Selected content from the Animal Health and Production Compendium (© CAB International 2013). Distributed under license by African Union – Interafrican Bureau for Animal Resources.
Whilst this information is provided by experts, we advise that users seek veterinary advice where appropriate and check OIE manuals for recent changes to regulations, diagnostic tests, vaccines and treatments.
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.
Identity Pathogen/s Overview Distribution Distribution Map for Africa Distribution Table for Africa Hosts/Species Affected Host Animals Pathology Diagnosis Disease Course Disease Treatment Table Vaccines Prevention and Control References Links to Websites OIE Reference Experts and Laboratories Images
Preferred Scientific Name
International Common Names
avian distemper, avian pneumoencephalitis, newcastle disease, rubulavirus, in birds
Newcastle disease virus
Newcastle disease (ND) is a highly contagious viral disease that affects birds all over the world. The disease has a huge economic impact and is classified as a notifiable disease by the World Organisation for Animal Health (formerly Office International des Epizooties, OIE). The disease is caused by Newcastle disease virus (NDV), which belongs to the genus Rubulavirus of the Family of Paramyxoviridae. Avian paramyxoviruses are classified into 9 serotypes designated avian paramyxovirus (APMV)-1 to APMV-9 (Alexander, 2000). NDV has been designated APMV-1. The virus contains two envelope proteins: the HN protein with haemagglutinating (H) and neuraminidase (N) activity, and the F protein that is responsible for cell fusion. The HN and F proteins induce protective immune responses. The susceptibility to ND varies between species, and strains of NDV also vary widely in the severity of disease they may produce. Lentogenic, mesogenic and velogenic strains are distinguished in increasing order of pathogenicity, based on the mean death time of an infected chick embryo. Strains may also vary in their tropism and transmission. Viscerotropic viruses, which usually kill birds quickly, are not distributed as widely as pneumotropic viruses, which kill birds more slowly. Sometimes the disease may go unnoticed, such as in duck and geese. After an incubation period of 2-15 days, general symptoms such as loss of appetite, huddling, weakness, and a decrease in egg production may occur. The symptoms may affect the respiratory tract (dyspnea and gasping), circulatory system (cyanosis of comb and wattle), gastrointestinal tract (crop dilatation, catarrh, and foamy mucus in the pharynx) and nervous system (ataxia, paralysis, and torticollis).
Domestic and free-living birds of many species are susceptible, as are caged or aviary birds, which are usually captured wild in countries where ND is endemic. Birds captured in the wild in endemic countries may introduce ND into a country free of the disease. Birds in poultry houses may be infected by humans and contaminated equipment, and also by sparrows, pigeons, game birds or other vectors. Studies have been published showing presence of NDV among waterfowl, but such birds seem to have a minor role in transmitting the virus to commercial poultry flocks (Astorga et al., 1994).
Control is based on strict hygiene, monitoring systems and stamping out or vaccination. Depending on the geographical area and the trade situation, countries may impose national monitoring and vaccination policies. Live vaccines are normally used; these are administered by eye, nose drop, spray or drinking water. Inactivated vaccines that are injected can also be used. Although live vaccines are highly effective, inactivated vaccines have the advantage that post-vaccinal respiratory reactions do not occur. The induction of haemagglutinating inhibition (HI) antibody titres is highly correlated with protection.
This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.
Newcastle disease (ND) is endemic in many countries of the world. However, some European countries have been free of the disease for years (OIE, 2000).
The first outbreaks of ND are thought to have occurred in 1926 in Java, Indonesia and in Newcastle-upon-Tyne, UK (Alexander, 1997). Different clinical representations of the disease gave rise to different names, such as pseudo-fowl pest, avian distemper or avian pneumo-encephalitis, until serological evaluations revealed that these syndromes were due to the same causative agent (Alexander, 1997). It is speculated that the first panzootic spread of NDV started in the 1920s in Southeast Asia, and took about 30 years to spread around the globe. A second panzootic may have begun in the Middle East in the late 1960s and global spread occurred much more rapidly due to the intensification of the poultry industry worldwide, reaching most countries in about a decade. Imported NDV-carrying psittacine birds captured in the wild are associated with this second panzootic of ND. A third panzootic spread of ND, around the late 1970s, has been related to pigeons and doves (Columba livia) that were kept for leisure. It reached Europe in the 1980s (Alexander, 1997).
International reporting and recording of ND is carried out by the Food and Agricultural Organisation (FAO) of the United Nations. Due to the widespread use of vaccines, the true prevalence of the disease is difficult to assess, but ND is still widespread in many countries in Asia, Africa, and the Americas (Marin et al., 1996). Only countries of Oceania, and some in Europe, are relatively free of the disease. During the 1980s most countries in Europe remained free of ND, but since 1991 many outbreaks have occurred in Western Europe. There have been outbreaks in Belgium, Scandinavia, Denmark, The Netherlands, Luxembourg, Germany, Switzerland, Italy, Spain, Portugal, Malta, the UK and France (Alexander, 1997; Alexander et al., 1998; Lomniczi et al., 1998; OIE, 2005; OIE, 2006). Importantly, outbreaks tend to occur increasingly in backyard flocks, rather than in large commercial flocks. This makes it even more difficult to control and prevent new outbreaks, and studies of backyard birds are scarce (Gutierrez-Ruiz et al., 2000).
For current information on disease incidence, see OIE's WAHID Interface.
Thirty one African countries covering west, east and southern Africa regions reported ND to the AU-IBAR in 2011. Overall, the disease affected a total of 1,031 epidemiological units involving 487,206 cases and 326,706, with a case fatality rate of 67.1% (see table below). The three countries with the highest number of outbreaks are Ghana (216), Benin (152) and Uganda (120). Sierra Leon and Liberia reported ND for the first time in 2010 and continued reporting in 2011 indicating the impacts of capacity building programs provided through SPINAP and VACNADA projects for improving disease surveillance and reporting. Generally, all other countries have consistently reported ND during the past four years, consistent with the known endemicity of the disease on the African continent.
Countries reporting ND to AU-IBAR in 2011
NS: Not specified
There appears to be no temporal trend for ND occurrence on the continent, suggesting the lack of seasonality for the risk factors that determine occurrence and maintenance of the disease.
