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Biomedical subjects

A M Fadly

Publications and source records attributed to A M Fadly.

At least 73 records · Page 4Linked to original sources
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Absence of influence on immune competence by the sex-linked gene (K) determining slow feathering in white leghorn chickens.

Males of white leghorn strain crosses heterozygous (Kk) for the sex-linked feathering locus genes were mated to rapid-feathering (k-) females to produce rapid- and slow-feathering chicks of both sexes. K did not influence humoral-mediated immunity against challenge with sheep erythrocytes, killed Brucella abortus, or killed infectious bursal disease virus. Chicks challenged at 3 weeks of age had higher primary responses and higher titers of 2-mercaptoethanol-resistant antibody (IgG) than those challenged at 1 week of age. K had no influence on levels of cell-mediated immunity based on responses in in vitro phytohemagglutinin tests of donors 2 to 126 days of age, on responses in in vitro one-way mixed-lymphocyte cultures, and on rejection rates of skin grafts on young chicks. Feathering type did not influence viremia or antibody to avian leukosis virus; the level of lymphoid leukosis tumors was higher in rapid-feathering females than in slow-feathering females at 28 weeks of age (53% vs. 72%; P less than or equal to 0.10). We conclude that K does not influence general immune competence. The possibility that it may influence specific immunity to ALV under conditions not met in this study, because of an endogenous virus recently associated with the K locus, is discussed.

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Field vaccination against hemorrhagic enteritis of turkeys by a cell-culture live-virus vaccine.

A cell-culture-propagated (CC) live-virus hemorrhagic enteritis (HE) vaccine was evaluated for efficacy and safety in two field trials conducted in North Carolina (NC) and Minnesota (MN). At 4 or 5 1/2 weeks of age, 9,839 poults in NC and 15,857 poults in MN were vaccinated with a CC HE vaccine administered via the drinking water. A comparable number of poults were maintained as unvaccinated controls. Vaccinated and unvaccinated poults were compared for seroconversion, response to laboratory challenge with a virulent HE virus at 3 weeks postvaccination, livability, percentage graded A, and average weight at marketing. In both trials, vaccination with the CC HE vaccine resulted in immunity against HE as indicated by seroconversion and by resistance to HE lesions following laboratory challenge with virulent HE virus. Compared with unvaccinated groups, vaccinated groups had a significantly higher percentage of turkeys graded A in the NC trial and in two of three flocks in the MN trial (P less than 0.005). Further, in the NC trial, livability was significantly higher (P less than 0.005) in vaccinated turkeys than in unvaccinated turkeys. These data indicate that the CC HE vaccine is efficacious and safe to use in the field.

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An enzyme-linked immunosorbent assay for detection of hemorrhagic enteritis virus and associated antibodies.

An enzyme-linked immunosorbent assay (ELISA) that detects antibodies specific for type II avian adenoviruses is described. Freon-treated extracts from spleens of hemorrhagic enteritis (HEV)-infected poults were a better source of antigen than the cell-culture-propagated virus. Antigen-coated microtiter wells treated with bovine serum albumin reduced nonspecific adsorption of immunoglobulins. The ELISA readily detected antibodies in hemorrhagic-enteritis- and marble-spleen-disease-infected field flocks of turkeys and pheasants. Antibody was also detected 1 week after vaccination of 2-week-old poults with cell-culture-prepared hemorrhagic enteritis vaccine. The assay was specific and more sensitive than agar-gel-precipitation and virus-neutralization tests. HEV-related antigens in infected spleens were also detected indirectly in a blocking ELISA by removal of HEV antibodies (Ab) from stock (Ab+) serum through antigen-antibody complex formation. Extracts from HEV-infected poults reduced specific antibody reactivities in HEV-antigen-coated wells, whereas extracts from HEV-challenged poults previously vaccinated with attenuated virus did not remove HEV antibodies.

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Influence of endogenous viral (ev) gene expression and strain of exogenous avian leukosis virus (ALV) on mortality and ALV infection and shedding in chickens.

