Newcastle disease is an infection of domestic poultry and other bird species with virulent Newcastle disease virus (NDV). It is a worldwide problem that presents primarily as an acute respiratory disease, but depression, nervous manifestations, or diarrhea may be the predominant clinical form. Severity depends on the virulence of the infecting virus and host susceptibility. Occurrence of the disease is reportable and may result in trade restrictions.
NDV, synonymous with avian paramyxovirus serotype 1 (PMV-1), is an RNA virus and the most important of the 11 known PMV serotypes as a pathogen for poultry. The original classification of NDV isolates into one of three virulence groups by chicken embryo and chicken inoculation as virulent (velogenic), moderately virulent (mesogenic), or of low virulence (lentogenic) has been abbreviated for regulatory purposes. Velogens and mesogens are now classified as virulent NDV (vNDV), the cause of Newcastle disease and reportable infection, whereas infections with lentogens, the low virulence NDV (loNDV) widely used as live vaccines, are not reportable. Clinical manifestations vary from high morbidity and mortality to asymptomatic infections. Severity of infection depends on virus virulence and age, immune status, and susceptibility of the host species. Chickens are the most and waterfowl the least susceptible of domestic poultry; however, some differences may be seen if the NDV strain is adapted to a particular species.
Virulent NDV strains are endemic in poultry in most of Asia, Africa, and some countries of North and South America. Other countries, including the USA and Canada, are free of those strains in poultry and maintain that status with import restrictions and eradication by destroying infected poultry. Cormorants, pigeons, and imported psittacine species are more commonly infected with vNDV and have also been sources of vNDV infections of poultry. NDV strains of low virulence are prevalent in poultry and wild birds, especially waterfowl. Infection of domestic poultry with loNDV contributes to lower productivity.
Infected birds shed virus in exhaled air, respiratory discharges, and feces. Virus is shed during incubation, during the clinical stage, and for a varying but limited period during convalescence. Virus may also be present in eggs laid during clinical disease and in all parts of the carcass during acute vNDV infections. Chickens are readily infected by aerosols and by ingesting contaminated water or food. Infected chickens and other domestic and wild birds may be sources of NDV. Movement of infected birds and transfer of virus, especially in infective feces, by the movement of people and contaminated equipment or litter are the main methods of virus spread between poultry flocks.
Onset is rapid, and signs appear throughout the flock within 2–12 days (average 5) after aerosol exposure. Spread is slower if the fecal-oral route is the primary means of transmission, particularly for caged birds. Young birds are the most susceptible. Observed signs depend on whether the infecting virus has a predilection for respiratory, digestive, or nervous systems. Respiratory signs of gasping, coughing, sneezing, and rales predominate in infections with loNDV. Nervous signs of tremors, paralyzed wings and legs, twisted necks, circling, clonic spasms, and complete paralysis may accompany, but usually follow, the respiratory signs in neurotropic velogenic disease. Nervous signs with diarrhea are typical in pigeons, and nervous signs are frequently seen in cormorants and exotic bird species. Respiratory signs with depression, watery greenish diarrhea, and swelling of the tissues of the head and neck are typical of the most virulent form of the disease, viscerotropic velogenic Newcastle disease, although nervous signs are often seen, especially in vaccinated poultry. Varying degrees of depression and inappetence are seen. Partial or complete cessation of egg production may occur. Eggs may be abnormal in color, shape, or surface and have watery albumen. Mortality is variable but can be as high as 100% with vNDV infections. Well-vaccinated birds may not show any signs of being infected except for a decrease in egg production, but these birds will shed virus in saliva and feces. Poorly vaccinated birds may develop torticollis, ataxia, or body and head tremors 10–14 days after infection and may recover with supportive care.
