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Among the consequences of the epidemic of highly pathogenic avian influenza which affected Italy between 1999 and 2000 was an epidemic of Newcastle disease in northern and central Italy. It affected industrially reared poultry, dealer flocks and backyard flocks, with a total of 254 outbreaks notified up to December 31, 2000. Virological investigations yielded virulent isolates of Newcastle disease virus, which produced intracerebral pathogenicity indices ranging from 1.6 to 2.0 and which, on the basis of their monoclonal antibody binding patterns, could be classified as belonging to group C1. The clinical, gross and microscopical findings were typical of Newcastle disease, and different avian species were susceptible to different degrees. Chickens and guinea fowl appeared to be the most susceptible, followed by pheasants, turkeys and ostriches. The epidemiological inquiry highlighted the crucial role of a broiler hatchery in initiating the epidemic, and of dealers in perpetuating it. The control measures imposed by Directive 92/66/EEC are discussed with reference to the outbreaks in backyard flocks.
Vet Rec 2002 May 04
PMID:Newcastle disease outbreaks in Italy during 2000. 1201 48

Outbreaks of highly pathogenic avian influenza caused by H5N1 viruses were reported almost simultaneously in eight neighbouring Asian countries between December 2003 and January 2004, with a ninth reporting in August 2004, suggesting that the viruses had spread recently and rapidly. However, they had been detected widely in the region in domestic waterfowl and terrestrial poultry for several years before this, and the absence of widespread disease in the region before 2003, apart from localised outbreaks in the Hong Kong Special Autonomous Region (SAR), is perplexing. Possible explanations include limited virus excretion by domestic waterfowl infected with H5N1, the confusion of avian influenza with other serious endemic diseases, the unsanctioned use of vaccines, and the under-reporting of disease as a result of limited surveillance. There is some evidence that the excretion of the viruses by domestic ducks had increased by early 2004, and there is circumstantial evidence that they can be transmitted by wild birds. The migratory birds from which viruses have been isolated were usually sick or dead, suggesting that they would have had limited potential for carrying the viruses over long distances unless subclinical infections were prevalent. However, there is strong circumstantial evidence that wild birds can become infected from domestic poultry and potentially can exchange viruses when they share the same environment. Nevertheless, there is little reason to believe that wild birds have played a more significant role in spreading disease than trade through live bird markets and movement of domestic waterfowl. Asian H5N1 viruses were first detected in domestic geese in southern China in 1996. By 2000, their host range had extended to domestic ducks, which played a key role in the genesis of the 2003/04 outbreaks. The epidemic was not due to the introduction and spread of a single virus but was caused by multiple viruses which were genotypically linked to the Goose/GD/96 lineage via the haemagglutinin gene. The H5N1 viruses isolated from China, including the Hong Kong SAR, between 1999 and 2004 had a range of genotypes and considerable variability within genotypes. The rising incidence and widespread reporting of disease in 2003/04 can probably be attributed to the increasing spread of the viruses from existing reservoirs of infection in domestic waterfowl and live bird markets leading to greater environmental contamination. When countries in the region started to report disease in December 2003, others were alerted to the risk and disease surveillance and reporting improved. The H5N1 viruses have reportedly been eliminated from three of the nine countries that reported disease in 2003/04, but they could be extremely difficult to eradicate from the remaining countries, owing to the existence of populations and, possibly, production and marketing sectors, in which apparently normal birds harbour the viruses.
Vet Rec 2005 Aug 06
PMID:Origin and evolution of highly pathogenic H5N1 avian influenza in Asia. 1608 21

The health of 22 free-ranging adult rheas (Rhea americana) examined and sampled during a translocation/reintroduction project and six juvenile rheas kept in semicaptivity was investigated, and details of their haematology and plasma biochemistry are presented. Serological testing for antibodies to infectious agents was negative for infectious laryngotracheitis, avian adenovirus, avian influenza, avian reovirus, infectious bursal disease, infectious bronchitis virus, paramyxovirus types 1, 2, and 3, fowlpox and Salmonella Pullorum. Antibodies to Chlamydophila species were found in 25 of 27 of the birds, and 22 of 25 had antibodies to Aspergillus species. Ova of gastrointestinal nematodes of the genus Capillaria were identified, and the anoplocephalid cestode Monoecocestus cf rheiphilus was identified in R americana for the first time.
Vet Rec 2006 Mar 04
PMID:Evaluation of the health of free-ranging greater rheas (Rhea americana) in Argentina. 1651 22