Two experiments were conducted to determine the influence of endogenous viral (ev) gene expression on the response of chicken to day-old inoculation with two laboratory and two field strains of avian leukosis virus (ALV). The ev2- and ev3-negative semi-congenic chickens had much higher mortality from a unique non-neoplastic syndrome (NNS) than ev2- and ev3-positive semi-congenic chickens after inoculation with ALV strain RAV-1. The three other ALV strains induced little NNS. All four strains of ALV induced higher incidences of neutralizing antibody and lower incidences of viremia in ev2- and ev3-negative chickens than ev2- and ev3-positive chickens. The semi-congenic ev2- and ev3-negative chickens were only slightly less likely to shed ALV in the cloaca. Chickens of line 0, an unrelated line lacking ev genes, had a much higher rate of antibody production and lower rate of viremia and shedding than the semi-congenic chickens. Surprisingly, line 0 failed to get NNS after RAV-1 inoculation. There were major differences among strains of ALV in induction of antibody response, viremia, and shedding in the cloaca. The two field strains of ALV tended to be less immunogenic than the laboratory strains. We conclude that both the genetics of the host, including variation in ev gene expression, and the strain of ALV can influence the probability of ALV shedding and congenital transmission after horizontal infection.

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Effect of endogenous leukosis virus genes on response to infection with avian leukosis and reticuloendotheliosis viruses.

We examined the effect of the presence or absence of endogenous viral gene (ev) 3, which controls expression of group-specific viral and envelope antigens (gs+chf+ phenotype), and ev2, which controls the production of a complete subgroup E virus (V-E+ phenotype), on the response of chickens to RAV-1, an exogenous avian leukosis virus (ALV) with an antigenic relationship to endogenous virus. After inoculation at one day of age, the chickens lacking either ev gene expression had a lower frequency of virus isolations and higher frequency and titer of neutralizing antibodies than those expressing ev genes. This relationship was not seen in groups inoculated with chick syncytial virus (CSV), a reticuloendotheliosis-associated virus with no relationship to endogenous virus, but the ev2+ birds tended to yield more CSV isolations than the ev2- birds. We suggest that chickens expressing ev genes may be immunologically tolerant to antigens common to exogenous and endogenous viruses. In addition, ev3- birds inoculated with RAV-1 at one day of age or as embryos died at a high rate between 6 and 12 weeks of age with a non-neoplastic syndrome characterized by severe atrophy of lymphoid organs, an inflammatory reaction in the liver, and a lower immune response to particulate antigens.

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Evidence for bursal involvement in the pathogenesis of hemorrhagic enteritis of turkeys.

The pathogenesis of hemorrhagic enteritis in turkey poults infected with hemorrhagic enteritis virus (HEV) at 3 days or at 2 or 5 weeks of age was compared with pathogenesis in poults that had been chemically bursectomized neonatally and exposed to cell-culture-propagated virus at 2 or 5 weeks of age. Conventional poults exposed to HEV at 2 or 5 weeks developed clinical disease, and mortality ranged from 38% to 100%. In addition to the splenic and intestinal lesions usually seen with HEV infection, the pancreas, bursa of Fabricius, and thymus were also affected. In contrast, although they were free from detectable maternal antibody, poults infected with HEV at 3 days of age failed to develop clinical disease or mortality; however, virus was demonstrated by histological and electron microscopic examinations in spleens of these poults. Neonatal chemical bursectomy completely prevented the clinical signs, gross lesions, and mortality induced by HEV in poults at 2 or 5 weeks of age. These findings strongly suggest that an intact bursa is necessary for HEV to induce disease in turkeys.

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Propagation of virulent and avirulent turkey hemorrhagic enteritis virus in cell culture.

Virulent and apathogenic isolates of turkey hemorrhagic enteritis virus (HEV) were successfully propagated in lymphoblastoid cell lines of turkey origin, whereas spleen and kidney cell cultures from HEV-infected turkeys failed to replicate the virus. The lymphoblastoid cell lines used were MDTC-RP16 and MDTC-RP19, which were previously established from tumors induced by Marek's disease virus in turkeys. Virus replication followed co-cultivation of lymphoblastoid cells with spleen cells from HEV-infected turkeys. Virus replication was demonstrated by immunofluorescence, by agar-gel-precipitin tests, and by electron microscopy. Supernatant fluid of cultures infected with virulent HEV caused death and specific lesions in turkey poults. Poults vaccinated with apathogenic HEV were protected against death and lesions after challenge with pathogenic HEV, which was recovered from infected cultures. The MDTC-RP19 cell line appeared far more susceptible than the MDTC-RP16 cell line to infection with HEV.

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