A suggested reclassification of avian mycoplasma serotypes.
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Biomedical subjects
J Fabricant
Publications and source records attributed to J Fabricant.
In vitro studies of hemorrhagic enteritis virus with immunofluorescent antibody technique.
Dissociated spleen lymphocytes from hemorrhagic enteritis virus (HEV)-free chickens, pheasants, and turkeys were infected with HEV in suspension cultures. Viral antigens were detected in cells of all three donor species by immunofluorescence. The age of chicken from which cells were obtained and the temperature of incubation influenced the development of viral antigens in cultured cells, which could be observed as early as 24 hr postinfection. This is the first time that HEV has been shown to infect cells in vitro.
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Immunofluorescence studies on the early pathogenesis of hemorrhagic enteritis virus infection in turkeys and chickens.
Chickens and turkeys not previously exposed to hemorrhagic enteritis virus (HEV) were inoculated orally with the virus. Birds were necropsied each day from the first to the eighth day following inoculation, and specimens from various tissues were collected for examination. Clinical illness was noted only in turkeys, although intestinal hemorrhages and swollen, necrotic spleens were seen in both species. The distribution and localization of viral antigens in various tissues and peripheral blood lymphocytes were studied by the immunofluorescent technique. The patterns of HEV infection in chickens and turkeys were similar, except there was a high level and persistence of viral antigen in the thymus of turkeys but not in chickens.
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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.
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Dose-dependent inhibition of virus rescue from lymphocytes latently infected with turkey herpesvirus or Marek's disease virus.
The number of plaque-forming units (PFU) of turkey herpesvirus (HVT) isolated per 10(6) latently infected splenic lymphocytes was determined by co-cultivation on permissive monolayer cultures in 35-mm-diameter Petri dishes. Doses of 1 x 10(6) spleen cells or less per culture gave uniform dose-related titers, whereas doses of 8 x 10(6) cells often yielded less than 1-2% of the expected number of PFU. Intermediate doses gave proportionally reduced virus yields. This dose-dependent inhibition was observed with spleen cells from birds within a week after infection and became more marked with time. A similar phenomenon occurred with a non-oncogenic Marek's disease virus (MDV) isolate (SB-1) but not with oncogenic MDV isolates (CU-2, JM-10, GA-5), except in genetically resistant birds. High numbers of uninfected spleen cells mixed with low numbers of HVT-infected cells during assay reduced titers only slightly. Immunosuppression by combined neonatal thymectomy and cyclophosphamide treatment before HVT infection prevented the inhibition, but embryonal bursectomy had no effect.
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Field trials with a bivalent vaccine (HVT and SB-1) against Marek's disease.
White leghorn chickens on five farms were given a bivalent Marek's disease (MD) vaccine consisting of turkey herpesvirus (HVT) and SB-1 (a nononcogenic MD virus); other chickens received only HVT. The farms had histories of "vaccination failures," presumably owing to an exceptionally virulent challenge MD virus. The bivalent vaccine uniformly protected chickens better than HVT alone between 12 and 16-20 weeks of age, when serious MD losses occurred. During that period, total mortality in groups given both viruses ranged from 0.39 to 1.26% (mean 0.86%), whereas that in HVT-vaccinated groups not exposed to SB-1 varied from 1.92 to 7.44% (mean 3.43%). Chickens in pens or rows with close contact to those given bivalent vaccine also had low MD mortality rates (0.46-1.06%, mean 0.77%), probably from the spread of SB-1.
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Marek's disease virus-induced tumor transplants: development and rejection in various genetic strains of chickens.
This study compares the ability of strains of chickens of varied genetic resistance to Marek's disease (MD) to resist or regress both local and general reactions to transplantable tumor cells induced by a variety of MD virus strains and to transmissible lymphoid tumor cells (Olson's TLT) induced by an avian leukosis-sarcoma retrovirus. Previous studies have dealt with only a single MD transplant. Three conclusions can be drawn from our data: 1) MD virus infection alone could induce progressive tumors at the site of inoculation. 2) Progression or regression of transplant tumors was independent of genetic susceptibility to MD. 3) Incidence of virus-induced host tumors was dependent upon genetic susceptibility to MD.
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The early history of infectious bronchitis.
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Animals↗