PATHOGENESIS, PATHOLOGY AND IMMUNITY

Susceptible birds contract NDV mainly from contami­nated feed and water and to a lesser extent by inhalation of virus-containing dust or dander.

Little is known about the minimal infectious dose of NDV for wild birds.

The portal of entry of NDV is the epithelium of the upper respiratory tract. Experimental instillation of NDV directly into the crop, thus circumventing the respiratory epithelium, does not initiate infection in the chicken. Fol­lowing initial virus replication in the epithelial layers, NDV is released from infected cells and phagocytosed by macrophages and thrombocytes. Subsequent virus transport in the bloodstream results in ND virus being detectable in all blood components: i) blood plasma; ii) macrophages; iii) attached to erythrocytes in intravasal agglutination of red blood cells with the formation of micro-emboli in various organs and infection of cells and cell cytolysis within organs. Consequently, death follows as a result of intravasal coagulopathy and organ dysfunction.

The development of disease and outcome of the infec­tion depends on the avian host species, its immunity and the virulence of the infecting virus strain. The incubation period for domestic poultry is 5 to 7 days, and it is likely to be similar for other susceptible birds. The mortality rate depends on the species of bird, being highest in terrestrial birds with case fatality rates close to 100% (in commercial poultry flocks), and low — if at all — in aquatic birds. The few survivors develop protective circulating antibodies that can be detected 5—7 days post- infection by HI tests or enzyme-linked immunosorbent assays (ELISA).

Antibodies in serum are transferred into the yolk during the growth of egg follicles. The quantity of antibodies in serum equates with that in yolk. During the last third of embryonic development, yolk antibodies pass into the small intestine of embryos, are absorbed by the mucosal cells and transferred to the blood circulation. A few days after hatching the antibody content in the blood of chicks reaches a maximal concentration and then declines there­after. The duration of persisting antibodies depends on the metabolic decay of IgY and the growth rate of the chicks. Calculations of the elimination of maternal antibodies from the circulation resulted in half-life times in the range of 4—5 days.

Owing to the relatively short period of illness, there is usually no loss of body condition. The gastrointestinal tract is almost empty or contains mucus, and the subcutis and muscles are dehydrated. The kidneys are enlarged and the ureters filled with whitish to yellow urates. Besides these non-specific lesions, haemorrhages in the epithelium of the nasal cavity, trachea and bronchi, on the serosal surfaces in the body cavity, and in the mucosa of the prov­entriculus, intestines and bursa of Fabricius can be observed, but may be mild or absent(⁹).

An infection during the moulting period results in mal­formation of feathers, which appear larger than normal, with thinner and fragile shafts and smaller vanes.

Virulent NDV strains cause rapid death, and histologi­cal lesions might be completely absent. In more protracted cases, perivascular cuffing by lymphocytes are seen mainly in the brainstem, the medulla oblongata and the spinal cord but also in the respiratory tract and the kidneys.

I n columbiform birds the pigeon variant of APMV1 (PPMVl) regularly causes spongiform lesions in the brain­stem along with gliosis and necrosis of neurons. Indirect immunofluorescence on thin sections using monoclonal antibodies directed against the F and HN proteins dem­onstrates the presence of viral antigens in many tissues(1⁰) with high specificity and sensitivity.