Horizontal transmission of lymphoid leukosis virus. Influence of age, maternal antibodies and degree of contact exposure.

Eight groups of 1-day-old or 8-week-old chickens were exposed by contact to lymphoid leukosis virus (LLV) infection. Five groups of about 60 spf chickens were used. Three groups of the same size were progeny from LLV vaccinated hens. Five groups were housed in one chicken house in close contact with a large number of immunologically tolerant chickens (virus "spreaders"). On two occasions infectious LLV was recovered from air/dust samples collected in this house. In the second house a small number of congenitally infected birds generated a mild degree of LLV exposure. It was demonstrated that infection by contact may lead to lymphoma formation and congenital virus transmission. The incidence of virus infection and LL mortality in the groups of birds exposed at 8 weeks of age were significantly lower than in chickens exposed at 1 day of age. In addition, about 100-fold differences in numbers of LLV-associated white blood cells were observed between both age groups. These results indicate that in addition to resistance to tumour formation, resistance to LLV infection develops in the chicken with increasing age. Maternal antibodies, present in three groups exposed at 1 day of age, reduced the rate of infection and the incidence of LL.

Age-related resistance to avian leukosis virus. I. Influence of age at exposure on mortality and congenital transmission.

Groups of White Leghorn chickens were inoculated at 1 day and at 2, 4, 6 and 8 weeks of age respectively with a mixture of leukosis viruses of subgroups A and B. The five infected groups were kept in a filtered air positive pressure house. A sixth group was accommodated separately in a similar house as a control. All birds which died or were removed were subjected to pathohistological examination; diagnosis of lymphoid leukosis was made upon either gross lesions plus microscopical lesions or microscopical lesions only. The incidence of lymphoid leukosis in the infected groups appeared inversely proportional to age of infection, i.e. the mortality due to lymphoid leukosis decreased from 54.3% in the group infected at 1-day-old to 7.4% in the group infected at 8 weeks of age. Prevalence of leukosis in the latter group may be attributed to a small number of chicks already infected vertically with the virus. Congenital transmission of leukosis virus was demonstrated in embryos in the groups infected at 1-day-old, 2, 4 and 6 weeks of age. In the latter group congenital transmission was extremely low; from 214 pooled embryo extracts (1007 embryos) only 2 (0.9%) contained leukosis virus. In the group infected at 8 weeks of age no virus was detected in the embryos. Congenital transmission of leukosis virus appeared to be related to age of infection, i.e. early infection went parallel with a high rate of transmission. The pattern of congenital transmission was erratic and the number of hens shedding leukosis virus continually was small. From the results in this trial it is concluded that both lymphoid leukosis and congenital transmission occur rarely if chickens (born free of leukosis virus) are kept free from infection during the first 6-8 weeks of life and subsequently are injected with a relatively high dose of leukosis virus.

Comparison of complement fixation and phenotypic mixing tests for the detection of lymphoid leukosis virus in egg albumen and embryos of individual eggs.

Individual eggs, collected from 14 hens over a period of 10 weeks, were tested for lymphoid leukosis (LL) virus by four methods. The chickens were selected from a conventional flock on the basis of virus recovery from embryos 3 months earlier. Albumen samples and extracts of embryos were examined by complement fixation (CFT) and phenotypic mixing tests (PMT). Most eggs positive for LL virus (LLV) and/or group specific (gs)-antigen were detected by testing of embryo extracts by PMT and CFT. Examination of albumens yielded less LLV and gs-antigen positive eggs. However, because a few birds produced eggs with predominantly gs-antigen in the albumen and less frequently with virus in the embryos from the same eggs, the combination of CFT on both albumen and embryo extract proved to be the most sensitive detection system. CFT on both albumen and embryo are easier to perform than PM tests and therefore may be useful in LL eradication programmes. The majority of the hens intermittently transmitted virus and/or gs-antigen to embryos. The results of this study indicate that congenital transmission patterns of LLV infections may be different in individual birds.

The control of lymphoid leukosis in a flock White Plymouth Rock chickens.

Lymphoid leukosis (LL) was successfully controlled in a commercial basic breeding line of White Plymouth Rock chickens. The control method has been developed for breeder flocks and consists of three elements: --In the flock under study, homogenates of embryos from all eggs collected during a number of 14-day periods are tested for the presence of LL viruses. --Only eggs from hens that have been shown not to shed virus in their eggs are used for the production of progeny. The offspring are reared in isolation during the first two months of life, at which time the age-related resistance against tumour formation by LL viruses appears to be sufficiently developed. --The chickens are subsequently inoculated intramuscularly with LL viruses of subgroups A and B transferred to a conventional chicken house. The vaccination raises a solid immunity to horizontal LL virus exposure and, due to the age-related resistance, tumour formation does not follow. No excretion of LL viruses could be detected in three generations of White Plymouth Rock chickens to which the three elements of the control procedure were applied. Clinical disease was not observed in any of the chickens under notice.

The control of lymphoid leukosis in a flock White Plymouth Rock chickens.

Summary Lymphoid leukosis (LL) was successfully controlled in a commercial basic breeding line of White Plymouth Rock chickens. The control method has been developed for breeder flocks and consists of three elements: - In the flock under study, homogenates of embryos from all eggs collected during a number of I4-day periods are tested for the presence of LL viruses. - Only eggs from hens that have been shown not to shed virus in their eggs are used for the production of progeny. The offspring are reared in isolation during the first two months of life, at which time the age-related resistance against tumour formation by LL viruses appears to be sufficiently developed. - The chickens are subsequently inoculated intramuscularly with LL viruses of subgroups A and B transferred to a conventional chicken house. The vaccination raises a solid immunity to horizontal LL virus exposure and, due to the age-related resistance, tumour formation does not follow. No excretion of LL viruses could be detected in three generations of White Plymouth Rock chickens to which the three elements of the control procedure were applied. Clinical disease was not observed in any of the chickens under notice.

Absence of Marek's disease virus antigen in the feather follicle epithelium of vaccinated chicks demonstrated by immunofluorescence.

In chickens vaccinated with MDV strain CVI 988, HVT strain FC 126 or PB-THV 1, no MDV-specific antigens could be demonstrated in the feather follicle epithelium by immunofluorescence (IF). In chickens given virulent MDV strains, the epithelium of the feather follicle was positive in IF. In an experiment where chickens were vaccinated with strain CVI 988, positive IF was observed in the lung, bursa and pancreas, but not in the feather follicle epithelium, kidney, cloaca, or caecal tonsils. Absence of IF antigen in the skin may be indicative of avirulence of the strain of MDV.