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.     

Methods of spread of velogenic viscerotropic Newcastle disease virus in the southern Californian epidemic of 1971-1973.

Data collected during the velogenic viscerotropic Newcastle disease (VVND) epidemic that occurred in southern California from 1971 to 1973 were analyzed to determine the methods of spread of the disease. Spread between chicken flocks was extensive and due mainly to the movement of live birds and mechanical transport of virus by man, especially by vaccination and poultry service crews. Spread to exotic birds was from contact with infected imported stock. Spread to other species was most probably through contact with infected chickens. Infection persisted in commercial chicken flocks because of intensive vaccination programs, heavy traffic and contact between layer operations, and the maintenance of multi-age flocks. These foci of infection probably led to spread of the disease to areas from which VVND had been eradicated several months before. There was no evidence of significant wind-borne spread of virus between flocks.     

Effects of certain stress factors on the re-excretion of infectious laryngotracheitis virus from latently infected carrier birds

Experiments were set up to assess the effects of 'natural' and 'artificial' stresses on the re-excretion of infectious laryngotracheitis (ILT) virus in latently infected chickens recovered from the acute phase of the disease. The stresses were rehousing with the addition of ILT-free contact birds, corticosteroid treatment and the onset of lay. The contact birds were also monitored for transmission of the virus from the carrier birds. Rehousing with unfamiliar birds induced ILT virus shedding in one of five birds and there was evidence of transmission from this bird to its mate. The onset of lay had a significant effect on the overall shedding rates of the carrier birds. Nine of 10 birds shed virus after onset of lay compared with only two in the three-and-a-half weeks before, and there was a highly significant increase (P less than 0.001) in the overall number of virus isolations during this period. Corticosteroid treatment did not affect virus shedding. These results may explain some of the apparently spontaneous outbreaks of ILT which occur in the field.     

An investigation of 11 outbreaks of foot-and-mouth disease in villages in northern Thailand

The results of investigations of 11 outbreaks of foot-and-mouth disease in villages in northern Thailand are described. The causative virus was Asia in one in seven outbreaks, Type O in two outbreaks and unknown in two outbreaks. The most probable sources of the outbreaks were co-mingling of cattle and/or buffalo with livestock from an infected neighbouring village (four) and recent introductions of infected cattle from a public livestock market (two) while the probable source could not be determined in five outbreaks. Attack rates in cattle and buffalo ranged from 0.28% to 50.9% but no pigs became sick during any of the outbreaks. Most outbreaks lasted 4 weeks or less. Adult cattle and buffalo were at higher risk of becoming a case when compared with work cattle. Beef cattle were at higher risk than buffalo and adult cattle and buffalo were at higher risk than calves less than 1 year of age. There was significant clustering of cases within households. Serological investigations indicated that many unaffected animals were probably not exposed to virus during the outbreaks. We concluded that close contact between animals was the main method of spread and that differences in attack rates between animal classes reflected differences in animal management. We further concluded that simple quarantine of early cases during outbreaks is likely to be effective in reducing spread within and between villages.     

Persistence of the V4 strain of Newcastle disease virus in an open-range flock of chickens

The V4 strain of Newcastle disease virus was introduced into a small open range flock of bantam chickens, by dosing half the birds directly into the crop. As indicated by rises in titres of haemagglutination inhibition antibody, the virus spread to the uninoculated birds and persisted in the flock for two years, infecting chickens that were introduced by natural brooding and rearing. All new clutches of chicks seroconverted by 80 days of age, and the titres of adult birds showed a concurrent rise, suggesting that the chicks were amplifying the virus. The modes of spread and of persistence of the virus were not determined; although cloacal swabs were taken regularly, only one yielded virus. Antibody titres of the inoculated birds remained above the presumptive protective level of 3 (log2) for over a year, whereas the titres of birds infected by contact were generally less than 3.     

