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Table of Contents:
Taxonomy Information
  1. Species:
    1. Newcastle Disease Virus (Website 1):
      1. Common Name: Avian paramyxovirus, , pseudofowl pest, pseudovogel-pest, atypische Geflugelpest, pseudo-poultry plague, avian pest, avian distemper, Ranikhet disease, Tetelo disease, Korean fowl plague, and avian pneumoencephalitis. The nomenclature may also be confusing as sometimes infection of birds with any strain of the NDV may be termed ND. Strictly speaking, ND should be reserved for infections falling within the internationally accepted definition.
      2. GenBank Taxonomy No.: 11176
      3. Description: Paramyxoviruses contain nonsegmented, single-stranded RNA genomes of negative polarity, and they replicate entirely in the cytoplasm(Lamb et al., 2002). Newcastle disease (ND), caused by avian paramyxovirus serotype 1 (APMV-1) viruses, is included in the List A of the Office International des Epizooties. ND has been a devastating disease of poultry, and in many countries the disease remains one of the major problems affecting existing or developing poultry industries. Eight other serotypes of avian paramyxoviruses are recognised, namely APMV-2 to APMV-9. Most of these serotypes appear to be present in natural reservoirs of specific feral avian species, although other host species are usually susceptible. Only AMPV-2 and APMV-3 viruses have made a significant disease and economic impact on poultry production. Strains of NDV have been distinguished on the basis of the clinical signs produced in infected chickens. Beard and Hanson defined the following five groups or pathotypes: 1) Viscerotropic Velogenic: viruses responsible for disease characterised by acute lethal infections, usually with haemorrhagic lesions in the intestines of dead birds. 2) Neurotropic Velogenic: viruses causing disease characterised by high mortality, which follows respiratory and neurological disease, but in which gut lesions are usually absent. 3) Mesogenic: viruses causing clinical signs consisting of respiratory and neurological signs, with low mortality. 4) Lentogenic: viruses causing mild infections of the respiratory tract. 5) Asymptomatic enteric: viruses causing avirulent infections in which replication appears to occur primarily in the gut(Alexander et al., 2000). NDV and other avian paramyxoviruses have been included in the Rubulavirus genus, primarily because of their nonconserved intergenic junctions and lack of a C-protein open reading frame, hallmarks specific to the Rubulavirus genus. However, the organization of the NDV P gene and its mRNA editing profile resemble those found for the species of the genera Morbillivirus and Respirovirus, but not for other species in the genus Rubulavirus. Thus, further consideration of the appropriate taxonomy of NDV and avian paramyxoviruses is required(Lamb et al., 2002). The definition of ND adopted at the 67th General Session of the Office Internationale des Epizooties held in Paris in May 1999 was: Newcastle disease is defined as an infection of birds caused by a virus of avian paramyxovirus serotype 1 (APMV-1) that meets one of the following criteria for virulence: a) The virus has an intracerebral pathogenicity index (ICPI) in day-old chicks (Gallus gallus) of 07 or greater. or b) Multiple basic amino acids have been demonstrated in the virus (either directly or by deduction) at the C-terminus of the F2 protein and phenylalanine at residue 117, which is the N-terminus of the F1 protein. The term multiple basic amino acids refers to at least three arginine or lysine residues between residues 113 to 116. Failure to demonstrate the characteristic pattern of amino acid residues as described above would require characterisation of the isolated virus by an ICPI test'(Alexander et al., 2001).
      4. Variant(s):
Lifecycle Information
  1. Newcastle Disease Virus
    1. Stage Information:
      1. Virion:
        • Size: Paramyxoviridae are generally spherical and 150 to 350 nm in diameter.
        • Shape: Paramyxoviridae are generally spherical, but they can be pleiomorphic, and filamentous forms can be observed. Inserted in to the envelope are glycoprotein spikes that extend about 8 to 12 nm from the surface of the membrane and that can be readily visualized by electron microscopy.
Genome Summary
  1. Genome of Newcastle Disease Virus(Seal et al., 2000)
    1. Description: The enveloped virus has a negative sense single-stranded genome of approximately 15 kb which codes for six proteins including an RNA directed RNA polymerase (L), hemagglutininneuraminidase (HN) protein, fusion (F) protein, matrix (M) protein, phosphoprotein (P) and nucleoprotein (N). Transcription occurs in the 3' to 5' direction with decreasing amounts of protein resulting with each subsequent gene (Fig. 1). Replication of a positive-sense intermediate genome also is synthesized by the NDV polymerase. Cleavage of a precursor F0 to the F1 and F2 products is necessary for viral spread to other cells. The F and HN surface glycoproteins are the principal antigens that elicit a protective immune response(Seal et al., 2000).
    2. NCDV-B1(Website 34)
      1. GenBank Accession Number: NC_002617
      2. Size: 15186 bp(Website 34).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Complete sequence for the B1 strain of Newcastle disease virus(Website 34).
  2. Genome of Newcastle disease virus (STRAIN ULSTER/67)
    1. Newcastle disease virus Ulster/67(Website 38)
      1. GenBank Accession Number: AY562991
      2. Size: 15186 bp(Website 38).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Newcastle disease virus isolate chicken/N. Ireland/Ulster/67, complete genome(Website 38).
  3. Genome of Newcastle disease virus strain U.S.-Largo-71
    1. Newcastle disease virus isolate mixed species/U.S./Largo/71(Website 39)
      1. GenBank Accession Number: AY562990
      2. Size: 15192 bp(Website 39).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Newcastle disease virus isolate mixed species/U.S./Largo/71, complete genome(Website 39).
  4. Genome of Newcastle disease virus strain Italy-2736-00
    1. Newcastle disease virus isolate dove/Italy/2736/00(Website 40)
      1. GenBank Accession Number: AY562989
      2. Size: 15192 bp(Website 40).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Newcastle disease virus isolate dove/Italy/2736/00, complete genome(Website 40).
  5. Genome of Newcastle disease virus strain U.S.(CA)-1083(Fontana)-72
    1. Newcastle disease virus isolate chicken/U.S.(CA)/1083(Fontana)/72(Website 41)
      1. GenBank Accession Number: AY562988
      2. Size: 15192 bp(Website 41).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Newcastle disease virus isolate chicken/U.S.(CA)/1083(Fontana)/72, complete genome(Website 41).
  6. Genome of Newcastle disease virus strain U.S.(CA)-211472-02
    1. Newcastle disease virus isolate chicken/U.S.(CA)/1083(Fontana)/72(Website 42)
      1. GenBank Accession Number: AY562988
      2. Size: 15192 bp(Website 42).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Newcastle disease virus isolate gamefowl/U.S.(CA)/211472/02, complete genome(Website 42).
  7. Genome of Newcastle disease virus strain NCDV-anhinga-U.S.(Fl)-44083-93
    1. Newcastle disease virus isolate anhinga/U.S.(Fl)/44083/93(Website 43)
      1. GenBank Accession Number: AY562986
      2. Size: 15192 bp(Website 43).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Newcastle disease virus isolate anhinga/U.S.(Fl)/44083/93, complete genome(Website 43).
  8. Genome of Newcastle disease virus strain NCDV-Cockatoo-Indonesia-14698-90
    1. Newcastle disease virus isolate cockatoo/Indonesia/14698/90(Website 44)
      1. GenBank Accession Number: AY562985
      2. Size: 15192 bp(Website 44).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Newcastle disease virus isolate cockatoo/Indonesia/14698/90, complete genome(Website 44).
  9. Genome of Newcastle disease virus strain NCDV-ZJ1
    1. Newcastle Disease virus strain ZJ1(Website 45)
      1. GenBank Accession Number: AF431744
      2. Size: 15192 bp(Website 45).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Newcastle Disease virus strain ZJ1, complete genome(Website 45).
  10. Genome of Newcastle disease virus strain NCDV-HB92-isolate-V4
    1. Newcastle disease virus strain HB92 isolate V4(Website 46)
      1. GenBank Accession Number: AY225110
      2. Size: 15186 bp(Website 46).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Newcastle disease virus strain HB92 isolate V4, complete genome(Website 46).
  11. Genome of Newcastle disease virus strain NCDV-B1-isolate-Takaak
    1. Newcastle disease virus strain B1 isolate Takaak(Website 47)
      1. GenBank Accession Number: AF375823
      2. Size: 15186 bp(Website 47).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Newcastle disease virus strain B1 isolate Takaaki, complete genome(Website 47).
  12. Genome of Newcastle disease virus strain NCDV-virusB1
    1. Newcastle disease virus B1, Second Entry(Website 48)
      1. GenBank Accession Number: AF309418
      2. Size: 15186 bp(Website 48).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Newcastle disease virus B1, complete genome (second entry)(Website 48).
  13. Genome of Newcastle disease virus strain NCDV-LaSota
    1. Newcastle disease virus strain LaSota(Website 49)
      1. GenBank Accession Number: AF077761
      2. Size: 15186 bp(Website 49).
      3. Gene Count: The NDV genome comprises six genes which encode the six known viral structural proteins. Three of these are associated with the lipid envelope of the virion: the haemagglutin-neuraminidase and fusion glycoproteins are anchored in the membrane and appear as protruding spikes on the virion surface, the matrix protein is non-glycosylated and is peripherally attached to the inner surface of the envelope. The remaining three proteins are associated with genomic RNA to form the viral nucleocapsid, these are the nucleocapsid protein, the phosphoprotein and the large protein(Millar et al., 1988).
