INTRODUCTION
History
The first outbreaks to be recognized and termed Newcastle disease (ND) occurred in poultry in 1926, in Java, Indonesia (Kraneveld, 1926), and in Newcastle-upon-Tyne, England (Doyle, 1927). However, there are earlier reports of similar disease outbreaks in Central Europe before this date. (Halasz, 1912). In particular, Macpherson (1956) attributes the death of all the chickens in the Western Isles of Scotland in 1896 as being due to Newcastle disease. It is possible, therefore, that ND did occur in poultry before 1926, but its recognition as a specifically defined disease of viral aetiology dates from the outbreaks during this year in Newcastle-upon-Tyne.
The name "Newcastle disease", (after the geographical location of the first outbreaks in Great Britain), was coined by Doyle as a temporary measure because he wished to avoid a descriptive name that might be confused with other diseases (Doyle, 1935). The name has, however, continued to be used although when referring to the ND virus (NDV), the synonym 'avian paramyxovirus type 1' (APMV-1) is now often employed.
Later it became clear that other less severe infections were caused by viruses almost identical to the original virus. In the United States, a relatively mild respiratory disease, often with nervous symptoms, was first reported in the 1930s and subsequently termed pneumoencephalitis (Beach, 1942). It was shown to be due to a virus indistinguishable from NDV in serological tests (Beach, 1944). Since then, numerous NDV isolations of viruses that produce an extremely mild disease or no evidence of disease in chickens, have been made around the world and it is now accepted that pools of such viruses are perpetuated in waterfowl and other wild birds.
The pattern of outbreaks which are due to virulent NDV throughout the world suggest that several panzootics have occurred in poultry since 1926. The first appeared to have spread very slowly across the globe, apparently from the Far East. It probably took over 20 years to become a true panzootic and probably never reached poultry in the USA. The beginning of the second ND panzootic was first recognised at the end of the 1960s and within four years had reached all corners of the earth. (Hanson, 1972). The reasons for the different spreading rates of the two panzootics appear to be the development of the world poultry industry and the commercialisation of poultry food production both of which lead to greater contact between separate farms because food delivery vehicles move from one to another. Another factor is the revolution that has occurred in world transport. Air transportation especially has led to a huge and growing trade in captive caged birds. There is no doubt that imported caged birds were responsible for introducing the panzootic virus into poultry in California (Hanson, 1972; Francis, 1973) and Walker et al., (1973) were able to link most of the outbreaks occurring in the USA during 1970-1972 to importations of exotic birds.
Antigenic and genetic evidence (Alexander et al., 1997; Lomniczi et al., 1998; Herczeg et al., 2001) has indicated that there was probably a worldwide spread of a third virulent virus during the late 1970s, the start and spread of which is unclear, presumably due to the masking of disease by the almost universal use of vaccines since the mid-1970s.
Another ND panzootic occurred in the 1980s, but in racing and show pigeons (Columba livia) rather than in poultry, although spread of the responsible virus did occur to poultry. The world population of racing or show pigeons is enormous and at the end of the 1970s these birds were still largely unvaccinated and fully susceptible to infection with NDV. Infections in pigeons with this variant NDV strain probably began in the Middle East in the late 1970s (Kaleta et al., 1985), and by 1984-5 had become a true panzootic. In many countries where outbreaks occurred there was also spread to feral pigeons and doves. The way pigeons are kept and raced has meant that this panzootic has proven difficult to control and in several countries it probably remains endemic in racing and possibly also in feral pigeons.
The effect panzootics of ND have had on the poultry populations of different countries has not always been well recorded. Alexander (2001) documented the history of ND in Great Britain in detail and considered it a good example of the effect ND may have on the poultry industry in a developed Western country where eradication policies have been employed.
Aetiology
The three virus families Rhabdoviridae, Filoviridae and Paramyxoviridae form the order Mononegavirales; i.e. viruses with negative sense, single stranded and non-segmented RNA genomes. ND is caused by avian paramyxovirus serotype 1 [APMV-1] viruses, which, with viruses of the other eight APMV serotypes [APMV-2 to APMV-9], have been placed in the genus Avulavirus, sub-family Paramyxovirinae, family Paramyxoviridae, in the current taxonomy (Lamb et al., 2000; Mayo 2002).
