[The susceptibility of certain species to Newcastle disease virus].
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Live B1 Newcastle disease virus was administered to young turkeys either intraocularly or by driniking water, or by both methods. Protection against egg production loss was evaluated by challenge-exposure to viscerotropic velogenic Newcastle disease virus in drinking water. During 22 days postchallenge (PC), none of the vaccinated hens had morbidity, whereas 44% of the unvaccinated controls died 6-13 days PC. Percent egg production (PEP) of all groups 1-5 and 6-22 days PC were compared with their levels 1-5 days before challenge. For days 1-5 PC, changes were not significant. For days 6-22 PC, changes for all groups were siginficant lower. The controls had 0 production. Hens vaccinated only at 4 days or at 4 days and again at 4 weeks averaged one-third or less of prechallenge levels but were recovering. Those revaccinated at 4 months maintained 84-91% of their prechallenge levels and were considered satisfactory. Broodiness was a detracting factor in one group of hens vaccinated at 4 days, 4 weeks, and 51/2 months. They averaged two-thirds of prechallenge levels but were in decline.
Drake, John W. (University of Illinois, Urbana). Multiplicity reactivation of Newcastle disease virus. J. Bacteriol. 84:352-356. 1962.-A very weak multiplicity reactivation occurs among Newcastle disease virus particles inactivated by ultraviolet irradiation. The preliminary steps in the infection of embryonic chicken fibroblasts are complex, and their relation to multiplicity reactivation is discussed.
Elution time of velogenic, mesogenic and lentogenic strains of Newcastle disease virus was determined. The differences in their elution time were also calculated. Four samples, each of a velogenic strain (VGF2), a mesogenic strain (Komarov) and a lentogenic strain (LaSota) were used for hemagglutination test with 0.6% chicken red blood cells. The time it took for wells of the end hemagglutination points (highest dilution that gave agglutination) to elute was recorded as elution time for each sample. The mean elution time of the three strains of Newcastle disease virus differed significantly (p < 0.05). The velogenic strain gave the highest mean elution time of 118 min, followed by the mesogenic strain with 59 min and the lentogenic strain with 25 min. Based on this result it appears that elution time could form a basis for rough characterization of isolates of Newcastle disease virus into the three major strains.
During 1993, outbreaks of Newcastle disease occurred on many farms in Tamilnadu, India. Six Newcastle disease virus (NDV) isolates were obtained from the chickens on five different farms and from the birds on one duck farm during outbreaks of the disease. All the isolates were characterized as velogenic, based on the mean death time, intravenous pathogenicity index, intracerebral pathogenicity index (ICPI), stability of haemagglutinin at 56 degrees C, agglutination of equine erythrocytes, haemagglutination elution pattern and adsorption of haemagglutinin by chick brain cells. The isolate obtained from ducks resembled a group D strain, based on its ICPI and its reaction with a panel of monoclonal antibodies. The other five NDV isolates obtained from chickens were placed in groups B(1), C1(2) and D(2) on the basis of their binding patterns with the panel of monoclonal antibodies. In challenge experiments, it was found that LaSota vaccine provided 100% protection against each of these field isolates and against a local NDV strain obtained from the Institute of Veterinary Preventive Medicine, Tamilnadu, India, while unvaccinated chickens succumbed to challenge. The possible origin of epizootic viruses causing outbreaks in vaccinated flocks is discussed.
The fatty acid acylation of Newcastle disease virus hemagglutininin-neuraminidase and fusion glycoproteins was assayed. [3H]palmitate label was associated with cytoplasmic fusion proteins (F0 and F1) and virion-associated F1. In contrast, there was no detectable [3H]palmitate label associated with the hemagglutin-neuraminidase protein in Newcastle disease virus-infected Chinese hamster ovary cells or chicken embryo cells or in virions released from these cells. Thus, fatty acid modification may not be important for the maturation of some glycoproteins.
Infection of chicken fibroblasts with Newcastle-disease virus indicates that cellular inositol is compartmented in at least two pools. Only the smaller pool is directly connected with the biosynthesis of phosphatidylinositol. Entrance of exogenous inositol into this pool is inhibited by phlorizin but not by the virus. Three hours after infection Newcastle-disease virus blocks the entrance of inositol from the small pool into one (or more) subsequent larger pool(s). About five hours after infection the virus enhances the catabolism of phosphatidylinositol in chicken cells and about seven hours after infection the permeability of the plasma membrane increases.