      4. Description: Newcastle disease virus strain LaSota, complete genome(Website 49).
Biosafety Information
Culturing Information
  1. Incubation of fertile eggs (Alexander et al., 2000):
    1. Description: Samples from dead birds should consist of oro-nasal swabs, as well as samples collected from lung, kidneys, intestine (including contents), spleen, brain, liver and heart tissues. These may be collected separately or as a pool, although intestinal samples are usually processed separately from other samples. Samples from live birds should include both tracheal and cloacal swabs, the latter should be visibly coated with faecal material. Small delicate birds may be harmed by swabbing. Collection of fresh faeces may serve as an adequate alternative. Where opportunities for obtaining samples are limited, it is important that cloacal swabs (or faeces) and tracheal swabs (or tracheal tissue) be examined as well as organs or tissues that are grossly affected or associated with the clinical disease. Samples should be taken in the early stages of the disease. Samples should be placed in isotonic phosphate buffered saline (PBS), pH 7.0-7.4, containing antibiotics. (penicillin (2000 units/ml), streptomycin (2 mg/ml), gentamycin (50 g/ml), and mycostatin (1000 units/ml) for tissues and tracheal swabs, but at five-fold higher concentrations for faeces and cloacal swabs) Readjust the solution to pH 7.0-7.4 following the addition of the antibiotics. Faeces and finely minced tissues should be prepared as 10-20% (w/v) suspensions in the antibiotic solution. Suspensions should be processed as soon as possible after leaving them for 1-2 hours at room temperature. When immediate processing is impracticable, samples may be stored at 4C for up to 4 days(Website 53). Virus isolation demands between 3 and 10 days for the result, especially with pigeon PMV-1 strains for which a second passage in embryonated eggs may be required to recover the virus (data not shown, observations in author's reference laboratory.)(Barbezange et al., 2002).
    2. Medium: Most virulent strains of NDV will grow in a wide range of cell culture systems and it is possible that in some instances, due to local conditions, inoculation of cell cultures may be the best method for attempting NDV isolation. However, the most widely recommended method is the treatment of samples with antibiotics and the inoculation of embryonated fowls' eggs. The choice of eggs is important, these should be obtained from a specific pathogen free flock or, at least, eggs from hens free of NDV antibodies, and used at 9 to 10 days old(Alexander et al., 1988B). The supernatant fluids of faeces or tissue suspensions obtained through clarification by centrifugation at 1000 g for about 10 minutes at a temperature not exceeding 25C are inoculated in 0.2 ml volumes into the allantoic cavity of each of at least five embryonated SPF fowl eggs of 9-11 days' incubation. After inoculation, these are incubated at 35-37C for 4-7 days. Eggs containing dead or dying embryos as they arise, and all eggs remaining at the end of the incubation period, should first be chilled to 4C and the allantoic fluids tested for haemagglutination (HA) activity. Fluids that give a negative reaction should be passaged into at least one further batch of eggs(Website 53).
    3. Optimal Temperature: incubated at 35-37C for 4-7 day(Website 53).
    4. Upper Temperature: 37C(Website 53).
    5. Lower Temperature: 35C(Website 53).
Epidemiology Information:
  1. Outbreak Locations:
    1. Outbreaks of Newcastle disease were first reported in poultry in Java, Indonesia and Newcastle-upon-Tyne in 1926. The disease currently has worldwide distribution(Seal et al., 2000).
    2. In Western Europe, reported outbreaks increased markedly during the early 1990s, peaking at 239 outbreaks in countries of the European Union in 1994. Between 1991 and 1995, the majority of outbreaks in the EU occurred in the Benelux countries and Germany, predominantly in backyard poultry. Most of the outbreaks since 1995 have also been in backyard poultry. One notable aspect of the outbreaks in Western Europe during the 1990s was the occurrence of outbreaks in countries, which had been free of the disease for many years. Since 1995, 18 outbreaks have been reported in Denmark, one in Sweden, two in Finland, one in Norway, one in the Republic of Ireland and twenty-six in Northern Ireland, all areas that had been declared free of ND and which were monitored regularly by serological testing with no evidence of ND virus infections. Although voluntary vaccination was permitted, Great Britain was also essentially free of ND, and the outbreak confirmed in pheasants in 1996 was the first in this country since 1984. The virus is still detected in racing pigeons. However in 1997, eleven outbreaks of ND were confirmed in Great Britain in commercial poultry, four in broiler chickens and seven in turkeys. Until 1998, Australia had been free of virulent NDV since the 1932 outbreak. Two outbreaks of virulent ND occurred in Australia in 1998 and further outbreaks were reported in 1999(Alexander et al., 2000).
    3. A sick chicken from a backyard flock appears to be the means of entry into California poultry flocks. When the bird exhibited signs of illness, it was taken, on September 25, 2002, to a private veterinary practitioner in Torrence, CA. The bird was found to have a very pathogenic strain (velogenic) of the exotic Newcastle disease (END). This bird or index case is considered to be the carrier of the very infectious and pathogenic virus that spread quickly into backyard poultry then moved from there into poultry production facilities in Southern California. This is the first time since the 1971-73 outbreak of END that the disease has been of epidemic proportions in California. The main methods of transmission of the disease from one location to another seem to have been via bird to bird contact, human activities, insects, rodents, cages, machinery equipment and infected eggs. It then spread to other areas of the state. Since this exotic strain of Newcastle disease was first identified, millions of birds have been sacrificed in California and as of May 2003, it has not been contained by depopulation and quarantine. At the time of publication, commercial flocks and back yard flocks in seven counties in California have been affected. Additional areas of the state are under quarantine. The disease had spread to adjacent states of Nevada, Arizona but the outbreak there seems to be under control through the use of depopulation and quarantine by government response teams. An outbreak of the virus had been detected in Texas, in May of 2003. DNA sequencing analysis confirmed that the Texas strain was caused by a separate introduction of the disease and not due by movement from affected areas in California, Nevada or Arizona. Intense surveillance, and early detection in El Paso County, seems to have contained and eliminated the disease in Texas(Website 50).
    4. Information received on 17 November 2003 from Dr Peter Fernandez, Associate Administrator, Animal and Plant Health Inspection Service, United States Department of Agriculture (USDA), Washington, DC: The exotic strain of Newcastle disease virus detected primarily in backyard flocks in the States of California, Nevada, Arizona, and Texas has been completely eradicated. The confirmation of this exotic strain of Newcastle disease virus triggered an emergency response resulting in the depopulation of almost 4.5 million birds. During the epizootic, 21 commercial operations and 911 backyard establishments were confirmed positive. The last infected commercial operation was found on 26 March 2003 and the last infected backyard establishment was found on 31 May 2003. During the peak of the eradication activities, over 19,000 establishments were quarantined and over 2,500 of these establishments were depopulated. With the successful eradication of the virus, effective 16 September 2003, all States and Federal quarantines in all areas were officially lifted. Enhanced surveillance in commercial flocks as well as targeted surveillance in backyard flocks has not detected any further evidence of the virus. Surveillance continues and efforts have now been shifted to prevention and mitigation through outreach and education programmes. The virus has been completely stamped out and, in accordance with Article 2.1.15.3 of the Terrestrial Animal Health Code, there are no further infected zones. All restrictive measures in relation to Newcastle disease in the United States of America have therefore been lifted(Website 35).
    5. The most recent outbreak reports as posted by the OIE include: Albania: 26 March 2004, Algeria: 14 February 2003, Australia: 27 June 2003, Austria: 14 November 2003, Bahrain: 30 January 2004, Belarus: 13 June 2003, Canada: 19 September 2003, Denmark: 7 March 2003, Italy: 6 February 2004, Kuwait: 31 January 2003, Namibia: 14 March 2003, Niger: 14 March 2003, Norway: 2 July 2004, Russia: 8 August 2003, Senegal: 16 July 2004, Serbia and Montenegro: 14 March 2003, Sudan: 18 April 2003, Sweden: 28 May 2004, Taipei China: 23 May 2003, Thailand: 16 July 2004, Turkey: 16 July 2004, and the United States of America: 21 November 2003 (see above)(Website 36).
  2. Transmission Information:
    1. From: Aves , To: Aves
      Mechanism: Although the administration of live vaccines by aerosol demonstrates clearly that infection may be established via the respiratory route, remarkably little experimental evidence exist to suggest that infected birds will pass on the virus to susceptible birds in this way, even over short distances. The success of this route of transmission will depend on many environmental factors, such as temperature, humidity, and stocking density(Alexander et al., 2000). Inhalation of infectious virus may occur as a result of the presence of either larger droplets or fine aerosols containing virus. The former may occur in the birds' environment due to the presence of infected hosts in which the virus is replicating in the respiratory tract or as a result of contaminated drinking water, e.g. as with vaccination by this medium. In addition, respiratory infection may produce fine aerosols containing virus, which may cover much greater distances before infecting susceptible hosts by inhalation. Faecal excretion may also result in the production of both large and small particles containing infectious virus, the latter most probably resulting from dried faeces(Alexander et al., 1988A).
