Biomedical subjects

A M Fadly

Publications and source records attributed to A M Fadly.

84 records · Page 5Linked to original sources

PubMedDate not supplied

Studies of reticuloendotheliosis virus-induced lymphomagenesis in chickens.

Seventy-three percent of chickens inoculated with the chick syncytial strain of reticuloendotheliosis virus (REV) at hatching developed lymphomas by 39 weeks of age. Neonatal treatment with cyclophosphamide or surgical bursectomy at 2, 4, 8, or 12 weeks of age significantly (P less than 0.01) reduced lymphoma development. In a further experiment, surgical bursectomy of REV-infected chickens followed by intravenous inoculation of the chickens with a single cell suspension of their own bursa cells at 2, 4, 9, or 13 weeks of age resulted in lymphoid tumors in chickens treated at 9 or 13 weeks but not in chickens treated at 2 or 4 weeks of age. Furthermore, this treatment did not shorten the incubation period for lymphoma development. These findings argue very strongly that transforming target cells are primarily in the bursa of Fabricius. The data also suggest that a minimum residency of 4 weeks in the bursa is required for infected bursa cells to become transformed. Therefore, lymphomagenesis induced by REV in chickens appears similar to that induced by the avian leukosis virus group.

Animals↗

PubMedDate not supplied

Avian leukosis virus infection and congenital transmission in lines of chickens resisting selection for reduced shedding.

Two lines (D and E) of three breeder lines of chickens that had resisted selection for reduced avian leukosis virus (ALV) congenital transmission on the breeder's premises did not resist the same selection procedures (tests for gs-antigen in albumen) under laboratory conditions. The incidence of ALV congenital transmission in the remaining third line (F) was spontaneously reduced from 13% to 0.9%. Environmental ALV exposure of uninfected chicks after hatching induced 7-10% of the progeny from lines E and F to become congenital transmitters but had negligible effects on line D. Neither errors in identifying dams nor horizontal transmission leading to congenital transmission were great enough to explain the lack of improvements in the three lines on the breeder's premises. Conditions of environmental exposure on the breeder's farm seem most likely to account for the resistance to reduced shedding. These findings suggest that the effectiveness of testing and selection procedures used to reduce ALV may be greatly influenced by the environment.

Animals↗

PubMedDate not supplied

Pathogenesis of infectious bursal disease in chickens infected with virus at various ages.

Chickens free from infectious bursal disease (IBD) maternal antibody were inoculated with a virulent strain of IBD virus at 1, 5, or 11 weeks of age. Chickens inoculated at 5 weeks developed severe clinical signs and had reduced levels of serum complement within 2-4 days postinoculation, but those inoculated at 1 or 11 weeks did not. However, at 1, 2, 4, and 8 days postinoculation, the rate of virus recovery from different tissues, severity of microscopic lesions, and frequency of detection of viral antigens in lymphoid organs of chickens inoculated at 5 weeks were comparable to those of chickens inoculated at 1 or 11 weeks of age. These findings suggest that age resistance to clinical manifestations of IBD is probably independent of the ability of virus to replicate and induce lesions in the host.

Age Factors↗

PubMedDate not supplied

Efficacy and safety of a cell-culture live virus vaccine for hemorrhagic enteritis of turkeys: laboratory studies.

Poults free from hemorrhagic enteritis (HE) antibody were vaccinated by gavage at 1 day or 2 weeks of age with a live HE vaccine virus that had been propagated in a Marek's disease (MD)-induced B-lymphoblastoid cell line of turkey origin. Vaccinated and unvaccinated poults were challenged with a virulent HE virus at various times postvaccination. One hundred tissue-culture-infectious doses of the vaccine virus per poult were sufficient to induce a serological response as well as to protect poults against HE lesions and mortality. Vaccinated poults were protected against the disease as early as 1 week and as late as 8 weeks PV. The vaccine was efficacious by several routes of application. The vaccine virus spread horizontally from vaccinated to contact-exposed poults, as indicated by seroconversion and resistance of contact-exposed poults to challenge. The vaccine had no detectable harmful effects on the humoral immune response to particulate antigens or on weight gain of vaccinated poults. The vaccine proved to be free from MD virus, as indicated by the absence of MD lesions and antibody in 8-week-old chickens inoculated intra-abdominally with the vaccine at hatching. These findings indicate that the cell-culture-propagated HE vaccine is efficacious and safe.

Adenoviridae Infections↗

PubMedDate not supplied

Comb lesions and mortality patterns in white leghorn layers affected by Marek's disease.

