- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Links to Websites
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Newcastle disease
International Common Names
- English: avian distemper; avian pneumoencephalitis; newcastle disease, rubulavirus, in birds
Local Common Names
- Germany: atypische geflugelpest
- Netherlands: pseudo-vogelpest
- UK: pseudo-poultry plague
- USA: pseudo-fowl pest
OverviewTop of page
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.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Alectoris rufa (red-legged partridge)||Domesticated host, Wild host||Poultry: All Stages|
|Anas (ducks)||Domesticated host, Wild host||Poultry: All Stages|
|Anser (geese)||Domesticated host, Wild host||Poultry: All Stages|
|Cairina (Muscovy ducks)||Domesticated host, Wild host||Poultry: All Stages|
|Columba livia (pigeons)||Wild host|
|Coturnix japonica (Japanese quail)||Domesticated host, Wild host||Poultry: All Stages|
|Gallus||Domesticated host, Wild host||Poultry: All Stages|
|Gallus gallus domesticus (chickens)||Domesticated host||Poultry: All Stages|
|Meleagris gallopavo (turkey)||Domesticated host, Wild host||Poultry: All Stages|
|Melopsittacus undulatus||Domesticated host, Wild host|
|Perdix perdix (grey partridge)||Domesticated host, Wild host||Poultry: All Stages|
|Phasianus colchicus (common pheasant)||Domesticated host, Wild host||Poultry: All Stages|
Hosts/Species AffectedTop of page
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*
Domestic and wild bird species
Variable: severe to subclinical
Passerines, turkeys, chickens, psittacines
egg production loss
Turkeys, psittacines, passerines
egg production loss
Encephalitis in psittacines
Ducks, geese, rails
Duck, geese, turkeys
Mortality in turkeys, otherwise subclinical
APMV-9 (only one isolate)
*adapted from Alexander, 1993, Alexander, 1997, Kouwenhoven, 1993.
** these APMVs have also been isolated from captive cage birds (Alexander, 1993)
Systems AffectedTop of page blood and circulatory system diseases of poultry
digestive diseases of poultry
nervous system diseases of poultry
reproductive diseases of poultry
respiratory diseases of poultry
DistributionTop of page
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.
Distribution TableTop of page
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 details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Afghanistan||Disease not reported||OIE, 2009|
|Armenia||Disease not reported||OIE, 2009|
|Azerbaijan||Disease not reported||OIE, 2009|
|Brunei Darussalam||Reported present or known to be present||OIE Handistatus, 2005|
|Cambodia||Disease not reported||OIE, 2009|
|China||Restricted distribution||OIE, 2009|
|-Hong Kong||Present||OIE, 2009|
|Georgia (Republic of)||Last reported||2001||OIE Handistatus, 2005|
|India||Restricted distribution||NULL||Alexander, 1997; OIE, 2009|
|Indonesia||Present||NULL||Alexander, 1997; OIE, 2009|
|Israel||Disease not reported||OIE, 2009|
|Japan||Present||NULL||OIE, 2004b; Alexander, 1997; OIE, 2009|
|Jordan||Disease not reported||OIE, 2009|
|Kazakhstan||Disease not reported||OIE, 2009|
|Korea, DPR||Disease not reported||OIE Handistatus, 2005|
|Korea, Republic of||Present||OIE, 2009|
|Kyrgyzstan||Disease not reported||OIE, 2009|
|Laos||No information available||OIE, 2009|
|-Peninsular Malaysia||Reported present or known to be present||OIE Handistatus, 2005|
