Persistence of velogenic viscerotropic Newcastle disease virus in litter.

Litter in a room which had housed chickens and turkeys actively infected with velogenic viscerotropic Newcastle disease was no longer infectious for susceptible chickens placed there 10 to 14 days later.     

Efficacy of a commercial Newcastle vaccine against velogenic viscerotropic Newcastle disease virus.

Effects of parental immunity and method of vaccination were studied in broiler chickens vaccinated with a commercial LaSota vaccine and challenged with the Fontana strain of velogenic viscerotropic Newcastle disease (VVND). Immunity was satisfactory from all methods of vaccination used.     

Response of congenitally immune chicks to viscerotropic velogenic Newcastle disease virus.

Separate groups of chicks of hen hyperimmune to viscerotropic velogenic Newcastle disease virus (VVNDV) were challenge-exposed to VVNDV by intraocular route at 1 day and 34 days old. Their response was evaluated by clinical symptoms, hemagglutination-inhibition (HI) titers, and virus isolations. Chicks exposed at 1 day old excreted VVNDV from the vent for up to 60 days; their active mean HI titers remained low (10-40); and deaths from VVNDV occurred early (5-16 days) and late (28-55 days). Chicks challenge-exposed at 34 days old excreted virus from the vent for 10 days; active HI titers developed quickly and remained high (891-1177); and deaths and signs of VVNDV occurred early (5-13 days).     

Dysgerminoma in an eastern rosella (Platycercus eximius eximius)

This report describes a case of dysgerminoma in a 21-year-old eastern rosella (Platycercus eximius eximius) that presented with dyspnea and a severely distended coelom. The bird was euthanatized, and a large, left-sided coelomic mass was identified. Microscopically, the mass was composed of sheets and nests of round to polygonal neoplastic cells with lacy cytoplasm. The neoplastic cells were weakly positive for vimentin and c-kit but negative for pancytokeratin, AE1, and inhibin. On the basis of the histomorphology and immunoreactivity, the neoplasm was determined to be a dysgerminoma. The variability of histologic appearance and immunohistochemical staining of dysgerminomas in humans compared with veterinary species is discussed.     

Scanning electron microscopy of tracheal epithelium of chickens infected with velogenic viscerotropic Newcastle disease virus

Ultrastructural changes in the tracheal epithelium of chickens infected intranasally with velogenic viscerotropic Newcastle disease virus were examined by scanning electron microscopy. Hypertrophy of the mucus-secreting, or goblet, cells was the first sign of change, followed by disoriented and deformed cilia, hemorrhage, and hyperplasia of goblet cells accompanied by an increase in mucus. By day 7 postinfection, there was a marked decrease in the number of ciliated cells. Submucosal glands and some collagen fibers were exposed to the surface, an indication of loss of the epithelial cells. Macrophages and cell debris were abundant, and hyperplasia of the basal cells was evident in the later stages of infection, probably in an attempt to regenerate the lost epithelium. However, all chickens died 10 days postinfection, before any further work could be done.     

Comparison of electrocardiograms of chickens infected with viscerotropic velogenic Newcastle disease virus and virulent avian influenza virus

Electrocardiograms of chickens infected with viscerotropic velogenic Newcastle disease virus (NDV) or virulent avian influenza virus (AIV) were characterized and compared. The ECG were monitored by radiotelemetry and were recorded twice daily before virus infection and during the course of the infection. Thirteen lead II intervals, segments, and amplitudes were measured and analyzed. The ECG of NDV-infected chickens were characterized by lengthened (P less than or equal to 0.05) ST segments and increased (P less than or equal to 0.05) P amplitudes. The ECG of AIV-infected chickens were characterized by lengthened (P less than or equal to 0.05) RS intervals, ST segments, TP intervals, and PR segments and by increased (P less than or equal to 0.05) P amplitudes. The TP intervals and PR segments of ECG of AIV-infected chickens were significantly (P less than or equal to 0.05) longer than those of NDV-infected chickens. The pronounced conduction delays indicated in the ECG of AIV-infected chickens may have diagnostic importance.     

Epizootiologic aspects of viscerotropic velogenic Newcastle disease in six pet bird species

Pet birds of 6 species were exposed to a psittacine isolate to viscerotropic velogenic Newcastle disease (VVND) virus to evaluate the impact of VVND in those species. Species examined were the budgerigar, yellow-headed Amazon parrot, canary, halfmoon conure, lesser hill mynah, and blackheaded nun. Five of the 6 species were highly susceptible to infection with VVND virus. Canaries were relatively refractory to infection with the virus. Contact birds of the same species developed infections almost as rapidly as did the birds directly exposed to nebulized VVND virus. Mortality was most marked for the conures. Less than half of the parrots exposed to nebulized virus died of VVND. Of the directly exposed budgerigars, mynahs, and nuns, 16% to 22% died during an observation period of postexposure days 0 through 28.     