    2. From: Aves , To: Aves
      Mechanism: Transmission of virus infection from one bird to another via contaminated faeces can be easily demonstrated. The pigeon variant virus, the asymptomatic enteric viruses, and other viruses which fail to induce significant respiratory signs in infected birds, are likely to be transmitted primarily this way(Alexander et al., 2000). Spread of the disease to chickens in Great Britain was shown to be due to food contaminated with faeces and carcasses of infected feral pigeons and Alexander et al., confirmed that virus presented in this way would result in infection in susceptible hens. A noticeable property of the disease seen in laying birds in Great Britain during the 1984 outbreaks was the extreme slowness of spread through a house. This was attributed by Alexander et al., to the barrier that battery cages would present to a virus dependent on fecal-oral route(Alexander et al., 1988A). It has been demonstrated that NDV will survive for period of six months or more in avian faeces under normal temperatures(Vindevogel et al., 1988).
    3. From: Aves , To: Aves
      Mechanism: The concept of vertical transmission in birds implies that the virus is passed directly from the parent to the progeny via the embryonated egg and excludes infection which may occur after the egg has been laid. The facts that virus may penetrate the shell of the egg after laying and that faecal contamination of eggs or the environment has frequently resulted in infection and disease early in the life of chicks hatched from infected parents have often confused the assessment of true vertical transmission. Experimental assessment has also been greatly hindered by the cessation of egg laying, which is usually associated with infection by pathogenic strains of NDV. There are many instances of infected embryos in eggs obtained from hens undergoing field infection but this generally results in death of the embryo long before hatching. In addition, the presence of infected eggs may further complicate assessment of vertical transmission in the field as cracked or broken infected eggs at the hatchery represents another source of virus that may result in early infection in chicks and apparent vertical spread. In contrast to infection of embryos with virulent viruses, lentogenic or vaccinal viruses may not cause death of the embryo and infected chicks may hatch from such eggs. Again it is not clear at what point such eggs become infected although La Sota vaccine has been shown to be present in the ovaries, oviduct and uterus after vaccination(Alexander et al., 1988A). The status of possible NDV egg transmission is similar to the situation for persistence, because both positive and negative results have been reported. Embryos that survived V4 strain infection in ovo hatched and the progeny were NDV positive. More recently virulent NDV was detected in uninfected cell cultures prepared from embryonated chicken eggs. However, chicks hatched from eggs collected from NDV infected flocks were virus negative even though dead embryos and infertile eggs in the same incubator contained NDV(Seal et al., 2000). Sporadic outbreaks of Newcastle disease (ND) occurred in Taiwan during 1998-2000. In some cases, the disease occurred in broilers less than 2 wk old that originated in a broiler breeder farm, so spread of the ND virus (NDV) from the infected breeder farm to broiler ranches was suspected. The purpose of the present study was to examine the possibility of the transmission of NDV through eggs. Both clinical and experimental evidence were used to prove that this is possible. From epidemiological investigation, the possibility of transmission through eggs was suggested in two separate ND cases from a breeder farm and its progeny because two identical NDVs were isolated from both cases. In order to clarify the possibility of the transmission through eggs, one mean egg lethal dose (ELD50) of NDV was inoculated into the allantoic cavity of 155 9-to-11-day-old specific-pathogen-free (SPF) chicken embryos. Seventy-one hatching chicks from the inoculated embryos were raised for 14 days. The cloacal swabs from those chicks at the ages of 1, 4, and 7 days and the tissues after necropsy at the ages of 14 days were taken for virus isolation. The same NDV was reisolated from three hatching chicks. This experiment confirms that a few chicken embryos infected in ovo with a low titer of NDV can hatch and contain NDV after hatching, which results in NDV spreading through eggs(Chen et al., 2002).
    4. From: Aves , To: Homo sapiens
      Mechanism: Many of the documented cases involved infections in laboratory workers who accidentally splashed high-titer NDV-infected egg fluids into their eyes, veterinary laboratory diagnosticians who performed postmortem examinations on infected birds or handled infectious tissues, workers in poultry processing plants, and poultry vaccination crews(Swayne et al., 2003).
    5. From: Homo sapiens , To: Aves
      Mechanism: Man may transfer NDV either mechanically on his person or equipment, or as a result of an infection, which is usually manifest as conjunctivitis(Alexander et al., 1988A). No evidence exists to support human-to-human transmission, but the potential for human-to-bird transmission exists(Swayne et al., 2003).
  3. Environmental Reservoir:
    1. Birds of various uses(Alexander et al., 2000):
      1. Description: FERAL BIRDS: Migratory feral birds may be responsible for the primary introduction of infection, but nearly all NDV isolates obtained from feral birds are of low virulence. A more significant role of such birds may be the transmission of virus within an area following NDV infection of poultry(Alexander et al., 2000). There appears to be two main reservoirs of NDV. The avirulent virus mainly associated with waterfowl and the highly virulent viruses associated with tropical birds, such as psitticines. Both are associated with growth in the intestine(McFerran et al., 1988). CAPTIVE CAGED BIRDS: World trade in captive caged birds is enormous, and in many countries virulent NDV has been isolated frequently from such birds held in quarantine. For example, 147 virulent NDV isolations were made from 2,274 lots of captive birds held in quarantine in the USA from 1974 to 1981. Some infected psittacines have been shown to excrete virulent virus intermittently for extremely long periods, in some cases for more than one year, which further emphasises the potential role these birds may have in the introduction of NDV to a country or area(Alexander et al., 2000). Smuggled pet birds, especially Amazon parrots from Latin America, pose a great risk of introducing exotic Newcastle into U.S. poultry flocks. Amazon parrots that are carriers of the disease but do not show symptoms are capable of shedding END virus for more than 400 days(Website 52). There appears to be a pool of highly virulent viruses maintained in exotic birds such as Psittacines. In the USA of 2.9 million quarantined birds examined, NDV was recovered from 173 lots. Of these isolates VVNDV was obtained from 141 lots, non-viscerotropic velogenic NDV was recognised in 6 lots, mesogenic in 3 lots and lentogenic NDV from 23 lots. The majority of velogenic isolates were from Psittaciformes, with Passeriformes next in importance. It appears some species can become carriers of infection. Thus whilst canaries appeared to eliminate the virus, nuns and conures excreted virus up to 84 days post exposure and parrots excreted the virus up to 84 days post exposure and parrots excreted for 376 days(McFerran et al., 1988). PRIVATELY OWNED GAME FOWL: Several premises in metropolitan Los Angeles were quarantined in early October after exotic Newcastle diseaseone of the most infectious poultry diseases knownwas detected in privately owned game fowl. The source of this outbreak isn't known, although it is speculated that infected birds were smuggled into California from Mexico. Birds carrying the virus have been confiscated at the border(Nolan et al., 2002). Game birds may also be implicated in the introduction of NDV to a country, since considerable trade occurs in these birds, which are often imported for immediate release(Alexander et al., 2000). RACING PIGEONS: The extremely rapid spread of the disease across Europe and the rest of the world probably resulted from contact associated with races, shows, trade and the gregarious nature of the sport. The practice of large transporters collecting birds in a wide area to take to the release point for races presents an excellent environment for the spread of NDV and was considered a prominent method of spread in Great Britain. In addition racing of disease birds offers opportunities for the wider dissemination of the disease as birds are expected to cover long distances and frequently fly widely off course (especially if sick). Such birds may be taken into other pigeon lofts to recuperate or mix with feral birds. In Great Britain, where there was no vaccination of domestic poultry at that time, the virus passed from racing pigeons to feral pigeons which resulted in the infection of domestic hens via food-stores infested with infected feral pigeons(Alexander et al., 1988A). Infected pigeons eliminate virus in the laryngeal secretions and faeces from the second day after infection for 10 to 15 days. Infection can thus be transmitted through direct and indirect contact with oro-nasal secretions and faeces even during the incubation period. It has been shown that in experimental infection of pigeons with velogenic NDV, virus persists for not more than 3 weeks in the intestine and 5 weeks in the brain. After they have been ill for 6 weeks, pigeons may be considered as no longer carriers of virus and thus are unlikely to transmit the infection(Vindevogel et al., 1988). POULTRY MARKETS: Modern methods of slaughter of commercial poultry, marketing of poultry meat and veterinary inspection, have reduced the movement of live commercial poultry (excluding day-old chicks) in many developed countries. However, in many countries, the normal method of trade is by live poultry markets. Such markets, where birds of many different species may be placed in close contact, represent ideal reservoirs of virus from which disease may be disseminated(Alexander et al., 2000). PERSONNEL AND EQUIPMENT: Secondary spread during most epizootics of ND in recent years has been the result of the movements of personnel or equipment. Humans may be infected with NDV, but the most likely role of personnel is in the transfer of infective faeces from one site to another on hair, clothing, footwear, crates, feed sacks, egg trays or vehicles(Alexander et al., 2000). Survives for long periods at ambient temperature, especially in faeces(Website 51). POULTRY WASTE: In the past, poultry meat has been incriminated as the main vehicle for the introduction and spread of NDV. For example, in 1947, one-third of the first 542 outbreaks in England and Wales were considered to be directly attributable to feeding poultry waste to chickens. Sampling of batches of frozen poultry imported into Great Britain in the same year produced an isolation rate of up to 66 percent. Modern methods of poultry carcass preparation and legislation on the feeding of untreated swill to poultry have greatly diminished the risk from poultry products, but the possibility of spread in this way nevertheless remains(Alexander et al., 2000). Poultry products contaminated with pathogenic strains of Newcastle disease virus are a source of virus transmission to susceptible poultry flocks. The probability of contamination varies according to the type of product. Research conducted by various laboratories in Europe has shown that pathogenic virus can be isolated from the carcasses of chickens, whether vaccinated or not, during a brief period after experimental infection. Eggs laid by hens infected with Newcastle disease virus present a very low risk. Furthermore, feathers, bones, blood and offal present potential risks if they are incorporated in poultry feed. Finally, poultry droppings used as a fertiliser can present a major risk of infection in certain circumstances(Guittet et al., 1997). FERAL PIGEONS: In countries of the British Isles, outbreaks of ND in commercial poultry have been associated with feed contaminated with infective faeces from feral pigeons infected with NDV. Similarly, water contaminated with infected faeces may introduce NDV to a flock(Alexander et al., 2000). AIR: Few studies have attempted to assess the survival of airborne virus, but Hugh-Jones were able to detect virus 64m but not 165 m downwind of an infected premises. These authors stressed the importance of environmental conditions, particularly relative humidity on the likelihood of airborne spread. When climatic conditions are favorable and poultry farms sufficiently concentrated, as in Northern Ireland in 1973, it is difficult not to conclude that airborne spread may play a significant role in epidemics of ND. However, in the majority of outbreaks there has been no evidence that airborne spread has played a major role and in recent years airborne spread has not been an issue in reported outbreaks and an alternative, more likely, cause has nearly always existed, particularly the movement of poultry and the agency of humans(Alexander et al., 2000). CONTAMINATED VACCINES: Good manufacturing practices should ensure that vaccines are highly unlikely to be carriers of virulent NDV. However, in the past, birds have become infected when vaccines against other disease have been contaminated with NDV, or as a result of failure to inactivate killed vaccines prepared from virulent NDV. In 1996 and 1997, a series of NDV isolates of low virulence were obtained from poultry flocks in Denmark, a country, which pursues a non-vaccinating policy for ND. These viruses were demonstrated to be the result of contamination of avian virus vaccines with vaccinal NDVs(Alexander et al., 2000). NON-AVIAN HOSTS: Non-avian hosts are likely to introduce NDV by mechanical transfer of infective faeces, e.g. by insects, rodents or scavenging animals. In hot countries, reptiles which may enter poultry houses should not be ignored as potential transmitters of NDV, as susceptibility to infection has been reported in reptiles(Alexander et al., 2000).