During an outbreak of avian influenza in the Netherlands in spring 2003, the disease was controlled by destroying all the poultry on the infected farms and on all the farms within a radius of 3 km. In total, 30 million birds were killed on 1242 farms and in more than 8000 hobby flocks, by using mobile containers filled with carbon dioxide, mobile electrocution lines and by gassing whole poultry houses with carbon monoxide or carbon dioxide. Observations of these methods were used to compare their effectiveness and capacity, and their effects on the welfare of the birds. Gassing whole poultry houses had a much greater capacity than mobile equipment, and catching live birds to bring them to a mobile killing device caused extra stress and could cause pain due to injuries inflicted when catching and handling them. Gassing whole poultry houses with carbon monoxide requires strict safety regulations and, therefore, gassing with carbon dioxide was considered preferable. However, this method is not suited to all types of housing, and in these circumstances mobile killing devices were a useful alternative.
Vet Rec 2006 Jul 08
PMID:Slaughter of poultry during the epidemic of avian influenza in the Netherlands in 2003. 1682 97

This case report describes the course of an outbreak of avian influenza on a Dutch turkey farm. When clinical signs were observed their cause remained unclear. However, serum samples taken for the monitoring campaign launched during the epidemic of highly pathogenic avian influenza in 2003, showed that all the remaining turkeys were seropositive against an H7 strain of avian influenza virus, and the virus was subsequently isolated from stored carcases. The results of a reverse-transcriptase pcr showed that a H7N3 strain was involved, and it was characterised as of low pathogenicity. However, its intravenous pathogenicity index was 2.4, characterising it as of high pathogenicity, suggesting that a mixture of strains of low and high pathogenicity may have been present in the isolate. The outbreak remained limited to three farms.
Vet Rec 2006 Sep 23
PMID:Outbreak of avian influenza H7N3 on a turkey farm in the Netherlands. 1699 95

The avian influenza (AI) vaccine designated TROVAC-AIV H5 (TROVAC-H5) contains a live recombinant fowlpox rec. (FP) recombinant (recFP), expressing the hemagglutinin (HA) gene of an AI H5 subtype isolate. This recombinant vaccine was granted a license in the United States for emergency use in 1998 and full registration in Mexico, Guatemala, and El Salvador where over 2 billion doses have been administered. One injection of TROVAC-H5 protects chickens against AI-induced mortality and morbidity for at least 20 weeks, and significantly decreases shedding after challenge with a wide panel of H5-subtype AI strains, regardless of neuraminidase subtype. Recently, excellent protection was demonstrated against 2003 and 2004 Asian highly pathogenic H5N1 isolates. Whereas TROVAC-H5 AI H5 efficacy was not inhibited by anti-AI or anti-fowlpox maternal antibodies (passive immunity), protection to AI was significantly decreased in chickens previously vaccinated or infected with FP (active immunity). Advantages of the TROVAC-H5 vaccine over inactivated AI vaccines are: (a) single administration at 1 day of age and early onset (1 week) of protection, (b) easy monitoring of AI infection in vaccinated flocks with agar gel precipitation (AGP) and enzyme-linked immunosorbent assay (ELISA) used as tests to differentiate infected from vaccinated animals (DIVA tests), and (c) no residue problem due to adjuvant. These features make TROVAC-H5 an ideal AI vaccine for routine administration of day-of-age chicks in hatcheries. RecFP expressing HA from three lineages of H7 subtype (Eurasian, American, and Australian) were also tested for efficacy against a highly pathogenic avian influenza (HPAI) Eurasian HPAI H7N1. Only the recFP expressing the Eurasian H7 gene provided sufficient protection indicating that the breadth of protection induced by recFP is apparently restricted for H7 isolates. The fowlpox vector technology can also be used for the production of an emergency vaccine: once the HA sequence of an emerging AI virus is known, recFP can be rapidly generated. TROVAC-H5 has recently been shown to be immunogenic in cats and could therefore also be considered for use in mammals.
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PMID:Development and use of fowlpox vectored vaccines for avian influenza. 1713 11