= Present, no further details = Widespread = Localised
= Confined and subject to quarantine = Occasional or few reports
= Evidence of pathogen = Last reported... = Presence unconfirmed
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further information for individual references may be available in the Animal Health and Production Compendium. A table for worldwide distribution can also be found in the Animal Health and Production Compendium.
|Country||Distribution||Last Reported||Origin||First Reported||Invasive||References||Notes|
|Algeria||Disease not reported||OIE, 2009|
|Botswana||Present, no further details||OIE, 2012|
|Burkina Faso||Present||OIE, 2012|
|Burundi||Present, no further details||OIE, 2012|
|Cameroon||Present, no further details||OIE, 2012|
|Cape Verde||Present, no further details||OIE, 2012|
|Central African Republic||Present, no further details||OIE, 2012|
|Chad||Present, no further details||OIE, 2012|
|Congo Democratic Republic||Present, no further details||OIE, 2012|
|Côte d'Ivoire||Present, no further details||OIE, 2012|
|Djibouti||Last reported||2003||OIE, 2012|
|Egypt||Disease not reported||OIE, 2009|
|Gabon||Disease not reported||OIE, 2009|
|Gambia||OIE, 2009||Disease suspected|
|Kenya||Present, no further details||OIE, 2012|
|Liberia||Present, no further details||AU-IBAR, 2011|
|Libya||Last reported||1976||OIE Handistatus, 2005|
|Mali||Present, no further details||OIE, 2012|
|Morocco||Disease not reported||OIE, 2009|
|Niger||Present, no further details||AU-IBAR, 2011|
|Réunion||Disease not reported||OIE Handistatus, 2005|
|Rwanda||Present, no further details||OIE, 2012|
|Sao Tome and Principe||Serological evidence and/or isolation of the agent||OIE Handistatus, 2005|
|Senegal||Present, no further details||OIE, 2012|
|Seychelles||OIE, 2012||Disease suspected|
|Somalia||No information available||OIE Handistatus, 2005|
|South Africa||Present||OIE, 2012|
|Sudan||Disease not reported||OIE, 2009|
|Tunisia||Disease not reported||OIE, 2009|
Many species of bird are susceptible to Newcastle disease virus (NDV). In addition to the domestic avian species, natural or experimental infection with NDV has been demonstrated in at least 236 species from 27 of the 50 orders of birds. It is generally agreed that aquatic birds such as ducks and geese are least susceptible to NDV (Bolte et al., 2001), while the most susceptible are chickens, and gregarious birds forming temporary or permanent flocks (Kaleta and Baldauf, 1988; Kouwenhoven, 1993). The breeds used in the poultry industry are equally susceptible, only some indigenous breeds are less susceptible (Kouwenhoven, 1993).
APMV-2 viruses are mainly found in passerines and turkeys as primary hosts, and furthermore in chickens, psittacines and rails. APMV-3 viruses are primary isolated from turkeys (see table).
Table: Avian paramyxoviruses (APMVs), main hosts and disease*
|APMV-1 (NDV)**||Domestic and wild bird species||Variable: severe to subclinical|
|APMV-2**||Passerines, turkeys, chickens, psittacines||Respiratory disease, egg production loss|
|APMV-3**||Turkeys, psittacines, passerines||Respiratory disease, egg production loss Encephalitis in psittacines|
|APMV-4||Ducks, geese, rails||Subclinical|
|APMV-6||Duck, geese, turkeys||Mortality in turkeys, otherwise subclinical|
|APMV-9 (only one isolate)||Duck||Subclinical|
*adapted from Alexander, 1993, Alexander, 1997, Kouwenhoven, 1993.
** these APMVs have also been isolated from captive cage birds (Alexander, 1993)
Blood and Circulatory System - Poultry
Digestive - Poultry
Nervous - Poultry
Reproductive - Poultry
Respiratory - Poultry
Infection takes place either by inhalation or by ingestion, and this mode of infection is also used for mass application of live vaccines by spray and aerosol generators (Alexander, 1997). In aerosols, particles of <5 microns disperse in the entire respiratory tract including the airsacs. Particles > 5 microns are caught in the conjunctivae, nose and trachea down to the bifurcation. Horizontal transmission between birds depends on the availability of the virus in infectious form and may occur through inhalation of fine aerosols or large droplets containing the virus. These droplets originate from the exhaled air of birds in which the virus has replicated in the respiratory tract. Virus may be transmitted by dust and other particles, including faeces. Spread of avirulent NDV may predominantly occur through ingestion of infected faeces; in this case respiratory signs are absent. Virus is shed during the incubation period and for a limited period during convalescence. As an exception, some psittacine birds have been demonstrated to shed NDV intermittently for over 1 year (OIE, 2000).
Vertical transmission is not important for transmission of the virus, and it has not been clearly demonstrated. Experimental infection of laying hens frequently stops them from laying, and chick embryos die very soon after infection with NDV. Furthermore, the virus may penetrate the shell of infected eggs, complicating the assessment of true vertical transmission (Alexander, 1997).
Outbreaks of ND may occur as a result of movement of infected live (caged) birds (Clavijo et al., 2000), transmission from infected water fowl (Takakuwa et al., 1998), contaminated people or equipment, infected poultry products (meat, feathers, blood, offal, poultry scraps and bones), airborne spread, contaminated poultry feed, drinking water (surface contamination or by seepage from infective faeces), and vaccines (Alexander, 1997, Kouwenhoven, 1993). However, the greatest risk of spread of NDV comes from the movement of people and equipment. Due to centralization of many processes in the poultry industry there is intensive traffic of personnel and vehicles (feed and chicken trucks, egg collectors, advisors, helpers, veterinarians, neighbours) moving from one flock to another (Kouwenhoven, 1993). The virus is easily spread by mechanical transfer, by people carrying the virus or transporting contaminated equipment, or by infective material (most probably faeces). Vaccination crews have also been implicated in the spread of NDV, as have incompletely inactivated and contaminated vaccines (Alexander, 1997).
Climate does not seem to have a significant effect on virus transmission, because the disease occurs in both hot and dry and moist temperate climate zones.
Newcastle disease has been one of the most important diseases of poultry since its discovery in the early 1920s. The regular outbreaks, high mortality and morbidity, worldwide distribution, its classification as a notifiable disease by the World Organisation for Animal Health (OIE), and the massive use of live and inactivated vaccines explain its huge economical importance. There are difficulties in controlling the disease because of the number of hosts. The implications of the constant variation of the causative virus make it unlikely that in the near future the disease will lose its importance.
Humans may be infected in the conjunctival sac with NDV, but this does not generate a systemic infection (Alexander, 1997). Even a wild-type NDV infection induces only mild disease, mainly mild conjunctivitis and laryngitis (Schirmacher et al., 1998). NDV does not pose a risk for food safety.
There are no pathognomonic gross lesions for NDV infections and the lesions are dependent on the strain and pathotype of the virus, in addition to the host and environmental factors, such as secondary E. coli infections, Ornithobacterium tracheale (Odor et al., 1997), or infections with Mycoplasmas.
Infections with viscerogenic velogenic NDV strains induce haemorrhages. These lesions predominantly occur in the proventriculus (concentrated around the orifices of the mucous glands), the posterior half of the duodenum, jejunum and ileum, and are nearly pathognomonic for VVNDV (Kowenhoven, 1993; OIE, 2000). The lesions can develop into diphtheroid inflammations, that later become necrotic. Intestinal lymphoid tissue, including the caecal tonsils, is swollen. Gut contents are grey-green. Catarrhal or serous conjunctivitis, rhinitis, sinusitis and caseous tracheitis can also be observed. Sprayed vaccines may cause a caseous exudate in the trachea. Airsacculitis may be observed, often complicated by E. coli or M. gallisepticum infections (Nakamura et al., 1994). In adult layers, egg yolk may be seen in the abdominal cavity. The ovaries are oedematous, and ovarian follicles are often flaccid, degenerative, and may contain haemorrhages.
Gross lesions are not normally found in the nervous system, regardless of the infecting pathotype.
In the respiratory system, cilia may be lost in 1-2 days after aerosol infection. The mucosa subsequently shows congestion, oedema, and infiltration of inflammatory cells such as the lymphocytes and macrophages. However, recovery may occur rapidly.