Time-dependent infection probability of classical swine fever via excretions and secretions

Several routes contribute to the spread of classical swine fever (CSF) during outbreaks of this disease. However, for many infected herds in recent epidemics, no route of virus introduction could be indentified. To obtain more insight into the relative importance of secretions and excretions in transmission of CSF virus, a model was developed. This model quantified the daily transmission probabilities from one infectious pig to one susceptible pig, using quantitative data on: (a) virus excretion by infected pigs, (b) survival of virus in the environment and (c) virus dose needed to infect susceptible pigs. Furthermore, the model predicted the relative contribution of secretions and excretions to this daily probability of infection of a susceptible pig. Three virus strains that differed in virulence were evaluated with the model: the highly virulent strain Brescia, the moderately virulent strain Paderborn and the low virulent strain Zoelen. Results suggest that it is highly probable that susceptible pigs in contact with Brescia or Paderborn infected pigs will be infected. For a pig in contact with a Zoelen infected pig, infection is less likely. When contact with blood is excluded, the predicted overall probability of infection was only 0.08 over the entire infectious period. The three strains differed in the relative contribution of secretions and excretions to transmission, although blood had a high probability of causing infection of a susceptible pig when in contact with a pig infected with any strain. This supports the statement that during outbreaks, control measures should ideally be based on the characteristics of the specific virus strain involved, which implies the development of strain-specific measures.     

The pathogenicity of four avian influenza viruses for fowls, turkeys and ducks

Groups of 10 two-week-old chicks, turkey poults and ducklings were each infected by the intranasal route with one of four avian influenza viruses: a/fowl/Germany/34 (Hav 1N))--Rostock, A/FPV/Dutch/27 (Hav 1 Neq 1)--Dutch, A/fowl/Victoria/75 (Hav 1 Neq 1)--Australian, and A/parrot/Ulster/73 (Hav 1 N1)--Ulster. Eight hours after infection 10 birds of the same age and species were placed in contact with each group and allowed to mix. The clinical signs of disease and onset of sickness and death were recorded. Ulster virus was completely avirulent for all birds. Rostock, Dutch and Australian viruses were virulent for fowls and turkeys causing death in all birds with the exception of 3/10 in contact fowls from the Rostock virus group and 2/10 in contact fowls from the Australian virus group. Only Rostock virus caused sicked sickness or death in ducks, 9/10 intranasally infected and 6/7 in contact birds showed clinical signs and 2/10 intranasally infected and 3/7 in contact ducks died. Intranasal and in contact pathogenicity indices were calculated for each virus in each bird species and indicated quantitatively the differences in virulence of the four virus strains. Virus isolation and immune response studies indicated that surviving in contact fowls in the Rostock virus group had never been infected but that surviving Australian virus in contact fowls had recovered from infection. Infection was not established in Ulster virus in contact fowls and Australian virus intranasally infected and in contact ducks. The birds in all other groups showed positive virus isolations and a high incidence of positive immune response. The last virus isolation was made at 22 days after intranasal infection of ducks with Ulster virus.     

Evaluation of risk factors for the spread of low pathogenicity H7N2 avian influenza virus among commercial poultry farms

OBJECTIVE: To identify risk factors associated with the spread of low pathogenicity H7N2 avian influenza (AI) virus among commercial poultry farms in western Virginia during an outbreak in 2002. DESIGN: Case-control study. PROCEDURE: Questionnaires were used to collect information about farm characteristics, biosecurity measures, and husbandry practices on 151 infected premises (128 turkey and 23 chicken farms) and 199 noninfected premises (167 turkey and 32 chicken farms). RESULTS: The most significant risk factor for AI infection was disposal of dead birds by rendering (odds ratio [OR], 73). In addition, age > or = 10 weeks (OR for birds aged 10 to 19 weeks, 4.9; OR for birds aged > or = 20 weeks, 4.3) was a significant risk factor regardless of poultry species involved. Other significant risk factors included use of nonfamily caretakers and the presence of mammalian wildlife on the farm. Factors that were not significantly associated with infection included use of various routine biosecurity measures, food and litter sources, types of domestic animals on the premises, and presence of wild birds on the premises. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that an important factor contributing to rapid early spread of AI virus infection among commercial poultry farms during this outbreak was disposal of dead birds via rendering off-farm. Because of the highly infectious nature of AI virus and the devastating economic impact of outbreaks, poultry farmers should consider carcass disposal techniques that do not require off-farm movement, such as burial, composting, or incineration.     

