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In October 2006, following an initially non-statutory disease investigation affecting 12-week-old grey partridges (Perdix perdix), an outbreak of Newcastle disease due to infection with the avian paramyxovirus type 1 virus responsible for the current panzootic in pigeons (PPMV-1) was confirmed in Scotland. Two pens of partridges were affected by signs including loss of condition, diarrhoea, progressive neurological signs and mortality totalling approximately 24 per cent, and laboratory evidence of the infection was obtained only in these groups. The premises had approximately 17,000 poultry including a collection of 375 birds of rare breeds, containing endangered breeds of significant conservation value, which were not culled but subjected to a health monitoring and testing programme. Investigations suggested that a population of feral pigeons living above the affected pens of partridges was the likely source of the outbreak. Laboratory and genetic analyses confirmed that the isolate recovered from the clinically affected partridges was PPMV-1, belonging to genetic lineage 4b. However, the virus could not be isolated from or detected in dead pigeons collected from the affected buildings.

During outbreaks of infectious animal diseases, composting may be an effective method of disposing of mortalities and potentially contaminated manure. Duplicate biosecure structures containing 16 cattle (Bos taurus) mortalities (343 kg average weight) were constructed with carcasses placed on a 40-cm straw layer and overlaid with 160 cm of feedlot manure. At a depth of 80 cm (P80), compost heated rapidly, exceeding 55 degrees C after 8 d and maintained temperatures of 55 to 65 degrees C for > 35 d. Temperatures at 160 cm (P160) failed to exceed 55 degrees C, but remained above 40 degrees C for >4 mo. To investigate rates of microbial inactivation, Escherichia coli O157:H7, Campylobacter jejuni, and Newcastle disease virus (NDV) were inoculated in manure (E. coli O157:H7 and C. jejuni approximately 10(8) CFU g(-1); NDV, approximately 10(6) EID(50) g(-1)), embedded at P80 and P160 and retrieved at intervals during composting. Escherichia coli O157:H7 and NDV were undetectable after 7 d at both depths. The C. jejuni DNA was detected up to 84 d at P80 and >147 d at P160. To estimate degradation of recalcitrant substrates, bovine brain, hoof, and rib bones were also embedded at P80 and P160 and retrieved at intervals. Residues of soft tissues remained in carcasses after opening at 147 d and bovine tissue decomposition ranked as brain > hoof > bone. More than 90% dry matter (DM) of brain disappeared after 7 d and 80% DM of hoof decomposed after 56 d. High degradation of cattle carcasses, rapid suppression of E. coli O157:H7 and NDV and reduction in viable cell densities of >6 logs for C. jejuni demonstrates that the biosecure composting system can dispose of cattle carcasses and manure in an infectious disease outbreak.

We developed a Bayesian approach to sample size calculations for studies designed to estimate disease prevalence that uses a hierarchical model for estimating the proportion of infected clusters (cluster-level prevalence) within a country or region. The clusters may, for instance, be villages within a region, cities within a state, or herds within a country. Our model allows for clusters with zero prevalence and for variability in prevalences among infected clusters. Moreover, uncertainty about diagnostic test accuracy and within-cluster prevalences is accounted for in the model. A predictive approach is used to address the issue of sample size selection in human and animal health surveys. We present sample size calculations for surveys designed to substantiate freedom of a region from an infectious agent (disease freedom surveys) and for surveys designed to estimate cluster-level prevalence of an endemic disease (prevalence estimation surveys). In disease freedom surveys, for instance, assuming the cluster-level prevalence for a particular infectious agent in the region is greater than a maximum acceptable threshold, a sample size combination consisting of the number of clusters sampled and number of subjects sampled per cluster can be determined for which authorities conducting the survey detect this excessive cluster-level prevalence with high predictive probability. The method is straightforward to implement using the Splus/R library emBedBUGS together with WinBUGS., (Copyright 2006 John Wiley & Sons, Ltd.)

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.

At present Denmark has the status of a 'non-vaccinating' country for Newcastle disease and its poultry population should therefore be free of antibodies to avian paramyxovirus 1 (APMV-1). Three live avian vaccines against infectious bronchitis, avian encephalomyelitis, and chick anaemia which had been found to be contaminated with APMV-1 viruses of low virulence for chickens were examined. The vaccines were produced by the same company and the affected batches had been used in Denmark in 1996/97. Furthermore, APMV-1 isolates of low virulence were obtained from three commercial broiler breeder flocks, one of which had been vaccinated with two of the contaminated vaccines. The flocks belonged to the same hatchery organisation. A comparison of viral F0 gene sequences and typing of virus isolates with a panel of monoclonal antibodies showed that the vaccine and field isolates were identical.

Between January 6 and April 23, 1997, 11 outbreaks of Newcastle disease were confirmed in Great Britain, four in broiler chickens and seven in turkeys. Although the viruses isolated gave intracerebral pathogenicity indices in day-old chicks between 1.65 and 1.95, the clinical signs of disease in field infections were variable and not always associated with high mortality, especially in turkeys. Epidemiological investigations indicated that the majority of the outbreaks occurred as a result of secondary spread by human agency from two or more primary infected flocks. The presence of similar outbreaks in Scandinavian countries in 1996 and the unusual patterns of movement of migratory birds at the end of 1996 and beginning of 1997 suggest they may have been responsible for the primary introduction of the causative virus into Great Britain.

Antigenic characterisation of two highly virulent virus isolates from outbreaks of Newcastle disease on two closely connected farms in County Monaghan, Republic of Ireland, in 1990 showed the viruses to be indistinguishable but unlike other Newcastle disease viruses so far tested. However, they appeared to be antigenically closest to avirulent viruses isolated from waterfowl from several countries and from chickens in Northern Ireland in 1986. Despite the antigenic differences, chickens vaccinated with a live commercial Hitchner B1 vaccine were protected against intramuscular challenge with one of the virulent isolates.

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.

The operation of the Importation of Captive Birds Order 1976 is described. In the first 24 months that the order was effective, a total of 183,189 birds were landed. Of these 5829 (3.18 per cent) were dead on arrival, 8643 (4.71 per cent) died in quarantine and 474 batches of carcases were submitted for post mortem examination. Chlamydia infections were diagnosed in birds from 14 quarantine/isolation lots and salmonellae were isolated from 23 lots. Thirty-six haemagglutinating agents were isolated from 17 quarantine/isolation lots. These were identified as eight influenza A viruses with Hav 7 Neq 2 subtypes (associated with two importations); 14 influenza A viruses with Hav 4 Nav 1 subtypes (six importations); four yucaipa-like paramyxoviruses (three importations); four 449-like paramyxoviruses (two importations); one unspecified paramyxovirus; five Newcastle disease viruses (NDV) (two importations). Four of the NDV isolates, associated with one importation, were shown to be velogenic viruses by intravenous pathogenicity index tests in six-week-old chickens.