The haemorrhages may be explained by microscopic lesions in the vascular system. The media may show hydropic degeneration, hyalinization of the capillaries and arterioles, development of hyaline thrombosis in small vessels, and necrosis of endothelial cells (Alexander, 1997). Lymphoid tissue may be depleted of lymphoid cells, and show degeneration and necrosis, particularly in the thymus, bursa and spleen.
In the nervous system, a non-purulent encephalomyelitis can be observed in the cerebellum, medulla, midbrain, brain-stem and spinal cord, with neuronal degeneration, foci of glial cells and perivascular infiltration of lymphocytes (Kouwenhoven, 1993; Alexander, 1997).
In the reproductive system, atresia may occur in the follicles, with infiltration of inflammatory cells and formation of lymphoid aggregates (Alexander, 1997).
Clinical diagnosis can be made upon respiratory or nervous signs. Birds may suddenly cough, gasp or may droop their wings. The animals may twist their head or neck, or show ataxia or paralysis. Diagnosis may also be made when egg production has decreased or completely stopped, and eggs are misshapen, rough-shelled, thin-shelled and contain watery albumen. Also when birds show greenish diarrhoea, and tissues around the neck are oedematous and swollen, NV may be suspected. However, a presumptive diagnosis of ND must always be confirmed by virus isolation and identification.
Laboratory diagnosis depends on the detection of the agent, because the widespread use of vaccines hampers the interpretation of serological results (OIE, 2008). Although direct detection of NDV antigen by immunohistological techniques may unequivocally reveal the presence of NDV, these methods, including immunofluorescence, impression smears or immunoperoxidase techniques, do not allow further characterization of the virus and are less sensitive than virus isolation. Therefore, virus isolation (VI) is preferred. Inoculation of specific-pathogen-free (SPF) or NDV-antibody free embryonated chicken eggs, incubated 9-11 days before use, is the most sensitive method for isolation of NDV (Kouwenhoven, 1993; Alexander, 1997). Samples to be used for VI are preferentially cloacal swabs or faeces of dead birds, intestinal contents, tracheal material or bone marrow. Whole carcasses should preferably be submitted, without freezing and thawing (Kouwenhoven, 1993; Alexander, 1997). About 0.2 ml supernatant of a clarified 20% w/v suspension of pooled organs containing antibiotics (10 minutes 1000 x g) is injected in the allantoic cavity of at least five embryonated eggs. The embryos frequently die within 3-6 days after inoculation and are subsequently tested for haemagglutinating activity. HI-positive isolates should be further typed with Avian paramyxovirus (APMV)-monospecific sera. In particular APMV-1 should be distinguished from APMV-3 and -7 (OIE, 2000). Blind passaging is seldom required (Alexander, 1997; Kouwenhoven, 1993; OIE, 2000).
The polymerase chain reaction (PCR) is frequently used to detect, and quantifiy, NDV (Fuller et al., 2009; Jang et al., 2011) in conjunction with virus isolation and biological characterization for index cases.
Virulence is traditionally determined using in vivo pathogenicity tests to distinguish between high, moderate and low virulence isolates (OIE, 2008). The pathogenicity of any newly isolated virus can be assessed by determining the mean death-time in eggs, the intracerebral pathogenicity index in 1-day old chickens or by the intravenous pathogenicity index in 6-week old chickens. Increasingly the polymerase chain reaction (PCR), in which the fusion protein (F0) gene is amplified followed by sequencing of that part of the F0 gene that encodes the cleavage site (between the F2 and F1 polypeptides) has been used to differentiate virulent from non-virulent strains (Kant et al., 1997; Nanthakumar et al., 2000; OIE, 2000; Aldous et al., 2001; Al-Garib et al., 2003). At the position where the F0 polypeptide is cleaved, to produce F2 and F1 polypeptides, there are a number of basic amino acid residues (arginine, R, and/or lysine, K) at the C-terminus of the F2 polypeptide. Most NDVs that are pathogenic for chickens have the sequence 112R/K-R-Q-K/R-R116 at the C-terminus of the F2 protein i.e. at least one pair of basic amino acids, whereas viruses of low virulence have the sequence 112G/E-K/R-Q-G/E-R116 i.e. the basic amino acids only occur singly. Furthermore, the virulent and non-virulent strains have a phenylalanine or leucine residue at position 117 (start of the F1 polypeptide), respectively.
PCR can be used to detect the virus in clinical specimens as well as following the growth of virus in embryos in the laboratory, the advantage being the extremely rapid demonstration of the presence of virus and even its virulence if primers covering the part of the genome coding for the F0 cleavage site are used (Creelan et al., 2002). However, some studies have shown lack of sensitivity of RT-PCR in detecting virus in some organs and particularly in faeces (Creelan et al., 2002). Multiplex PCR tests have been developed to allow simultaneous detection and differentiation of several avian viruses, such as NDV, avian pneumovirus and avian influenza (Malik et al., 2004). Multiplex PCR techniques have also been used experimentally to differentiate between velogenic, mesogenic and lentogenic strains from chickens (Shan et al., 2003). Real-time RT-PCR techniques have been developed in which detection is faster than conventional RT-PCR, partly because of automation and in part because the PCR product is detected during the actual PCR reaction; a separate detection stage is not required (Jang et al., 2011). Fuller et al. (2009) have developed a real time PCR which simultaneously detects and pathotypes strains of NDV. As with virulence determination, it is important that molecular techniques alone are not used to record a negative result in investigations of suspected ND (OIE, 2004f). Indeed, isolation of virus and assessment of pathogenicity in vivo is an international obligatory requirement at the start of each outbreak.
Table: Methods to determine the pathogenicity of NDV isolates*
|Mean death time||Intracerebral pathogenicity index||Intravenous pathogenicity index||Molecular basis for pathogenicity|
|Sample||Fresh infective allantoic fluid||Fresh infective allantoic fluid||Fresh infective allantoic fluid||cDNA by RT-PCR|
|Method||Inoculation of embryonated eggs||Intracerebral injection into 24 hours –60 hours old SPF chickens||Intravenous injection into 6-week old SPF chickens||Determination of the deduced amino acid sequence of the F0 cleavage site of the isolate|
|Time required||7 days of observation||8 days of observation||10 days of observation||= 24 hours, dependent on RNA isolation method and interpretation of obtained sequence|
|Interpretation||Mean time in hours for the minimum lethal dose to kill all the inoculated embryos||Mean score per bird per observation over the 8-day period (0=normal, 1=sick, 2=dead)||Mean score per bird per observation over the 10-day period (0=normal, 1=sick, 2=nervous signs, 3=dead)||Pathogenic sequence**: 112 R/K-R-Q-K/R-R116 at the C-terminus of the F2 protein; F (phenylalanine) at residue 117 at the N terminus of the F1 protein Apathogenic sequence**: 112 G/E-K/R-Q-G/E-R116 at the C-terminus of the F2 protein; L (leucine) at residue 117 at the N terminus of the F1 protein|
|Score||velogenic (<60 hours); mesogenic (60-90 hours); lentogenic (>90 hours)||least virulent=0, most virulent=2||least virulent=0, most virulent=3||Pathogenic or apathogenic sequence|
* adapted from Anonymous, 2000, ** there seems to be overall the requirement of at least one pair of basic amino acids at residues 116 and 115 plus a phenylalanine at residue 117, and a basic amino acid at (R) at 113 if the virus is to show virulence in chickens (OIE, 2000).
