| Etiology and Epidemiology Newcastle disease is caused by an RNA virus, paramyxovirus-1 (PMV-1), that can be categorized into three groups: the velogenic strains, which are highly pathogenic and easily transmitted; the mesogenic strains, which show intermediate pathogenicity; and the lentogenic strains, which show low pathogenicity in chickens. Isolates that cause the respiratory-nervous syndrome, even those that are highly pathogenic, usually produce few or no distinctive gross lesions; however, isolates that cause the viscerotropic syndrome often do. Velogenic and mesogenic virus isolates kill injected 10-day-old chicken embryos in 2-4 days, lentogenic isolates usually in 4-6 days or not at all. Virus is shed during incubation, during the clinical stage, and for a varying but limited period during convalescence. It is present in exhaled air, respiratory discharges, feces, eggs laid during clinical disease, and all parts of the carcass during acute infection and at death. Chickens are readily infected by aerosols and by ingesting contaminated water or food. While the chicken is the primary source of virus, other domestic birds and certain wild birds are susceptible and may be sources. Parrots, mynahs, and such caged birds as pittas that moved in commercial channels were the principal source of infection during the 1970-72 pandemic (USA) of the velogenic viscerotropic form of Newcastle disease. An outbreak of PMV-1 occurred in pigeons in the USA and the UK during 1984. This pigeon paramyxovirus is lentogenic for chickens and occurs worldwide in some pigeon populations. |
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| Clinical Findings The signs depend greatly on whether the virus is neurotropic or viscerotropic. The neurotropic viruses result in respiratory and nervous signs. The viscerotropic viruses, which predominate worldwide, cause respiratory signs with peracute disease, watery-greenish diarrhea, and swelling of the tissues of the head and neck. Nervous signs are also frequently seen in exotic bird species (parrots, etc) infected with viscerotropic viruses and in poultry species that survive beyond the acute phase of the disease. Onset is rapid, and signs appear simultaneously throughout the flock 2-12 days (average 5) after exposure. Young chickens are more susceptible and show signs sooner than older ones. Respiratory signs include gasping, coughing, sneezing, and rales. Nervous signs include drooping wings, dragging legs, twisting of the head and neck, circling, depression, inappetence, and complete paralysis; they may accompany but usually follow the respiratory signs. Clonic spasms are seen in moribund birds. Laying flocks may have partial or complete cessation of production and not recover. Eggs from infected flocks may be abnormal in color, shape, or surface, and have watery albumen. Mortality from either type of virus depends on virulence of the virus, species infected, environmental conditions, and the immune status of the flock. In general, mortality is higher in young flocks, but 100% mortality may occur in adult flocks as well. |
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 A number of dead chickens seen in an outbreak of ND |
 Nervous signs, such as paralysis of legs and wings, twisting of head and neck, etc. |
 Hyperemia and edema on mucous membrane of the trachea |
 Hemorrhages and ulcers of proventricular mucosa |
| Lesions Lesions are highly variable, reflecting the variation in tropism and pathogenicity of the virus. Petechiae may be seen on the serous membranes; hemorrhages of the proventricular mucosa and intestinal serosa are accompanied by hemorrhagic and necrotic areas on the mucosal surface, especially at lymphoid foci such as cecal tonsils. Congestion and mucoid exudates may be seen in the respiratory tract, with opacity and thickening of the air sacs. |
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 Hemorrhages and ulcers seen on mucous membrane of the intestine |
 Enlargement of the spleen having white spots due to degeneration or necrosis |
 Hematic ovarian follicles in ovary |
 Perivascular cell infiltration and non-purulent encephalitis with slight increase of glia cells at the cerebrum (HE staining) |
| Diagnosis Tentative diagnosis of a rapidly spreading, respiratory-nervous disease may be confirmed by isolation of the hemagglutinating virus identified by inhibition with Newcastle disease antiserum. A rise in hemagglutination-inhibition antibodies in paired serum samples also confirms the disease. The acute form should be differentiated from highly pathogenic avian influenza (Influenza: Introduction, Equine Influenza, Swine Influenza, Avian Influenza Viruses). Although it is difficult to differentiate between Newcastle strains other than by the rapidity with which they kill injected embryonating chicken eggs and adult chickens, grouping strains according to their geographic and temporal appearance using monoclonal antibodies has had some success. Oligonucleotide gfingerprintingh of the viral RNA has been used to differentiate between strains similar in all other respects. |
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| Prevention and Treatment Proper administration of a high-titered vaccine is essential for induction of a good immune response. Live virus vaccines are widely used. Lentogenic strains, chiefly B1 and LaSota in the New World, are administered in drinking water or in spray. Sometimes, administration is via the nares or eye. Healthy chicks are vaccinated as early as day 1-4 of life. However, delaying vaccination until the second or third week avoids interference with an active immune response by maternal antibody. Mycoplasma and some other bacteria, if present, may act synergistically with some vaccines to aggravate the vaccine reaction after spray administration. Failure to follow instructions (eg, use of sprays in open or windy houses, or use of chemically treated water to dilute the virus) may result in incomplete or no protection after vaccination. When other infections are present in the flock, and where required by law, killed vaccines should be used. Killed vaccines with oil adjuvants give the longest protection. Whether killed vaccines, lentogenic mass vaccines, or IM-injected mesogenic strains are used, repeated vaccination is required to protect chickens throughout life. The frequency of revaccination largely depends on the risk of exposure and virulence of the field virus. Disease control officials in the USA and some other countries use import restrictions and eradication methods to prevent establishment of the highly virulent, viscerotropic form of the disease; other countries depend on vaccination. |
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| Zoonotic Risk Newcastle disease virus can produce a transitory conjunctivitis in man, but the condition has been limited primarily to laboratory workers and vaccination teams exposed to large quantities of virus and, before vaccination was widely practiced, to crews eviscerating poultry in processing plants. The disease has not been reported in people who rear poultry or consume poultry products. |
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| Quoted from "The Merck Veterinary Manual" | |||