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Marek’s Disease

Chickens are the most important natural host for Marek’s disease virus, but quail can be naturally infected and turkeys can be infected experimentally. Turkeys are commonly infected with turkey herpesvirus, an avirulent strain related to Marek’s disease virus. Other birds and mammals appear to be refractory to the disease or infection.

Marek’s disease is one of the most ubiquitous avian infections; it is identified in chicken flocks worldwide. Every flock, except for those maintained under strict pathogen-free conditions, may be presumed to be infected. Although clinical disease is not always apparent in infected flocks, a subclinical decrease in growth rate and egg production may be economically important.

Etiology:

Three serotypes of the cell-associated herpesvirus are recognized. Serotypes 1 and 2 designate virulent and avirulent chicken isolates, respectively; serotype 3 designates the related avirulent turkey herpesvirus. Serotypes 2 and 3, as well as attenuated serotype 1 viruses, have been used as vaccines. Serotypes are identified by reaction with type-specific monoclonal antibodies or by biological characteristics such as host range, pathogenicity, growth rate, and plaque morphology.

Transmission and Epidemiology:

The disease is highly contagious and readily transmitted among chickens. The virus matures into a fully infective, enveloped form in the epithelium of the feather follicle, from which it is released into the environment. It may survive for months in poultry house litter or dust. Dust or dander from infected chickens is particularly effective in transmission. Infection usually occurs via aerosol exposure through the respiratory tract. Once infected, chickens continue to be carriers for long periods and act as sources of infectious virus. Shedding of infectious virus can be reduced, but not prevented, by prior vaccination. Unlike serotypes 1 and 2, which are highly contagious, turkey herpesvirus is not readily transmissible among chickens (although it is easily transmitted among turkeys, its natural host). Attenuated serotype 1 strains vary greatly in their ability to be transmitted among chickens; the most highly attenuated are not transmitted. Marek’s disease virus is not vertically transmitted.

Pathogenesis:

Three types of interactions between viruses and host cells are recognized in vivo: productive infection, latent infection, and neoplastic transformation. Productive infection may occur transiently in B lymphocytes within a few days after infection with virulent serotype 1 strains and is characterized by antigen production, which leads to cell death. Because few if any virions are produced, this has also been termed a restrictive-productive infection. Productive infection also occurs in the feather follicle epithelium, in which enveloped virions are produced. Latent infection of activated T cells is responsible for the long-term carrier state. No antigens are expressed, but virus can be recovered from such lymphocytes by co-cultivation with susceptible cells in tissue cultures. Some T cells, latently infected with oncogenic serotype 1 strains, undergo neoplastic transformation. These transformed cells, provided they escape the immune system of the host, may multiply to form characteristic lymphoid neoplasms. Cell-mediated and humoral immune responses are both directed against viral antigens, with cell-mediated immunity probably being the most important.

Clinical Findings and Lesions:

Typically, affected birds show only depression before death, but a transient paralysis syndrome has been associated with Marek’s disease; chickens become ataxic for periods of several days and then recover. This syndrome is rare in immunized birds.

Enlarged nerves are one of the most consistent gross lesions in affected birds. Various peripheral nerves, but particularly the vagus, brachial, and sciatic, become enlarged and lose their striations. Diffuse or nodular lymphoid tumors may be seen in various organs, particularly the liver, spleen, gonads, heart, lung, kidney, muscle, and proventriculus. Enlarged feather follicles (commonly termed skin leukosis) may be noted in broilers after defeathering during processing and are a cause for condemnation. The bursa is only rarely tumorous and more frequently is atrophic. Histologically, the lesions consist of a mixed population of small, medium, and large lymphoid cells plus plasma cells and large anaplastic lymphoblasts. These cell populations undoubtedly include both tumor cells and reactive inflammatory cells. When the bursa is involved, the tumor cells typically appear in interfollicular areas.

Diagnosis:

Usually, diagnosis is based on enlarged nerves and lymphoid tumors in various viscera. The absence of bursal tumors helps distinguish this disease from lymphoid leukosis (see Lymphoid Leukosis); also, Marek’s disease occurs at any age >3 wk. Reticuloendotheliosis, although rare, can easily be confused with Marek’s disease because both diseases feature enlarged nerves and T-cell lymphomas in visceral organs. A diagnosis based on typical gross lesions may be confirmed histologically or, better, by demonstration of predominant T-cell populations and Marek’s viral DNA in lymphomas by histochemistry and polymerase chain reaction assays, respectively. Furthermore, Marek’s disease lymphomas will usually lack evidence of clonally integrated avian retroviruses or alteration of the cellular oncogene c-myc.

Control:

Vaccination is the principal method of control. The efficacy of vaccines can be improved, however, by strict sanitation to reduce or delay exposure and by breeding for genetic resistance. Probably the most widely used vaccine consists of turkey herpesvirus. Bivalent vaccines consisting of turkey herpesvirus and either the SB-1 or 301B/1 strains of serotype 2 Marek’s disease virus have been used to provide additional protection against challenge with virulent serotype 1 isolates. Several attenuated serotype 1 Marek’s disease vaccines are also available; of these, the CV1988/Rispens and R2/23 strains appear particularly effective. A synergistic effect on protection, noted mainly between serotype 2 and 3 strains, has prompted the empirical use of other virus mixtures. Because all vaccines are administered at hatching and require 1-2 wk to produce an effective immunity, exposure of chickens to virus should be minimized during the first few days after hatching. Cell-associated vaccines are generally more effective than cell-free vaccines because they are neutralized less by maternal antibodies. Under typical conditions, vaccine efficacy is usually >90%. Since the advent of vaccination, losses from Marek’s disease have been reduced dramatically in broiler and layer flocks. However, disease may become a serious problem in individual flocks or in selected geographic areas, eg, the Delmarva broiler industry. Of the many causes proposed for these excessive losses, early exposure to very virulent virus strains appears to be among the most important.

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