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Induction of lymphomas and tumor antigen by Marek's disease virus in turkeys.

Pathogenic Marek's disease (MD) virus (MDV) induced a high incidence of mortality and gross and microscopic lesions in turkey poults. Inoculated turkey poults became persistently viremic with MDV, although the levels of detectable circulating MDV were generally lower in turkeys than in similarly inoculated chickens. The early lytic phase of MD characterized by lymphoid cell destruction and the appearance of viral antigen in lymphoid organ was not as prominent in turkeys as in chickens. Gross MD lesions in turkeys were most prevalent in liver and spleen; peripheral nerves were involved infrequently. MD tumors in turkeys contained cells that reacted with antiserum prepared against chicken MD-tumor-associated surface antigen (MATSA); this result indicated that MDV induced cellular transformation in turkeys and the tumor-associated antigen in chicken and turkeys cross-reacted. Several in vitro-propagating B-cell lines were developed from the turkey lymphomas. As in chickens, MD in turkeys also resulted in immunodepression. Circulating lymphocytes from turkeys that eventually died of MD or had gross tumors at the end of the experiment were deficient in mitogenic response to Concanavalin A.

Animals↗

Marek's disease in turkeys: lack of protection by vaccination.

Herpesvirus of turkeys, a highly effective vaccine against Marek's disease (MD) in chickens, was ineffective in protecting turkeys against MD. Another tissue-culture attenuated vaccine virus also protected chickens, but not turkeys, from MD. Intact and immunosuppressed turkey poults inoculated with herpesvirus of turkey developed a persistent viremia, but did not have detectable gross or microscopic lesions.

Animals↗

AUS in the prevention of Marek's disease.

Aminoureidosulfone (AUS) was used as a feed additive to prevent mortality in Marek's disease (MD)-infected chickens in the laboratory. Chicks infected with MD virus (5000 plaque-forming units) at 1 day of age were given AUS in the feed from 1 day of age until the experiment was terminated. AUS, at all concentrations tested, reduced mortality due to Marek's disease. Chickens receiving AUS at the 0.002% level had a 4% mortality rate, those receiving 0.005% had 9% mortality, and those receiving 0.01% had 2% mortality; mortality rates in the respective controls were 44%, 49%, and 50%. However, lesion reduction in surviving chicks was minimal. When AUS was withdrawn from the feed, MD-induced mortality increased within two weeks; average body weight decreased also.

Animal Feed↗

Experimental infection of laying chickens with adenovirus 127 and with a related virus isolated from ducks.

Infection of commercially reared white leghorn and white rock hens with adenovirus 127 was associated with decreases in total egg production, external egg quality, egg weight (P less than 0.01), and eggshell thickness (P less than 0.01). The egg-production and egg-quality disturbances were transient, and production returned to normal approximately 4 weeks postinfection. Infection of white leghorns with a hemagglutinating adenovirus isolated from Missouri ducks did not adversely affect egg production, external egg quality, or eggshell thickness, but it was associated with decreased egg weight (P less than 0.01). Prior infection with the duck adenovirus prevented the adverse egg-production effects of adenovirus 127 infection. Mean hemagglutination-inhibition antibody titers of chickens infected with adenovirus 127 or with duck adenovirus ranged from 1:588 to 1:10809, and mean titers of uninfected chickens did not exceed 1:2.

Adenoviridae Infections↗

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↗

[Effects of Mycoplasma synoviae infection on the state of health, reactions to vaccination and results of fattening in broiler chickens (author's transl)].

Four cases in which contact infection was experimentally induced in broilers by Mycoplasma synoviae (M.s.) are reported. The chickens were inoculated against Newcastle disease (NCD) and infectious bronchitis (IB) in accordance with the Netherlands vaccination programme. Fattening was continued for six weeks. The rate of horizontal transmission of M. synoviae infection varied with the severity of the virus infection (i.e. vaccination). There was a close correlation between this finding and the adverse effects of M. synoviae infection on the severity of the reactions to vaccination, the final weight, the table quality and feed conversion. Moreover, there was evidence to suggest that M. synoviae accelerates the appearance of dyschondroplasia in broilers.

