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Biomedical subjects

N Yuasa

Publications and source records attributed to N Yuasa.

At least 55 records · Page 3Linked to original sources
PubMed1983

Isolation of chicken anemia agent with MDCC-MSB1 cells from chickens in the field.

An attempt was made to isolate chicken anemia agent (CAA) from chickens suffering from anemia in the field by using MDCC - MSB1 , which was an established cell line derived from Marek's disease lymphoma. When 99 chickens of 15 flocks were examined, CAA was isolated from 58 chickens of 12 flocks. The rate of CAA isolation with MDCC - MSB1 cells was almost the same as that determined by an in vivo method by chick inoculation. It was shown that CAA was more closely concerned with anemic diseases of chickens in the field than fowl adenoviruses.

Adenoviridae Infections↗
PubMed1983

Distribution of chicken anemia agent (CAA) and detection of neutralizing antibody in chicks experimentally inoculated with CAA.

When chicks were inoculated experimentally with chicken anemia agent (CAA) at 1 day of age, CAA was consistently recovered from all the organs, including the brain, up to 28 days postinoculation (PI). It was recovered from the brain and rectal contents even 49 days PI, when the experiment was finished. In chicks inoculated with CAA at 28 or 42 days of age, CAA was also proved to multiply in all the organs, except the brain. It disappeared from these chicks earlier than from the chicks inoculated at 1 day of age. Neutralizing antibody against CAA began to be detected 21 days PI in the chicks inoculated at 1 day of age, and 7 days PI in the chicks inoculated at 28 or 42 days of age.

Anemia↗
PubMed1983

Experimental egg transmission of chicken anemia agent.

When inoculated with chicken anemia agent (CAA) via the yolk sac at 6 days of age, chick embryos could develop normally into chicks. All the chicks hatched suffered from anemia and died at 10 to 15 days of age with bone marrow aplasia. Specific pathogen free laying hens were inoculated with CAA, and eggs were collected from them over a period from 1 to 28 days after inoculation. Two of 67 chicks hatched from the eggs revealed anemia at 14 days of age. CAA was recovered from 3 of 40 chicks. From the results, a possibility of egg transmission of CAA from dams to their progeny was experimentally suggested.

Anemia↗
PubMed1983

Chronological observations on hemato-pathological changes in chicks inoculated with chicken anemia agent.

Chicks were inoculated with the Gifu-1 strain of the chicken anemia agent (CAA) on the day of hatching. They manifested distinct anemia accompanied with pancytopenia 8--20 days after inoculation. Discoloration of the bone marrow and atrophy of the thymus began to be seen 6 days after inoculation. Histologically, hematopoietic cells began to decrease and large blastic cells to appear in the bone marrow 4--6 days after inoculation. Hypoplasia and subsequently aplasia occurred to all over the bone marrow 8 days after inoculation. In the bone marrow erythrocytopoiesis was noticed first 16--18 days after inoculation, granulocytopoiesis later, and transient hyperplasia finally. At last, the bone marrow returned to a normal condition 32 days after inoculation or later. In the thymus the depletion of cortical lymphocytes became distinct 4--6 days after inoculation, and lobular atrophy 8 days after inoculation or later. The depletion of lymphocytes in the other lymphatic tissues and hemorrhage in the lamina propria of the proventriculus were observed only in the anemic phase. The results mentioned above indicated that the anemia induced by CAA was caused by the disorder of hematopoietic cell formation in the bone marrow. It was also noteworthy that cortical lymphocytes in the thymus began to decrease remarkably soon after inoculation.

Anemia↗
PubMed1983

Propagation and infectivity titration of the Gifu-1 strain of chicken anemia agent in a cell line (MDCC-MSB1) derived from Marek's disease lymphoma.

Chicken anemia agent (CAA) propagated in an established cell line derived from Marek's disease (MD) lymphoma (MDCC-MSB1). When passaged 19 times in MDCC-MSB1 cell cultures, it produced anemia of the same severity in chicks as it did before passage. Titration of the infectivity of CAA was performed successfully with subcultures of MDCC-MSB1 cell cultures which had been inoculated with serial tenfold dilutions of infected material. In it, no infected cultures could be subcultured. The propagation of CAA was also proved in the MD cell line, MDCC-JP2, and the avian lymphoid leukosis (LL) cell line, LSCC-1104B1, but not in the two MD cell lines, MDCC-RP1 and MDCC-BP1, or in the two LL cell lines, LSCC-1104X5 and LSCC-TLT. No CAA propagated in cell cultures prepared from skin and muscle, liver, or brain of chick embryos, or kidney, thymus, bursa of Fabricius, bone marrow, or white blood cells of chickens.