Antigenic variation of ND viruses [APMV-1] detectable by conventional haemagglutination inhibition [HI] tests has been reported, although only rarely (Arias-Ibarrondo et al., 1978; Hannoun, 1977, Alexander et al., 1984). One of the most noted variations of this kind has been the virus responsible for the panzootic in racing pigeons. This ND virus, referred to as 'pigeon APMV-1 [PPMV-1]', was demonstrably different from standard strains in haemagglutination inhibition tests, but not sufficiently different antigenically that conventional ND vaccines were not protective (Alexander and Parsons, 1986). In recent years antigenic variations detected by monoclonal antibodies and genetic variations detected by nucleotide sequencing of the virus genome have proved invaluable in understanding the epidemiology of ND (Alexander et al., 1997; 1999; Herczeg et al., 1999; 2001).
CURRENT WORLD SITUATION
In many respects, it is extremely difficult to assess the prevalence of ND in the world at any given time. In some countries or areas disease is not reported at all or only if it occurs in commercial poultry, while its presence in village chickens or backyard flocks is ignored. Even in poultry reared commercially, estimations of the geographical distribution of NDV are confused by the use of live vaccines in all but a few countries throughout the world. In some countries the distribution is especially complicated by using, as live vaccines, viruses that are considered sufficiently virulent in other countries to warrant the current definition of ND.
When countries or areas are declared free of ND, further complications are caused by the definition of the type of ND virus described as harmless although this is being be addressed by the new definitions and codes to be adopted by the Office International des Epizooties. Even in countries that have long been recognised as free of ND, monitoring surveys often reveal symptomless infections with avirulent viruses which have presumably spread from waterfowl or other wild birds. However, there can be little doubt that the highly pathogenic form of ND is a serious problem, either as an enzootic disease or as a cause of regular, frequent epizootics throughout Africa, Asia, Central America and parts of South America (Copland, 1987; Spradbrow, 1988; Rweyemamu et al., 1991; Alders & Spradbrow, 2001a). In other areas such as Europe, the situation appears to be one of sporadic epizootics occurring despite vaccination programmes (Kaleta & Heffels-Redmann, 1992).
In Western Europe there was a marked increase in reported outbreaks during the early 1990s, peaking with 239 outbreaks in European Union [EU] countries in 1994. The distribution overtime suggests a single epidemic from the early to mid-1990s, but, in fact, antigenic and phylogenetic evidence indicates that several strains of virus were responsible for these outbreaks. During 1991-1995 the majority of outbreaks in the EU occurred in the Benelux countries and Germany, predominantly in backyard poultry and most of the outbreaks since 1995 have been in these types of birds. One of the most extensive epidemics in Western Europe occurred in Italy in 2000 when 254 outbreaks of ND were confirmed, again mainly in backyard poultry.
One notable aspect of the outbreaks during the 1990s concerned those that occurred in countries that had been free of the disease for many years. Between 1995 and 1999, there were 18 outbreaks in Denmark, 2 in Finland and 27 in Northern Ireland. There was also 1 in Sweden, 1 in Norway and 1 in the Republic of Ireland.. These were all areas of Western Europe that had been declared free of ND and which were monitored regularly by serological testing and had no evidence of ND virus infections other than occasional incursions of avirulent viruses typical of spread from wild birds.
From the time of the 1932 outbreak (Albiston & Gorrie, 1942) to 1998, Australia had been free of virulent ND virus. Since 1966, however, it has been recognised that viruses similar to those placed in the "asymptomatic enteric" pathotype group (Westbury, 1981; Spradbrow, 1987) are present in wild birds in Australia and on occasions have spread to commercial poultry flocks. Two outbreaks of virulent ND occurred in Australia in 1998 and further outbreaks were reported in 1999 and 2000 (Kirkland, 2000; Westbury, 2001).
DISEASE AND PATHOGENICITY
Newcastle disease
The clinical signs seen in birds infected with NDV vary widely and are dependent on factors such as: the virus, the host species, age of host, infection with other organisms, environmental stress and immune status. In some circumstances infection with the extremely virulent viruses may result in sudden, high mortality with comparatively few clinical signs. Although none of the variable clinical signs can be regarded as pathognomonic, certain signs do appear to be associated with particular viruses. This has resulted in the grouping of viruses into five "pathotypes" on the basis of the predominant signs in affected chickens (Beard and Hanson, 1984):
Viscerotropic velogenic: viruses responsible for disease characterised by acute lethal infections, usually with haemorrhagic lesions in the intestines of dead birds.