As an example, the Ulster NDV isolate is an avirulent NDV representative with MDT, IVPI and ICPI values of 0. The well known lentogenic LaSota NDV strain has MDT, IVPI and ICPI values of 103, 0 and 0.15, respectively. An example of an extremely virulent strain is the Herts '33 NDV strain. However, there is no consequent correlation between the MDT, IVPI and ICPI, and interpretation may be difficult. Notably, the MDT is imprecise in particular for strains of low virulence. The IVPI is particularly useful for classifying moderately and highly virulent NDV isolates (Kouwenhoven, 1993).
Serological tests may be useful for diagnosis provided the vaccination status of the animals is known. Virus neutralisation, HI and ELISA tests are available, and new ELISAs have been described for use with future marker and subunit vaccines (Mackay et al., 1999). As with PCR, rapid field and multiplex versions of serological tests are being developed, for example an immunocomb-based dot-enzyme-linked immunosorbent test for detection of ND, infectious bursal disease and infectious bronchitis (Manoharan et al., 2004). At present, the HI test is most widely used. SPF chicken red blood cells are routinely used, with some variations in test procedures between laboratories. HI tests can also be used to assess the immune status of a flock (OIE, 2000).
The virus enters the body via the respiratory or intestinal tract. In the trachea, the virus is spread by ciliary activity and by cell-to-cell spread. The incubation period of ND varies from 2 to 15 days (average 5-6 days). The variation depends on the strain, the host species, its age and immune status, intercurrent infections, environmental conditions, the route of exposure and the dose (Alexander, 1997; Parede and Young, 1990). After initial multiplication at the introduction site, the virulent virus is carried by viraemia to the spleen, liver, kidney and lung. While lentogenic NDV strains are present only at low titres in the circulation, mesogenic NDV strains spread rapidly to the kidneys, lung, bursa and spleen. Virulent virus can therefore be found virtually within 22-24 hours in practically all tissues, titres being most elevated in the thymus (Kouwenhoven, 1993; Brown et al., 1999). The virus multiplication is then usually interrupted for 12-24 hours and the virus titres drop. During the second multiplication of the virus, after the arrest period, the virus is once again released into the circulation. This release is associated with the appearance of general disease signs, and the virus is released into the environment by exhaled air and faeces. Virus cells invade the brain after multiplication in non-nervous tissue has stopped, whereupon death is imminent (Kouwenhoven, 1993).
Clinical signs are loss of appetite, listlessness, abnormal thirst, huddling, weakness and somnolence. There is a sudden decrease in egg production (40% to occasionally 100%) together with de-pigmentation, and loss of the eggshell and albumen quality in layers (Kouwenhoven, 1993). The severity of the disease in chickens depends largely on the strain and host immune status. Some NDV strains may kill fully susceptible, unvaccinated chickens within 3-4 days, whereas the low virulence virus may circulate without clinical signs in unvaccinated birds. The signs may affect the respiratory (gasping and coughing), circulatory (cyanosis of comb and wattle), gastrointestinal (crop dilation, catarrh, and foamy mucus in the pharynx) and nervous systems (drooping wings, dragging legs, twisting head and neck, circling, ataxia, paralysis, and torticollis). Egg production may be reduced or cease altogether.
Consequently, NDVs have been classified into pathotypes, referring to their pathogenicity in chickens (Lopaticki et al., 1998).
Table: Pathotypes of Newcastle disease viruses in chickens (Alexander, 1997)
|Viscerotropic velogenic||highly pathogenic with haemorrhagic intestinal lesions|
|Neurotropic velogenic||high mortality following respiratory and nervous signs|
|Mesogenic||respiratory signs, occasional nervous signs, but low mortality|
|Lentogenic or respiratory||mild or subclinical respiratory infection|
|Asymptomatic enteric||subclinical enteric infection.|
Infections of chickens with viscerotropic velogenic NDV strains (VVNDV) may lead to listlessness, increased respiration and weakness, ending in prostration and death. Mortality may be up to 100% in fully susceptible flocks. In the 1970s, VVDNV outbreaks induced marked respiratory distress in the UK and including Northern Irish flocks. Oedema around the eyes and head, and greenish diarrhoea may also be present. Before death, muscular tremors, torticollis, opisthotonus and paralysis may be apparent (Alexander, 1993).
Infections of chickens with neurotropic velogenic NDV strains (NVNDV) may lead to the sudden onset of severe respiratory distress followed by neurological signs 1-2 days later. Egg production drops dramatically, but mortality is much lower than after VVNDV infections, and usually reaches a maximum of 50% in adult chickens (Alexander, 1997).
Infection of chickens with mesogenic strains of NDV usually causes respiratory disease. In adult chickens, egg production will drop greatly, which may last for several weeks. Nervous signs are uncommon. Mortality is low, and only marked in young birds (Alexander, 1997).
Infection with lentogenic strains of NDV does not usually cause disease in adult birds. In young birds infections with LaSota strains may cause respiratory disease, often resulting in mortality (Alexander, 1997).
Egg production may return to normal after 3-4 months, except after infection with velogenic NDV strains. Embryos from acutely infected flocks often die within 5 days of hatching and hatchability is reduced. In turkeys, the disease signs are usually less severe than in chickens. Ducks and geese are even more resistant to NDV infections than turkeys. Disease signs in turkeys are predominantly respiratory with airsacculitis and nervous signs (Kouwenhoven, 1993).
Antibodies against NDV can be detected in serum about 4-6 days after infection. Antibodies can be detected using virus neutralization tests (VNT) or haemagglutination tests (HI). The VN responses appear to parallel the HI responses, HI antibody responses are frequently used to determine the protective antibody response. Neutralizing antibodies are mainly directed against the F and HN proteins, but neutralizing antibodies against the F protein induces greater neutralization than against the HN protein (Alexander, 1997; Reynolds and Maraqa, 2000a).
Cell mediated immunity against NDV without detectable HI antibodies is not sufficient to protect against virulent NDV challenge (Reynolds and Maraqa, 2000b). Early systemic antibody responses are IgM, followed by IgG, which peak around 3-4 weeks after infection (Kouwenhoven, 1993; Alexander, 1997). At about the time systemic antibody responses can be detected, IgA with some IgG can be detected in secretions of the upper respiratory tract and the intestinal tract (Alexander, 1997). Only live vaccines administered via the respiratory route stimulate antibody in all secreta, as well as in serum (Kouwenhoven, 1993). Recently, it has been shown that NDV can induce IL-15 (Azimi et al., 2000).
Immune hens will pass antibodies via the egg yolk and passive immunity will prevent haematogenous spread of virulent vaccine virus during the first 7 days of life (Kouwenhoven, 1993; Alexander, 1997). The half-life of maternal antibodies measured by HI is estimated as 4.5 days (Alexander, 1997).
There are no reports of successful treatment of ND and no antiviral drugs are commercially available. Because ND is an OIE notifiable disease, it is unlikely that such drugs will be developed in the near future.
Good management and hygiene remain the basis for prevention of ND, but in areas with an intensive poultry industry control of ND without vaccination is uncommon. Only in geographically isolated areas, with a very low risk of introduction of NDV and a relatively small economic impact of an outbreak, may vaccination be reserved for emergency or ring vaccinations (Kouwenhoven, 1993).
