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).

Viscerotropic velogenic Newcastle disease in turkeys: immune response following vaccination with either viable B1 strain or inactivated vaccine.

When used as a vaccine, live letogenic B1 Newcastle disease virus (NDV) protects turkeys against challenge-exposure to viscerotropic velogenic NDV (VVNDV). Low-level passively-immune poults were vaccinated one, two, or three times at various intervals and their immunity challenged at various times from 1 to 10 months of age. Newcastle disease virus was isolated readily from either the blood, trachea, or vent of turkeys in all challenge groups (through 5 months of age) on the 3rd to 6th days postchallenge (PC) but after 14 days PC was isolated rarely. Virus was isolated from turkeys that had high titers of serum hemagglutination-inhibition antibodies at the time of challenge. The anamnestic antibody response appeared to be stronger in poults that had low antibody titers prior to challenge-exposure to VVNDV. In a small-scale study with an inactivated VVNDV vaccine, vaccinated poults were protected against challenge with the homologous viscerotropic virus. Parallel control studies on the infectivity of viscerotropic NDV for turkeys indicated that resistance to VVNDV increased with age.

Viscerotropic velogenic Newcastle disease in Turkeys: virus shedding and persistence of infection in susceptible and vaccinated poults.

Susceptible turkeys and turkeys vaccinated with live lentogenic B1 strain Newcastle disease virus (NDV) were inoculated intracularly with viscerotropic velogenic (VV) Fontana strain NDV and studied for virus shedding and persistence of infection. Susceptible poults that survived infection (15%) continued to shed NDV from the intestinal tract up to 46 days postinoculation. Turkeys that were vaccinated with B1 strain NDV did not develop clinical signs when their immunity was challenged with VV Fontana strain virus. Virus was covered up to 53 days postchallenge (PC) from the cloaca of poults that were vaccinated once at 4 days of age and challenged at 1 month of age. Older turkeys that had been vaccinated one to three times did not generally shed virus after 4 days PC. Newcastle disease virus was recovered later in convalescence by the organ-culture method when swabs of trachea and cloaca were negative for virus. Persistent infection was detected as long as 88 days PC in organ cultures of cecal tonsil. Five of seven NDV isolants from organ cultures or from swabs caused fatal disease in chickens.

Viscerotropic velogenic Newcastle disease in turkeys: isolation of Newcastle disease virus from tracheal and cecal tonsil organ cultures.

Tracheal and cecal-tonsil organ cultures were made from vaccinated turkeys that had survived challenge of immunity with viscerotropic velogenic strain of Newcastle disease virus (NDV). Culture fluids were tested to show that latent infections did exist in the vaccinated and challenged turkeys, thus indicating a possible carrier state. NDV was recovered from 6 of 159 turkeys examined. Preliminary tests indicate that 4 isolants are velogenic and 2 are lentogenic.

Viscerotropic velogenic Newcastle disease in turkeys: vaccination against loss of egg production.

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.

Isolation of bovine adenovirus type 1 without an adenovirus-associated virus.

This report describes the isolation and identification of a strain of bovine adenovirus type 1 from a cow in a herd that had undergone an episode of diarrhea and abortions. This strain of bovine adenovirus type 1 did not agglutinate either guinea pig or human 0 erythrocytes, and no 20-nm virus particles were evident by electron microscopy, further indicating that it was not contaminated by adenovirus-associated virus.

Effects of incubation temperatures and bovine viral diarrhea virus immune serum on bovine turbinate cells persistently infected with a noncytopathogenic isolate of bovine viral diarrhea virus.

Noncytopathogenic bovine viral diarrhea virus (BVDV) on initial inoculation in receptive cells induced a persistence in vitro at incubation temperatures of 33, 37, and 39 C. The mechanisms of this persistence were not the result of the induction of defective interfering particles or the selection of temperature-sensitive mutants, but were the result of a naturally occurring noncytopathogenic isolate of BVDV. Persistently infected cells were not freed of the infection by continuous passage in media containing homologous antibody. Persistently infected cells appeared to undergo an earlier senescence than did noninoculated cells of the same passage level and age. This phenomenon was reversed by renewal of the culture media.

Isolation and identification of a bovine adenovirus type 3 with an adenovirus-associated virus.