Neurotropic velogenic: viruses causing disease characterised by high mortality which follows respiratory and neurological disease, but where gut lesions are usually absent.
Mesogenic: viruses causing clinical signs consisting of respiratory and neurological signs, with low mortality.
Lentogenic: viruses causing mild infections of the respiratory tract.
Asymptomatic enteric: viruses causing avirulent infections in which replication appears to be primarily in the gut.
These groupings are by no means clear-cut, and even in experimental infections of specific pathogen-free [SPF] chickens, considerable overlapping occurs (Alexander & Allan, 1974). In addition, in the field exacerbating factors may result in the clinical signs induced by the milder strains mimicking those of the more pathogenic viruses.
In general terms, ND may consist of signs of depression, diarrhoea, prostration, oedema of the head and wattles, nervous signs, such as paralysis and torticollis, and respiratory signs (McFerran & McCracken, 1988). Fall in egg production, perhaps leading to complete cessation of egg laying, may precede more overt signs of disease and deaths in egg-laying birds. Virulent ND strains may still replicate in vaccinated birds, but the clinical signs will be greatly diminished in relationship to the antibody level achieved (Allan et al., 1978).
As with clinical signs, no gross or microscopic lesions can be considered pathognomonic for any form of ND (McFerran & McCracken, 1988). Carcasses of birds dying as a result of virulent ND usually have a fevered, dehydrated appearance. Gross lesions vary with the infecting virus. Virulent panzootic ND viruses typically cause haemorrhagic lesions of the intestinal tract. These are most easily seen if the intestine is opened and may vary considerably in size. Some authors have reported lesions most typically in the proventriculus, while others consider them to be most prominent in the duodenum, jejunum and ileum. Even in birds showing neurological signs prior to death, there is usually little evidence of gross lesions in the central nervous system. Lesions are usually present in the respiratory tract when clinical signs indicate involvement. These generally appear as haemorrhagic lesions and congestion; airsacculitis may be evident. Egg peritonitis is often seen in laying hens infected with virulent NDV.
Microscopic lesions are not considered to have any diagnostic significance. In most tissues and organs where changes occur, they consist of hyperaemia, necrosis, cellular infiltration and oedema. Changes in the central nervous system are those of nonpurulent encephalomyelitis.
Molecular basis of pathogenicity of ND
During replication, NDV particles are produced with a precursor glycoprotein, F0, which has to be cleaved to F1 and F2 for the virus particles to be infectious (Rott and Klenk 1988). This post translation cleavage is mediated by host cell proteases (Nagai et al. 1976a). Trypsin is capable of cleaving F0 for all NDV strains and in vitro treatment of noninfectious virus will induce infectivity (Nagai et al., 1976b).
The cleavability of the F0 molecule was shown to be related directly to the virulence of viruses in vivo (Rott, 1979; Rott, 1985). It would appear that the F0 molecules of viruses virulent for chickens can be cleaved by a host protease or proteases found in a wide range of cells and tissues. This allows these viruses to spread throughout the host, damaging vital organs. In contrast F0 molecules in viruses of low virulence appear to be restricted in their sensitivity to host proteases resulting in restriction of these viruses to growth only in certain host cell types.
Since the initial studies comparing the deduced amino acid sequences at the cleavage site of the F0 precursor of a number of virulent and avirulent ND strains (Collins et al, 1993), a large number of studies has confirmed the presence of multiple basic amino acids at that site in virulent viruses. Usually the sequence has been 113RQK/RR ¯ F117 in virulent viruses and most have had a basic amino acid at position 112 as well. In contrast, viruses of low virulence usually have the sequence 113K/RQG/ER ¯ L117.
The major influence on the pathogenicity of NDV is therefore the amino acid motif at the F0 cleavage site, the presence of basic amino acids at positions 113, 115 and 116 and phenylalanine at 117 in virulent strains means that cleavage can be effected by protease or proteases present in a wide range of host tissues and organs. For viruses of low virulence, cleavage can occur only with proteases recognizing a single arginine, i.e. trypsin-like enzymes. Such viruses are therefore restricted in the range of sites where they are able to replicate to areas with trypsin-like enzymes, such as the respiratory and intestinal tracts, whereas virulent viruses can replicate in a range of tissues and organs resulting in a fatal systemic infection (Rott, 1979).