Vaccines available against NDV consist of live NDV strains of low virulence or inactivated strains, and recombinant vectored vaccines (OIE, 2008).
|Vaccine||Dosage, Administration and Withdrawal Times||Life Stages||Adverse Affects|
|inactivated virus vaccine||Intramuscular or subcutaneous injection.||Poultry: All Stages||Tissue reaction at site of injection.|
|live virus vaccine||Spray, aerosol, drinking water, eyedrop or intransal application.||Poultry: All Stages||Respiratory signs of distress.|
|Recombinant live vectored vaccine comprising herpesvirus of turkeys expressing a surface antigen of NDV.||Injection into amniotic sac of 18-day-old embryos. Injection subcutaneously in one-day-old chicks.||Embryo (in ovo) and poultry at all stages|
|Recombinant live vectored vaccine comprising fowl pox virus expressing surface antigens of NDV.||Subcutaneously in one-day-old chicks or wing web in older birds. Sub-cutaneously in turkeys aged four weeks or older.||Poultry: All stages|
Among live avirulent strains Clone 30, Hitchner-B1, La Sota, Queensland V4, Poulvac NDW and F (Asplin) are used extensively worldwide as primary vaccines. Occasionally, new lentogenic field isolates are evaluated as vaccine candidates (Rehmani and Spradbrow, 1996; Murakawa et al., 2000). Live vaccines should contain = 106.5-107, 50% egg infectious dose (EID50). Mesogenic strains used in vaccines include Roakin, Mukteswar and Komarov, and are used for secondary vaccinations (Agoha et al., 1992; Kouwenhoven, 1993; Alexander, 1997; Roy et al., 1999; OIE, 2000). The challenge for every vaccine manufacturer is the timing of vaccination, and the balance between attenuation and immunogenicity. For instance, in young birds vaccination with LaSota and Clone strains will usually lead to strong immunity and can overcome certain levels of maternal antibodies, but may also result in adverse effects, as opposed to the Hitchner-B1 strain. For inactivated vaccines, a high virus yield is important to produce a potent vaccine and the Ulster 2C strain has proven very suitable for this purpose (OIE, 2000). The potency of inactivated vaccines is greatly dependent on the antigen dose (Maas et al., 1999; Maas et al., 2000), and it is proposed that inactivated vaccines should preferably contain 50 x 50% protective doses (PD50) per 0.5 ml dose (Kouwenhoven, 1993). A combination of live and inactivated ND vaccine, administered simultaneously, is shown to provide better protection against virulent NDV and has been successfully used in control programmes in areas of intense poultry production (Senne et al., 2004).
Immunosuppression, notably after infectious bursal disease infection or vaccination, may reduce the response to ND vaccination (Montgomery et al., 1997). However, some IBD and ND vaccines may provide good immunity after simultaneous vaccination (Kouwenhoven, 1993). The effect of ND on E. coli infections is unclear. It has been reported that NDV vaccination stimulates innate immunity, suppressing the multiplication of E. coli in chickens for a period of 2-8 days post vaccination (Huang and Matsumoto, 2000). However, there are also studies suggesting that ND vaccination may enhance an E. coli infection, if both occur simultaneously (Nakamura et al., 1992).
Live vaccines may be administered by eye drop or intranasal instillation, spray, or drinking water. The administration route has a significant effect on the induced immune response (Mutalib and Boyle, 1994). Eye drop and intranasal installation is laborious, but is more likely to lead to a uniformly high degree of long lasting protection. Furthermore, maternal antibodies do not interfere at the mucosal surfaces of the nose, the Harderian and paranasal glands. Vaccination by aerosol, using sprays, can be administered in coarse or fine droplets. Coarse droplets are bigger and birds must be hit directly. This spray method is usually performed using hand-sprayers, knapsack sprayers or spray cabinets in hatcheries. The 'Atomist' atomizer is frequently used for fine-droplet spraying (Kouwenhoven, 1993). One should consider that, for successful immunization using these administration routes, sufficient virus replication is required in the upper respiratory tract, which is a characteristic of many lentogenic isolates. Vaccination via the drinking water gives heterogeneous results due to the variations in water intake by the birds. Essentially, intestinal replication is required for this type of administration. After aerosol vaccination with live lentogenic vaccines clinical signs are inevitable. Coughing, wet tracheas and incidental plugging of the bifurcation of the trachea can occur. Adverse reactions are usually less significant after vaccination via eyedrop or drinking water. Also, lighter breeds such as white layers are more prone to adverse reactions than heavier breeds. Research using both live and inactivated vaccines showed that the ocular route of administration was superior to the drinking water route, which was in turn superior to the spray technique. However, the ocular route may not be economically viable for small flocks (Degefa et al., 2004).
Inactivated vaccines are usually based on oil emulsions and administered by intramuscular or, more seldom, subcutaneous injection (Deguchi et al., 1998). The vaccine in a dose of approximately 0.5 ml per chicken is deposited in the breast or leg muscles. When injecting in the breast, care should be taken not to inject internal organs such as the heart, liver or lungs as this will cause rapid death of the bird. Inactivated vaccines are mainly used as secondary vaccinations at the end of the rearing period (Kouwenhoven, 1993).
The immune status of a flock can be determined using the level of HI antibodies, because there is a strong correlation between protection and HI antibody level in birds older than 6 weeks. This is the basis for the widespread use of blood testing to determine the proper vaccination schedule. Young birds with maternal antibodies, vaccinated at an early age, will respond with low or no rise in HI titre, and are protected less well and for a shorter period than older birds. Re-vaccinations can be timed using HI titres, because re-vaccination of flocks with high HI titres will not result in a titre rise, and the titre may even drop due to antibody consumption.
Because maternal antibodies protect well during the first week of life, vaccination of parent stock with inactivated vaccines is widely practised (van Eck, 1990). Subsequently, young chickens are vaccinated with a lentogenic strain the first week of life, which should provide protection during the next few weeks. Subsequent re-vaccinations should be timed based on the infection pressure and HI titre of the flock (Kouwenhoven, 1993).
Recombinant vectored vaccines against ND that are commercially available include herpesvirus of turkeys (HVT, a Marek's disease vaccine) and fowl pox virus, both of which express a protective surface antigen of NDV. The HVT+ND vaccine can be given in ovo as well as to chicks.
African Union-Interafrican Bureau for Animal Resources, 2011. Panafrican Animal Health Yearbook 2011. Pan African Animal Health Yearbook, 2011:xiii + 90 pp. http://www.au-ibar.org/pan-african-animal-health-yearbook
Agoha NJ, Akpavie SO, Durojaiye OA, Adene DF, 1992. Pathogenicity of two strains of Newcastle disease virus in the grey-breasted helmet guinea fowl. Veterinary Quarterly, 14(2):51-53; 9 ref.
Ahlert T et al., 1997. Tumor-cell number and viability as quality and efficacy parameters of autologous virus-modified cancer vaccines in patients with breast or ovarian cancer. J. Clin. Oncol., 15:1354-1366.
Ahmad J, Sharma JM, 1992. Evaluation of a modified-live virus vaccine administered in ovo to protect chickens against Newcastle disease. American Journal of Veterinary Research, 53(11):1999-2004; 28 ref.
