with high rates of losses in many avian species, particularily in chickens and turkeys. Also susceptible to disease are quails, guinea fowl, ducks, geese, ostriches, passerine birds, and birds of prey whereas conflicting reports on the susceptibility of the domestic pigeon exist. Based on literature reports and on own experiments, and applying as criteria for judgements clinically overt forms of disease, virus multiplication plus shedding and seroconversion, it is concluded that domestic pigeons are only partially susceptible to influenza A viruses of the haemagglutinin subtype H7. Infection of pigeons with H7 viruses results only in some of them in signs, virus shedding and seroconversion. Using the same criteria, pigeons appear to be even less susceptible to infection with influenza A viruses of the H5 subtype. Only one of five publications describe in 1/19 pigeons exposed to H5 influenza A virus depression one day before death, and only 2/19 multiplied and excreted virus, and 1/19 developed circulating antibodies. Consequently, pigeons play only a minor role in the epidemiology of H5 influenza viruses. In contrast, following infection with influenza A virus of the subtype H7 clinical signs in pigeons consist of conjunctivitis, tremor, paresis of wings and legs, and wet droppings. H7-infected pigeons multiply and excrete H7 viruses and develop circulating antibodies. Albeit of the status of infection, free-flying domestic pigeons can act as mechanical vectors and vehicles for long-distance transmission of any influenza A virus if plumage or feet were contaminated.     

Continuing presence of rinderpest virus as a threat in East Africa, 1983-1985

The re-emergence of rinderpest virus in East Africa in 1979 caused widespread outbreaks of disease and subclinical infection throughout the region until mid-1983. Subsequent massive emergency vaccination campaigns have been successful in eliminating clinical rinderpest from Tanzania and preventing its spread southwards. Unfortunately the virus is still endemic in north-eastern Uganda and has recently caused epidemic outbreaks with high mortality in cattle in that country. In Kenya, buffaloes (Syncerus caffer) in and around the Masai Mara game reserve have developed antibodies to rinderpest virus as recently as late 1984. Although there have been no outbreaks of clinical disease in Tanzania or Kenya from April 1983 to the end of 1985 this serological evidence plus the increasing incidence of clinical outbreaks in Uganda indicate that rinderpest virus still threatens East Africa. The substantial aid which has been provided to the region for rinderpest control must be maintained.     

Avian paramyxovirus type 1 infection in pigeons: recent changes in clinical observations

Since its first appearance in 1984, avian paramyxovirus type 1 has remained an enzootic disease in racing pigeons on Long Island, New York. The clinical presentation of the disease in the autumn of 1987 suggests a decrease in the severity and incidence of neurological signs, with the chief complaint being watery droppings accompanied by poor racing performance. Diagnosis is based upon serology, using hemagglutination-inhibition tests with Newcastle disease or paramyxovirus type 1 virus.     

Characterization of Newcastle disease virus (avian paramyxovirus-1) isolated from pigeons

Newcastle disease virus (avian paramyxovirus-1) was isolated from pigeons in 12 states between May 1984 and December 1985. One of the isolates was from a feral pigeon; the remainder were from privately owned pigeon lofts. Use of monoclonal antibodies showed seven of the eight isolates tested to be indistinguishable from the 1982 and 1983 Great Britain and European isolates. Clinical signs were paralysis, torticollis, tremors, incoordination, and death. Pigeons inoculated with the paramyxovirus-1 isolates intravenously or intramuscularly developed clinical disease identical to that described for natural infection; however, only one pigeon inoculated intranasally developed clinical signs. The mean death time for inoculated pigeons was 9.5 days, with a range of 4 to 25. Virus was shed for up to 20 days. Primary lesions observed on necropsy were gastroenterocolitis and pancreatic necrosis. Chickens experimentally infected by the cloacal, intranasal, or caudal thoracic air-sac route remained healthy. However, the intracerebral pathogenicity index (ICPI) in day-old chickens was similar to that observed with velogenic Newcastle disease virus isolates. Four of six isolates inoculated intravenously into 6-week-old chickens induced neurotropic disease.     

Survey of the pathologic findings in a large production colony of pigeons, with special reference to pseudomembranous stomatitis and nephritis

Pathologic evaluations of pigeons dying between September 1984 and August 1985 are reported for a production colony of 1200-1800 White Carneau and Show Racer pigeons ranging in age from hatchlings to 12 years. Infectious diseases were the common causes of death in pigeons younger than 1 year; salmonellosis and nephritis were the common causes in pigeons 1-3 years old; and neoplasia and reproductive organ disorders were the common causes in pigeons older than 3 years. Monthly mortality was 2-4% in pigeons fed a cholesterol-containing diet and 0.9% in those fed noncholesterol-containing pellet diets. The increased deaths in the cholesterol-fed birds were attributed primarily to end-stage renal disease and atherosclerosis with secondary complications. The most frequently observed clinical entity in pigeons younger than 6 months was pseudomembrane formation on the oral and pharyngeal mucosa, termed pseudomembranous stomatitis. The definitive etiologic factor was not determined. Although all affected pigeons had similar gross lesions, the cases fell into one of three subsets, suggestive of bacterial, fungal, or viral etiologies. Chronic nephritis occurring as end-stage renal disease was more severe in pigeons fed a cholesterol-containing diet.     