A comparison of the onset of protection induced by Newcastle disease virus strain B1 and a fowl poxvirus recombinant Newcastle disease vaccine to a viscerotropic velogenic Newcastle disease virus challenge

Four-week-old specific-pathogen-free white rock chickens were immunized with either a commercial recombinant fowl poxvirus-vectored Newcastle disease vaccine (FPN) expressing the hemagglutinin-neuraminidase and fusion protein genes of Newcastle disease virus (NDV) strain B1 or live NDV B1. Vaccinates and controls were challenged by eyedrop and intranasal (E/I) route with a viscerotropic velogenic NDV at 14 days postvaccination to determine the time of clearance of challenge virus. In a subsequent experiment, chickens were challenged at 3, 6, or 10 days postvaccination to determine the onset of immunity. Chickens that received a recommended field dose (1x) or a 0.01x dose of FP-N subcutaneously (s.c.) and were seropositive by hemagglutination-inhibition test at 14 days postvaccination cleared the challenge virus by 14 days postchallenge. Clinical Newcastle disease and high challenge virus titers in tissues were seen only in seronegative FP-N 0.01x dose vaccinates and controls. In a comparison of vaccination with FP-N (1x, 10(4,9) median tissue culture infective dose) s.c., B1 (10(6) median egg infective dose [EID50]) s.c., or B1 (10(6) EID50) E/I, chickens vaccinated at 6 or 10 days before challenge with all vaccines were protected against clinical disease, but only those vaccinated with B1 E/I 10 days before challenge were protected against infection with the challenge virus. Vaccination at 3 days before challenge with B1 E/I provided early protection, but severe nervous signs developed later and reduced overall protection to 60%, whereas disease in chickens vaccinated with B1 s.c. and FP-N s.c. 3 days before challenge was similar to the challenge controls.     

Velogenic viscerotropic Newcastle disease virus strains in Morocco

Isolates of Newcastle disease virus (NDV) in Morocco were characterized as velogenic. Two isolates were from tracheal swabs taken at a Moroccan live poultry market, and four isolates were from field cases. Infection of 8-week-old chickens showed that these isolates and previously characterized Moroccan isolates were of the viscerotropic pathotype. Based on hemagglutinin thermostability and the capacity to agglutinate equine erythrocytes, the Moroccan velogenic viscerotropic NDV isolates were classified as belonging to at least three distinct strains.     

Methods of spread of velogenic viscerotropic Newcastle disease virus in the southern Californian epidemic of 1971-1973.

Data collected during the velogenic viscerotropic Newcastle disease (VVND) epidemic that occurred in southern California from 1971 to 1973 were analyzed to determine the methods of spread of the disease. Spread between chicken flocks was extensive and due mainly to the movement of live birds and mechanical transport of virus by man, especially by vaccination and poultry service crews. Spread to exotic birds was from contact with infected imported stock. Spread to other species was most probably through contact with infected chickens. Infection persisted in commercial chicken flocks because of intensive vaccination programs, heavy traffic and contact between layer operations, and the maintenance of multi-age flocks. These foci of infection probably led to spread of the disease to areas from which VVND had been eradicated several months before. There was no evidence of significant wind-borne spread of virus between flocks.     

Pathology of velogenic Newcastle Disease virus infection in turkeys.

Twenty-four 4-week-old poults, free from Mycoplasma meleagridis and M. gallisepticum, were inoculated with a velogenic viscerotropic strain of Newcastle disease virus. Clinical signs (gasping, coughing, and dyspnea) developed 4-5 days postinoculation, continued until nervous derangement appeared, and then (usually 3 days after initial clinical signs appeared) declined in severity. Prominent nervous signs were paresis and paralysis of the extremities, with pronounced head-shaking. The most constant gross lesions detected involved the airsacs. The abdominal sacs of a few poults contained a large accumulation of yellowish, cheesy exudate and there was cloudiness of the thoracic airsacs of all inoculated poults. A few turkeys had tracheitis with some catarrhal exudates and casts in the lower part of the tracheal lumen. Congestion of lepto-meningeal vessels usually correlated with the severity of the nervous signs. The histologic lesions were characterized by both degenerative and proliferative changes with predominantly mononuclear cell and heterophil infiltrations throughout the body. The obvious lesion seen in the recovery stage of the disease was proliferation of lymphofollicular nodules in the parenchymatous organs.     

Failure to demonstrate viscerotropic velogenic Newcastle disease in psittacine birds in the Republic of the Philippines

Birds on the islands of Luzon, Mindanao, and Palawan in the Republic of the Philippines were surveyed for viscerotropic velogenic Newcastle disease (VVND). Virus isolation was attempted on 728 cloacal samples from native and exotic psittacine birds, non-psittacine birds, and domestic chickens and ducks. A VVND virus isolate was obtained from a single domestic chicken that had exhibited ocular discharge and diarrhea 3 days before sampling. All other birds were negative for VVND.     

Interactions between viscerotropic velogenic Newcastle disease virus and pet birds of six species. II. Viral evolution through bird passage

Following in vivo studies in pet birds of 6 species, 279 Newcastle disease virus (NDV) reisolates were selected for characterization by the embryonated-chicken-egg mean-death-time, plaque-assay, hemagglutination-elution, and hemagglutinin-thermostability techniques. Initially, the 279 isolates were screened by the mean-death-time and plaque-assay techniques, and 5 sequential isolates were chosen for each of 3 budgerigars and 2 parrots for characterization by the other 2 in vitro assays to determine whether the Colorado Psittacine Isolate of viscerotropic velogenic (VV) NDV (COPI-VVNDV) had evolved during passage through pet birds. Nineteen isolates were then selected for chicken back-passage studies. Fifteen of the 19 isolates were chosen for potential avirulence for 8-week-old domestic chickens. The 4 remaining isolates produced large red plaques when assayed and were therefore used as virulent virus controls likely to be VVNDV. Subsequent in vitro characterization of selected back-passage chicken NDV isolates demonstrated little change in the 4 parameters originally evaluated for the pet-bird isolates used for the back-passage studies. Although the psittacine isolate slowly evolved to relatively avirulent strains of NDV by passage in pet birds, reversion did not occur during the chicken back-passage studies.