Twelve Newcastle disease virus (NDV) strains were isolated from chickens involved in outbreaks of Newcastle disease (ND) in western China (Shaanxi, Gansu, Xinjiang, Qinghai and Guangxi provinces) between 1979 and 1999. All strains were determined to be velogenic by plaque formation, the mean death time (MDT) of embryonated eggs, and the intracerebral pathogenicity index (ICPI). For preparation of virus RNA, the acid guanidinium-thiocyanate method was used. A 908bp fragment of nucleotide was amplified by RT-PCR starting from the N terminal of the F gene and the PCR segments were cloned into the PGEM-T vector and sequenced. The similarities of the nucleotide sequences (1-519bp) and predicted amino acid sequences of the F gene (1-125) were analyzed by comparing the 12 NDV isolates with the NDV vaccine strains Lasota, B1, H1 and V4, with classical NDV strains and recent epizootic strains. Phylogenetic analysis demonstrated that all strains were of two novel genotypes; the NDV strains that caused the outbreak of ND in western China during 1998-1999 was of the genotype VIIa, whereas the strains from the Qinghai province (1979-1985) were of genotype VIII, which has been found predominately in southern Africa.
Chickens inoculated with inactivated-virus Newcastle disease vaccines containing different emulsion adjuvants were challenge exposed with viscerotropic velogenic Newcastle disease virus. Adjuvant activity was evident in all of 9 vaccines containing mineral oil emulsion (OE), but was not evident in 2 vaccines which contained a metabolizable lipid emulsion (LE) adjuvant consisting of peanut oil, glycerol, and lecithin. Serologic responses of chickens inoculated with OE vaccines were 10- to 100-fold higher than those of chickens inoculated with LE vaccines. One of 106 chickens given OE vaccine, 12 of 24 given LE vaccine, and all of 24 nonvaccinated control chickens were clinically affected or died after challenge exposure. Five OE vaccines emulsified only by brief vigorous shaking had adjuvant activity similar to 4 OE vaccines emulsified by conventional homogenization.
During an epornitic of velogenic viscerotropic Newcastle disease (VVND) in southern California, free-flying wild birds, captive and free-ranging semidomestic birds, and exotic birds were collected from the quarantine area to determine their role in the epizootiology of the disease. The VVND virus was isolated from 0.04% of 9,446 free-flying wild birds, 0.76% of 4,367 semidomestic birds, and 1.01% of 3,780 exotic birds examined. Three house sparrows and 1 crow directly associated with infected poultry flocks were the only free-flying wild birds from which VVND virus was isolated. Among semidomestic species, ducks, quail, chukars, pheasants, peafowl, pigeons, and doves were found to be infected. Psttacines, pittas, and toucans accounted for 92% of the VVND virus isolations from exotic birds. In addition, domestic Newcastle disease virus (NDV) was isolated from 0.29% of the free-flying wild birds, from 1.65% of the semidomestic birds, and from 0.19% of the exotic birds collected. Hemagglutination-inhibition against domestic NDV was demonstrated in 0.24% of 3,796 wild bird serums, 8.28% of 2,004 semidomestic bird serums, and 3.90% of 231 exotic bird serums tested. Although few free-flying wild birds were infected with VVND virus in this epornitic, the isolation of domestic NDV strains from free-flying wild ducks and mourning doves suggests the potential for transportation of NDV over long distances by migratory birds.
An experimental vaccine containing the avirulent Australian V4 strain of Newcastle disease virus was used to vaccinate 3-or 6-week-old chickens by aerosol and drinking water application. The chickens lacked maternally derived antibody to Newcastle disease virus. When the vaccine virus was diluted in tap water more than 90% of the infectivity was destroyed immediately. The addition of 0.25% skim milk prevented this loss and there was no loss in distilled water. Rates of inactivation at 37 degrees C were similar in tap water and distilled water and were unaffected by the addition of skim milk. Both methods of vaccination resulted in the production of haemagglutination-inhibition antibodies which persisted for at least 8 to 12 weeks. The antibody response to aerosol vaccination was significantly better than that following drinking water vaccination. No clinical disease was induced by exposure to vaccine virus. Serum neutralisation antibodies paralleled those detected by haemagglutination-inhibition in chicks vaccinate once by drinking water. After revaccination through the drinking water, haemagglutination-inhibition antibodies were boosted temporarily while neutralising antibodies were maintained at an enhanced level. From chickens vaccinated by aerosol, Newcastle disease virus was recovered for 10 days from lungs and for 7 days from tracheas and caecal tonsils. Peak viraemia was detected 2 and 3 days after vaccination while both neutralising and haemagglutination-inhibition antibodies became detectable 5 days after vaccination.
Inactivation of Newcastle Disease Virus (NDV) by binary ethylenimine (BEI) is reported. The activity of an oil vaccine prepared with BEI-inactivated NDV was compared to a vaccine prepared with formalin-inactivated NDV. The BEI inactivated vaccine had almost twice the efficacy.
The MET95 strain of a lentogenic Newcastle disease virus (NDV) isolated from a broiler in Japan, showed unique hemagglutination (HA) activity. The MET95 strain failed to show HA when examined by rapid glass plate method although they showed HA titer of 1:1,024 by micro-plate method. This unique HA was also observed after the MET95 strain was passaged ten times in chickens. The failure of HA by rapid glass plate method was not shown in any other NDVs examined.
