Pathogenesis of a Local Nigerian Velogenic Newcastle Disease Virus Infection in Vaccinated and Unvaccinated Chicken Layers

ABSTRACT Velogenic Newcastle disease (VND) has been very much associated with drop in egg production and the production of poor quality eggs. The aim of this project was to study the pathological, biochemical and haematological changes that led to the poor egg production and quality. Two hundred and forty Isa-Brown pullets were purchased from Zartech, Ibadan, Oyo State, Nigeria at day old. They were reared to point of lay. At 16 weeks of age they were divided into two groups of 120 layers each. One group was vaccinated intramuscularly (IM) with an oil emulsion inactivated Komarov vaccine. Both groups were kept in different locations. At the peak of egg production, 32 weeks of age, the vaccinated layers were divided into groups, A and B of sixty layers each while the unvaccinated were divided into groups C and D also of 60 layers each. Groups A and C layers were each inoculated with 0.2 ml of a local strain of VND virus (VNDV) IM. Layers in groups B and D were each given 0.2 ml of the phosphate buffered saline IM. The clinical signs including changes in weight of the layers and egg production performance were studied. Gross and microscopic lesions and the presence of the virus in the female reproductive tract were studied with histopathological and immunohistochemical stainings respectively. The Newcastle disease antibody levels, changes in the blood cells, serum calcium and phosphorus levels were also assayed in the four groups. Clinical signs were first observed in group C layers on day 2 PI and lasted upto day 18 PI. The clinical signs included depression, greenish diarrhoea and later torticollis. Mortality was 89.58 %. Group A birds showed little drop in feed and water consumption on days 3 and 4 PI only but there was no depression. Mortality was zero. The body weights of the group C layers were consistently and significantly (p < 0.05) lower than those of group A layers from days 6 to 21 PI. The two uninfected groups, B and D showed no clinical signs. Groups A and C showed significant (p < 0.05) drop in egg production from week 1 to the end of the experiment on week 7 PI. The lowest drop was weeks 2 and 3 PI. From week 4 PI, the production started rising gradually. Only group C layers produced white-coloured, softshelled and cracked eggs. The gross lesions included proventricular haemorrhages, intestinal and caecal tonsil ulcers in group C layers which initially showed swollen, oedematous, hyperaemic reproductive tract with ruptured yolk materials in the abdominal cavity. Later there was atrophy of the tract with atresia of the ovarian follicles. The histopathological changes followed same pattern as the gross. The initial inflammatory phase was characterized by oedema, hyperaemia, deciliation, infiltration by lymphoplasmacytic and macrophagic inflammatory cells, necrosis of epithelia and glandular cells. The later atrophic phase showed fibrosis or fibroplasias and hyperplasia of repair. Group A layers showed mild inflammatory changes in the oviduct and increased lymphoid follicles and infiltrations but there was no gross lesion in the reproductive tract. Immunohistochemical staining showed extensive presence of the virus in the ovary, infundibulum, magnum, isthmus, uterus and vagina of group C layers only. The geometrical mean antibody titers were higher in group C than in group A layers on days 10, 15 and 21 PI. There was significant (p < 0.05) hypophosphotaemia on days 7, 14, 21, 28, 42 and 49 PI in the infected groups. The red blood cell (RBC) count was significantly (p < 0.05) lower in group C than group D layers on days 6 and 15 PI. Infection in group C layers produced significant (p < 0.05) leukocytosis on days 3 and 6 PI and significant (p < 0.05) leukopenia on days 10, 15 and 21 PI. The above observations showed that the drop in egg production seen in VND could be due to damage to the female reproductive tract and hypophosphotaemia. The virus replicates strongly in the ovarian follicles of unvaccinated layers and true transovarian infection is possible. Vaccination of layers can protect against most of these lesions except drop in egg production.