Neurotropism of highly pathogenic avian influenza virus A/chicken/Indonesia/2003 (H5N1) in experimentally infected pigeons (Columbia livia f. domestica)

This investigation assessed the susceptibility of experimentally infected pigeons to the highly pathogenic avian influenza virus (HPAIV) H5N1 that caused recent outbreaks of avian influenza in birds and humans in several countries of Asia. For this purpose 14 pigeons were infected ocularly and nasally with 10(8) EID50 and clinical signs were recorded and compared with five chickens infected simultaneously as positive controls. The chickens demonstrated anorexia, depression, and 100% mortality within 2 days postinoculation. Three of the pigeons died after a history of depression and severe neurological signs consisting of paresis to paralysis, mild enteric hemorrhage, resulting in a mortality of 21%. Gross lesions in these pigeons were mild and inconsistent. Occasionally subcutaneous hyperemia and hemorrhage and cerebral malacia were observed. Microscopic lesions and detection of viral antigen were confined to the central nervous system of these pigeons. In the cerebrum and to a minor extent in the brain stem a lymphohistiocytic meningoencephalitis with disseminated neuronal and glial cell necrosis, perivascular cuffing, glial nodules, and in one bird focally extensive liquefactive necrosis could be observed. The remaining nine pigeons showed neither clinical signs nor gross or histological lesions associated with avian influenza, although seroconversion against H5 indicated that they had been infected. These results confirm that pigeons are susceptible to HPAIV A/chicken/Indonesia/2003 (H5N1) and that the disease is associated with the neurotropism of this virus. Although sentinel chickens and most pigeons did not develop disease, further experiments have to elucidate whether or not Columbiformes are involved in transmission and spread of highly pathogenic avian influenza.     

Paramyxovirus type 1 infections of racing pigeons: 1 characterisation of isolated viruses

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.     

Encephalomyocarditis virus disease of pigs associated with a plague of rodents

An epizootic of encephalomyocarditis virus (EMCV) disease in pigs in the central west of New South Wales in association with a plague of mice (Mus musculus) in 1984 is described. The disease was confirmed in 47 outbreaks in 37 piggeries and 1152 pigs died, representing an overall death rate of 17.4% in pigs considered at risk. The disease was diagnosed in both intensively housed pigs and pigs farmed outdoors, with mortality rates higher in piggeries with less than 50 sows. The age at which pigs died ranged from 4 days to 24 weeks with higher death rates in younger pigs. Serological testing of pigs slaughtered at Blayney abattoir indicated EMCV infection to be more widespread than the disease reported. Mice were present in all piggeries reporting the disease while rats were present in 66% of the outbreaks. The role of rodents as natural reservoirs of EMCV and the possibility of variations in pathogenicity amongst strains of the virus are discussed.     

Serologic detection of the occurrence of avian paramyxoviruses in pigeons

447 blood-serum samples of racing and free living pigeons collected in 11 districts of Czechoslovakia from August 1983 till March 1984 were examined by the haemagglutination inhibition test to the Newcastle disease virus, strain Roakin, to the pigeon PMV-1 and to the PMV-3; 121 of the samples were tested to other serotypes, PMV-2--PMV-9, and to the avian influenza A virus. 58.4% of samples were positive (greater than or equal to 2 log2) to the Roakin strain with the mean titre 3.6 log2 and 65.1% to the pigeon PMV-1 with the mean titre 4.5 log2. All samples tested were negative to other serotypes except two samples of one group positive to PMV-8 with the mean titre 4.3 log2. The titres of HI antibodies to the Roakin strain and to the pigeon PMV-1 were compared. The risk of the transmission and of the readaptation of pigeon virus to poultry was discussed.     