The infection of turkey poults with Histomonas meleagridis by contact with infected birds or contaminated cages

The conditions under which infection with Histomonas meleagridis could spread from directly inoculated turkey poults to uninoculated poults without the aid of invertebrate hosts or vectors was investigated in several experiments. In three experiments in battery cages, uninoculated poults were commingled with directly infected birds on pine-shaving litter. Directly exposed birds were inoculated per cloaca with H. meleagridis by means of a plastic pipette tip attached to a 10-ml syringe or orally gavaged with fresh cecal droppings from donor turkeys 4 days postinoculation (PI). Of the cloacally inoculated controls in these experiments, 31 of 44 (70.5%) birds had severe lesions ofhistomoniasis at 14 days PI, whereas none of the orally gavaged birds became infected. Histomoniasis developed in 11 of 36 (30.5%) birds allowed to commingle with inoculated birds. In other treatments, poults were allowed only contact with droppings from directly inoculated birds after the infected birds were removed from the cages. This was done for a single period of 1 hr or repeated five times. Four of 32 birds (12.5%) became infected in this way after the single exposure, whereas only four of 44 birds (9.1%) exposed five times developed lesions. In a comparison of floor materials, 35 of 35 control birds inoculated per cloaca developed severe liver and cecal lesions, irrespective of litter. Uninoculated birds allowed to commingle with infected birds on paper or pine shavings became severely infected in all cases (12/12 and 12/12 birds, respectively), whereas only 33% of those on wire-floored cages became infected (4/12). These results suggest that transmission of infection is more likely to occur as a result of direct contact between birds than from contact with litter or fecal material.     

Experimental pathogenesis for chickens, turkeys, and pigeons of exotic Newcastle disease virus from an outbreak in California during 2002-2003

Exotic Newcastle disease virus (NDV) isolated from chickens during the 2002-2003 California outbreak (CA exotic Newcastle disease [END] virus) was inoculated into 4-week-old specific-pathogen-free (SPF) White Leghorn chickens, 3-week-old SPF Beltsville White turkeys, 6-week-old commercial Broad Breasted White turkeys, and 10- to 20-week-old racing pigeons, and the clinicopathologic features of disease were compared. Birds were monitored clinically and euthanized sequentially with collection of tissues. Tissues were examined by histopathology, by immunohistochemistry to detect viral nucleoprotein, and by in situ hybridization to detect viral mRNA. Clinically, infected chickens and SPF turkeys showed severe depression, and all died or were euthanized because of severe clinical signs by day 5 postinoculation. In these birds, histologic lesions were widespread and virus was detected in multiple organs. All infected commercial turkeys showed mild depression, and incoordination was observed in some birds. Histologic lesions were mild, and viral distribution was limited. In pigeons, only 1 bird showed overt clinical disease, and histologic lesions and viral distribution were present in limited organs. Consequently, susceptibility to highly virulent NDV was shown to vary among chickens, SPF turkeys, commercial turkeys, and pigeons. Additionally, we have evidence of CA END virus subclinical infections that suggest pigeons could be subclinical carriers of other virulent NDV.     

Latency sites and reactivation of duck enteritis virus

Duck virus enteritis (DVE) is a contagious disease caused by herpesvirus in waterfowl populations. Recovered birds become carriers and shed the virus periodically. Reactivation of latent duck enteritis virus (DEV) has been implicated in outbreaks of DVE in domestic and migrating waterfowl populations. In this study, the sites for virus latency were determined in white Pekin ducks infected with the DEV-97 strain. At 3 wk postinfection, infectious virus was not detectable in tissues or cloacal swabs (CSs). At 7 and 9 weeks postinfection, the viral DNA was detected by polymerase chain reaction in the trigeminal ganglia (TG), suggesting that the virus is latent. Viral DNA was detected in the peripheral blood lymphocytes (PBL), spleen, thymus, bursa, and CSs only after in vitro cocultivation. In vivo virus reactivation was demonstrated when dexamethasone or a combination of dexamethasone and cyclophosphamide was inoculated in latently infected ducks. The reactivation of DEV occurred without any clinical evidence of the disease, but the virus was detected in PBL and CSs. We conclude from this study that DEV establishes latency in TG and lymphoid tissues including PBL.     

