Epidemiology and Transmission:
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 f***s. 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 f***s, by the movement of people and contaminated equipment or litter are the main methods of virus spread between poultry flocks. Clinical Findings:
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. 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 f***s. Poorly vaccinated birds may develop torticollis, ataxia, or body and head tremors 10–14 days after infection and may recover with supportive care. Lesions:
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. Diagnosis:
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). Prevention:
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