Studied was the immunization pattern against Newcastle disease in birds with the use of a spray method on broilers obtained congenitally from their mothers, having antihemagglutinins. All birds on one of the premises ( a total of 14, 000) were vaccinated when 5 days old with a liquid vaccine of strain B1 (one fourth dose per bird) using the Dutch pulverizing apparatus Flox-10 -- group I. Other 14,000 birds of another of the premises of the same batch were treated at the same age with the same dose via the same route of application of a liquid vaccine of the La Sota strain --group II. All birds of the two groups were revaccinated in the same way at the age of 25 days with a vaccine of the La Sota strain at the rate of a whole dose per bird. The birds were kept under equal conditons of feeding and management. It was found that they built immunity which protected them fully from Newcastle disease up to the end of the fattening period (2 months). This was demonstrated by the test for establishing resistance to a control infection with a highly virulent strain of the Newcastle disease virus (challenge) as well as serologically by the hemagglutination inhibition reaction. At the slaughter by the end of the fattening period all period all birds of the two groups sshowed almost equal average body weight, however, those of group I manifested 0.97 per cent lower mortality rate and lower forage intake per kg weight (by 23 g on an average).
A local virulent strain, VLT, of Newcastle disease virus formed 3- to 4-mm plaques on monolayers of primary chicken embryo cultures on the 4th day after inoculation. It agglutinated chicken and human 0 erythrocytes. Its hemagglutinin was stable at 56 C when compared with those of Komarov (K) and F vaccinal strains of the same virus. The viral titer of infected allantoic fluid dropped from 10(8.1) plaque-forming units to 10(1.0) plaque-forming units/ml within 2 hours when incubated at 56 C. The strain was ether-sensitive; it adsorbed readily on monolayers of chicken embryo cells and did not diffuse through agar. Its intracerebral pathogenicity index, chicken dose LD50, and embryo mean death time (hours) were 1.8, 9.0, and 48, respectively. Two virulent strains isolated in 1974 and 1975 were found to be identical to the VLT strain in terms of certain physical and biological properties. On the basis of plaque morphologic characteristics, hemagglutination spectrum, and hemagglutinin inactivation at 56 C, it was possible to identify readily the field isolate when it was compared with vaccinal strains (K and F) commonly used in Lebanon.
Forty-five velogenic Newcastle disease virus strains isolated in Germany between 1939 and 1995 were analysed by restriction enzyme digestion and sequencing to shed light on the relationships of past epizootics. Viruses derived from the period prior to 1970 belonged to a clade (IVea) of genotype IV comprising the earliest isolates from Europe, and could be isolated until the late seventies from poultry. Essex'70-like viruses, the prototype of genotype V, were already present at the beginning of the 1970-74 epizootic and in sporadic cases thereafter, indicating that these Newcastle disease outbreaks started in Western Europe. A genotype VI (subtype VIc) isolate was obtained in the early 1980s from a single outbreak in poultry. Outbreaks between 1993-95 were again part of a Western European epizootic caused by a genotype VIIa virus that was prevalent in the Far East.
Durand, D. P. (University of Missouri, Columbia). Interference between viable strains of Newcastle disease virus. J. Bacteriol. 82:979-983. 1961.-Strains of Newcastle disease virus (NDV) which differed in their ability to produce plaques on monolayers of chicken embryo cells were studied during conditions of dual infection. Interference with NDV plaque formation by a nonplaque-forming NDV strain was observed. The primary mechanism involved with this type of interference appears to be due to the viable infectious virus, and is not associated with interferon production or the hemagglutinin of NDV.
Following the introduction of routine vaccination regimes with different types of Newcastle disease (ND) vaccines, the incidence of velogenic viscerotropic Newcastle disease (VVND) in commercial poultry worldwide has declined dramatically. Unfortunately, these vaccination regimes are not feasible in free-range and backyard systems of poultry production practiced in many developing countries. In this study, we sought to develop a single vaccination regime in chickens with ND vaccines to elicit a long-lasting high level of ND virus (NDV) antibodies adequate to protect chickens against ND. The level of antibody response, as measured by the hemagglutination-inhibition (HI) test, and the degree of protection against the virulent strain of NDV were studied in chickens immunized with different vaccines. The vaccines used were: killed-in-oil emulsion (subcutaneous; s.c.) plus live virus (oculanasal; o.n.), given concurrently; experimental vaccine (s.c.) plus live virus (o.n.), given concurrently; killed-in-oil (s.c.); experimental vaccine prepared by homogenizing commercial live vaccine and oil emulsion (s.c.); and live virus (o.n.). The results obtained in this study indicate that concurrent administration of oil emulsion and live NDV vaccines induced the best antibody response, but there was no significant difference in protection among the vaccinated groups.