Avian influenza presents both challenges and opportunities to leaders around the world engaged in pandemic influenza preparedness planning. Most resource-poor countries will be unable to stockpile antivirals or have access to eventual human vaccines for pandemic flu. Preparedness plans, directed at controlling avian influenza at the source, enable countries simultaneously to promote national and global health, animal welfare and international development. Improving the veterinary infrastructure and capacity of resource-poor countries is one way to prevent potential pandemic flu deaths in resource-rich countries. In this article, Amanda Martinot, James Thomas, Alejandro Thiermann and Nabarun Dasgupta argue that national health leaders need to consider more comprehensive strategies that incorporate veterinary surveillance and improvements in veterinary infrastructure for the control of avian influenza epizootics as part of national pandemic preparedness planning. This, they argue, will require a shift in attitude, from thinking in terms of preparation for an inevitable pandemic to pre-emption of the potential pandemic through prevention measures in the animal population.
Vet Rec 2007 Mar 10
PMID:Prevention and control of avian influenza: the need for a paradigm shift in pandemic influenza preparedness. 1735 Nov 79

Recent outbreaks of the H5N1 strain of avian influenza in Europe have highlighted the need for continuous surveillance and early detection to reduce the likelihood of a major outbreak in the commercial poultry industry. In Great Britain (gb), one possible route by which H5N1 could be introduced into domestic poultry is through migratory wild birds from Europe and Asia. Extensive monitoring data on the 24 wild bird species considered most likely to introduce the virus into GB, and analyses of local poultry populations, were used to develop a risk profile to identify the areas where H5N1 is most likely to enter and spread to commercial poultry. The results indicate that surveillance would be best focused on areas of Norfolk, Suffolk, Lancashire, Lincolnshire, south-west England and the Welsh borders, with areas of lower priority in Anglesey, south-west Wales, north-east Aberdeenshire and the Firth of Forth area of Scotland. These areas have significant poultry populations including a large number of free-range flocks, and a high abundance of the 24 wild bird species.
Vet Rec 2007 Dec 08
PMID:Risk-based surveillance for H5N1 avian influenza virus in wild birds in Great Britain. 1806 12

A matched case-control study was carried out to identify risk factors for highly pathogenic avian influenza A virus (subtype H5N1) infection in commercial chickens in Bangladesh. A total of 33 commercial farms diagnosed with H5N1 before September 9, 2007, were enrolled as cases, and 99 geographically matched unaffected farms were enrolled as control farms. Farm data were collected using a pretested questionnaire, and analysed by matched-pair analysis and multivariate conditional logistic regression. Two factors independently and positively associated with H5N1 infection remained in the final model. They were 'farm accessible to feral and wild animals' (odds ratio [OR] 5.71, 95 per cent confidence interval [CI] 1.81 to 18.0, P=0.003) and 'footbath at entry to farm/shed' (OR 4.93, 95 per cent CI 1.61 to 15.1, P=0.005). The use of a designated vehicle for sending eggs to a vendor or market appeared to be a protective factor (OR 0.14, 95 per cent CI 0.02 to 0.88, P=0.036).
Vet Rec 2009 Jun 13
PMID:Risk factors for infection with highly pathogenic influenza A virus (H5N1) in commercial chickens in Bangladesh. 1952 22

Tetanus toxoid (TT) was assessed as a positive marker for avian influenza (AI) virus vaccination in chickens, in a vaccination and challenge study. Chickens were vaccinated twice with inactivated AI H5N2 virus vaccine, and then challenged three weeks later with highly pathogenic AI H5N1 virus. Vaccinated chickens were compared with other groups that were either sham-vaccinated or vaccinated with virus with the TT marker. All sham-vaccinated chickens died by 36 hours postinfection, whereas all vaccinated chickens, with or without the TT marker, were protected from morbidity and mortality following exposure to the challenge virus. Serological testing for H5-specific antibodies identified anamnestic responses to H5 in some of the vaccinated birds, indicating active virus infection.
Vet Rec 2010 Oct 30
PMID:Use of a tetanus toxoid marker to allow differentiation of infected from vaccinated poultry without affecting the efficacy of a H5N1 avian influenza virus vaccine. 2125 85


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