A bovine adenovirus with agglutinating activity was isolated from feedlot calves and classified as serotype 3. The agglutinating activity was shown to be the property of an adenovirus-associated virus (AAV). The AAV was isolated from the bovine adenovirus by isopycnic centrifugation in CsCl; the AAV had a density of 1.4 g/cm2. This AAV is serologically related to bovine AAV-TR-15, but is distinct from bovine parvovirus-1 and primate AAV types 1 to 4, using counterimmunoelectrophoresis and hemagglutination-inhibition.

Lesions in clinically healthy cattle persistently infected with the virus of bovine viral diarrhea--glomerulonephritis and encephalitis.

Four clinically healthy cattle persistently infected with the virus of bovine viral diarrhea were examined for viral antigen and lesions. Antigen was seen by direct immunofluorescence in cytoplasm of the neurons of the brain and cervical part of the spinal cord, cells and basement membrane of renal glomeruli, reticular cells of lymph nodes and spleen, epithelial cells of small intestinal crypts and renal and testicular tubules, and endothelial cells of blood vessels. Infected neurons were pyknotic and surrounded by astrocytes and macrophages. A few blood vessels in the brains were cuffed with mononuclear cells. Basement membranes of renal glomeruli were irregularly thick with eosinophilic material, and mesangial cells in the glomeruli were plentiful. The virus had a direct effect on some tissues, but was restricted in its cytopathogenicity and was not eliminated by defense mechanisms of the host. Renal glomerular lesions were believed to have an immunologic basis.

Effects of bovine viral diarrhea virus on the percentages and absolute numbers of circulating B and T lymphocytes in cattle.

The percentage and absolute numbers of circulating B and T lymphocytes were determined for 10 healthy cattle by labeling mononuclear cells with anti-bovine immunoglobulin or peanut agglutinin. The cattle were then inoculated with a cytopathogenic isolate of bovine viral diarrhea (BVD) virus, and B- and T-lymphocyte populations were again quantitated at given intervals. Seemingly, BVD virus caused a decrease in the absolute numbers of B and T lymphocytes and in the percentage of T lymphocytes. Although these effects lasted through 7 days, all of the cattle recovered from infection and had detectable BVD virus-neutralizing antibodies in their sera 17 days after exposure.

Frequency of persistent bovine viral diarrhea virus infection in selected cattle herds.

Sera and blood buffy coat samples were obtained from 3,157 cattle in 66 selected herds. Antibodies to bovine viral diarrhea (BVD) virus were detected in 89% of the serum samples by immunoprecipitation or virus-neutralization tests. Cytopathic or noncytopathic BVD viruses were isolated from blood buffy coat samples from 60 cattle in 6 herds. A second blood buffy coat sample was obtained from 54 of the 60 cattle 2 months after the initial sampling, and BVD virus was isolated again from each cow. The 54 cattle were considered persistently infected with BVD virus. The frequency of persistent infection was 1.7%.

Total protein and immunoglobulins G1, G2, and M in serum of calves persistently infected with bovine viral diarrhea virus.

Total serum protein and immunoglobulins (Ig) G1, G2, and M concentrations were investigated in 11 calves persistently infected with bovine viral diarrhea virus. These calves were allowed to suckle from their dams until weaned. A gradual increase in total protein was observed from birth to 12 months of age. There was a wide variation in Ig concentrations in pre- and postcolostrum sera. The IgG1 increased from the time of delivery of the calves to the 5th month, decreased by the 10th month, and then stabilized through the 12th month. The IgG2 increased from birth to 10 months and remained stable through 12 months. The IgM increased from birth to the 11th month, and then decreased sharply by the 12th month.

Severe clinical disease induced in cattle persistently infected with noncytopathic bovine viral diarrhea virus by superinfection with cytopathic bovine viral diarrhea virus.

Eight healthy cattle that were persistently infected with noncytopathic bovine viral diarrhea virus (BVDV) were inoculated with cell culture fluids that contained noncytopathic or cytopathic BVDV. A severe disease occurred after inoculation with cytopathic BVDV. The clinical signs, lesions, and immune response were consistent with those of clinical BVDV infections.

Response of cattle persistently infected with noncytopathic bovine viral diarrhea virus to vaccination for bovine viral diarrhea and to subsequent challenge exposure with cytopathic bovine viral diarrhea virus.