Aldous EW, Collins MS, McGoldrick A, Alexander DJ, 2001. Rapid pathotyping of Newcastle disease virus (NDV) using fluorogenic probes in a PCR assay. Vet. Microbiol., 80:201-212.
Alexander DJ, 1993. Paramyxovirus infection. Virus infections of birds., 321-340; 86 ref.
Alexander DJ, 1997. Newcastle disease and other avian paramyxovirus infections. In: Calnek BW, Barnes HJ, Beard CW, McDougald LR, Saif YM, eds.. Diseases of Poultry, 10th edn. Iowa, USA: Iowa State University Press, 541-570.
Alexander DJ, 2000. Newcastle disease and other avian paramyxoviruses. Rev. Sci. Tech., 19:443-462.
Alexander DJ, 2001. Gordon memorial lecture: newcastle disease. British Poultry Science, 42(1):5-22.
Alexander DJ, Morris HT, Pollitt WJ, Sharpe CE, Eckford RL, Sainsbury RMQ, Mansley LM, Gough RE, Parsons G, 1998. Newcastle disease outbreaks in domestic fowl and turkeys in Great Britain during 1997. Veterinary Record, 143(8):209-212; 10 ref.
Al-Garib SO, Gielkens ALJ, Gruys E, Koch G, 2003. Review of Newcastle disease virus with particular references to immunity and vaccination. World's Poultry Science Journal, 59(2):185-200.
Astorga RJ, Cubero MJ, León L, Maldonado A, Arenas A, Tarradas MC, Perea A, 1994. Serological survey of infections in waterfowl in the Guadalquivir Marshes (Spain). Avian Diseases, 38(2):371-375; 24 ref.
Azimi N, Tagaya Y, Mariner J, Waldmann TA, 2000. Viral activation of interleukin-15 (IL-15): characterization of a virus- inducible element in the IL-15 promoter region. J. Virol., 74:7338-7348.
Bar-Eli N, Giloh H, Schlesinger M, Zakay-Rones Z, 1996. Preferential cytotoxic effect of Newcastle disease virus on lymphoma cells. J. Cancer Res. Clin. Oncol., 122:409-415.
Baron S et al., 1998. A host defense role for a natural antiviral substance in the nervous system. J. Neuroimmunol., 85:168-173.
Bolte AL, Voss M, Vielitz E, Kaleta EF, 2001. Response of domestic geese to lentogenic and velogenic strains of Newcastle disease virus. Dtsch. Tierarztl. Wochenschr., 108:155-159.
Brown C, King DJ, Seal BS, 1999. Pathogenesis of Newcastle disease in chickens experimentally infected with viruses of different virulence. Veterinary Pathology, 36(2):125-132; 27 ref.
Cattoli G, Fusaro A, Monne I, Molia S, Menach Ale, Maregeya B, Nchare A, Bangana I, Maina AG, Koffi JNN, Thiam H, Bezeid OEMA, Salviato A, Nisi R, Terregino C, Capua I, 2010. Emergence of a new genetic lineage of Newcastle disease virus in West and Central Africa - implications for diagnosis and control. Veterinary Microbiology, 142(3/4):168-176. http://www.sciencedirect.com/science/journal/03781135
Chen L et al., 2001. The Structure of the Fusion Glycoprotein of Newcastle Disease Virus Suggests a Novel Paradigm for the Molecular Mechanism of Membrane Fusion. Structure, 9:255-266.
Clavijo A, Robinson Y, Booth T, Munroe F, 2000. Velogenic Newcastle disease in imported caged birds. Can. Vet. J., 41:404-406.
Creelan JL, Graham DA, McCullough SJ, 2002. Detection and differentiation of pathogenicity of avian paramyxovirus serotype 1 from field cases using one-step reverse transcriptase-polymerase chain reaction. Avian Pathology, 31:493-499.
Crennell S, Takimoto T, Portner A, Taylor G, 2000. Crystal structure of the multifunctional paramyxovirus hemagglutinin- neuraminidase. Nat. Struct. Biol., 7:1068-1074.
Crossley BM, Hietala SK, Shih LM, Lee L, Skowronski EW, Ardans AA, 2005. High-throughput real-time RT-PCR assay to detect the exotic Newcastle Disease virus during the California 2002-2003 outbreak. Journal of Veterinary Diagnostic Investigation, 17(2):124-132.
Degefa T, Dadi L, Yami A, Gmariam K, Nassir M, 2004. Technical and economic evaluation of different methods of Newcastle disease vaccine administration. Journal of Veterinary Medicine Series A, 51(7/8):365-369.
Deguchi K, Honda T, Matsuo K, Fujikawa H, Iwamoto T, Sakanoue Y, 1998. Influence of inoculation site of combined oil-adjuvanted vaccine on the antibody response in chickens. Journal of Veterinary Medical Science, 60(7):831-835; 13 ref.
Eck JHHvan, 1990. Protection of broilers against Newcastle disease by hyperimmunisation of the dams. Veterinary Quarterly, 12(3):139-145; 10 ref.
Fuller CM, Collins MS, Alexander DJ, 2009. Development of a real-time reverse-transcription PCR for the detection and simultaneous pathotyping of Newcastle disease virus isolates using a novel probe. Archives of Virology, 154(6):929-937. http://springerlink.metapress.com/content/am370688650705g1/?p=dea4510eea9b4eddb17bc420ed240f58&pi=2
Gutierrez-Ruiz EJ et al., 2000. A serological survey for avian infectious bronchitis virus and Newcastle disease virus antibodies in backyard (free-range) village chickens in Mexico. Trop. Anim. Health Prod., 32:381-390.
Heckert RA, Riva J, Cook S, McMillen J, Schwartz RD, 1996. Onset of protective immunity in chicks after vaccination with a recombinant herpesvirus of turkeys vaccine expressing Newcastle disease virus fusion and hemagglutinin-neuraminidase antigens. Avian Diseases, 40(4):770-777; 19 ref.
Hilgers LA et al., 2000. Alkyl-polyacrylate esters are strong mucosal adjuvants. Vaccine, 18:3319-3325.
Huang HJ, Matsumoto M, 2000. Nonspecific innate immunity against Escherichia coli infection in chickens induced by vaccine strains of Newcastle disease virus. Avian Dis, 44:790-796.
Jang J, Hong SH, Kim IH, 2011. Validation of a real-time RT-PCR method to quantify Newcastle Disease Virus (NDV) titer and comparison with other quantifiable methods. Journal of Microbiology and Biotechnology, 21(1):100-108.
Kaleta EF, Baldauf C, 1988. Newcastle disease in free-living and pet birds. Newcastle disease., 197-246; 247 ref.
Kant A et al., 1997. Differentiation of virulent and non-virulent strains of Newcastle disease virus within 24 hours by polymerase chain reaction. Av. Pathol., 26:837-849.
King DJ, 1999. A comparison of the onset of protection induced by Newcastle disease virus strain B1 and a fowl poxvirus recombinant Newcastle disease vaccine to a viscerotropic velogenic Newcastle disease virus challenge. Avian Diseases, 43(4):745-755; 23 ref.
Kouwenhoven B, 1993. Newcastle disease. Virus infections of birds., 341-361; 37 ref.