|-Sabah||Reported present or known to be present||OIE Handistatus, 2005|
|-Sarawak||Reported present or known to be present||OIE Handistatus, 2005|
|Mongolia||Disease not reported||OIE, 2009|
|Saudi Arabia||Present||OIE, 2009|
|Singapore||Disease not reported||OIE, 2009|
|Sri Lanka||Present||OIE, 2009|
|Syria||Disease not reported||OIE, 2009; OIE, 2009|
|Syria||Present||OIE, 2009; OIE, 2009|
|Taiwan||Reported present or known to be present||OIE Handistatus, 2005|
|Tajikistan||Disease not reported||OIE, 2009|
|Thailand||Disease not reported||2004||OIE, 2004c; OIE, 2009|
|Turkey||Present||NULL||OIE, 2004d; OIE, 2009|
|Turkmenistan||Last reported||1994||OIE Handistatus, 2005|
|United Arab Emirates||Disease not reported||OIE, 2009|
|Uzbekistan||Last reported||1993||OIE Handistatus, 2005|
|Yemen||No information available||OIE, 2009|
|Algeria||Disease not reported||OIE, 2009|
|Burkina Faso||Present||OIE, 2012|
|Cape Verde||Present||OIE, 2012|
|Central African Republic||Present||OIE, 2012|
|Congo Democratic Republic||Present||OIE, 2012|
|Côte d'Ivoire||Present||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|
|Libya||Last reported||1976||OIE Handistatus, 2005|
|Morocco||Disease not reported||OIE, 2009|
|Réunion||Disease not reported||OIE Handistatus, 2005|
|Sao Tome and Principe||Serological evidence and/or isolation of the agent||OIE Handistatus, 2005|
|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|
|Bermuda||Disease not reported||OIE Handistatus, 2005|
|Canada||Restricted distribution||OIE, 2009|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Restricted distribution||OIE, 2009|
|USA||Disease not reported||2003||OIE, 2003; OIE, 2009|
Central America and Caribbean
|Barbados||Last reported||1972||OIE Handistatus, 2005|
|British Virgin Islands||Disease never reported||OIE Handistatus, 2005|
|Cayman Islands||Disease never reported||OIE Handistatus, 2005|
|Costa Rica||Disease not reported||OIE, 2009|
|Cuba||Disease not reported||OIE, 2009|
|Curaçao||Disease not reported||OIE Handistatus, 2005|
|Dominica||Disease not reported||OIE Handistatus, 2005|
|Dominican Republic||Present||OIE, 2009|
|El Salvador||Disease not reported||OIE, 2009|
|Guadeloupe||Disease not reported||OIE, 2009|
|Guatemala||Disease not reported||OIE, 2009|
|Honduras||Disease not reported||OIE, 2009|
|Jamaica||Disease not reported||OIE, 2009|
|Martinique||Disease not reported||OIE, 2009|
|Nicaragua||Disease not reported||OIE, 2009|
|Panama||Disease not reported||OIE, 2009|
|Saint Kitts and Nevis||Last reported||2002||OIE Handistatus, 2005|
|Saint Vincent and the Grenadines||Disease never reported||OIE Handistatus, 2005|
|Trinidad and Tobago||Last reported||1997||OIE Handistatus, 2005|
|Argentina||Disease not reported||OIE, 2009|
|Bolivia||Restricted distribution||OIE, 2009|
|Brazil||Disease not reported||OIE, 2009|
|Chile||Disease not reported||OIE, 2009|
|Ecuador||Disease not reported||OIE, 2009|
|Falkland Islands||Disease never reported||OIE Handistatus, 2005|
|French Guiana||Disease never reported||OIE, 2009|
|Guyana||Disease never reported||OIE Handistatus, 2005|
|Paraguay||Last reported||1997||OIE Handistatus, 2005|
|Peru||Absent, reported but not confirmed||OIE, 2009|
|Uruguay||Disease not reported||OIE, 2009|
|Venezuela||Present||NULL||OIE, 2004e; OIE, 2009|
|Albania||Restricted distribution||OIE, 2009|