The role of rodents in avian influenza outbreaks in poultry farms: a review

Wild migratory birds are associated with global avian influenza virus (AIV) spread. Although direct contact with wild birds and contaminated fomites is unlikely in modern non-free range poultry farms applying biosecurity measures, AIV outbreaks still occur. This suggests involvement of other intermediate factors for virus transmission between wild birds and poultry. This review describes current evidence of the potential role of rodents in AIV transmission from wild birds to poultry and between poultry houses. Rodents can be abundant around poultry houses, share their habitat with waterfowl and can readily enter poultry houses. Survival of AIV from waterfowl in poultry house surroundings and on the coat of rodents suggests that rodents are likely to act as mechanical vector. AIVs can replicate in rodents without adaptation, resulting in high viral titres in lungs and nasal turbinates, virus presence in nasal washes and saliva, and transmission to naïve contact animals. Therefore, active AIV shedding by infected rodents may play a role in transmission to poultry. Further field and experimental studies are needed to provide evidence for a role of rodents in AIV epidemiology. Making poultry houses rodent-proof and the immediate surroundings unattractive for rodents are recommended as preventive measures against possible AIV introduction.     

Classic fowl plague--a review

Highly pathogenic avian influenza (HPAI) represents a severe form of generalized avian influenza which is characterized by a rapid and severe course of disease and a very high mortality. All poultry species are susceptible. Turkeys and chickens are most vulnerable. There are no pathognomonic symptoms or specific pathological alterations. The disease is caused by avian influenza virus strains of the subtypes H5 or H7. These viruses arise spontaneously from apathogenic progenitors by insertional mutation in the HA gene. Until recently, outbreaks of HPAI were rare events, however, they have been found to cause increasing losses over the past few years. Since 2003, a widespread occurrence of HPAI has been registered in southeast Asia, and some countries are endemically infected with HPAIV strain H5N1. In six countries this virus has also caused fatal human infections. This has sparked fears that this agent may be the progenitor of a new pandemic influenza virus. During summer 2005 the disease has slowly spread westward. Isolated outbreaks have been reported from Kazakhstan, Russia, Romania, Turkey, Croatia and Ukraine. Migratory birds have been tentatively accused for spreading the infection along their flyways.     

Comparison of different control strategies for foot-and-mouth disease: a study of the epidemics in Canada in 1951/52, Hampshire in 1967 and Northumberland in 1966

The measures used to control the epidemics of foot-and-mouth disease in Canada in 1951/52 (29 outbreaks) were compared with those used in the epidemic in Hampshire in 1967 (29 outbreaks). In both epidemics the disease spread more from premises where the disease was reported late and the imposition of quarantine or restrictions on infected premises was delayed. In Hampshire, area restrictions were imposed, susceptible livestock on infected premises and on premises in direct contact were slaughtered, and contacts were traced. In Canada, the initial diagnosis was vesicular stomatitis, no area restrictions were imposed, no tracing was carried out and the animals on infected premises were allowed to recover. However, apart from the disease's spread through infected meat and by unknown or airborne routes, it did not spread from infected premises once quarantine was imposed, partly owing to the low population density of livestock in the area. The effects of the slaughter of infected premises and direct contacts in the Fareham area of Hampshire in 1967 and in the Chathill area of Northumberland in 1966 were compared with what might have happened if, in addition, culling on contiguous premises or culling on premises within 3 km or emergency vaccination had been put into effect. The slaughter of cattle, sheep, goats and pigs on premises within 3 km two days after confirmation of the first outbreak would have resulted in fewer outbreaks and a shorter period to complete slaughter, but more animals would have been slaughtered. In the Chathill area, the slaughter of sheep, goats and pigs only on premises within 3 km two days after confirmation of the first outbreak would not have resulted in fewer outbreaks and more animals would have been slaughtered. Fewer premises and animals would have been slaughtered by a contiguous cull than by a 3 km cull but more than by the slaughter of infected premises and direct contacts. Emergency vaccination within 3 km, providing protection at four days (but not to animals already infected before the development of immunity), would have resulted in the fewest animals being slaughtered and could have reduced the number of outbreaks in the Fareham area by one and in the Chathill area by two or three. All the procedures would have had a greater effect the sooner they were introduced. However, with many foci of infection, priorities for action would have had to have been established. Earlier tracing of the last outbreak in the Fareham area could have shortened the Hampshire epidemic. Surveillance of a farm identified as at risk through animal movements and by the use of an airborne-prediction model could have eliminated the source of further outbreaks in the Chathill area.     

Surveillance for highly pathogenic avian influenza in migratory shorebirds at the terminus of the East Asian-Australasian Flyway

AIM: To determine if migratory birds arriving in New Zealand in the Southern Hemisphere spring of 2004 were infected with the highly pathogenic avian influenza (AI) virus, H5N1.