Marek's disease was diagnosed as the cause of prolonged high mortality in two commercial flocks of white leghorn layers by gross and microscopic examination of affected tissues and by immunofluorescent study of live tumor cells using anti-Marek's disease tumor-associated surface antigen, anti-immunoglobulin M, and monoclonal antibodies. The disease was characterized by swollen, necrotic, lymphomatous combs and mortality that rose above normal at 28 weeks of age, peaked at 35-36 weeks, and returned to normal by 45-46 weeks.

Animals↗

PubMedDate not supplied

Hatchery-related contact transmission and short- term small-group-rearing as related to lymphoid-leukosis-virus-eradication programs.

Pathogen-free chickens highly susceptible to lymphoid leukosis virus (LLV) were used to study the role of hatchery-related contact transmission of LLV. In one experiment, the efficiency of short-term small-group-rearing in conventional-type rearing units to prevent contact transmission of LLV from infected to uninfected groups was evaluated. Results obtained from these experiments suggest that LLV is not transmitted by congenitally infected chicks to uninfected hatchmates in the hatcher. However, LLV can be transmitted by congenitally infected chicks to uninfected hatchmates during standard manual vent sexing. Rate of contact transmission was lower in chickens reared on wire-mesh floors than in chickens reared on solid floors. Short-term procedures in which chicks were reared in colony cages and brooder batteries effectively reduced the transmission of LLV by infected groups of hatching chicks to uninfected groups. All these procedures should facilitate the rearing of small groups of chicks with little risk of infection for a period sufficient to conduct virus assays, an essential step in LLV eradication.

Animals↗

PubMedDate not supplied

Characteristics of CVI988/Rispens and R2/23, two prototype vaccine strains of serotype 1 Marek's disease virus.

Studies were focused on two attenuated serotype 1 Marek's disease (MD) vaccine viruses, CVI988/Rispens (passage 42) and R2/23 (passage 105). Both serotype 1 vaccine viruses provided much higher levels of protection than the prototype MD vaccine, turkey herpesvirus (HVT); the best protection was generally provided by CVI988/Rispens when compared with other vaccines. The efficacy of neither serotype 1 vaccine was improved by mixture with viruses of other serotypes (synergism). No differences between the two serotype 1 vaccines were revealed by cross-neutralization tests, thus excluding preferential in vivo neutralization by maternal antibodies as an explanation for differences in protective efficacy. Neither vaccine strain induced MD lesions or reduced growth rates in 8- or 18-week trials. Neither virus depressed humoral or cellular immune responses to antigenic challenge at 3 or 15 days after vaccination. Both virus strains exhibited altered characteristics during serial backpassage; R2/23 acquired increased oncogenic potential, and CVI988/Rispens acquired the potential for increased viremia titers, accompanied by an increased frequency of both histologic nerve lesions and gross thymic atrophy. During backpassage trials, contact spread was not observed for R2/23 and, surprisingly, seemed relatively limited for CVI988/Rispens. Studies on these two serotype 1 strains generally support the safety and efficacy of the serotype 1 class of MD vaccines.

Animals↗

PubMedDate not supplied

Multicentric histiocytosis in young chickens. Gross and light microscopic pathology.

During 1991-94, tissue specimens from 262 young chicken carcasses condemned at slaughter contained novel multicentric proliferations of histiocytelike cells. These tissues had been submitted to the USDA FSIS Eastern Laboratory because of grossly enlarged spleens, livers, or kidneys. The spleens were two to three times normal diameter and contained miliary white or yellow 1-3-mm foci. Similar miliary foci were present throughout the enlarged livers and kidneys. Microscopic examination of these tissues revealed discrete circular nodules expanding splenic periarteriolar lymphoid sheaths, hepatic periportal nodules, and discrete perivascular and more diffuse interstitial nodules replacing renal tubules. Nodules also were present in the pancreas, bone marrow, proventriculus, and lung, with more diffuse infiltrates in intestinal lamina propria. The cells composing these nodules contained irregularly oval, folded, or pleomorphic nuclei and relatively abundant eosinophilic cytoplasm. Mitotic figures and pyknotic nuclei were common. These cells were interpreted to be histiocytes (tissue macrophages or dendritic cells) and did not resemble lymphocytes. These proliferating cells also did not resemble the cell population of commonly diagnosed lymphoid neoplasms of young chickens. No intralesional organisms were detected and polymerase chain reaction analysis failed to detect Marek's herpesvirus DNA or leukosis/sarcoma and reticuloendotheliosis proviral DNA.

Animals↗

PubMedDate not supplied

Effect of serotype 2 and 3 Marek's disease vaccines on the development of avian leukosis virus-induced pre-neoplastic bursal follicles.