|Andorra||Disease not reported||OIE Handistatus, 2005|
|Austria||Disease not reported||OIE, 2009|
|Belarus||Disease not reported||200305||OIE, 2003; OIE, 2009|
|Belgium||Disease not reported||OIE, 2009|
|Bosnia-Hercegovina||Last reported||1998||OIE Handistatus, 2005|
|Bulgaria||Present||NULL||OIE, 2005a; OIE, 2009|
|Croatia||Disease not reported||OIE, 2009|
|Cyprus||Disease not reported||NULL||OIE, 2005b; OIE, 2009|
|Czech Republic||Disease not reported||OIE, 2009|
|Denmark||Disease not reported||OIE, 2009|
|Estonia||Disease not reported||OIE, 2009|
|Finland||Present||NULL||OIE, 2004a; OIE, 2009|
|France||Disease not reported||OIE, 2009|
|Greece||Disease not reported||20071206||OIE, 2005c; OIE, 2009|
|Hungary||Restricted distribution||OIE, 2009|
|Iceland||Disease never reported||OIE, 2009|
|Ireland||Disease not reported||OIE, 2009|
|Isle of Man (UK)||Disease never reported||OIE Handistatus, 2005|
|Italy||Disease not reported||OIE, 2009|
|Jersey||Disease never reported||OIE Handistatus, 2005|
|Latvia||Disease not reported||OIE, 2009|
|Liechtenstein||Disease not reported||OIE, 2009|
|Lithuania||Disease not reported||OIE, 2009|
|Luxembourg||Disease not reported||OIE, 2009|
|Macedonia||Disease not reported||OIE, 2009|
|Malta||Disease not reported||OIE, 2009|
|Moldova||Last reported||1993||OIE Handistatus, 2005|
|Montenegro||Disease not reported||OIE, 2009|
|Netherlands||Disease not reported||OIE, 2009|
|Norway||Disease not reported||OIE, 2009|
|Poland||Disease not reported||OIE, 2009|
|Portugal||Disease not reported||OIE, 2009|
|Russian Federation||Present||OIE, 2009|
|-Russia (Europe)||Widespread||Alexander, 1997|
|Serbia||Disease not reported||OIE, 2009|
|Slovakia||Disease not reported||OIE, 2009|
|Slovenia||Disease not reported||OIE, 2009|
|Spain||Disease not reported||OIE, 2009|
|Sweden||Present||NULL||OIE, 2003; OIE, 2009|
|Switzerland||Disease not reported||OIE, 2009|
|UK||Disease not reported||OIE, 2009|
|-Northern Ireland||Last reported||1997||OIE Handistatus, 2005|
|Ukraine||Disease not reported||OIE, 2009|
|Yugoslavia (former)||Last reported||2003||OIE Handistatus, 2005|
|Yugoslavia (Serbia and Montenegro)||Last reported||2002||OIE Handistatus, 2005|
|Australia||Disease not reported||OIE, 2009|
|French Polynesia||Disease not reported||OIE, 2009|
|New Caledonia||Disease never reported||OIE, 2009|
|New Zealand||Disease never reported||OIE, 2009|
|Samoa||Disease never reported||OIE Handistatus, 2005|
|Vanuatu||Disease never reported||OIE Handistatus, 2005|
|Wallis and Futuna Islands||No information available||OIE Handistatus, 2005|
PathologyTop of page
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).
DiagnosisTop of page
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
Fresh infective allantoic fluid
Fresh infective allantoic fluid
Fresh infective allantoic fluid
cDNA by RT-PCR
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
7 days of observation
8 days of observation
10 days of observation
= 24 hours, dependent on RNA isolation method and interpretation of obtained sequence
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)
at the C-terminus of the F2 protein; F (phenylalanine) at residue 117 at the N terminus of the F1 protein
at the C-terminus of the F2 protein; L (leucine) at residue 117 at the N terminus of the F1 protein
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).