Nine steers persistently infected with noncytopathic bovine viral diarrhea (BVD) virus were allotted into 3 groups (3 cattle/group). Cattle in group A were vaccinated with a modified-live BVD virus vaccine of porcine cell origin, cattle in group B with a modified-live BVD virus vaccine of bovine cell origin, and cattle in group C with a killed BVD virus vaccine of bovine cell origin. Detrimental effects due to vaccination were not seen. Six weeks after vaccination, the steers were challenge exposed with a cytopathic BVD virus. All steers developed mucosal disease after challenge exposure, produced antibodies that neutralized various isolates of BVD virus, and remained persistently infected until death. Steers given killed virus vaccine had a minimal neutralizing-antibody response and developed mucosal disease as quickly as reported for challenge-exposed, nonvaccinated, persistently infected cattle. Steers given modified-live virus vaccines had higher neutralizing-antibody response and longer intervals from challenge exposure to development of mucosal disease. The specificity of the neutralizing-antibody response differed between groups of vaccinated cattle.

Differentiation of cytopathic and noncytopathic isolates of bovine viral diarrhea virus by virus neutralization.

Soluble antigens of cytopathic and noncytopathic isolates of bovine viral diarrhea virus were resolved by high-performance liquid gel-permeation chromatography into 4 major and 3 minor peaks. The 2 peaks with the larger molecular weights (240,000 and 140,000 daltons) were immunogenic when inoculated into rabbits. Virus neutralizing antibodies were specific for the homologous virus. The soluble antigens were determined to be greater than 100,000 daltons by filtration.

Infectivity of bovine adenovirus type 5 recovered from a polyarthritic calf with weak calf syndrome.

Bovine adenovirus type 5, isolated from newborn calves with a polyarthritic disease known as "weak calf syndrome" caused a mild, self-limiting illness in susceptible calves. The induced illness was characterized by marked pyrexia and occasionally by mild diarrhea. It was concluded that the virus may contribute to morbidity and mortality associated with the weak calf syndrome by adding to the stress and debilitation caused by cold wet weather and by bovine viral diarrhea (BVD) virus, which has also been isolated from tissues of calves affected with weak calf syndrome.

Isolation of cytopathic and noncytopathic bovine viral diarrhea virus from the spleen of cattle acutely and chronically affected with bovine viral diarrhea.

Both cytopathic and noncytopathic bovine viral diarrhea virus (BVDV) were isolated from 16 of 17 bovine spleens representing 11 herds that had experienced acute BVD and from 12 of 21 bovine spleens from 1 herd affected with chronic BVD. It was concluded that isolation of cytopathic and noncytopathic BVDV from the same spleen probably indicates that an animal with a persistent, noncytopathic BVDV infection was superinfected with a cytopathic BVDV. The prevalence (greater than 70%) of 2 viruses in the spleen of cattle with acute or chronic BVD suggested that persistent infection with noncytopathic BVDV may be an important factor in the pathogenesis of BVD.

Reproductive performance of apparently healthy cattle persistently infected with bovine viral diarrhea virus.

A Holstein-Friesian bull and three Holstein-Friesian cows were seronegative for bovine viral diarrhea (BVD) virus but were persistently infected with the virus. Virus was isolated from buffy coat cells and nasal and lacrimal secretions during their lifetime, and they remained free of clinical signs of BVD. The three cows were pregnant when purchased, and they gave birth to full-term calves. One calf lived only a few hours, one calf became ill and died within a few days, and one calf became ill and was euthanatized within a few weeks. One cow was then bred and became pregnant but aborted a 7-month fetus. A second cow was bred approximately 5 months after parturition but did not conceive. The third cow was necropsied 6 weeks after calving, because of loss of weight. Although the bull's semen contained BVD virus when seropositive cows were bred, normal calves were born. When seronegative heifers were bred, they became seropositive to BVD virus within two weeks, with higher titers in six weeks. On heifer conceived after one service but aborted a 6-month fetus. Three others continued to have estrous cycles until their titers rose to 1:128, then they conceived and gave birth to normal calves. Another heifer conceived on the first service, had a titer of 1:128 two weeks after breeding, and gave birth to a normal calf.