Definition of Newcastle Disease
Although it is likely that the vast majority of birds are susceptible to infection with ND viruses of both high and low virulence for chickens, the disease seen with any given virus may vary enormously from one species to another. Many other factors also affect the course of disease (see above). ND viruses show a considerable range of virulence for susceptible hosts such as chickens. Generally, variation consists of clusters around the two extremes in tests used to assess virulence, but, for a variety of reasons, some viruses may show intermediate virulence [mesogenic]. Equally, the very virulent viruses may infect and replicate in vaccinated birds without causing clinical disease (Parede & Young, 1990; Guittet et al., 1993; Capua et al., 1993). This enormous variation in virulence and clinical signs means that none can be regarded as pathognomonic and that it is necessary to define carefully what constitutes ND for the purposes of trade, control measures and policies.
The current OIE definition (OIE, 2000a) is:
Newcastle disease is defined as an infection of birds caused by a virus of avian paramyxovirus serotype 1 (APMV-1) that meets one of the following criteria for virulence:
a) The virus has an intracerebral pathogenicity index (ICPI) in day-old chicks (Gallus gallus) of 0.7 or greater.
or
b) Multiple basic amino acids have been demonstrated in the virus (either directly or by deduction) at the C-terminus of the F2 protein and phenylalanine at residue 117, which is the N-terminus of the F1 protein. The term 'multiple basic amino acids' refers to at least three arginine or lysine residues between residues 113 to 116. Failure to demonstrate the characteristic pattern of amino acid residues as described above would require characterisation of the isolated virus by an ICPI test.
In this definition, amino acid residues are numbered from the N-terminus of the amino acid sequence deduced from the nucleotide sequence of the F0 gene, 113-116 corresponds to residues -4 to -1 from the cleavage site."
Origins of Virulent ND Viruses
The emergence of ND as a highly pathogenic disease in poultry since 1926, (initially predominantly in South East Asia), suggests that some sudden major change has occurred either in the virus or in its hosts. Hanson (1972) considers that the various hypotheses which have been put forward can be grouped into three categories:
The virulent virus has always existed in poultry in South East Asia, but it was not until the beginning of the commercialisation of the industry in that part of the world that the disease, with its enormous economic impact, was noticed as a significant problem.
The virus is enzootic in different species, possibly inhabiting tropical rain forests, and spread to domestic poultry because of the incursion of man into that habitat.
There is a major mutation of a precursor virus of low virulence.
The first explanation remains a possibility. Some consider it unlikely that the disease would have gone unreported if it was enzootic in village chickens, but even today village chickens throughout Africa, Asia and the Americas often show high levels of mortality, either regularly or as large die-offs every few years which go largely undiagnosed. Similarly, there have been occasional descriptions of disease outbreaks prior to 1926 that are very similar to ND.
The second explanation has, until recent years, been generally accepted as the most likely. The reason is mainly the discovery that during the 1970-73 panzootic, movement of captive caged birds, particularly psittacines which may be resistant excreters of NDV, was, to some extent, responsible for the introduction and spread in some countries, particularly California (Francis, 1973, Walker et al., 1973). However, as discussed above, viruses isolated from feral birds are usually of low virulence and it has been suggested that caged birds are most probably infected after they have been trapped. Maintenance of the virus in any feral bird species seems unlikely because of the effect that infection is likely to have on the bird's survival.
The third explanation has usually been dismissed out of hand as probably representing a mutation too big to be within the bounds of probability, especially without any apparent evolutionary advantage that would result from such selection. However, viruses isolated from ND outbreaks in Ireland and Australia during the 1990s have suggested that this may be how some virulent ND viruses emerge.
In 1990 in Ireland two outbreaks of ND occurred in egg laying birds. The viruses isolated were highly virulent and apparently identical (Alexander et al., 1992). They were very closely related antigenically and genetically (Collins et al., 1998) to viruses of low virulence normally isolated from feral waterfowl but known to have infected chickens in Ireland in 1987 (McNulty et al., 1988). The group formed by these viruses was both antigenically and genetically distant from all other ND viruses. Collins et al (1993) has shown that the virulent virus had four nucleotide differences at the site coding for the F0 cleavage site compared to the related viruses of low virulence (Table 1.1.), which would explain the higher virulence for chickens. However, the distinctiveness of this group of viruses from other ND viruses support the theory that the virulent viruses arose by mutation from those of low virulence.
