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Biomedical subjects

B W Calnek

Publications and source records attributed to B W Calnek.

At least 91 records · Page 5Linked to original sources
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An adenovirus survey of poultry flocks during the growing and laying periods.

Chicken adenoviruses were isolated from asymptomatic chickens on each of 7 farms tested; a majority of them induced cytopathology by the second serial passage. Although adenoviruses were isolated from chickens ranging in age from 8 to 34 weeks, the highest isolation rate was from those 8 to 14 weeks. Eight serotypes (1, 2, 4, 5, 6, 7, 8, and 9) were identified in a relatively small geographic area; serotypes 1, 4, 7, and 9 were isolated most frequently. Multiple serotypes were found on 6 of 7 farms, with 1 farm having 4 serotypes identified. Repeat isolations of the same serotypes were noted on 2 farms. The pattern of virus isolations was generally related to age but varied according to farm. Although new serotypes kept appearing, even after birds came into lay, no clinical problems were associated with them. The incidence of precipitin reactors tended to be low (10-40%) in immature birds but reached 80% or more after sexual maturity. The "antiserum pool" modification of the VN test was found to be accurate and less cumbersome than the conventional procedure for typing isolants.

Adenoviridae↗
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Avian adenoviruses: effect on egg production, shell quality, and feed consumption.

Four avian adenovirus isolants (Indiana C, DPI-2, IBH-2, and B-3)were examined for pathogenicity in laying birds. None affected shell quality, and only one (IBH-2) had even a minimal effect on egg production (faster decline). Of three isolants tested (Indiana C, DPI-2, and IBH-2), only IBH-2 caused feed intake to be reduced. No other clinical signs were observed during these experiments. Egg transmission, virus excretion, and antibody production were found to mimic patterns reported for serotype-1 avian adenoviruses.

Adenoviridae Infections↗
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In vitro inactivation of cell-free Marek's disease herpesvirus by immune peripheral blood lymphocytes.

The effect of peripheral blood lymphocytes (PBL) on cell-free Marek's disease virus (MDV) was studied in vitro in PBL from intact or embryonal bursectomized (Bx) chicks infected with the apathogenic SB-1 isolate of MDV. The PBL were harvested purified and were mixed, 200 or 2,000 to 1, with cell-free GA-5 of MDV. Virus survival was assayed after incubation for 1 hour at 36 C by the standard assay for cell-free MDV. PBL from intact but not Bx chickens were able to inactivate virus. When the effective suspension of PBL was depleted of macrophages, inactivation no longer occurred, suggesting that it resulted from cooperation between macrophages and B-cells.

Animals↗
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In vitro isolation, propagation, and characterization of duck hepatitis virus type III.

The in vitro isolation, propagation, and characterization of duck hepatitis virus Type III (DHV-III), is described. This virus, which is serologically distinct from the classical (Type I) DHV, replicated in liver and kidney cell cultures of duck origin. Replication was limited in chicken and quail kidney and duck embryo fibroblast cultures. It did not replicate in a variety of other cell cultures of avian or mammalian origin. The virus was grown successfully in embryonating eggs of ducks, but not of chickens. DHV-III passed through a 50-nm membrane filter, was stable at pH 3.0 and resisted treatment with 5% chloroform. Virus growth was not inhibited by treatment with 5-iodo-2-deoxyuridine. Electron-microscope examination revealed crystalline arrays in the cytoplasm; virus particles had cubic symmetry, and were about 30 nm in diameter. By these properties, this virus can be classified as a member of the picornavirus group.

Animals↗
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Marek's disease tumor-associated surface antigen (MATSA) in resistant versus susceptible chickens.