  4. Intentional Releases:
    1. Intentional Release Information:
      1. Description: Even before Newcastle disease was identified in the United States, its potential threat to the poultry industry was acknowledged by the War Department Commission during World War II. To be prepared for its possible use in biological warfare, a war research project was initiated to explore methods of protecting poultry by use of inactivated virus vaccines or by enhancing the immunity with a modified live virus vaccine(Hitchner et al., 2004). As of October 2001, the potential for use of infectious agents, such as anthrax, as weapons has been firmly established. It has been suggested that attacks on a nations' agriculture might be a preferred form of terrorism or economic disruption that would not have the attendant stigma of infecting and causing disease in humans. Highly pathogenic avian influenza virus is on every top ten list available for potential agricultural bioweapon agents, generally following foot and mouth disease virus and Newcastle disease virus at or near the top of the list(Perdue et al., 2003).
      2. Emergency Contact: Poultry or pet bird owners or veterinarians who suspect a bird may have END should immediately contact State or Federal animal health authorities or call 1-866-536-7593 (toll-free)(Website 52).
      3. Containment: To prevent END from being introduced into U.S. poultry flocks, USDA's Animal and Plant Health Inspection Service (APHIS) requires that all imported birds (poultry, pet birds, birds exhibited at zoos, and ratites) be tested and quarantined for diseases before entering the country. In addition to international import restrictions, APHIS has increased surveillance efforts to detect END if it is accidentally introduced into the United States. APHIS and State veterinarians trained to diagnose foreign animal diseases regularly conduct field investigations of suspicious disease conditions. This surveillance is enhanced by efforts from university personnel, State animal health officials, USDA-accredited veterinarians, and industry representatives. If END were detected in domestic poultry or pet birds, APHIS would work quickly with its State and industry counterparts to implement aggressive measures, including quarantine, control, and cleanup, to prevent opportunities for the disease to spread(Website 52). The infectivity of NDV and other avian paramyxoviruses may be destroyed by physical and chemical treatments such as heat, irradiation (including light and ultraviolet rays), oxidation processes, pH effects and various chemical compounds. The rate at which infectivity is destroyed depends on the strain of virus, the length of time of exposure, the quantity of virus, the nature of the suspending medium, and the interactions between treatments. No single treatment can guarantee destruction of all viruses but may result in low probability of infective virus remaining(Alexander et al., 1993).
Diagnostic Tests Information
  1. Immunoassay Test:
    1. Haemagglutination Inhibition (Website 53):
      1. Time to Perform: unknown
      2. Description: ND virus may be employed as an antigen in a wide variety of serological tests, enabling neutralisation or enzyme-linked immunosorbent assays (ELISA) to be used for diagnosis. At present, the HI test is most widely used. Chicken sera rarely give nonspecific positive reactions in this test and any pretreatment of the sera is unnecessary. Sera from species other than chickens may sometimes cause agglutination of chicken red blood cells (RBCs), so this property should first be determined and then removed by adsorption of the serum with chicken RBCs. This is done by adding 0.025 ml of packed chicken RBCs to each 0.5 ml of antisera, shaking gently and leaving for at least 30 minutes; the RBCs are then pelleted by centrifugation at 800 g for 2-5 minutes and the adsorbed sera are decanted. The value of serology in diagnosis is clearly related to the expected immune status of the affected birds. HI titres may be regarded as being positive if there is inhibition at a serum dilution of 1/16 (24 or log2 4 when expressed as the reciprocal) or more against 4 HAU of antigen. Some laboratories prefer to use 8 HAU in HI tests. While this is permissible, it affects the interpretation of results so that a positive titre is 1/8 (23 or log2 3) or more. Back titration of antigen should be included in all tests to verify the number of HAU used. HI titres may be used to assess the immune status of a flock. In vaccinated flocks that are being monitored serologically, it may be possible to identify anamnestic responses as the result of a challenge infection with field virus, but great care should be exercised as variations may occur from other causes. For example, it has been demonstrated that APMV-3 virus infections of ND-virus-vaccinated turkeys will result in substantially increased titres to ND virus(Website 53).
    2. Haemagglutination Assay (Website 53):
      1. Time to Perform: unknown
      2. Description: HA activity detected in bacteriologically sterile fluids harvested from inoculated eggs may be due to the presence of any of the 15 haemagglutinin subtypes of influenza A viruses or of the eight other paramyxovirus serotypes. (Nonsterile fluid could contain bacterial HA.)(Website 53).
      3. False Positive: The haemagglutination test is not specific for Newcastle disease virus and other viruses will agglutinate red blood cells. Therefore a sample of allantoic fluid testing positive for haemagglutinin will need further testing to confirm the presence of Newcastle disease virus. The presence of Newcastle disease virus in the sample is confirmed by using the haemagglutination inhibition (HI) test(Website 54).
    3. ELISA (Website 53):
      1. Time to Perform: unknown
      2. Description: Antibodies to NDV may be detected in poultry sera by a variety of tests including single radial immunodiffusion, single radial hemolysis, agar gel precipitin, VN in chick embryos, and plaque neutralization. ELISAs, which lend themselves to semiautomated techniques have become popular, especially as part of a flock screening procedures. Good correlation has been reported between ELISA and HI tests. Sera from other species (including turkeys) may cause low-titer, nonspecific agglutination of chicken RBCs, complicating the test. Such agglutination may be removed by adsorption with chicken RBCs before testing(Alexander et al., 1993). There are a variety of commercial ELISA kits available and these are based on several different strategies for the detection of ND virus antibodies, including indirect, sandwich and blocking or competitive ELISAs using MAbs. At least one kit uses a subunit antigen. Usually such tests have been evaluated and validated by the manufacturer, and it is therefore important that the instructions specified for their use be followed carefully(Website 53). ELISA procedures based on whole virus as coating antigen have also been developed. However, these ELISAs were of limited use, mainly because of non-specific reactions in the chicken sera(Kho et al., 2000).