List of Symptoms/SignsTop of page
|Digestive Signs / Abnormal colour of stool in birds, white, green, yellow faeces||Poultry:All Stages||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Diarrhoea||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Poultry:All Stages||Sign|
|General Signs / Cyanosis, blue skin or membranes||Sign|
|General Signs / Dehydration||Sign|
|General Signs / Discomfort, restlessness in birds||Poultry:All Stages||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Poultry:All Stages||Sign|
|General Signs / Haemorrhage of any body part or clotting failure, bleeding||Poultry:All Stages||Sign|
|General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass||Sign|
|General Signs / Inability to stand, downer, prostration||Poultry:All Stages||Sign|
|General Signs / Increased mortality in flocks of birds||Poultry:All Stages||Sign|
|General Signs / Laryngeal, tracheal, pharyngeal swelling, mass larynx, trachea, pharynx||Poultry:All Stages||Sign|
|General Signs / Opisthotonus||Poultry:All Stages||Sign|
|General Signs / Pale comb and or wattles in birds||Poultry:All Stages||Sign|
|General Signs / Pale mucous membranes or skin, anemia||Sign|
|General Signs / Petechiae or ecchymoses, bruises, ecchymosis||Sign|
|General Signs / Polydipsia, excessive fluid consumption, excessive thirst||Sign|
|General Signs / Torticollis, twisted neck||Poultry:All Stages||Sign|
|General Signs / Trembling, shivering, fasciculations, chilling||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weakness, paresis, paralysis of the legs, limbs in birds||Sign|
|General Signs / Weakness, paresis, paralysis, drooping, of the wings||Sign|
|General Signs / Weight loss||Sign|
|Musculoskeletal Signs / Contracture of the toes of birds, curly toe||Sign|
|Musculoskeletal Signs / Spasms of the limbs, legs, foot, feet in birds||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Poultry:All Stages||Sign|
|Nervous Signs / Head shaking, headshaking||Sign|
|Nervous Signs / Seizures or syncope, convulsions, fits, collapse||Sign|
|Nervous Signs / Tremor||Sign|
|Ophthalmology Signs / Cataract, lens opacity||Sign|
|Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling||Sign|
|Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Sign|
|Ophthalmology Signs / Purulent discharge from eye||Sign|
|Pain / Discomfort Signs / Colic, abdominal pain||Poultry:All Stages||Sign|
|Reproductive Signs / Decreased hatchability of eggs||Poultry:Mature female||Sign|
|Reproductive Signs / Decreased, dropping, egg production||Sign|
|Reproductive Signs / Defective, misshapen, soft, rough, absent egg shell||Poultry:Mature female||Sign|
|Reproductive Signs / Flabby egg yolk, thin albumin||Poultry:Mature female||Sign|
|Reproductive Signs / Soft, thin egg shell||Poultry:Mature female||Sign|
|Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring||Sign|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Sign|
|Respiratory Signs / Change in voice, vocal strength||Sign|
|Respiratory Signs / Coughing, coughs||Poultry:All Stages||Sign|
|Respiratory Signs / Decreased, muffled, lung sounds, absent respiratory sounds||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Poultry:All Stages||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Poultry:All Stages||Sign|
|Respiratory Signs / Purulent nasal discharge||Sign|
|Respiratory Signs / Sneezing, sneeze||Sign|
|Skin / Integumentary Signs / Ruffled, ruffling of the feathers||Sign|
|Skin / Integumentary Signs / Skin edema||Sign|
|Skin / Integumentary Signs / Skin erythema, inflammation, redness||Sign|
|Skin / Integumentary Signs / Skin ulcer, erosion, excoriation||Sign|
|Skin / Integumentary Signs / Skin vesicles, bullae, blisters||Sign|
Disease CourseTop of page
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)
highly pathogenic with haemorrhagic intestinal lesions
high mortality following respiratory and nervous signs
respiratory signs, occasional nervous signs, but low mortality
Lentogenic or respiratory
mild or subclinical respiratory infection
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).
EpidemiologyTop of page
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.
Impact: EconomicTop of page
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.
Zoonoses and Food SafetyTop of page
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.
Disease TreatmentTop of page
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.
Prevention and ControlTop of page
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).
Dosage, Administration and Withdrawal Times
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.
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