An occurrence of Newcastle disease in pigeons: Virological and serological studies on the isolatesFoyers de maladie de Newcastle chez le pigeon: Etudes virologiques et serologiques sur des souches isolees

The antigenic and pathogenetic relationship between pigeon Newcastle disease virus (NDV) isolates during outbreaks of 1982 in Italy and reference pathogen and non-pathogen NDV-strains were investigated.The pigeon-isolates were slow-eluters and showed a thermostability at 56°C of over 30 min. They proved to be lentogenic as measured by the mean-death-time in chicken-embryos, and between lentogenic and mesogenic as measured by the Hanson test. They failed to produce plaques in chicken-embryo-fibroblasts and showed high pathogenicity for experimentally infected pigeons, low-pathogenicity for quails and were not pathogenic for chickens. They were antigenically different from the LaSota strain as measured by the cross-HI-test and induced considerable seroconversion in inoculated animals. The existence of a lentogenic neurotropic pigeon-pathogenic strain was considered.     

Outbreaks of classical swine fever in Great Britain in 1986

Classical swine fever was confirmed in 10 herds in Britain between April 10 and June 25, 1986 and typical acute disease was seen in nine of them. Serological evidence of exposure to classical swine fever virus was found in a further seven herds which, together with another nine, were slaughtered as dangerous contacts. Altogether 7781 pigs in 26 herds were slaughtered at a cost of 450,101 pounds for compensation alone. In order to detect subclinical disease, the majority of traced herds were blood sampled as well as inspected. A total of 119,169 pigs were inspected in 506 herds and 8302 blood samples were collected. Three primary outbreaks were identified, all attributed to the feeding of unprocessed waste food containing imported pig meat products. There was no spread of disease from two of these primary outbreaks.     

Paramyxovirus-1 in feral pigeons (Columba livia) in Ontario

Paramyxovirus-1 (PMV-1) infection was diagnosed in racing pigeons in Ontario during 1985, but it was not until January 1989, that the virus was isolated from feral pigeons (Columba livia) in this province. During an 18 month period beginning January 1988, a total of 43 feral pigeons was submitted to the Wildlife Diseases Laboratory, Pathology Department, Ontario Veterinary College. A history of neurological signs accompanied most of the birds. Tissues from 29 birds were submitted for PMV-1 isolation. Allantoic inoculation of embryonated chicken eggs yielded PMV-1 in 10 of the pigeons submitted. On the basis of histological criteria, we believe that 12 other birds were also infected with PMV-1.

Gross pathological changes were unremarkable. Lymphplasmacytic interstitial nephritis was observed histologically in all birds from which PMV-1 was isolated. Other lesions seen, in decreasing frequency of occurrence, were lymphoplasmacytic interstitial hepatitis and multifocal hepatic necrosis, lymphoplasmacytic interstitial pancreatitis, nonsuppurative encephalitis and myelitis.

The existence of PMV-1 in feral pigeons poses a potential threat to the poultry population since there is ample opportunity for mingling with poultry under open housing management. There is also a concern that pigeons may harbor the virus, perhaps in the kidney, and become chronic carriers and potential long-term disseminators of the disease.

     

Protection against respiratory disease in calves induced by vaccines containing respiratory syncytial virus, parainfluenza type 3 virus, Mycoplasma bovis and M dispar

A field trial to assess the ability of two vaccines to protect calves against respiratory disease was carried out on a large beef rearing unit in southern England over the two winters of 1983 to 1984 and 1984 to 1985. A quadrivalent vaccine containing the killed antigens of respiratory syncytial virus, parainfluenza virus type 3, Mycoplasma bovis and M dispar or a vaccine containing only the respiratory syncytial virus component were inoculated into 246 and 245 calves, respectively; 245 calves remained as unvaccinated controls. The calves were reared in seven batches and outbreaks of disease occurred in five; significant protection was achieved in the four batches in which disease was associated with respiratory syncytial virus and M bovis infection, together or independently. The death rate from pneumonia was 9 per cent in the control group, 2 per cent in the calves inoculated with the quadrivalent vaccine (P less than 0.001), a protection rate of 77 per cent, and 3 per cent in the calves inoculated with the respiratory syncytial virus vaccine (P less than 0.01), a protection rate of 68 per cent. The proportion of calves receiving treatment for respiratory disease was 38 per cent in the control group, 25 per cent in the calves inoculated with the quadrivalent vaccine (P less than 0.001) and 27 per cent in the calves inoculated with the respiratory syncytial virus vaccine (P less than 0.01). The results show that protection against respiratory disease can be achieved by parenteral vaccination of calves with the appropriate inactivated microorganisms.     

3株鸽源新城疫病毒的分子特征及对鸽的致病性

2011-2013年在新城疫流行病学调查中分离到3株鸽源新城疫病毒(SDS,SD01和SD02),为了进一步了解其生物学特性和遗传进化规律,对3株病毒进行了测序和生物活性分析,并对分离株SDS对鸽的致病性进行了评价.结果表明,毒株SDS基因组全长为15 192 bp,基因排列方式为3'-NP-P-M-F-HN-L-5'...