  2. Nucleic Acid Detection Test:
  3. Other Test:
    1. Intracerebral pathogenicity index (Website 53):
      1. Time to Perform: unknown
      2. Description: The extreme variation in virulence of different NDV isolates and the widespread use of live vaccines means that the identification of an isolate of NDV from birds showing clinical signs does not confirm a diagnosis of ND. As indicated in the (OIE) definition (of Newcastle disease), an assessment of the virulence of the isolate by the ICPI test or amino acid sequencing is also required(Alexander et al., 2000). 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 chicks or by the intravenous pathogenicity index in 6-week-old chickens. In some countries, variations of these standard techniques are used. The pathogenicity of isolates can also be evaluated using molecular biological techniques, i.e. reverse-transcription polymerase chain reaction and sequencing(Website 53). Confirmed diagnosis may be slow, taking several days to isolate the virus and carry out the pathogenicity test. It assumes viruses always show their potential pathogenicity for chickens, which does not always appear to be the case(Aldous et al., 2001). 1) Fresh infective allantoic fluid with a HA titre greater than 24 (greater than 1/16) is diluted 1/10 in sterile isotonic saline with no additives, such as antibiotics. 2) 0.05 ml of the diluted virus is injected intracerebrally into each of ten chicks hatched from eggs from an SPF flock. These chicks must be over 24-hours and under 40-hours old at the time of inoculation. 3) The birds are examined every 24 hours for 8 days. 4) At each observation, the birds are scored: 0 if normal, 1 if sick, and 2 if dead. (Dead individuals must be scored as 2 at each of the remaining daily observations after death). 5) The intracerebral pathogenicity index (ICPI) is the mean score per bird per observation over the 8-day period. The most virulent viruses will give indices that approach the maximum score of 2.0, whereas lentogenic strains will give values close to 0.0(Website 53).
    2. Intravenous pathogenicity index (Website 53):
      1. Time to Perform: unknown
      2. Description: 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 chicks or by the intravenous pathogenicity index in 6-week-old chickens. In some countries, variations of these standard techniques are used. The pathogenicity of isolates can also be evaluated using molecular biological techniques, i.e. reverse-transcription polymerase chain reaction and sequencing(Website 53). 1) Freshly collected infective allantoic fluid (which should be no older than 24-48 hours and should have tested negative for bacterial contamination) with a HA titre of greater than 24 (greater than 1/16) is diluted 1/10 in sterile isotonic saline. 2) 0.1 ml of the diluted virus is injected intravenously into each of ten 6-week-old SPF chickens. 3) Birds are examined at 24-hour intervals for 10 days and scored at each observation: 0 if normal, 1 if sick, 2 if paralysed or showing other nervous signs, and 3 if dead. (Dead individuals must be scored as 3 at each of the remaining daily observations after death). 4) The intravenous pathogenicity index (IVPI) is the mean score per bird per observation over the 10-day period. Lentogenic strains and some mesogenic strains will have IVPI values of 0, whereas the indices for virulent strains will approach 3.0. Some variations have been recommended in these tests. Swabbing of the cloaca and conjunctiva of 8-week-old chickens with undiluted allantoic fluid has been substituted for the IVPI test. The intention is to distinguish between viscerotropic velogenic and other velogenic viruses(Website 53).
    3. Intracloacal inoculation pathogenicity test (Seal et al., 2000):
      1. Time to Perform: unknown
      2. Description: In the United States the intracloacal innoculation pathogenicity test is used to distinguish viscerotropic velogenic NDV from neurotropoic velogenic viruses(Seal et al., 2000). 1) Freshly collected infective allantoic fluid (which should be no older than 24-48 hours and should have tested negative for bacterial contamination) with a HA titre of greater than 24 (greater than 1/16) is diluted 1/10 in sterile isotonic saline. 2) 0.1 ml of the diluted virus is injected intravenously into each of ten 6-week-old SPF chickens. 3) Birds are examined at 24-hour intervals for 10 days and scored at each observation: 0 if normal, 1 if sick, 2 if paralysed or showing other nervous signs, and 3 if dead. (Dead individuals must be scored as 3 at each of the remaining daily observations after death). 4) The intravenous pathogenicity index (IVPI) is the mean score per bird per observation over the 10-day period. Lentogenic strains and some mesogenic strains will have IVPI values of 0, whereas the indices for virulent strains will approach 3.0. Some variations have been recommended in these tests. Swabbing of the cloaca and conjunctiva of 8-week-old chickens with undiluted allantoic fluid has been substituted for the IVPI test. The intention is to distinguish between viscerotropic velogenic and other velogenic viruses(Website 53).
    4. Mean Death in Eggs (Website 53):
      1. Time to Perform: unknown
      2. Description: 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 chicks or by the intravenous pathogenicity index in 6-week-old chickens. In some countries, variations of these standard techniques are used. The pathogenicity of isolates can also be evaluated using molecular biological techniques, i.e. reverse-transcription polymerase chain reaction and sequencing(Website 53). 1) Fresh infective allantoic fluid is diluted in sterile saline to give a tenfold dilution series between 10-6 and 10-9. 2) For each dilution, 0.1 ml is inoculated into the allantoic cavity of each of five 9-10-day-old embryonated SPF fowl eggs, which are then incubated at 37C. 3) The remaining virus dilutions are retained at 4C and another five eggs are inoculated with 0.1 ml of each dilution 8 hours later and left at 37C. 4) Each egg is examined twice daily for 7 days and the times of any embryo deaths are recorded. 5) The minimum lethal dose is the highest virus dilution that causes all the embryos inoculated with that dilution to die. 6) The mean death time (MDT) is the mean time in hours for the minimum lethal dose to kill all the inoculated embryos. 7) The MDT has been used to classify ND virus strains into velogenic (taking under 60 hours to kill); mesogenic (taking between 60 and 90 hours to kill); and lentogenic (taking more than 90 hours to kill)(Website 53).
    5. Monoclonal Antibodies (Alexander et al., 2000):
      1. Time to Perform: unknown
      2. Description: Mouse mAbs directed against strains of NDV have been used in HI tests to allow rapid identification of NDV without the possible cross reactions with other PMV serotypes that may occur with polyclonal sera. Some workers have used mAbs to distinguish between the common vaccine strains, Hitchner B1 and La Sota, while other mAbs can separate vaccine viruses from epizootic virus in a given geographical area. Panels of mAbs have been used to establish antigenic profiles of NDV isolates based on their ability to react or not with the viruses. This has proven to be a valuable method for grouping and differentiating isolates of NDV which has been particularly valuable in understanding the epizootiology of outbreaks(Alexander et al., 2000).
Infected Hosts Information
  1. Birds
    1. Taxonomy Information:
      1. Species:
        1. Aves (Website 55):
          • Common Name: Aves
          • GenBank Taxonomy No.: 8782
          • Description: Newcastle disease viruses have been reported to infect animals other than birds, ranging from reptiles to humans. Kaleta and Baldauf concluded that NDV infections have been established in at least 241 species of birds representing 27 of the 50 orders of the class. All birds are probably susceptible to infection, but , as stressed by Kaleta and Baldauf, the disease observed with any given virus may vary enormously form one species to another(Alexander et al., 2000). Table 1 of this reference contains data on all available species and a record of ND along with their taxonomic status in the class Aves and in brief, information on the mode of infection (natural or experimental) as well as clinical signs and pathological lesions observed by the authors. The host range of NDV represents approximately 236 species of pet and free-living birds in addition to domestic avian species (chicken, turkey, goose, duck and pigeon.)(Kaleta et al., 1988).
    2. Infection Process:
      1. Infectious Dose: To be added later - check,
      2. Description: TEXT,
    3. Disease Information:
      1. Newcastle Disease Virus :
        1. Incubation: Incubation period is four to six days(Website 51),
        2. Prognosis:
            In poultry the disease can cause high mortality (up to 100 percent). Surviving birds show impaired growth, poor food utilization, reduced egg production, and impairment of eggshell formation. Fertility and hatchability of eggs are also reduced(Gallili et al., 1998), In ducks and geese even when infected by mesogenic or velogenic viruses, infections are normally subclinical. Morbidity in geese, swans and ducks was 10 percent or less, with about 10 percent mortality in the ducks and geese and no mortality in swans. In pigeons, mortality can reach 40 percent in infections with the pigeon PMV-1 isolates in which nervous signs and diarrhea are the dominant features(McFerran et al., 1988),
        3. Diagnosis Summary: The objectives in the diagnosis of NDV infections are to reach a decision on whether or not to impose control measures and to obtain evidence to support epidemiological investigations. None of the clinical signs or lesions of ND may be regarded as pathognomonic, and the wide variation in disease with virus strain, host species, and other factors means that at best, these can serve as only suggestion of infection with NDV. Similarly, the presence of lentogenic NDV strains in birds in most countries and the almost universal use of live vaccines means that mere demonstration of infection, without definition of the infecting virus, is rarely adequate cause for control measures to be imposed(Alexander et al., 1993), Differential diagnosis of NDV involves hemagglutination inhibition with polyclonal NDV specific antisera or use of the ELISA. Oligonucleotide probes and viral genomic RNA fingerprint analysis have been used to identify and differentiate NDV strains, but with limited success. Monoclonal antibodies are now used to identify antigenic groups, but pathotyping NDV isolates still involves labor-intensive procedures. Pathotype prediction initially involves NDV inoculation of embryonated eggs to determine mean death time of the embryo (MDT). Further testing entails inoculation of chickens to determine the intracerebral pathogenicity index (ICPI) and the intravenous pathogenicity index (IVPI). In the United States the intracloacal inoculation pathogenicity test is used to distinguish viscerotropic velogenic NDV from neurotropic velogenic viruses. Additionally, virulent NDV can be differentiated by its ability to replicate in most avian and mammalian cell types without the addition of trypsin. Although all NDV isolates will replicate in chicken embryo kidney cells, lentogens require trypsin for replication in avian fibroblasts or mammalian cell types(Seal et al., 2000),
        4. Symptom Information :
          • Syndrome -- Viscerotropic-velogenic (Alexander et al., 1993):
            • Description: With extremely virulent viruses , the disease may appear suddenly, with high mortality occurring in the absence of other clinical signs. In outbreaks in chickens due to the VVND pathotype, clinical signs often begin with listlessness, increased respiration, and weakness, ending with prostration and death. During the panzootic caused by this type of virus in 1970-1973, disease in some countries like Great Britain and Northern Ireland was marked by severe respiratory signs, but in many other countries these were absent. This type of ND may cause edema around the eyes and head. Green diarrhea is frequently seen in birds that do not die early in infection, and prior to death, muscular tremors, torticollis, paralysis of legs and wings, and opisthotonos may be apparent. Mortality reaches 100 percent in flocks of fully susceptible chickens(Alexander et al., 1993). In outbreaks involving velogenic virus, birds may be found dead without any signs(McFerran et al., 1988).
