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Marek's disease: a model for protection against herpesvirus-induced tumours.

Marek's disease (MD) is a lymphoproliferative disease of chickens caused by a herpesvirus (MDV). Several effective vaccines have been developed and MD is therefore often considered as a model for studying antitumour vaccines. Key factors for the understanding of vaccine-induced immunity are discussed. Three serotypes have been characterized: serotype 1 or oncogenic MDV, serotype 2 or non-oncogenic MDV and serotype 3 or herpesvirus of turkeys. The three serotypes have clearly different genomes and proteins. The pathogenesis of infection with serotype 1 MDV can be divided into an early cytolytic phase, a latent phase and a second cytolytic infection combined with the development of tumours and permanent immunosuppression. The activation of T cells during the early cytolytic phase is important for establishing infection in the target cells for latency and transformation. Immune responses by B cells, and especially by T cells, are directed against viral infection. Evidence is presented that Marek's disease tumour-associated surface antigen is not involved in the antitumour responses. Moreover, the importance of antitumour immune responses in MD is questioned. Vaccinal immunity is dependent more on T cells than B cells and is directed against virus antigens. It is proposed that the evidence claimed for an antitumour response induced by vaccination actually relates to an antiviral response. The relevance of new, highly oncogenic strains causing MD in vaccinated chickens is discussed.

Animals↗

A study of breeder vaccination programs and problems in the broiler progeny in Saskatchewan utilizing enzyme-linked immunosorbent assay.

A survey of antibodies against infectious bursal disease virus (IBDV), infectious bronchitis virus (IBV), Newcastle disease virus (NDV), and reovirus (RV) was conducted in broiler-breeder flocks and selected progeny broiler flocks utilizing the enzyme-linked immunosorbent assay. Marked differences in antibody titers between different breeder flocks were related to differences in vaccination programs. Poor performance in some progeny broiler flocks was related to low antibody titers against IBDV in the source breeder flocks. Progeny broiler flocks in which there was a high incidence of condemnations for airsacculitis had elevated antibody titers against IBV. A few progeny broiler flocks that experienced high mortality due to gangrenous dermatitis had no antibody titers against IBDV at processing. Antibody titers against RV were very variable and could not be related to any production problems.

Animals↗

Effects of concurrent infections on growth, development, distribution, and infectivity of adult Philophthalmus megalurus and Philophthalmus gralli.

Chickens were infected concurrently with 10 and 20 metacercariae/eye of Philophthalmus megalurus and Philophthalmus gralli. After 14 and 34 days of growth, the adults were removed and worm lengths, return rates, stage of development, and distribution within the host recorded. In a second experiment, chickens infected on day 1 with 10 metacercariae/eye of P. megalurus were concurrently infected with a similar dose of P. gralli on day 14. At day 34, the worms were removed and evaluated for the same parameters as in the first study. The effect of concurrent infections on worm length of P. gralli but not P. megalurus was significant when compared to single species control groups. In all cases recovery rates of P. megalurus in concurrent infections were significantly lower than controls, whereas P. gralli adults were recovered at lower rates only in 20-metacercariae--14-day infections. Maturation of eggs was delayed in both species in concurrent infections at the higher infection levels. Normal distribution was disrupted more for P. gralli at the higher infection levels and longer growth periods. Philophthalmus megalurus adults rarely left their normal habitat in the conjunctival sac. A delayed infective dose of P. gralli affected both species by disrupting normal distribution patterns, delaying egg development, and, in the case of P. megalurus, reducing the recovery rate. The possible role of crowding and antagonistic effects is discussed.

Animals↗

Marek's disease in Japanese quails (Coturnix coturnix japonica): a study of natural cases.

Marek's disease was observed in quails. Gross lesions were confined mostly to the spleen and liver. Microscopic lesions were commonly seen in spleen, proventriculus, liver, and duodenum. Skin, peripheral nerves, and other visceral organs were also involved. Of 123 quails examined, 39 had serum antibodies against Marek's disease. These antibodies were detected from 11 to 17 weeks of age; the highest incidence was recorded at 15 weeks. Feather follicular antigen detected in 30 of the 95 quails was comparable to that of chicken. The disease was experimentally reproduced in susceptible quails. Marek's-disease-tumor-associated surface antigens (MATSA) were demonstrated in the peripheral leukocytes and spleen cells of affected quails. The possible source of infection and its epidemiological importance are discussed.

Age Factors↗

Embryo vaccination with infectious bursal disease virus alone or in combination with Marek's disease vaccine.