Animals↗

Prediction of the occurrence of Marek's disease in chickens on the basis of the quantitation of cell-mediated immunity.

Cell mediated immunity was assayed in chickens on the basis of the dinitrochlorobenzene skin test, T lymphocyte numbers in peripheral blood and the graft-versus-host reaction. It was found that chickens that were to develop clinical Marek's disease following exposure to Marek's disease virus had significantly lower prechallenge levels of cell mediated immunity than those that were resistant to Marek's disease. The graft-versus-host reaction had a smaller coefficient of variation than the other two tests, and it was concluded that this test is likely to be the most reliable indicator of the outcome of infection with Marek's disease virus.

Animals↗

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↗

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↗

Marek's disease in field chickens: correlation between incidence of Marek's disease and nuclear-inclusion formation in the feather-follicle epithelium.

The present study confirmed that Marek's disease (MD)-associated nuclear-inclusion (NI) formation in the feather-follicle epithelium (FFE) is related to mortality from MD; it also presented useful data on the epidemiology of MD in HVT-vaccinated field chickens. Incidence of NI formation in the FFE of chickens on six rearing farms varied greatly by age and flock, but most of the field flocks showed biphasic peaks of incidence of NI in chickens consisting of a small peak at an early age (usually at 2-4 weeks of age) and a large peak between 13 and 16 weeks of age. MD tended to occur in chickens over 20 weeks old, and almost all MD-affected chickens showed NI formation persistently in the FFE, usually between 13 and 20 weeks of age. Chickens that were healthy at the end of observation showed either transient NI formation, usually between 13 and 16 weeks of age, or no detectable NI formation. Incidence of NI formation in the FFE of chickens at 19-20 weeks of age was related to mortality from MD: chickens with NI formation had a MD mortality rate of 66.7%, whereas chickens without NI formation had MD mortality of only 0.8%.

Age Factors↗

[Experimental induction of the cutaneous form of Marek's disease in broilers].

Straight-run chickens of the Ross broiler hybrid were experimentally infected with the skin homogenates of sound broilers, broilers conditionally edible, and broilers confiscated for alternations in skin. The chickens infected with the homogenates of healthy skin were negative in the Marek's disease test. In 17% of the chickens infected with the skin from the conditionally edible broilers, macroscopically observable cutaneous lesions were induced and 60% of the infected chickens had microscopic changes in the skin; visceral organs were always affected by the infection. In the chickens infected with the skin of a confiscated bird, the long storage exerted its unfavourable effect and the infected birds were negative in the Marek's disease test. Our results indicate that the active form of Marek's disease was induced.

Animals↗

Avian ocular neoplasia--a description of spontaneously occurring cases.

Twenty-one cases of ocular neoplasia were studied in birds submitted for diagnosis. Eighteen of these were lymphocytic tumors in chickens affecting various parts of the globe and retrobulbar tissues. Two cases of rhabdomyosarcoma in chickens were recorded. One of these was located in the anterior uvea and the other in the orbit. One adenocarcinoma was seen in a budgerigar.

Adenocarcinoma↗

Experimentally induced fatty liver and kidney syndrome in the young turkey.

Turkeys were fed up to four weeks of age on diets of low biotin content and then fasted for 18 hours. Three birds developed clinical signs of fatty liver and kidney syndrome (FLKS) and on autopsy had pale and swollen livers and kidneys. Morphological studies showed fatty accumulations in liver, kidney, heart and proventriculus but no signs of inflammatory or degenerative changes. The infiltrated lipid had an abnormal fatty acid composition, with an increased proportion of monounsaturated fatty acids. Affected birds suffered from severe hypoglycaemia and hepatic glycogen was depleted. These findings demonstrate that FLKS can be induced experimentally in turkeys.

Animals↗