            • Symptom -- Generalised Signs (McFerran et al., 1988):
              • Description: loss of appetite progressing to failure to eat and abnormal thirst, and severe dehydration and emaciation may occur in association with fever. Fuffled feathers, huddling, listlessness, somnolence, progressing to complete depression are features. Birds often sit on their hocks with their eyes half to fully closed. Oedema of the face (especially of the eyelids) is sometimes seen with velogenic strains and therefore can no longer be considered diagnostic for Fowl Plague. Change of voice, becoming harsh, is sometimes followed by complete silence in the house due to the depression of birds. Diffuse congestion of the skin with localised areas of petechiation, especially in the wattles can be a feature. Combs and wattles can become cyanotic and oedematous due to a combination of respiratory and circulatory involvements(McFerran et al., 1988).
          • Syndrome -- Neurotropic Velogenic (Alexander et al., 1993):
            • Description: In chickens, it is marked by sudden onset of severe respiratory disease followed a day or two later by neurologic signs. Egg production falls dramatically, but diarrhea is usually absent. Morbidity may reach 100 percent. Mortality is generally considered much lower, although up to 50 percent in adult birds and 90 percent in young chickens has been recorded(Alexander et al., 1993).
            • Symptom -- Generalised Signs (McFerran et al., 1988):
              • Description: loss of appetite progressing to failure to eat and abnormal thirst, and severe dehydration and emaciation may occur in association with fever. Fuffled feathers, huddling, listlessness, somnolence, progressing to complete depression are features. Birds often sit on their hocks with their eyes half to fully closed. Oedema of the face (especially of the eyelids) is sometimes seen with velogenic strains and therefore can no longer be considered diagnostic for Fowl Plague. Change of voice, becoming harsh, is sometimes followed by complete silence in the house due to the depression of birds. Diffuse congestion of the skin with localised areas of petechiation, especially in the wattles can be a feature. Combs and wattles can become cyanotic and oedematous due to a combination of respiratory and circulatory involvements(McFerran et al., 1988).
          • Syndrome -- Mesogenic (Alexander et al., 1993):
            • Description: Mesogenic strains of NDV usually cause respiratory disease in field infections. In adult birds, there may be a marked drop in egg production that may last for several weeks. Nervous signs may occur but are not common. Mortality in fowl is usually low, except in very young and susceptible birds, but may be considerably affected by exacerbating conditions(Alexander et al., 1993).
            • Symptom -- Generalised Signs (McFerran et al., 1988):
              • Description: Loss of appetite progressing to failure to eat and abnormal thirst, and severe dehydration and emaciation may occur in association with fever. Fuffled feathers, huddling, listlessness, somnolence, progressing to complete depression are features. Birds often sit on their hocks with their eyes half to fully closed. Oedema of the face (especially of the eyelids) is sometimes seen with velogenic strains and therefore can no longer be considered diagnostic for Fowl Plague. Change of voice, becoming harsh, is sometimes followed by complete silence in the house due to the depression of birds. Diffuse congestion of the skin with localised areas of petechiation, especially in the wattles can be a feature. Combs and wattles can become cyanotic and oedematous due to a combination of respiratory and circulatory involvements(McFerran et al., 1988).
            • Symptom -- Reproductive (McFerran et al., 1988):
              • Description: The effect on egg production is usually marked. There can be a reduction in egg numbers associated with smaller eggs, misshapen and rough shelled eggs and shell-less eggs and a decrease in the quality of albumen. In other outbreaks the egg production can rapidly cease or fall to very low levels. This is usually preceded by the production of shell-less eggs. Egg production often returns to normal levels after 3-4 weeks, but in some outbreaks it never returns. In some cases surviving birds may go into moult(McFerran et al., 1988).
            • Symptom -- Respiratory (McFerran et al., 1988):
              • Description: Respiratory signs may occur as mild rales and snicks which only can be detected with careful observation. This is best heard at night when birds are settled. Signs may be more severe with sneezing, coughing, nasal discharge and laboured breathing to frank respiratory distress with open mouthed breathing. Inspiration can be accompanied by a rattling sound. Head shaking, with birds trying to dislodge mucus from the respiratory passages can be a feature. There may be a uni or bilateral mucopurulent conjunctivitis(McFerran et al., 1988).
            • Symptom -- Diarrhea (McFerran et al., 1988):
              • Description: Greenish-yellow diarrhea is a feature of some outbreaks but is by no means a universal sign(McFerran et al., 1988).
            • Symptom -- Nervous (McFerran et al., 1988):
              • Description: Nervous signs are variable and usually are not seen until the disease is advanced. They include tremors, torticollis, opisthotonus, convulsions which are steady and rhythmic incordinated movement and paralysis of wings or legs(McFerran et al., 1988).
          • Syndrome -- Lentogenic (Alexander et al., 1993):
            • Description: Lentogenic viruses usually do not cause disease in adults. In young, fully susceptible birds, serious respiratory disease problems can be seen, often resulting in mortality, following infection with more pathogenic LaSota strains complicated by infections with one or more of a range of other micro-organisms. Vaccination or infection of broilers close to slaughter with these viruses can lead to colisepticemia or airsacculitis, with resulting condemnation(Alexander et al., 1993).
            • Symptom -- Respiratory (McFerran et al., 1988):
              • Description: Respiratory signs may occur as mild rales and snicks which only can be detected with careful observation. This is best heard at night when birds are settled. Signs may be more severe with sneezing, coughing, nasal discharge and laboured breathing to frank respiratory distress with open mouthed breathing. Inspiration can be accompanied by a rattling sound. Head shaking, with birds trying to dislodge mucus from the respiratory passages can be a feature. There may be a uni or bilateral mucopurulent conjunctivitis(McFerran et al., 1988).
          • Syndrome -- Pigeon Panzootic (Alexander et al., 1993):
            • Description: The virus responsible for the panzootic in pigeons during the 1980s induced clinical signs in field infections of pigeons and chickens unlike those from other viruses. In both species, the predominant clinical features were diarrhea and nervous signs. In adult chickens, precipitous falls in egg production were seen, and high mortality was recorded in younger birds. This virus did not induce respiratory signs in uncomplicated infections of pigeons or chickens(Alexander et al., 1993).
            • Symptom -- Diarrhea (McFerran et al., 1988):
              • Description: Greenish-yellow diarrhea is a feature of some outbreaks but is by no means a universal sign(McFerran et al., 1988).
            • Symptom -- Nervous (McFerran et al., 1988):
              • Description: Nervous signs are variable and usually are not seen until the disease is advanced. They include tremors, torticollis, opisthotonus, convulsions which are steady and rhythmic incordinated movement and paralysis of wings or legs(McFerran et al., 1988).
            • Symptom -- Reproductive (McFerran et al., 1988):
              • Description: The effect on egg production is usually marked. There can be a reduction in egg numbers associated with smaller eggs, misshapen and rough shelled eggs and shell-less eggs and a decrease in the quality of albumen. In other outbreaks the egg production can rapidly cease or fall to very low levels. This is usually preceded by the production of shell-less eggs. Egg production often returns to normal levels after 3-4 weeks, but in some outbreaks it never returns. In some cases surviving birds may go into moult(McFerran et al., 1988).
          • Syndrome -- Other Species (Alexander et al., 1993):
            • Description: The clinical signs produced by specific viruses in other hosts may differ widely from those seen in chickens. In general, turkeys are as susceptible as chickens to infection with NDV, but clinical signs are usually less severe. Although readily infected, ducks and possibly geese usually are regarded as clinically resistant even to the strains of NDV most virulent for chickens. However, outbreaks of severe disease in ducks infected with NDV have been described. Outbreaks of ND have been reported in most game species, and the disease appears similar to that in chickens. In ostriches and other rarities, ND viruses virulent for chickens do not produce pathogenic disease(Alexander et al., 1993).