The appearance of MATSA-bearing cells in the spleens of genetically susceptible (P-line) and resistant (N-line) chickens followed similar patterns at 4 and 6 days postinoculation (PI), with 4 to 10% of the cells positive in indirect fluorescent-antibody tests. Levels of MATSA-positive cells at 10, 14, and 21 days PI continued at 6-8% in P-line birds but dropped from about 8% to below 1 or 2% in N-line birds. This pattern was seen also in virus-isolation rates from the same spleen samples. Viral internal antigens (VIA) were seen equally and with decreasing incidence in both groups at 4-10 days PI. VIA were not detected at 14 days but reappeared at 21 days, with higher levels in P-lines than inN-lines. It was concluded that genetic resistance to Marek's disease is not related to events which result in production of the putative tumor antigen, MATSA, but rather to host-controlled factors which terminate those events.

Animals↗
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Pathogenesis of Marek's disease virus-induced local lesions. 1. Lesion characterization and cell line establishment.

Subcutaneous (wing-web) or intramuscular inoculation of chickens with allogeneic normal or Marek's disease virus (MDV)-infected chicken kidney cells induced local lesions visible by 3-4 days postinoculation (PI). Lesions were slightly larger (P less than 0.05) in infected than uninfected chickens 5 and 8 days PI. They persisted and grew past 9 days PI only when infected. Infiltrating lymphocytes in infected and uninfected early lesions were similar; they included B-cells and also T-cells with and without Ia antigen. Up to 42% of lymphocytes from infected or uninfected lesions had the surface antigen MATSA. At 3 to 6 days PI, infected lesions contained lymphocytes with viral internal antigen, especially in Ia-bearing cells and MATSA-bearing cells, but thereafter infection was latent. Cells harvested daily from local lesions induced with allogeneic MDV-infected cells were cultured; MD tumor cell lines were established from lesions as early as 4 days PI, with a total success rate of about 50% thereafter. Either transformed tumor cells were already present during the early cytolytic infection period or else appropriate target cells were present that became infected in vivo and/or in vitro and then became transformed in vitro.

Animals↗
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Gallid-1 herpesvirus infection in the chicken. 3. Reinvestigation of the pathogenesis of infectious laryngotracheitis in acute and early post-acute respiratory disease.

Specific-pathogen-free chickens were infected via the trachea when 4 weeks old with 2000 plaque-forming units (PFU) of the virulent Australian infectious laryngotracheitis (ILT) virus strain CSW-1. Titers of ILT virus in the trachea were greatest (10(7.0) PFU/ml in washings, 10(6.0) PFU/g of tissue) 2-4 days postinfection (PI). Infectivity then declined rapidly, to become undetectable by 7 days PI, although highly localized areas of ILT antigen in the tracheal epithelium were occasionally observed by fluorescent antibody staining at 7 and 8 days PI. Tracheal organ cultures established 7 and 8 days PI provided no evidence of latent ILT virus infection at this immediate post-acute stage of pathogenesis. ILT virus was not isolated from peripheral blood leukocytes or lymphoid organs (spleen, bursa, thymus). ILT virus was found in the trigeminal ganglia and/or brain in 14 of 36 chickens (40%) examined between 4 and 7 days after intratracheal inoculation, but it was not in these tissues in five chickens examined at 8 days PI. Virus was also detected at 6 days PI in the trigeminal ganglia in one of five chickens infected by the conjunctival route. These data indicate that the early pathogenesis of ILT (CSW-1) infection frequently involves the tissues of the nervous system. In acute ILT in 4-week-old chickens, interferon-alpha/beta activity was not detectable in serum or tracheal exudates within 14 days PI, but tracheal washings contained significant virus-neutralizing activity by 7 and 8 days PI. In 3-day-old chickens infected via the trachea with 200 PFU of ILT CSW-1, the clearance of ILT virus from the trachea was similar to that observed in 4-week-old chickens, but ILT virus spread systemically to the livers of 20% by 5-7 days PI.

Animals↗
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In vitro infection studies with infectious laryngotracheitis virus.