Remarkable gross lesions are usually seen only with viscerotropic velogenic Newcastle disease. Petechiae may be seen on the serous membranes; hemorrhages of the proventricular mucosa and intestinal serosa are accompanied by multifocal, necrotic hemorrhagic areas on the mucosal surface of the intestine, especially at lymphoid foci such as cecal tonsils. Splenic necrosis and hemorrhage and edema around the thymus may also be seen. In contrast, lesions in birds infected with loNDV strains may be limited to congestion and mucoid exudates seen in the respiratory tract with opacity and thickening of the air sacs. Secondary bacterial infections increase the severity of respiratory lesions.
NDV can be isolated from oropharyngeal or cloacal swabs or tissues from infected birds by inoculation of the allantoic cavity of 9- to 11-day-old SPF embryonated chicken eggs. Infection is confirmed by recovery of a hemagglutinating virus that is inhibited with NDV antiserum or by detection of NDV RNA by reverse transcriptase PCR. A rise in NDV antibody titer by hemagglutination-inhibition or ELISA of paired serum samples indicates NDV infection. To confirm diagnosis, identification of an isolate such as vNDV is established by the rapidity of killing day-old SPF chicks inoculated by the intracerebral route, the intracerebral pathogenicity index, or by the presence of a specified amino acid motif at the cleavage site of the fusion protein (F) precursor (FO). Reference laboratories use nucleotide sequence analysis to detect genetic differences for comparison of isolates from different outbreaks and to identify the source of those infections. The acute form of ND should be differentiated from other diseases known to cause high mortality, such as highly pathogenic avian influenza (see Avian Influenza).
Vaccines are available for chickens, turkeys, and pigeons and are used to induce an antibody response, so vaccinated bids must be exposed to a larger dose of vNDV to be infected. Unfortunately, ND vaccines do not provide sterile immunity, and in many areas of the world vaccines are used to prevent losses from sickness and death. Live lentogenic vaccines, chiefly B1 and LaSota strains, are widely used and typically administered to poultry by mass application in drinking water or by spray. Mucosal immunity induced in birds vaccinated by live vaccines applied by these routes decreases the amount of vNDV the vaccinated birds will shed if infected with vNDV, compared with the immune response induced by an inactivated vaccine. Mass vaccination methods are less labor intensive but if not applied properly may lead to <85% of the flock being immunized, which is needed for herd immunity. Alternatively, individual administration of live vaccines is via the nares or conjunctival sac. Healthy chicks are vaccinated as early as day 1–4 of life. However, delaying vaccination until the second or third week avoids maternal antibody interference with an active immune response. Mycoplasma, some other bacteria, and other viruses affecting the respiratory tract, if present, may act synergistically with some vaccines to aggravate the vaccine reaction after spray administration.
Oil-adjuvanted inactivated vaccines are also used after live vaccine in breeders and layers and may be used alone in situations where use of live virus may be contraindicated (eg, in pigeons). In countries where vNDV is endemic, a combination of live virus and inactivated vaccine can be used; or alternatively, if permitted by law, a live mesogenic strain vaccine may be used in older birds. The frequency of revaccination to protect chickens throughout life largely depends on the risk of exposure and virulence of the field virus challenge. Administering inactivated vaccines is more labor intensive, because each bird has to be handled individually. Accidental inoculation of human tissues with oil-based vaccines requires prompt medical treatment.
Fowlpox or turkey herpesvirus–vectored NDV vaccines are commercially available for chickens and have the advantage of being able to be administered in ovo at the hatchery. These vaccines must be reconstituted as directed by the manufacturer and, because they take 3–4 wk to produce a protective level of immunity, biosecurity is even more important. A commercial kit to detect levels of antibodies induced by these vaccines is not yet available.
All NDV strains can produce a transitory conjunctivitis in people, but the condition has been limited primarily to laboratory workers and vaccination teams exposed to large quantities of virus. Before poultry vaccination was widely practiced, conjunctivitis from NDV infection occurred in crews eviscerating poultry in processing plants. The disease has not been reported in people who rear poultry or consume poultry products.