Leeuw Ode, Peeters B, 1999. Complete nucleotide sequence of Newcastle disease virus: evidence for the existence of a new genus within the subfamily Paramyxovirinae. Journal of General Virology, 80(1):131-136; 19 ref.
Locke DP et al., 2000. Newcastle disease virus phosphoprotein gene analysis and transcriptional editing in avian cells. Virus Res., 69:55-68.
Lomniczi B et al., 1998. Newcastle disease outbreaks in recent years in western Europe were caused by an old (VI) and a novel genotype (VII). Arch. Virol., 143:49-64.
Lopaticki S, Morrow CJ, Gorman JJ, 1998. Characterization of pathotype-specific epitopes of newcastle disease virus fusion glycoproteins by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and post-source decay sequencing. J. Mass. Spectrom, 33:950-960.
Maas RA et al., 2000. Antigen quantification as in vitro alternative for potency testing of inactivated viral poultry vaccines. Vet. Q., 22:223-227.
Maas RA, Oei HL, Venema-Kemper S, Koch G, Bongers J, 1999. Dose-response effects of inactivated Newcastle disease vaccines: influence of serologic assay, time after vaccination, and type of chickens. Avian Diseases, 43(4):670-677; 26 ref.
Makkay AM, Krell PJ, Nagy é, 1999. Antibody detection-based differential ELISA for NDV-infected or vaccinated chickens versus NDV HN-subunit vaccinated chickens. Veterinary Microbiology, 66(3):209-222; 34 ref.
Malik YS, Patnayak DP, Goyal SM, 2004. Detection of three avian respiratory viruses by single-tube multiplex reverse transcription-polymerase chain reaction assay. Journal of Veterinary Diagnostic Investigation, 16(3):244-248.
Manoharan S, Parthiban M, Prabhakar TG, Ravikumar G, Koteeswaran A, Chandran NDJ, Rajavelu G, 2004. Rapid serological profiling by an immunocomb-based dot-enzyme-linked immunosorbent test for three major poultry diseases. Veterinary Research Communications, 28(4):339-346.
Marcus PI, Heide Lvan der, Sekellick MJ, 1999. Interferon action on avian viruses. I. Oral administration of chicken interferon- ameliorates Newcastle disease. Journal of Interferon & Cytokine Research, 19(8):881-885; 28 ref.
Marín MC, Villegas P, Bennett JD, Seal BS, 1996. Virus characterization and sequence of the fusion protein gene cleavage site of recent Newcastle disease virus field isolates from the Southeastern United States and Puerto Rico. Avian Diseases, 40(2):382-390; 36 ref.
McGinnes L, Sergel T, Reitter J, Morrison T, 2001. Carbohydrate modifications of the ndv fusion protein heptad repeat domains influence maturation and fusion activity. Virology, 283:332-342.
McMillen JK et al., 1994. The safe and effective use of fowlpox virus as a vector for poultry vaccines. Dev. Biol. Stand., 82:137-145.
Mishra S, Kataria JM, Sah RL, Verma KC, Mishra JP, 2001. Studies on the pathogenicity of Newcastle disease virus isolates in guinea fowl. Tropical Animal Health and Production, 33(4):313-320.
Montgomery RD, Maslin WR, Boyle CR, 1997. Effects of Newcastle disease vaccines and Newcastle disease/infectious bronchitis combination vaccines on the head-associated lymphoid tissues of the chicken. Avian Diseases, 41(2):399-406; 27 ref.
Mori H, Tawara H, Nakazawa H, Sumida M, Matsubara F, Aoyama S, Iritani Y, Hayashi Y, Kamogawa K, 1994. Expression of the Newcastle disease virus (NDV) fusion glycoprotein and vaccination against NDV challenge with a recombinant baculovirus. Avian Diseases, 38(4):772-777; 22 ref.
Murakawa Y et al., 2000. Characterization of a lentogenic Newcastle disease virus isolated from broiler chickens in Japan. Avian Dis., 44:686-690.
Mutalib A, Boyle CR, 1994. Influence of site of inoculation of inactivated vaccines on the immune response in chickens. Avian Diseases, 38(4):857-860; 8 ref.
Nakamura K, Narita M, Imai K, Matsumura T, Maeda M, Tanimura T, 1992. The effect of mixed live vaccines of Newcastle disease and infectious bronchitis on the chicken respiratory tract. Journal of Comparative Pathology, 106(4):341-350; 14 ref.
Nakamura K, Ueda H, Tanimura T, Noguchi K, 1994. Effect of mixed live vaccine (Newcastle disease and infectious bronchitis) and Mycoplasma gallisepticum on the chicken respiratory tract and on Escherichia coli infection. Journal of Comparative Pathology, 111(1):33-42; 13 ref.
Nanthakumar T et al., 2000. Pathotyping of Newcastle disease viruses by RT-PCR and restriction enzyme analysis. Vet. Res. Commun., 24:275-286.
Odor EM, Salem M, Pope CR, Sample B, Primm M, Vance K, Murphy M, 1997. Isolation and identification of Ornithobacterium rhinotracheale from commercial broiler flocks on the Delmarva Peninsula. Avian Diseases, 41(1):257-260; 13 ref.
OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.
OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.
OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004). Paris, France: Office International des Epizooties.
OIE, 2000. Newcastle disease. In: OIE Manual of standards for diagnostic tests and vaccines, edition 4. Paris, France: Office International des Epizooties, 221-232.
OIE, 2003. Newcastle disease in Belarus (follow-up report No. 1) lifting of quarantine measures. Disease Information, 16, No. 24.
OIE, 2003. Newcastle disease in Norway. Disease Information, 16, No. 44.
OIE, 2003. Newcastle disease in Sweden. Disease Information, 16, No. 44.
OIE, 2003. Newcastle disease in United States of America. Final Report. Disease Information, 16(47).
OIE, 2004. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. Paris, France: World Organisation for Animal Health. http://www.oie.int/eng/normes/mmanual/A_summry.htm.
OIE, 2004. Newcastle disease in Finland. Disease Information, 30(17).
OIE, 2004. Newcastle disease in Japan. Disease Information, 17(53).
OIE, 2004. Newcastle disease in Thailand. Disease Information, 17(29).
OIE, 2004. Newcastle disease in Turkey. Disease Information, 17(28).
OIE, 2004. Newcastle disease in Venezuela. Follow-up report No. 1. Disease Information, 17(36).
OIE, 2005. Newcastle disease in Bulgaria. Follow-up report No. 1 (final report). Disease Information, 18(4).
OIE, 2005. Newcastle disease in Cyprus. Follow-up report No. 2. Disease Information, 18(6).
OIE, 2005. Newcastle disease in Denmark. Follow-up report no. 3. Paris, France: Office International des Epizooties, Disease Information, 18(51).
OIE, 2005. Newcastle disease in Finland. Follow-up report no. 3 (final report). Paris, France: Office International des Epizooties, Disease Information, 18(4).
OIE, 2005. Newcastle disease in France. Final report. Paris, France: Office International des Epizooties, Disease Information, 18(51).
OIE, 2005. Newcastle disease in Greece. Follow-up report No. 2 (final report). Disease Information, 18(7).
OIE, 2005. Newcastle disease in Israel. Immediate notification report. Paris, France: Office International des Epizooties, Disease Information, 18(44).