METHODS: Cloacal and faecal samples were collected from migratory red knots following their arrival in New Zealand in October 2004. Two species of resident sympatric birds, wrybill and mallard duck, were sampled prior to, and following, the arrival of migratory birds.

RESULTS: No AI viruses were isolated from migratory or resident shorebirds. Non-pathogenic AI viruses were isolated from six resident mallard ducks, comprising the endemic subtypes H4 (n=2), H7 (non-pathogenic), H10, and H11 (n=2).

CONCLUSIONS: Highly pathogenic AI H5N1 virus was not detected in migratory shorebirds or sympatric water birds in the Firth of Thames, New Zealand, in 2004-2005, despite the possible proximity of migratory birds to outbreaks of the disease in East Asia in 2004.     

Epidemiology of classical swine fever in Germany in the 1990s

In Germany, 424 outbreaks of CSF in domestic pigs and a great number of cases in wild boar were recorded between 1990 and 1998. Most of the federal states ('Bundesl?nder') were affected. Epidemiological data from field investigations combined with genetic typing allowed to distinguish seven unrelated epidemics and a number of sporadic outbreaks in domestic pigs. Detailed epidemiological data was available for 327 outbreaks. It was found that 28% of these were primary outbreaks. Most of them were due to indirect or direct contact to wild boar infected with CSF virus or swill feeding. Infected wild boar remain the main risk for domestic pigs. The most frequent sources of infection in secondary or follow up outbreaks were the trade with infected pigs, neighbourhood contacts to infected farms and other contacts via contaminated persons and vehicles, respectively. An increased risk of virus transmission from infected herds to neighbourhood farms was observed up to a radius of approximately 500m. More than two thirds of the infected herds were discovered due to clinical signs. About 20% were identified by epidemiological tracing on and back. These were scrutinised because contacts to infected herds were evident. In conclusion, tracing of contact herds and clinical examination combined with carefully targeted virological testing of suspicious animals is likely to be the most important measure to immediately uncover secondary outbreaks. Obligatory serological screening in the surveillance and the restriction zones do not seem to be efficient measures to detect follow-up outbreaks.     

Paramyxovirus disease in racing pigeons. Clinical aspects and immunization. A report from the Netherlands

Since 1981 a highly contagious viral disease causing high morbidity and low mortality in racing pigeons has spread over Europe. The virus belongs to the avian paramyxovirus sero group I. Clinical signs include watery droppings, polydypsia and neurologic signs in a high proportion of infected animals. Definitive diagnosis can be made by virus isolation in cell cultures or chicken embryos, and virus identification by haemagglutination and haemagglutination inhibition (HI) tests. The HI test, using sera from suspected animals, is a useful clinical tool to confirm the diagnosis. The most important differential diagnosis is salmonellosis. Good immunity against this disease can be acquired by subcutaneous vaccination with an inactivated oil adjuvant poultry NDV-vaccine. For the benefit of pigeon racing a plea is made for compulsory vaccination in countries in which the disease is endemic.     

Infectivity and transmissibility of H9N2 avian influenza virus in chickens and wild terrestrial birds

Genetic changes in avian influenza viruses influence their infectivity, virulence and transmission. Recently we identified a novel genotype of H9N2 viruses in widespread circulation in poultry in Pakistan that contained polymerases (PB2, PB1 and PA) and non-structural (NS) gene segments identical to highly pathogenic H7N3 viruses. Here, we investigated the potential of these viruses to cause disease and assessed the transmission capability of the virus within and between poultry and wild terrestrial avian species. Groups of broilers, layers, jungle fowl, quail, sparrows or crows were infected with a representative strain (A/chicken/UDL-01/08) of this H9N2 virus and then mixed with naïve birds of the same breed or species, or different species to examine transmission. With the exception of crows, all directly inoculated and contact birds showed clinical signs, varying in severity with quail showing the most pronounced clinical signs. Virus shedding was detected in all infected birds, with quail showing the greatest levels of virus secretion, but only very low levels of virus were found in directly infected crow samples. Efficient virus intra-species transmission was observed within each group with the exception of crows in which no evidence of transmission was seen. Interspecies transmission was examined between chickens and sparrows and vice versa and efficient transmission was seen in either direction. These results highlight the ease of spread of this group of H9N2 viruses between domesticated poultry and sparrows and show that sparrows need to be considered as a high risk species for transmitting H9N2 viruses between premises.