Anemia↗
PubMed1982

Hematopathological changes in dead and moribund chicks induced by chicken anemia agent.

Fifty day-old chicks were inoculated wit the Gifu-1 strain of chicken anemia agents. They began to show anemia and a drop in body weight 10 days postinoculation. Thirty-five of them died over a period of 12 to 23 days, mostly between 14 and 18 days postinoculation. Hematocrit value and red and white blood cell counts were markedly reduced in moribund birds. Polychromatic erythrocytes and granulocytes dropped in incidence in the peripheral blood accompanied with a fall in hematocrit value, and gained again with recovery from anemia. Macroscopically, dead and moribund birds revealed yellow bone marrow, marked atrophy of the thymus and bursa of Fabricius, discoloration and swelling of the liver, spleen and kidneys. In some cases, there were partially well-defined necrotic foci in the liver, round heart, fresh hemorrhages in the proventricular mucosa, erosion on the gizzard mucosa, and subcutaneous edema. Microscopically, marked hypoplasia or aplasia of hematopoietic cells in the bone marrow and severe depletion of lymphocytes in lymphoid organs, such as the thymus, bursa of Fabricius, spleen, and cecal tonsils, were commonly seen in affected birds. The changes described above suggested that the anemia induced by chicken anemia agent might closely be related to the bone marrow function.

Anemia↗
PubMed1981

Modification of low virulent Newcastle disease virus infection in chickens infected with reticuloendotheliosis virus.

One-day-old SPF chicks were inoculated with reticuloendotheliosis virus (REV) which had been isolated from contaminated Marek's disease vaccine. Then they were subjected to super infection with the B1 or TCND strain of Newcastle disease virus (NDV) and examined for virus recovery, antibody response and the appearance of symptoms. Regardless of the time, from 0 to 8 weeks, of inoculation with the NDV-B1 strain after the REV infection, the antibody response was suppressed and the duration of the NDV recovery prolonged. Specific death preceded by severe respiratory or neural signs occurred more frequently to chicks inoculated with REV than to uninoculated controls after inoculation with the NDV-B1 strain in the neonatal stage or with the NDV-TCND strain at 5 weeks of age.

Animals↗
PubMed1977

Pathological changes in chickens inoculated with reticuloendotheliosis-virus-contaminated Marek's disease vaccine.

A disease characterized by delayed growth, anemia, abnormal feathers, and leg paralysis occurred among chickens inoculated with Marek's disease vaccine over a period from spring to fall in 1974. These chickens were recognized among flocks inoculated with the vaccine produced by two vaccine makers. The affected ones were examined pathologically. Gross examination revealed a slight enlargement of peripheral nerves and atrophy of the spleen, thymus, and bursa of Fabricius. Histopathologically, the peripheral nerves had a mild cell infiltration of lymphoid and plasma cells, edema, degeneration of nerve fibers with Schwann's cell proliferation. Perivascular cuffings consisting mainly of lymphoid cells were seen in the brain and spinal cord. Atrophic changes displayed by prominent reduction of lymphocytes were recognized in the spleen, thymus, and bursa of Fabricius. Etiological examination suggested that most of the chickens examined might have been infected with reticuloendotheliosis virus and not with Marek's disease virus. The pathological changes observed in the peripheral nerves and central nervous system, however, were not distinguishable from those of Marek's disease.

Animals↗
PubMed1976

Isolation of a reticuloendotheliosis virus from chickens inoculated with Marek's disease vaccine.

Over a period from spring to fall in 1974, a disease with delayed growth, anemia, abnormal feathers, and leg paralysis as main symptoms broke out in flocks of chickens inoculated with Marek's disease vaccine. A virus was isolated from affected birds in the field and the same lot of Marek's disease vaccine as inoculated into these birds. It had a common antigenicity to the T strain of reticuloendotheliosis virus (REV) and could not be discriminated from this strain on the basis of morphology or property. When chicks were inoculated with it, they presented essentially the same symptoms as the birds affected in the field. Since the disease was reproduced in this manner, it was presumed to have been caused by REV contained in the vaccine as contaminant. The virus persisted in the body for long time and also induced horizontal infection.

Animals↗
PubMed1975

Effect of maternal immunity against development of Marek's disease and protective ability of vaccine.