The effect of serotype 2 and 3 Marek's disease virus (MDV) vaccines on the development of pre-neoplastic bursal lesions induced by two strains of subgroup A avian leukosis virus (ALV) was studied. Chickens of line 15I5 x 7(1) susceptible to ALV-induced lymphoma were inoculated at hatch with Rous-associated virus-1 (RAV-1) or strain RPL-40 of subgroup A ALV. All chickens, except for negative controls, were also inoculated at hatch with strain 301B/1 of serotype 2 MDV or strain FC126 of turkey herpesvirus (HVT), a serotype 3 MDV. At 11 and 14 weeks of age, serial sections of bursal tissues from chickens in various treatment groups were stained with methyl green pyronin and examined for ALV-induced pre-neoplastic bursal lesions, also known as hyperplastic follicles. At 6 days and at 11 and 14 weeks of age, bursal tissues from groups of chickens inoculated with serotype 2 MDV and ALV at hatch were also examined for the presence of MDV genome by in situ hybridization. The number of ALV-induced hyperplastic follicles was significantly higher in chickens inoculated with serotype 2 MDV than in unvaccinated chickens or in chickens vaccinated with HVT. In contrast, the lowest number of hyperplastic follicles was noted in chickens vaccinated with HVT, regardless of strain of ALV used. These results suggest that enhancement of lymphoid leukosis may result from an increase in the number of ALV-induced hyperplastic follicles caused by the MDV and also that the enhancing effect of MDV on ALV-induced lymphomagenesis may occur at the stage of formation of hyperplastic follicles in the bursa.

Animals↗

PubMedDate not supplied

Comparative evaluation of in vitro and in vivo assays for the detection of reticuloendotheliosis virus as a contaminant in a live virus vaccine of poultry.

Indirect immunofluorescence (IFA), polymerase chain reaction (PCR), and enzyme-linked immunosorbent assay (ELISA) were used for detection of reticuloendotheliosis virus (REV) as a contaminant in a live virus fowl pox (FP) vaccine of poultry. A FP vaccine known to be contaminated with REV was tested by in vitro and in vivo assays in chicken embryo fibroblasts (CEFs) and day-old specific-pathogen-free (SPF) chicks, respectively. Using in vitro assays, IFA and PCR were more sensitive than ELISA in detection of REV in CEFs inoculated with REV-contaminated FP vaccine. However, when the vaccine was tested by in vivo assays using SPF chickens, the sensitivity of ELISA was comparable with that of IFA and PCR. Antibody to REV was not detected in SPF chickens within 4 wk postinoculation with REV-contaminated FP vaccine at hatch. Filtration of vaccine to eliminate vaccine virus from the inoculum before testing in CEFs resulted in a significant reduction in the frequency of REV detection by PCR or IFA. The data suggest that the sensitivity of IFA, PCR, and ELISA depends on the concentration of REV in the vaccine and that in vivo assays of vaccines for contamination with REV should include a test for virus because a negative antibody test may be misleading.

Animals↗

PubMedDate not supplied

Detection of avian leukosis virus subgroup J using the polymerase chain reaction.

A polymerase chain reaction (PCR) assay was developed for the detection of avian leukosis virus strain J (ALV-J) in chickens. Primers were based in the E element and the 3' terminus of the long terminal repeat of proviral ALV-J. PCR products were amplified from genomic DNA extracted from chicken embryo fibroblasts (CEF) infected with either strain HPRS-103, the prototype of ALV-J, or field isolates of ALV-J obtained from broiler breeder flocks in the United States that exhibited myeloid leukosis. The newly developed PCR detected ALV-J in DNA prepared from CEF inoculated with ALV-J but not from CEF inoculated with subgroup A, B, C, D, or E. The PCR also detected ALV-J in DNA prepared from blood, combs, and toes obtained from chickens experimentally infected with ALV-J and in DNA obtained from peripheral blood monocytes from naturally infected broiler breeder chickens. The PCR described here offers a specific and sensitive alternative to conventional virus isolation tests for ALV-J.

Animals↗

PubMedDate not supplied

Response of chickens carrying germline insert ALVA11 to challenge with a field strain of subgroup A avian leukosis virus.

The ALVA11 germline insert in chickens is a defective subgroup A avian leukosis virus (ALV) proviral insert that expresses a low-to-moderate level of subgroup A ALV envelope glycoprotein. Chicks carrying or lacking ALVA11 were evaluated for response to challenge by RPL-42, a pathogenic field strain of subgroup A ALV, by either exposure to chicks shedding RPL-42 or direct injection with various doses of RPL-42. Chicks carrying ALVA11 were significantly more resistant, as measured by infectious virus and viral antibody status, to horizontal infection and direct injection of RPL-42 than chicks lacking ALVA11.

Animals↗