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.     

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.     

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.     

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.     

Investigation of an outbreak of velogenic viscerotropic Newcastle disease in pet birds in Michigan, Indiana, Illinois, and Texas.

An outbreak of velogenic viscerotropic Newcastle disease in exotic pet birds in the United States from April through July 1991 was investigated. More than 2,000 pet birds in 5 states (Michigan, Indiana, Illinois, Texas, and Maryland) were tested. Infected birds were found in Michigan, Illinois, Indiana, and Texas. This disease was eradicated without spread to domestic poultry. Epidemiologic investigations revealed the source of infection to be double yellow-headed Amazon parrots suspected to be illegally imported into Texas.     

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).     

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.     

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.     

Pathogenesis of chicken-passaged Newcastle disease viruses isolated from chickens and wild and exotic birds

The pathogenesis of six Newcastle disease virus (NDV) isolates recovered from chickens (Ckn-LBM and Ckn-Australia) and wild (Anhinga) and exotic (YN parrot, pheasant, and dove) birds was examined after the isolates had been passaged four times in domestic chickens. Groups of 10 4-wk-old specific-pathogen-free white leghorn chickens were inoculated intraconjunctivally with each one of the isolates. The infected birds were observed for clinical disease and were euthanatized and sampled at selected times from 12 hr to 14 days postinoculation or at death. Tissues were examined by histopathology, by immunohistochemistry (IHC) to detect viral nucleoprotein (IHC/NP), and by in situ hybridization to detect viral mRNA and were double labeled for apoptosis (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling ([TUNEL] or IHC/caspase-3) and viral nucleoprorein (IHC/NP). Birds infected with the three low virulence viruses (Ckn-LBM, YN parrot, and Ckn-Australia) did not develop clinical disease. Microscopic lesions were observed only at the inoculation site and in organs of the respiratory system. The detection of viral nucleoprotein (N) was restricted to the inoculation site. The pheasant and dove isolates were highly virulent for chickens with marked tropism for lymphoid tissues, confirmed by the presence of large numbers of cells positive for viral N protein and viral mRNA. Viral N protein was detected early in the cytoplasm of cells in the center of the splenic ellipsoids. The apoptosis assays (TUNEL and IHC/caspase-3) showed increased apoptosis in the splenic ellipsoids as well. Apparently, apoptosis is an important mechanism in lymphoid depletion during NDV infection.     

Interactions between viscerotropic velogenic Newcastle diseases virus and pet birds of six species. I. Clinical and serologic responses, and viral excretion

Clinical and serologic responses to a psittacine isolate of viscerotropic velogenic Newcastle disease virus (VVNDV) were evaluated in pet birds of six species: budgerigar, yellow-headed Amazon parrot, halfmoon conure, lesser hill mynah, black-headed nun, canary. The clinical response was most marked in the budgerigars, parrots, and conures, and only minimal in the nuns. Between post-exposure days (PED) 3 and 5 some birds developed ruffled plumage, conjunctivitis, and central nervous system dysfunction: ataxia, wing tremors, paralysis of the extremities, and tremors of the head accompanied by nodding and jerking. Mortality by PED 203 was 55% (29/52) in the halfmoon conures, 22% (23/105) in budgerigars, 29% (12/42) in parrots, and 21% (15/71) in nuns. The only clinical signs in canaries and mynahs were progressive death losses, respectively 25% (33/132) and 21% (10/48). The visceral lesions common in chickens with VVNDV were not observed in these six species. Canaries rapidly eliminated Newcastle disease virus (NDV), whereas it was detected for protracted periods in the oral and cloacal secretions of the other five species (for more than a year in parrots). Serologic evaluation by the hemagglutination-inhibition and neutralization tests also indicated prolonged NDV infections in 5 of the 6 species. The seroconversion rate observed in canaries was minimal (13%).     

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.     

Newcastle disease in wild water birds in western Canada, 1990

This report describes the investigation of mortality of double-crested cormorants (Phalacrocorax auritus), white pelicans (Pelecanus erythrorhynchos), and gulls (Larus spp.) in Alberta, Saskatchewan, and Manitoba during late summer 1990. Techniques used varied among areas, but virological and histopathological examination of birds was done in each area. The major clinical sign in cormorants was inability to fly, often with unilateral wing or leg paralysis. Focal nonsuppurative inflammation was present in the brain and spinal cord of cormorants and pelicans. Newcastle disease virus (NDV) was isolated from cormorants, a pelican, and a ring-billed gull (Larus delawarensls) from Saskatchewan. Cormorants from Alberta were positive for NDV in an immunofluorescent test. Most of the viruses were classed as velogenic and all had a similar monoclonal antibody profile to viruses from the 1970 to 1974 panzootic. Approximately half of cormorant, pelican, and gull eggs collected from affected colonies in the spring of 1991 had antibody to NDV. Antibody was also present in cormorant eggs from the Great Lakes. No unusual mortality was detected at any colony in 1991. Fledgling cormorants and gulls from colonies where mortality occurred in 1990 did not have antibody to NDV in June-July 1991. The overall extent of mortality among water birds and the source of the virus were not determined.     

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.     

Experimental pathogenesis for chickens, turkeys, and pigeons of exotic Newcastle disease virus from an outbreak in California during 2002-2003

Exotic Newcastle disease virus (NDV) isolated from chickens during the 2002-2003 California outbreak (CA exotic Newcastle disease [END] virus) was inoculated into 4-week-old specific-pathogen-free (SPF) White Leghorn chickens, 3-week-old SPF Beltsville White turkeys, 6-week-old commercial Broad Breasted White turkeys, and 10- to 20-week-old racing pigeons, and the clinicopathologic features of disease were compared. Birds were monitored clinically and euthanized sequentially with collection of tissues. Tissues were examined by histopathology, by immunohistochemistry to detect viral nucleoprotein, and by in situ hybridization to detect viral mRNA. Clinically, infected chickens and SPF turkeys showed severe depression, and all died or were euthanized because of severe clinical signs by day 5 postinoculation. In these birds, histologic lesions were widespread and virus was detected in multiple organs. All infected commercial turkeys showed mild depression, and incoordination was observed in some birds. Histologic lesions were mild, and viral distribution was limited. In pigeons, only 1 bird showed overt clinical disease, and histologic lesions and viral distribution were present in limited organs. Consequently, susceptibility to highly virulent NDV was shown to vary among chickens, SPF turkeys, commercial turkeys, and pigeons. Additionally, we have evidence of CA END virus subclinical infections that suggest pigeons could be subclinical carriers of other virulent NDV.