Experiments were conducted to determine the susceptibility of chicks to Marek's disease and the protective effect of the vaccine prepared from herpesvirus of turkey (HVT) on progeny from dams infected with Marek's disease virus (MDV), or HVT, or both when they were young. Chicks from dams infected with MDV or HVT-MDV were protected from the development of Marek's disease when challenged at 3 days of age. The degree of protection decreased when the time of challenge was delayed; no protection was recognized when chicks from MDV-infected dams were challenged at 10 days of age and chicks from HVT-MDV-infected dams at 21 days of age. When inoculated either with cell-free or cell-associated HVT vaccine, sufficient protection against Marek's disease developed within 10 days in chicks from uninfected or MDV-infected dams. On the contrary, the protective effect of HVT vaccine decreased in chicks from HVT- or HVT-MDV-infected dams when challenge was done at 10 days of age; especially, the effect of cell-free HVT seemed to be inferior to that of cell-associated. The effect was improved in some degree at 21 days of age, so far as the examination for cell-free HVT is concerned. It is considered that the progeny from dams infected with MDV may have maternal immunity against Marek's disease and that the progeny from dams infected with HVT may have immunity against HVT.

Age Factors↗
PubMedDate not supplied

Detection of chicken anaemia virus DNA from formalin-fixed tissues by polymerase chain reaction.

Chicken anaemia virus (CAV) DNA was detectable from various samples such as cell-free virus, infected MDCC-MSB1 cells, unfixed liver homogenates, formalin-fixed liver homogenate or formalin-fixed paraffin-embedded (FFPE) tissues from experimental or field infected chicks using PCR assay. The detection limit of the first PCR assay was 1 infected cell or 10(-1.5) TCID50 of cell-free virus (strain A2). The nested PCR assay increased the sensitivity 10- or 100-fold. CAV DNA was detectable in the other 14 Japanese strains isolated from 1976 to 1994 by the PCR assay. All the amplified products were digested with BglII, HindIII, PstI and SacI. These results suggest that the region amplified was highly conserved among the strains. The nested PCR assay was very sensitive. However, CAV DNA was detectable in most field samples using the first PCR assay. Therefore, the nested PCR assay may not always be necessary. In contrast, the nested PCR assay was necessary to detect CAV DNA in FFPE tissues or formalin-fixed material. Use of the PCR assay in CAV DNA detection from FFPE tissues may be most valuable in diagnosis of diseases caused by or associated with CAV, because it allows detection of both microscopic lesions and CAV DNA.

Animals↗
PubMedDate not supplied

Pathologic study of specific-pathogen-free chicks and hens inoculated with adenovirus isolated from hydropericardium syndrome.

The mortality and pathology caused by serotype 4 adenovirus, isolated from chickens with hydropericardium syndrome (HPS) in Japan, was investigated in specific-pathogen-free (SPF) chickens. One-day-old to 15-mo-old SPF chickens were inoculated intramuscularly, orally, and intranasally with liver homogenates from HPS chickens or isolated serotype 4 adenovirus. There were no clinical signs before death. The mortality rate in all groups of 1-day-old chicks was 100%, irrespective of the inoculum or inoculation route. Four-week-old chickens inoculated with liver homogenate also had a 100% mortality rate. Five-week-old chickens inoculated with cell culture of HPS adenovirus had a 40% mortality rate. The mortality rates of 7-mo-old hens inoculated with liver homogenates intramuscularly and orally were 75% and 25%, respectively. In 15-mo-old hens inoculated with liver homogenates intramuscularly, the mortality rate was 70%. Gross lesions were hydropericardium and swelling and congestion of the liver with occasional petechial hemorrhages. Histologically, the liver had diffuse or multifocal hepatic necrosis and hemorrhage with intranuclear inclusion bodies noted within hepatocytes. In the spleen, macrophages containing erythrocytes and yellow pigment were prominent in the red pulp. In the lung, a moderate diffuse macrophage infiltration was noted throughout the lung parenchyma, and these macrophages contained yellow pigment. In the pancreas of the chicks inoculated at 1 day old, there was multifocal necrosis of glands with intranuclear inclusion bodies. Intranuclear inclusion bodies were seen also in the gizzard, proventriculus, duodenum, cecum, kidney, and lung of the chicks inoculated at 1 day old. Immunohistochemically, the intranuclear inclusion bodies of various organs showed positive reactions against group I avian adenovirus. Adenovirus was recovered from the liver of chickens with HPS. This study indicates that HPS adenovirus is able to reproduce HPS lesions and mortality in SPF chicks and even adult chickens and that it is a highly pathogenic strain.

Adenoviridae↗