Phylogenetic studies have shown all the virulent viruses responsible for the outbreaks in Australia from 1998 to 2000 are extremely closely related to each other and to the endemic virus of low virulence. This suggests their emergence by mutation which, in this instance, required only two point mutations (Table 1.2., Westbury, 2001).
If mutations to virulence do occur, it is not clear whether these take place in feral birds and are then passed to poultry or whether they occur once the virus has been introduced to poultry. The lack of virulent isolations from feral birds, however, suggests that the latter is the more likely.
If virulent ND strains can emerge from those of low virulence by mutation, this may have important repercussions on the current methods of control of ND - mainly because of the enormous amounts of live vaccines used throughout the world.
Table 1.1. Nucleotide/amino acid sequences at F0 cleavage site of virus of high virulence [34/90] isolated from poultry in Ireland compared to antigenically and genetically closely related virus of low virulence isolated from ducks
|
Virus |
Virulence |
Nucleotide/amino acid sequence at F0 cleavage site |
|
MC110 |
low |
GAA CGG CAG GAG CGT CTG |
|
112ERQER*L117 |
||
|
34/90 |
high |
AAA CGG CAG AAG CGT TTT |
|
112KRQKR*F117 |
Table 1.2. Nucleotide/amino acid sequence at F0 cleavage site of virus of high and low virulence isolated in Australia in 1998
|
Virus |
Virulence |
Nucleotide/amino acid sequence at F0 cleavage site |
|
1154/98 |
low |
GGA AGG AGA CAG GGG CGT CTT |
|
111GRRQGR*L117 |
||
|
1238/98 |
high |
GGA AGG AGA CAG AGG CGT TTT |
|
111GRRQRR*F117 |
||
|
1249/98 |
high |
GGA AGG AGA CAG AGG CGT TTT |
|
111GRRQRR*F117 |
EPIDEMIOLOGY
Host Range
ND viruses have been reported to infect animals other than birds, ranging from reptiles to man (Lancaster 1966). Kaleta and Baldauf (1988) concluded that NDV infections have been established in at least 241 species of birds representing 27 of the 50 Orders of the class. It seems probable that all birds are susceptible to infection but, as stressed by Kaleta and Baldauf, the disease seen with any given virus may vary enormously from one species to another.
Wild birds
NDV isolates have been obtained frequently from migratory feral waterfowl and other aquatic birds. Most of these isolates have been of low virulence for chickens and similar to viruses of the "asymptomatic enteric" pathotype. The most significant outbreaks of virulent NDV in feral birds have been those reported in double-crested cormorants (Phalacrocorax auritus) in North America during the 1990s. Earlier reports of ND in cormorants and related species had been in the late 1940s in Scotland (Blaxland, 1951) and in Quebec in 1975 (Cleary, 1977). Recent outbreaks in cormorants in North America were first seen in 1990 in Alberta, Saskatchewan and Manitoba in Canada (Wobeser et al., 1993). In 1992 the disease re-appeared in cormorants in western Canada, around the Great Lakes and North mid-west USA, in the latter case spreading to domestic turkeys (Mixson & Pearson, 1992; Heckert, 1993). Antigenic and genetic analyses of the viruses suggested that all the 1990 and 1992 viruses were very closely related despite the geographical separation of the hosts. Disease in double-crested cormorants was observed again in Canada in 1995 and in California in 1997 and in both instances NDV was isolated from dead birds; as before, these viruses appear to be closely related (Kuiken, 1998).
Thirty-eight outbreaks of ND in commercial poultry were confirmed in 1997 in the United Kingdom (Alexander et al., 1998). There were also outbreaks caused by genetically similar viruses in Scandinavian countries in 1996 (Alexander et al., 1999). These, linked to the unusual patterns of movement of migratory birds at the end of 1996 and the beginning of 1997, suggest that migratory birds may have been responsible for the primary introduction of the causative virus into Great Britain (Alexander et al., 1998).
Caged "pet birds"
Virulent NDV isolates have often been obtained from captive caged birds (Senne et al., 1983). Kaleta and Baldauf (1988) thought it unlikely that infections of recently imported caged birds resulted from enzootic infections in feral birds in the countries of origin. They considered that the infections probably originated at holding stations before export, either as a result of enzootic NDV at those stations or of spread from nearby poultry such as backyard chicken flocks. Panigrahy et al., (1993) described outbreaks of severe ND in pet birds in six states in USA in 1991. Illegal importations were assumed to be responsible for the introductions of the virus.