Infectious laryngotracheitis (ILT) virus strains were studied for their ability to infect chicken macrophages, lymphocytes, and kidney cells in vitro. Although macrophages were as susceptible as chicken kidney cells to infection, replication of most virus strains in macrophages was markedly restricted. Only a few isolates induced progressive infections in macrophages, and even with these the donor of the macrophages influenced replication. Thus, it appears that both cell genotype and virus genotype may help determine the extent of restriction of virus replication. Macrophages were more susceptible to an attenuated vaccine strain of ILT virus than to virulent virus strains. Spleen lymphocytes, peripheral blood lymphocytes, thymocytes, bursal lymphocytes, buffy coat leukocytes, and activated T-cells were nearly or totally refractory to infection by ILT virus.

Animals↗
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Papovavirus infection in hand-fed parrots: virus isolation and pathology.

Papovavirus infection was diagnosed in 44 parrots of at least 18 species exclusive of the budgerigar (Melopsittacus undulatus). The birds were 14 days to 4 months old and had been removed from parental care and hand-fed as nestlings. The birds had been unexpectedly found dead after having evidenced no premonitory signs of illness, or they died following a short (12-to-48-hour) period of lassitude and anorexia. In most cases, necropsies revealed pallor, multiple hemorrhages, splenomegaly, and hepatomegaly with multifocal necrosis. Histological lesions included multifocal to diffuse hepatic necrosis that spared the periportal hepatocytes, karyomegaly of splenic reticuloendothelial cells and cells in other tissues, membranous glomerulopathy, and necrosis of bursal medullary lymphocytes. Papovaviruses were isolated from two cases, and papovavirus infection was confirmed in 27 of the birds by the fluorescent-antibody test using a conjugate against a papovavirus isolated from a budgerigar.

Animals↗
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Characterization of paramyxo-, herpes-, and orbiviruses isolated from psittacine birds.

Isolates of paramyxo-, herpes-, and orbiviruses from psittacine birds were characterized in the course of studies in cell cultures. The LBD-1 isolate, from a lovebird, was grown in chick kidney (CK) cells. It had the properties of a paramyxovirus but was found tobe serologically distinct from known avian paramyxoviruses. This virus was pathogenic for Japanese quail but not for young chickens or budgerigars. RSL-1 and -2, isolated from diseased rosellas, were propagated in chicken embryo fibroblasts and CK cells, and were found similar to other herpesviruses in physicochemical and morphological properties. They were immunologically related to the psittacine herpesvirus which causes Pacheco's parrot disease, and when inoculated into budgerigars produced clinical disease and death with hepatic lesions. The CKT-1 and PKT-1 isolates, from a cockatiel and a budgerigar, grew in fibroblastic cell cultures from several species. Their physicochemical properties suggested that they should be classified as members of the orbivirus group. They were mildly pathogenic for budgerigars.

Animals↗
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Difference between influences of homologous and heterologous maternal antibodies on response to serotype-2 and serotype-3 Marek's disease vaccines.

Marek's disease (MD) vaccines representing serotypes 2 (SB-1 strain of MD virus) and 3 (FC-126 strain of turkey herpesvirus) were administered to 1-day-old MD-susceptible chicks that either were free of antibodies or carried maternally derived antibodies against SB-1, FC-126, or a serotype-1 MD virus, CU-2 strain. Homologous antibodies delayed the development of vaccine virus viremias and inhibited vaccinal immunity, as judged by protection against challenge with the virulent JM-10 strain of MD virus 7 days postvaccination. Heterologous antibodies had little effect on vaccine responses. Antibodies were shown to interfere with both cell-associated and cell-free vaccine virus.

Animals↗
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The early pathogenesis of turkey herpesvirus infection in chickens and turkeys.

The early responses of chickens and turkeys to infection with two strains of turkey herpesvirus (FC 126 and a recent field isolate, T-5A) were compared. All birds had similar virus rescue patterns from the spleen, regardless of virus strain used for infection. Productive-restrictive infections as indicated by the presence of viral antigens were found only in the spleens of infected turkeys. Viral antigens were not found in bursa or thymus but were found intermittently and at low levels in the skin. Small focal accumulations of lymphocytic cells were found in the nerves of all groups of birds 7 and 14 days postinoculation.

Animals↗