    4. Prevention:
      1. Biosecurity Measures(Alexander et al., 2000)
        • Description: Biosecurity aimed at preventing disease should commence at the planning stage of commercial poultry farms. Farms and flocks should be well separated, hatcheries should be isolated from poultry farms, different species should be reared on different sites, and an adequate fresh water supply should be available, preferably one that does not draw on surface water. On poultry farms the following points should be observed: a) birdhouses, feed stores and water tanks should be bird-proofed. b) movements in and off the farm should be kept to a minimum. c) all equipment, especially vehicles, should be disinfected before access to the site is permitted. d) movements between different farms for egg collection, carcass collection, feed delivery and similar should be to and from a specified collection and delivery point away from the poultry flocks. Visits from personnel such as bleeding or vaccination teams, inseminators and veterinarians are the most likely method of introduction of ND. If such visits are unavoidable, regimens of clothing change, equipment disinfection and other basic hygiene controls must be enforced(Alexander et al., 2000), Newcastle disease can be controlled without vaccination, with vaccination of breeders and layers only, by using both policies in combination with a stamping out policy, by ring vaccinations in case of an outbreak, or with vaccination of the complete population combined with stamping out. The choice of the policy depends on the geographical location of an area or country, trade contacts with other areas that would favor import of virulent virus and risks of trade blockades in case of an outbreak(Kouwenhoven et al., 1993),
      1. Live Vaccines(Kouwenhoven et al., 1993)
        • Description: Live vaccines are based on lentogenic NDV strains (Hitchener B1, LasSota, Clone 30, QueenslandV4 and Poulvac NDW). A good vaccine should contain greater than or equal 10 (6.5) to 10 (7.0) EID50 per bird dose. The ICPI of the virus should not exceed 0.7, preferably not 0.4. The Hitchner B1 vaccine causes less post-vaccinal reactions than LaSota- and Clone 30-based preparations, but it is less immunogenic in birds with maternal antibody. The NDW vaccine causes no post-vaccinal reactions. Live vaccines are administered by eye or nose drop, spray or via the drinking water. Large numbers of birds are preferably vaccinated using spray and aerosol methods. The vaccine reaches eye, nose and pharynx(Kouwenhoven et al., 1993), Mesogenic live vaccines tend to be used only in countries where virulent NDV is widespread and it is important to maintain high antibody titres to prevent serious disease. The presence of enzootic disease is usually linked to severe economic restrictions, which rule out the use of oil emulsion vaccine. The most popular live vaccines have evolved from field isolates of low virulence. Most are based on lentogenic viruses Hitchner B1 or La Sota or similar viruses, although some asymptomatic enteric viruses have also been used as live vaccines(Alexander et al., 1995),
        • Efficacy:
          • Rate:
          • Duration:
        • Contraindicator: Vaccination must be regarded as complementing good management, biosecurity and hygiene in rearing domestic poultry. Vaccination against ND must never be considered an alternative to these other measures. National or international legislation or agreements that give the farmer and advisers little choice may control vaccination policies. For example, in the Netherlands vaccination is compulsory, but in countries such as Finland, Sweden and Norway vaccination is banned(Alexander et al., 2000), Mesogenic vaccines may have serious clinical effects if given to birds that have not been immunized previously, and are sufficiently virulent to be regarded as viruses for which the EC eradication policy would be invoked(Alexander et al., 1995),
        • Complication: Vaccinated birds challenged with virulent NDV may become infected and excrete virus, although in relatively small amounts, while remaining apparently healthy. This disadvantage must be fully understood when planning the role of vaccination in the control of ND(Alexander et al., 2000), Eye drop application is best to obtain a uniformly high degree of long lasting protection but is laborious and therefore limited to small flocks. When vaccinating using spray and aerosol methods, smaller droplets penetrate deeper, elicit better immunity but also result in more serious post-vaccinal reactions. Course droplets are short-lived in the air, birds must be hit directly and spraying must be carried out at close quarters from a distance of about 40 cm. Drinking water vaccination gives varying results due the variations in water intake between birds. Most lentigenic vaccines have an affinity for the respiratory epithelium rather than for the intestinal tract epithelium. Vaccination via automatic drinker systems often gives bad results since the vaccine has to pass long tubes before it reaches the birds. Birds kept in batteries with a nipple drinker system cannot be vaccinated via the drinking water. The only alternative in such cases is spray vaccination(Kouwenhoven et al., 1993), Postvaccinal reactions with live lentogenic vaccines are inevitable. These vary from slightly wet tracheas to production of much mucus and incidental plugging of the bifurcation of the trachea. Concurrent E. coli infections and Mycoplasma gallisepticum infections can aggravate postvaccinal reactions so that spray vaccination is not possible. Also low relative humidity can cause severe postvaccinal reactions. Lighter breeds are more sensitive than heavier ones. Reactions are more serious after vaccination at 14 days than at 7 days of age because of the lower concentration of circulating antibody(Kouwenhoven et al., 1993), One difficulty associated with live vaccines is that the immune response appears to be related to the virulence of the virus strain. La Sota, for example, gives better protective antibody titres than Hitchner B1 but is more likely to cause reactions(Alexander et al., 1995),
      1. Inactivated Vaccines(Kouwenhoven et al., 1993)
        • Description: Inactivated vaccines should not be prepared from virulent viruses and should contain greater than or equal to 50 PD50 per 0.5 ml dose. Inactivated oil emulsion vaccines provide uniform and long lasting protection, without post-vaccinal respiratory reactions. Other (non-replicating) antigens can be incorporated into the vaccine that can be administered together with live vaccines that require individual handling. Since priming is needed for the best effect they are mainly applied at the end of the rearing period(Kouwenhoven et al., 1993),
        • Efficacy:
          • Rate:
          • Duration: In older birds primed by previous vaccinations with live vaccines, immunity induced by oil emulsion vaccines lasts for the whole production period. But also 2 vaccinations with inactivated vaccine only, afford life long immunity(Kouwenhoven et al., 1993).
        • Contraindicator: Vaccination must be regarded as complementing good management, biosecurity and hygiene in rearing domestic poultry. Vaccination against ND must never be considered an alternative to these other measures. National or international legislation or agreements that give the farmer and advisers little choice may control vaccination policies. For example, in the Netherlands vaccination is compulsory, but in countries such as Finland, Sweden and Norway vaccination is banned(Alexander et al., 2000),
        • Complication: Intramuscularly or subcutaneous applied inactivated oil emulsion vaccines only sometimes cause necrosis in breast or leg muscles. Exceptionally residual vaccine may be found between the muscles for a long time after vaccination. There is experience of sudden mortality, most likely by shock, in a small proportion of birds in a flock after a second injection of inactivated vaccine in about 4 weeks after the first. In these cases the first vaccine contained no NDV but inactivated EDS virus. Supposedly some components of the emulsion cause hypersensitivity in these birds. In pigeons, intramuscular applied oil emulsion vaccine causes dramatic necrosis and mortality(Kouwenhoven et al., 1993),
      1. Stamping Out(Alexander et al., 2000)
      1. Prohibition of Importation of Susceptible Poultry and Poultry Meat(Alexander et al., 2000)
  2. Human
    1. Taxonomy Information:
      1. Species:
        1. Homo sapiens (Website 56):
          • Common Name: Homo sapiens
          • GenBank Taxonomy No.: 9606
          • Description: Humans are among the many species that can be infected with NDV. Many of the documented cases involved infections in laboratory workers who accidentally splashed high-titer NDV-infected egg fluids into their eyes, veterinary laboratory diagnosticians who performed postmortem examinations on infected birds or handled infectious tissues, workers in poultry processing plants, and poultry vaccination crews. The absence of many recent reports suggests that such infections may be commonplace and that when they occur, they are mild and self-limiting(Swayne et al., 2003).