Studies with specific-pathogen-free chickens revealed that chicks hatching from eggs inoculated at the 18th day of embryonation with infectious bursal disease (IBD) vaccine viruses of low virulence (isolates TC-IBDV and BVM-IBDV) developed antibody against IBD virus (IBDV) and resisted challenge with virulent IBDV at 3 weeks of age or older. Embryo vaccination did not adversely affect hatchability of chicks or survival of hatched chicks. Chicks embryonally vaccinated with TC-IBDV had transient histologic lesions in the bursa of Fabricius at hatch. Similar but milder lesions were also noted in chickens that received TC-IBDV at hatch. The level of protection following embryo vaccination with TC-IBDV and BVM-IBDV was similar to that following vaccination with the same vaccines at hatch. Vaccine viruses of moderate virulence (isolates BV-IBDV and 2512-IBDV) were not suitable as vaccines in embryos lacking maternal antibody to IBDV, because the vaccinated chicks developed acute IBD after hatch. Isolate 2512-IBDV was not pathogenic for embryos bearing maternal antibody to IBDV. Maternal antibody against IBDV interfered with efficacy of embryo vaccination with BVM-IBDV but not with 2512-IBDV. Embryo vaccination with a mixture of vaccines against IBD and Marek's disease resulted in protection of hatched chicks against challenge with virulent IBDV and Marek's disease virus.

Animals↗

Rapid serological profiling by enzyme-linked immunosorbent assay. IV. Association of infectious bursal disease serology with broiler flock performance.

Breeder and broiler flocks were serologically evaluated using a multiple enzyme-linked immunosorbent assay (M-ELISA). The serologic status of two commercial broiler-breeder flocks and their progeny was monitored, and 840 sera were promptly assessed for antibodies against six infectious agents using the M-ELISA. Breeder flocks were sampled at lay, and broiler chicks were hatched from fertile eggs collected on the scheduled lay date of the breeders. The broiler chicks were placed for growout as eight separate flocks (four from each breeder), and the serologic survey of broilers included sequentially sampling each flock five times between 1 day of age and market. Association of broiler vaccination schedules, mortality, and condemnation data with the temporal serologic data obtained indicated that the earlier appearance of active antibody against infectious bursal disease (IBD) in some unvaccinated flocks was associated with subsequent higher growout mortality and with the poorer overall performance that these flocks experienced. The results of this serologic survey also demonstrated that if a constant, well-timed monitoring program had not been used, major serologic differences between flocks would not have been detected. Serologic profiles of selected broiler flocks by virus-neutralization (VN) tests for infectious bronchitis virus (IBV) and reovirus or by hemagglutination-inhibition (HI) tests for Newcastle disease virus (NDV) compared favorably with the serologic profiles obtained by M-ELISA. Comparison of vaccination histories with serologic results derived from M-ELISA, VN or HI tests indicated that response to vaccination for IBV and NDV at 1 day was either blocked or significantly delayed by moderate levels of maternal antibody and/or were suppressed by an apparent field outbreak of IBD that occurred in all eight broiler flocks.

Animals↗

Cataracts and optic nerve hypoplasia in turkey poults.

Newly hatched commercial turkey poults culled because of grossly visible cataracts were studied. A total of 43 affected and 23 unaffected control poults at various ages were necropsied, and the ocular changes in affected poults were compared with those of aged-matched controls. Affected poults had consistent cataracts coupled with a marked depletion in retinal inner plexiform, ganglion cell, and optic nerve fiber layers, with a resultant reduction in the size of the optic nerves. Lesions were seen in 1-day-old poults. Lens changes included microphakia and lens fiber degeneration throughout the lens, with nuclear liquefaction. The depletion in the numbers of retinal ganglion cells did not appear to progress over several weeks time. The ganglion cell depletion was not uniform within the retina. The cause for these ocular changes is unknown.

Animals↗

Skeletal muscle lesions in turkeys associated with the feeding of monensin.

The feeding of monensin as a coccidiostat in three separate flocks of turkeys was associated with increased mortality, posterior paresis, and a skeletal muscle myopathy. Mortality attributed to the disease was 1.65%, 1.86%, and 4.80% in the three flocks. Samples of monensin-supplemented feed fed to the flocks when showing clinical signs contained 88, 85, and 106 g/ton of complete feed, respectively. Clinically, the turkeys showed posterior paresis, inability to rise, incoordination, reluctance to move, and leg trembling and weakness. Necropsy findings included consistent lesions of pallor within the type I muscles of the legs, wings, and backs. Microscopic lesions included myofiber degeneration and necrosis with massive cellular proliferation interpreted as sarcolemmal nuclei proliferation. Occasional axonal degeneration with loss of axons was present in peripheral nerves embedded in the damaged musculature. In the youngest flock, multifocal areas of acute coagulation necrosis of the myocardium were also present. These outbreaks occurred following intake of monensin in the complete feed at levels considered therapeutic; however, no associated predisposing clinical condition, drug/toxin interaction, or excessive monensin levels in the feed could be demonstrated.

Animals↗

Sub-gastrocnemial ischemic myopathy in broiler breeders.

Five male broiler grandparent males developed lameness early in the breeding period. The lameness was shown to be due to a myopathy affecting muscles deep to the gastrocnemius. It is believed that the condition was precipitated by the vigorous activity associated with mating. Similarities to previously reported pectoral myopathy of chickens and other exercise-induced myopathies were noted.

Animals↗