OIE, 2005. Newcastle disease in Japan. Immediate notification report. Paris, France: Office International des Epizooties, Disease Information, 18(49).
OIE, 2005. Newcastle disease in Romania. Follow-up report no.7. Paris, France: Office International des Epizooties, Disease Information, 19(5).
OIE, 2005. Newcastle disease in the Former Yugoslav Republic of Macedonia. Immediate notification report. Paris, France: Office International des Epizooties, Disease Information, 18(45).
OIE, 2005. Newcastle disease in Turkey. Final report. Paris, France: Office International des Epizooties, Disease Information, 18(52).
OIE, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.
OIE, 2006. Newcastle disease in Azerbaijan. Immediate notification and final report. Paris, France: Office International des Epizooties, Disease Information, 19(3).
OIE, 2006. Newcastle disease in Bulgaria. Immediate notification report. Paris, France: Office International des Epizooties, Disease Information, 19(4).
OIE, 2006. Newcastle disease in Greece. Follow-up report no. 2 (final report). Paris, France: Office International des Epizooties, Disease Information, 19(4).
OIE, 2006. Newcastle disease in Sweden. Follow-up report. Paris, France: Office International des Epizooties, Disease Information, 19(3).
OIE, 2008. Newcastle Disease. In: OIE Manual of diagnostic tests and vaccines for terrestrial animals, edition 6. Paris, France: Office International des Epizooties, 576-589.
OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int
OIE, 2012. World Animal Health Information Database. Version 2. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int/wahis_2/public/wahid.php/Wahidhome/Home
OLESIUK OM, 1951. Influence of environmental factors on viability of Newcastle disease virus. American Journal of Veterinary Research, 12:152-155.
Panshin A et al., 1997. Antigenic epitope characterization of matrix protein of Newcastle disease virus using monoclonal antibody approach: contrasting variability amongst NDV strains. Comp. Immunol. Microbiol. Infect. Dis., 20:177-189.
Panshin A et al., 1998. Variability of antigenic epitopes of the fusion protein of Newcastle disease virus. Comp. Immunol. Microbiol. Infect. Dis., 21:51-63.
Panshin A et al., 2000. Antigenic characterization of the nucleocapsid protein of Newcastle disease virus by means of a new panel of monoclonal antibodies. Comp. Immunol. Microbiol. Infect. Dis., 23:209-220.
Parede L, Young PL, 1990. The pathogenesis of velogenic Newcastle disease virus infection of chickens of different ages and different levels of immunity. Avian Diseases, 34(4):803-808; 12 ref.
Parimal Roy, Venugopalan AT, Koteeswaran A, 1999. Efficacy of live adjuvanted mesogenic Newcastle disease vaccine in chickens. Vaccine, 17(20/21):2674-2676; 8 ref.
Peeters BP, de Leeuw OS, Koch G, Gielkens AL, 1999. Rescue of Newcastle disease virus from cloned cDNA: evidence that cleavability of the fusion protein is a major determinant for virulence. J. Virol., 73:5001-5009.
Peeters BPH, Leeuw OSde, Verstegen I, Koch G, Gielkens ALJ, 2001. Generation of a recombinant chimeric Newcastle disease virus vaccine that allows serological differentiation between vaccinated and infected animals. Vaccine, 19(13/14):1616-1627; 65 ref.
Rehmani SF, Spradbrow PB, 1996. Receptors for the V4 strain of Newcastle disease virus in the digestive tract of chickens. Veterinary Microbiology, 50(1/2):157-160; 9 ref.
Reynolds DL, Maraqa AD, 2000. Protective immunity against Newcastle disease: the role of antibodies specific to Newcastle disease virus polypeptides. Avian Diseases, 44(1):138-144; 32 ref.
Sakaguchi M, Nakamura H, Sonoda K, Hamada F, Hirai K, 1996. Protection of chickens from Newcastle disease by vaccination with a linear plasmid DNA expressing the F protein of Newcastle disease virus. Vaccine, 14(8):747-752; 17 ref.
Schirmacher V et al., 1998. Immunisation with virus-modified tumor cells. Sem. Oncology, 25:677-696.
Senne DA, King DJ, Kapczynski DR, 2004. Control of Newcastle disease by vaccination. In: Control of Infectious Animal Diseases by Vaccination. Basel, Switzerland: S Karger AG, 165-170.
Shan SongHua, Shao ChaoGang, Xu CaoZhe, Zou Jian, Hu YongQiang, Wu JianHua, Gong ZuXun, 2003. Differentiation of velogenic, mesogenic and lentogenic strains of Newcastle disease virus by multiplex RT-PCR. Annals of Applied Biology, 142(1):49-54.
Steward M, Vipond IB, Millar NS, Emmerson PT, 1993. RNA editing in Newcastle disease virus. J. Gen. Virol., 74:2539-2547.
Takakuwa H, Ito T, Takada A, Okazaki K, Kida H, 1998. Potentially virulent Newcastle disease viruses are maintained in migratory waterfowl populations. Japanese Journal of Veterinary Research, 45(4):207-215; 28 ref.
Wise MG, Suarez DL, Seal BS, Pedersen JC, Senne DA, King DJ, Kapczynski DR, Spackman E, 2004. Development of a real-time reverse-transcription PCR for detection of Newcastle disease virus RNA in clinical samples. Journal of Clinical Microbiology, 42(1):329-338.
(http://www.oie.int, accessed 5 June 2013)
Dr Sam Mccullough
Australian Animal Health Laboratory
Division of Animal Health
Institute of Animal Production & Processing
5 Portarlington Road
Private Bag 24
Geelong, Victoria 3220
Tel: +61-3 52 27 50 00 Fax: +61-3 52 27 55 55
Dr Zhiliang Wang
National Diagnostic Center for Exotic Animal Diseases
China Animal Health and Epidemiology Center
Ministry of Agriculture
369 Nanjing Road
CHINA (PEOPLE'S REP. OF)
Tel: +86-532 184.108.40.206 Fax: +86-532 220.127.116.11
Dr Christian Grund
Federal Research Centre for Virus Diseases of Animals (BFAV)
Institute of Diagnostic Virology
Tel: +49-383 51 711 52 Fax: +49-383 51 712 26
Dr Ilaria Capua
Istituto Zooprofilattico Sperimentale delle Venezie
Via Romea 14/A
35020 Legnaro, Padova
Tel: +39-049 808 43 79 Fax: +39-049 808 43 60
Dr Kang-Seuk Choi
National Veterinary Research & Quarantine Service
Ministry of Food, Agriculture, Forestry and Fisheries (MIFAFF)
KOREA (REP. OF)
Tel: +82-31 467 1821 Fax: +82-31 467 1814
Prof. Ian Brown
Animal Health and Veterinary Laboratories Agency
New Haw, Addlestone
Surrey KT15 3NB
Tel: +44-1932 35 73 39 Fax: +44-1932 35 72 39
Ms Janice Pedersen
National Veterinary Services Laboratories
USDA, APHIS, Veterinary Services
P.O. Box 844
Ames, Iowa 50010
UNITED STATES OF AMERICA
Tel: +1-515 337 72 66 Fax: +1-515 337 73 97
Date of report: 03/06/2013
© CAB International 2013. Distributed under license by African Union – Interafrican Bureau for Animal Resources.
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.