    2. Infection Process:
      1. Infectious Dose: TEXT,
      2. Description: Check it out later(McFerran et al., 1988),
    3. Disease Information:
      1. Newcastle Disease Virus :
        1. Incubation: The incubation period of human cases has usually been 1 to 2 days(Chang et al., 1981),
        2. Prognosis:
            Reported infections have not been life threatening and usually have not been debilitating for more than one or two days(Alexander et al., 2000), The course of human NDV infection varies from 51 days to as long as 3 weeks and in all reported cases, patients have spontaneously recovered(Chang et al., 1981),
        3. Diagnosis Summary: Human infection usually results in production of low levels of neutralizing antibodies but frequently of no detectable HI antibodies. Evans has suggested that the poor immune response reflects limited multiplication of NDV in the conjunctiva or other tissues. The controversy as to whether mumps virus and NDV share a common antigen or antigens has not been settled. Jungherr et al., showed that neutralizing and HI antibodies against NDV were present in one half of a group of patients convalescing from mumps. The authors suggested that the reaction might have been due to nonspecific serum factors arising as a result of infection. Kilham et al., showed sera from mumps patients had NDV antibodies when tested by VN. Evans showed corresponding rises in HI titers to both mumps and NDV in paired sera. Jordan and Felter found that the presence of HI and complement fixing factors against NDV were dependent on the coexistence of mumps antibodies, but that sera containing mumps antibodies did not necessarily contain NDV antibodies. Miller and Yates tested 112 human sera for the presence of mumps and NDV HI antibodies. Of the sera, 43% reacted to both viruses and 52% were positive for NDV, but negative for mumps. The authors suggested that the HI activity against NDV was not due to cross reactions with mumps antibodies. Hsiung et al., were not able to show heterotypic serum reaction between mumps and NDV. Wenner et al., found that cross reactions observed in HI reactions between mumps and NDV were not due to common antigens shared by these viruses. A nonspecific substance in human and rhesus monkey sera which inhibited the agglutination of chicken erythrocytes was considered to cause the cross reactions. Evans reported that NDV antibodies existed independently of mumps antibodies and that mumps virus also failed to adsorb NDV antibodies out of such sera. Because of these many controversies, it has been suggested that serological diagnosis of NDV in human patients must be made with caution in the absence of virus isolation(Chang et al., 1981), A comparison of haemagglutination inhibition and enzyme-linked immunosorbent assay techniques for the detection of antibodies against Newcastle disease virus in sera from persons working in poultry farms and veterinary vaccine institutes and from the general population revealed that 22 percent more sera were positive by ELSA compared to HI. No samples were negative by ELSA but positive by HI. While HI titres of positive sera were found in the range of 8-64, ELISA titres were between 16 and 512. It was interesting that though 78 percent of sera had concordant results by the two tests, titres obtained by ELISA were nearly six times higher than those by HI.`(Charan et al., 1981),
        4. Symptom Information :
          • Syndrome -- Eye Infections (Swayne et al., 2003):
            • Description: The most frequently reported and best substantiated clinical signs in human infections have been eye infections, usually consisting of unilateral or bilateral reddening, excessive lachrymation, oedema of the eyelids, conjunctivitis and sub-conjunctival haemorrhage. Although the effect on the eye may be quite severe, infections are usually transient and the cornea is not affected. Reports of other clinical symptoms in humans infected with NDV are less well substantiated, but suggest that a more generalised infection may sometimes occur, resulting in chills, headaches and fever, with or without conjunctivitis. Both vaccinal and strains virulent for poultry may infect and cause clinical signs in humans(Alexander et al., 2000).
            • Observed:
                A review of ND as a zoonosis recorded thirty-five published reports of ND virus infections in humans between 1948 and 1971. Since that time, few additional reports have been published, which probably reflects the lack of serious, lasting effects resulting from such infections and the fact that such infections are common place(Alexander et al., 2000),
        5. Treatment Information:
    4. Prevention:
      1. Biosecurity Measures(Alexander et al., 2000)
        • Description: The use of personal equipment and biological safety cabinets in laboratories has undoubtedly reduced the exposure of current laboratory workers(Swayne et al., 2003),
Phinet: Pathogen-Host Interaction Network
Not available for this pathogen.
Lab Animal Pathobiology & Management

NA
References:
Aldous et al., 2001: Aldous EW, Alexander DJ. Detection and differentiation of Newcastle disease virus (avian paramyxovirus type 1). Avian Pathology. 2001; 30(2); 117-128.
Alexander et al., 1988A: Alexander DJ. Newcastle Disease: Methods of Spread. 256-272. In: . Newcastle Disease. 1988. Kluwer Academic Publishers, Netherlands.
Alexander et al., 1988B: Alexander DJ. Newcastle Disease Diagnosis. 147-160. In: . Newcastle Disease. 1988. Kluwer Academic Publishers, Netherlands.
Alexander et al., 1993: Alexander DJ. Newcastle Disease, Other Avian Paramyxoviruses, and Pneumovirus Infections. 63-80. In: . Diseases of Poultry, Volume 11. 1993. Iowa State Press, Ames, Iowa.
Alexander et al., 1995: Alexander DJ. The epidemiology and control of avian influenza and Newcastle disease. Journal of Comparative Pathology. 1995; 112; 105-126. [PubMed: 7769142].
Alexander et al., 2000: Alexanderi DJ. Newcastle Disease and other avian paramyxoviruses. Rev Sci Tech. 2000; 19(2); 443-462. [PubMed: 10935273].
Barbezange et al., 2002: Barbezange C, Jestin C. Development of a RT-nested PCR test detecting pigeon Paramyxovirus-1 directly from organs of infected animals. Journal of Virological Methods. 2002; 106(2); 197-207. [PubMed: 12393150].
Chang et al., 1981: Chang PN. Newcastle Disease. 261-274. In: . Series in Zoonosis: Viral Zoonosis, Volume 2. 1981. CRC Press, Boca Raton, Fla.
Charan et al., 1981: Charan S, Rai A, Mahajan VM. Comparison of enzyme-linked immunosorbent assay and haemagglutination inhibition test for the detection of Newcastle disease virus antibodies in human sera. Journal of Clinical Pathology. 1981; 34(1); 90-92. [PubMed: 7193219].
Chen et al., 2002: Chen JP, Wang CH. Clinical epidemiologic and experimental evidence for the transmission of Newcastle disease virus thorugh eggs. Avian Diseases. 2002; 46(2); 461-454. [PubMed: 12061659].
Gallili et al., 1998: Gallili GE, Ben-Nathan D. Newcastle Disease Vaccines. Biotechnology Advances. 1998; 16(2); 343-366. [PubMed: 14538149].
Guittet et al., 1997: Guittet M, Le Coq H, Picault JP. Risk for the transmission of Newcastle disease by contaminated poultry products. Rev Sci Tech. 1997; 16(1); 79-2. [PubMed: 9537744].
Hitchner et al., 2004: Hitchner SB. History of biological control of poultry diseases in the USA. Avian Diseases. 2004; 48(1); 1-8. [PubMed: 15077792].
Kaleta et al., 1988: Kaleta EF, Baldauf C. Newcastle Disease in Free-Living and Pet Birds. 197-246. In: . Newcastle Disease. 1988. Kluwer Academic Publishers, Netherlands.
Kho et al., 2000: Kho CL, Mohdazmi ML, Arshad SS, Yusoff, K. Performance of an RT-nested PCR ELISA for detection of Newcastle disease virus. J. Virol. Methods. 2000; 86(1); 71-83. [PubMed: 10713378].
Kouwenhoven et al., 1993: Kouwenhoven B. Newcastle Disease. 341-361. In: . Virus Infections of Birds. 1993. Elsevier Science, Amsterdam and New York.
McFerran et al., 1988: McFerran JB, McKracken RM. Newcastle Disease. 161-183. In: . Newcastle Disease. 1988. Kluwer Academic Publishers, Netherlands.
Millar et al., 1988: Miller NS, Emerson PT. Molecular Cloning and Nucleotide Sequencing of Newcastle Disease Virus. 79-97. In: . Newcastle Disease. 1988. Kluwer Academic Publishers, Netherlands.
Nolan et al., 2002: Nolan SR. Exotic Newcastle Disease Strikes Game Birds in California. JAVMA. 2002; 221(10); 1369-1370. [PubMed: 12458599].
Perdue et al., 2003: Perdue ML. Molecular diagnostics in an insecure world. Avian Dis.. 2003; 47(3 Suppl); 1063-1068. [PubMed: 14575112].
Seal et al., 2000: Seal BS, King D, Sellers HS. The Avian Response to Newcastle Disease Virus. Developmental and Comparative Immunology. 2000; 24; 257-268. [PubMed: 10935273].
Swayne et al., 2003: Swayne DE, King DJ. Avian Influenza and Newcastle Disease. Journal of the American Veterinary Association. 2003; 11; 1534-1540. [PubMed: 12784958].
Vindevogel et al., 1988: Vindevogel H, Duchatel JP. Panzootic Newcastle Disease Virus in Pigeons. 184-196. In: . Newcastle Disease. 1988. Kluwer Academic Publishers, Netherlands.
Website 34: Newcastle disease virus, complete genome
Website 35: Newcastle Disease in the United States of America
Website 36: OIE: Disease Information
Website 38: Newcastle Disease Virus isolate chicken/N. Ireland/Ulster/67, Complete Genome
Website 39: Newcastle Disease Virus isolate chicken/N. Ireland/Ulster/67, Complete Genome
Website 40: Newcastle disease virus isolate dove/Italy/2736/00, Complete Genome
Website 41: Newcastle disease virus isolate chicken/U.S.(CA)/1083(Fontana)/72, complete genome
Website 42: Newcastle disease virus isolate chicken/U.S.(CA)/1083(Fontana)/72, complete genome
Website 43: Newcastle disease virus isolate anhinga/U.S.(Fl)/44083/93, complete genome
Website 44: Newcastle disease virus isolate cockatoo/Indonesia/14698/90, complete genome
Website 45: Newcastle Disease virus strain ZJ1, complete genome
Website 46: Newcastle disease virus strain HB92 isolate V4, complete genome
Website 47: Newcastle disease virus strain B1 isolate Takaaki, complete genome
Website 48: Newcastle disease virus B1, complete genome (second entry)
Website 49: Newcastle disease virus strain LaSota, complete genome
Website 50: Information Resources on Newcastle Disease in Birds
Website 51: OIE Disease Information: Newcastle disease
Website 52: APHIS: Biosecurity for the Birds
Website 53: OIE: Manual of standards Diagnostic Tests and Vaccines 2000
Website 54: FAO: Isolation of virulent Newcastle disease virus
Website 55: Aves
Website 56: Homo sapiens
 
Data Provenance and Curators:
PathInfo: Meg Conlon, Bryan Lewis
HazARD: (for the section of Lab Animal Pathobiology & Management)
PHIDIAS: Yongqun "Oliver" He

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