Domestic poultry
Virulent NDV strains have been isolated from all types of commercially reared poultry, ranging from pigeons to ostriches.
Racing and show pigeons
In the late 1970s, an NDV strain, PPMV-1, showing some antigenic differences from classical strains, appeared in pigeons. It,, probably arose in the Middle East and subsequently produced a true panzootic, spreading in racing and show pigeons to all parts of the world (Alexander, 1997).
Introduction and spread
Transmission between birds
Apart from predatory birds or the practice of feeding poultry with untreated swill containing poultry meat, spread from bird to bird appears to occur as the result of either inhalation of excreted droplet particles or the ingestion of infective material such as faeces. Although it is clear from the administration of live vaccines by aerosol that infection may be established via the respiratory route, there is remarkably little experimental evidence that infected birds pass on the virus to susceptible birds in this way, even over short distances. The success of this route of transmission depends on many environmental factors, such as temperature, humidity, and stocking density. In contrast, it is easily demonstrated that virus infection can be passed from one bird to another via contaminated faeces. It seems most likely that the pigeon variant virus, the "asymptomatic enteric" viruses, and other viruses which fail to induce significant respiratory signs in infected birds, are transmitted primarily in this way (Alexander et al., 1984).
Several reviews have dealt with the way in which the ND virus may be introduced into a country or area and then subsequently spread from flock to flock (Lancaster, 1966; Lancaster and Alexander, 1975; Alexander 1988b, 1995). In summary, the main methods by which virus can be spread are:
Movement of live birds
Migratory feral birds may be responsible for the primary introduction of infection, but nearly all NDV isolates obtained from feral birds have been of low virulence. A more significant role of such birds may be the spread within an area once NDV infections have already occurred in poultry. Exceptions to the presence of the virus of low virulence in migratory birds have been discussed in the Host Range section above.
World trade in captive caged birds is enormous and in many countries virulent NDV has been isolated frequently from such birds held in quarantine. For example, 147 virulent NDV isolations were made from 2 274 lots of captive birds held in quarantine in the USA during 1974-1981 (Senne et al,. 1983). Some infected psittacines have been shown to excrete virulent virus intermittently for extremely long periods, in some cases for more than one year (Erickson et al., 1977). This further emphasises the potential role these birds may have in the introduction of NDV to a country or area.
There is also considerable international trade in game birds, which are often imported for immediate release.
The potential for racing pigeons to carry and introduce ND into a country or area has been highlighted by the panzootic in such birds over the last ten years.
Trade in backyard flocks and other birds kept for recreational purposes (hobby birds) has been implicated in the introduction and spread of ND in the outbreaks in European Union countries during 1991-1994.
Modern methods of slaughter of commercial poultry, marketing of poultry meat and veterinary inspection, have reduced the movement of live commercial poultry (with the exception of day-old chicks) in many European and other developed countries. However, in many countries, the normal method of trade is by live poultry markets. Such markets, where birds of many different species may be placed in close contact with each other, represent ideal opportunities for viruses to be disseminated. The movement of village chickens from one village to another, whether directly or through live bird markets, is the main method of spread of ND [see below].
Movement of people and equipment
Secondary spread during most epizootics of ND in recent times has been the result of the movements of personnel or equipment. Human beings may be infected with NDVs, but their most likely role is the transfer of infective poultry faeces from one site to another via clothing, footwear, crates, feed sacks, egg trays or vehicles.
Movement of poultry products
In the past, poultry meat has been seen as the main vehicle for the introduction and spread of NDV. Modern methods of poultry carcass preparation as well as legislation on the feeding of untreated swill to poultry have greatly diminished the risk from poultry products, but the possibility of spread in this way still remains.
Contaminated poultry food or water
In the British Isles, outbreaks of ND in commercial poultry have been associated with food contaminated with infective faeces from feral pigeons infected with the ND virus (Alexander et al., 1985; O'Reilly et al., 1994). Similarly, water contaminated with infective faeces may introduce NDV to a flock.
Airborne spread
In recent years, the significance of airborne transfer of viruses has been the subject of some debate. During the 1960s and 1970s, this was considered a major method of spread and Smith (1964) considered it the most logical explanation of spread in outbreaks occurring in 1960 and 1962 in Great Britain. In the same country, Dawson (1973) considered windborne spread to be of major significance during the 1970-1972 outbreaks that were noted for the severe respiratory signs and unusual patterns of spread. But in the 1971-1973 epizootic in California, with ostensibly the same virus, respiratory signs were not especially prominent and Utterback and Schwartz (1973) considered airborne spread to be of little significance.
There have been few attempts to assess the survival of airborne virus, but Hugh-Jones et al., (1973) were able to detect virus 64 metres but not 165 metres downwind of infected premises. These authors stressed the importance of environmental conditions, particularly relative humidity, with regard to the likelihood of airborne spread.
It is possible that when climatic conditions have been right and poultry farms sufficiently concentrated, as in Northern Ireland in 1973 (McFerran, 1989), airborne spread may have played a significant role in epidemics of ND. But in recent years, airborne spread has not been an issue in reported outbreaks and there has nearly always been an alternative and more likely cause, particularly the movement of poultry and humans.
VACCINES
Good manufacturing practices should ensure that vaccines are highly unlikely to be carriers of virulent ND virus. However, in the past, birds have become infected by vaccines for other diseases being contaminated with ND and also as a result of failure to properly inactivate vaccines prepared from virulent ND virus. In 1996-1997, a series of ND isolates of low virulence were obtained from poultry flocks in Denmark, a country which pursues a non-vaccinating policy for ND. It was demonstrated that these viruses were the result of contamination of avian virus vaccines with vaccinal ND viruses (Jorgensen et al., 2000). This episode further emphasises the potential of spread of ND in this way.
Non-avian hosts
This is likely to be by mechanical transfer of infective faeces, for example, by insects, rodents or scavenging animals. In hot countries, reptiles may enter poultry houses and should not be ignored as potential spreaders of NDV, as their susceptibility to infection has been reported.
BIOSECURITY AND HYGIENE IN THE CONTROL OF ND
In countries or areas that are free of virulent NDV, the primary aim should be to prevent the introduction of the virus. Because migratory and other feral birds frequently carry NDV strains of low virulence, which spread from time to time to domestic poultry, it is usual to exclude such viruses from control policies. Vaccinal viruses are somewhat different, as some are sufficiently virulent to cause disease in fully susceptible birds.
In some countries there is legislation designed to reduce the likelihood of outbreaks from specific sources. For example, on the island of Ireland there has been a legal requirement to heat treat poultry feed to reduce the possibility of introduction of NDV by this route.
On commercial farms, control measures should attempt to prevent viruses from infecting the flock. It is of paramount importance that good hygiene and biosecurity measures aimed at preventing the introduction of viruses by the routes described above are practised at all times on poultry farms.
Biosecurity aimed at preventing disease should begin at the planning stage of commercial poultry farms. Farms and flocks should be well separated, hatcheries should be isolated from poultry farms, different species should be reared on different sites, and there should be an adequate fresh water supply, preferably one that does not draw on surface water. Often in developed countries such practices are difficult to impose as the poultry industry may already be established in areas with high concentrations of poultry flocks and with little opportunity to change due to limitations of available land. But in countries where the commercialisation of poultry farming is at a developmental stage, these points should be adopted.
On the farms the following points should be observed:
Houses, food stores and water tanks should be bird-proofed.
Movements on and off the farm should be kept to a minimum.
All equipment, especially vehicles, should be disinfected before access to the site is permitted.
Movements between different farms for egg collection, carcass collection, food delivery and the like should be confined to a specified collection and delivery point away from the poultry flocks. Unfortunately, as poultry farming has become industrialised and its profits marginalised, the move has been away from such precautions which are often considered an expensive luxury.
Visits by personnel such as bleeding or vaccination teams, inseminators and veterinarians are the most likely method of introduction of ND and if such visits are unavoidable, regimens of clothing change, equipment disinfection and other basic hygiene controls must be enforced.
Possibly the greatest aid to implementing biosecurity and hygiene measures that will assist in the prevention or control of ND is the education of farmers and those working with poultry with respect to the spread of virus and measures to avoid it. The best tool for the control of ND at any level, international, national or local farm, may well be an efficient, well-manned poultry extension service.
