Marek’s Disease - Selina Blogs

Marek’s Disease (MD) is a lympho-proliferative, highly contagious disease of poultry and caused by a highly cell associated Herpes B virus.

Distribution

The disease was first described by Hungarian veterinarian Jozsef Marek in 1907. Outbreak were reported in USA in 1914 and subsequent observations came from Netherlands, Great Britain and many other countries. In 1950s, he lymphomatous form of the disease became more evident in USA, to which the terms ‘Visceral lymphomatosis” and “acute leukosis” were applied. A new virulent form of the disease appeared in 1960’s which spread rapidly and caused high mortality and morbidity in young chickens in USA and in many other countries. In 1970, the live virus vaccine against Marek’s disease became available in USA, that greatly reduced the economic loss. In certain areas of USA, such as Delmarva, there were appearance of variant strains of Marek’s disease virus (MDV). Similar variant viruses appeared in Europe.

Paralysis in poultry was reported from India in 1933, but these cases were labelled as avian leukosis complex. Prevalence of MD was established in this country in 1969 by Paliwal. In Haryana, 85 outbreaks were recorded during 1970 to 1978. In 22 outbreaks of MD in Haryana, the average mortality and seroprevalence was 32.4% and 78.4% respectively. Mild infection of this disease with respiratory viruses have been recorded in this subcontinent. The disease is now prevalent in almost, all the states of the country as sporadic outbreak.

Aetiology

MD is caused by a herpes virus which is hexagonal in shape having double stranded DNA. Size of the virus as naked is 85 to 100 micrometre and as enveloped is 13 to 17 micrometre. Three serotypes are recognised, serotypes 1 and 2 designate virulent and avirulent chicken isolates respectively, serotype 3 designates the related avirulent turkey herpesvirus. Serotypes 2 and 3 and attenuated serotype-1 virus are used for vaccine preparation. Serotype 1 strain vary markedly in pathogenicity and have been subdivided into mildly virulent and very virulent pathotypes.

Virus remains stable for about 24 hours at 30° C. Virus is destroyed by formalin and ether. Serotype-1 viruses are isolated by co-cultivation of lymphocytes with chicken kidney cells or duck embryo fibroblasts, while chick embryo fibroblasts are preferred for isolation of serotypes 2 and 3.

Susceptible Hosts

Chickens are the most important natural host. Besides quail has been found to suffer from the disease, mostly ocular in type. Experimental production of the disease in Japanese quail have been reported. Turkey may also suffer. Wild birds like jungle fowl, great horn owls, pheasants, budgerigars suffer from such disease. Disease has also been recorded in pigeons, geese, canaries and swans.

Mode of Transmission

Infection is transmitted through inhalation of infected material from the environment. Virus particle can persist for a considerable period of time in the dandruff of feather follicles, which are released in environment. Virus is also present in oral, nasal and tracheal secretions. Poultry litter may remain infected up to several weeks and thus can remain as a source of transmission through inhalation. Virus may enter from infected droppings or from infected bird. The darkling beetle can carry the virus for several weeks. Stress has been the main environmental factor. The disease is not transmitted through eggs.

Pathogenesis

Chickens of 12 to 24 weeks of age are mostly susceptible to Marek’s disease and generally it does not occur in chickens below 6 weeks of age and older birds above 24 weeks of age. Purchase (1985) observed that, clinical signs in egg type flock are often not seen until 16-20 weeks and rarely as late as 24-30 weeks.

Three phases of viral infection have observed; productive – restrictive infection, latent infection and neoplastic transformation. Virus initially replicate in lungs followed by cytolytic infection of lymphoid system mostly in bursa and thymus. Productive-restrictive infection occurs in lymphocytes mainly of BZ-cell origin and characterized by antigen production leading to cell death. Long term carrier state of he disease occurs due to latent infection of T-cells and sometimes these cells undergo neoplastic transformation. These transformed cells multiply in peripheral nerves, other tissues and organs to form lymphoid neoplasms.

Though transformed T-cell contain the viral genome, the synthesis of viral antigen and particles is restricted. A new antigen, MATSA (Marek’s disease associated tumour specific antigen) appears in the transformed T-cells. Immune responses are of both cell-mediated and humoral type, but cell-mediated immunity against viral antigen is most important. Gupta (1978) was of the opinion that thymus derived lymphocyte may play an important role in development of immunity against HVT vaccination.

Clinical Findings

The disease appears in several forms:

(a) Classical form or Neural form: Marek in 1907 reported this form of the disease from Hungary. Birds of 16 to 20 weeks of age ususally suffer. Mortality rate is comparatively low and mostly noted at onset of sexual maturity i.e. about 16 weeks and at the time of peak laying i.e. about 30 weeks of age. Signs are mostly concerned with the affections of the nerves. There is paralysis of legs, dropping of the wings. The nerves like sciatic of leg, branches of wings, coeliac of intestine and vagus running through neck are affected. Birds are unable to stand. They remain in recumbent position. Legs and wings may be stretched in either direction. The “Split leg” stance is the usual feature. In many of the infected birds the vents remain soiled with green diarrhoea. The mortality is high during environmental or physiological stress. In chronic condition one or two birds may die every day over a considerable period of time.

(b) Acute or Visceral form: In acute form, the internal organs of the birds are affected. Birds will show depression, droopiness, unthriftyness, dehydration, emaciation and anaemia. Generally 3 to 4 weeks old birds suffer from this form. Mortality rate may go as high as 60%. Chicks may die all on a sudden without showing any clinical manifestation. Ovaries of the affected layers and pullets look like cauliflower and mulberry fruit respectively. Regressed bursa has been considered to be a post mortem finding in some birds.

(c) Transitional paralytic form: This form occurs in chicken at the age of 5 to 18 weeks of age and characterized by sudden development of paresis or paralysis of the legs, wings and neck. The signs usually disappear within 24-48 hours.

(d) Ocular form: Blindness develops in the birds due to mononuclear cell infiltration in the iris causing grey eye or pearl eye.

(e) Skin or cutaneous form: Distinct white nodules are found on the skin and in extreme cases it look as brownish scales. Lesions may coalesce.

(f) Muscular form: Both superficial and deep muscles like pectoral muscles are affected. Muscles look lustreless, whitish grey and there are tiny whitish streaks to nodular tumours.

Lesions

Affected nerve is thickened to more than 2-3 times than normal. Striation and glistering appearance of nerve is lost and looks oedematous. Celiac, cranial, mesenteric, brachial and sciatic plexus and greater splanchnic nerves are mostly affected.

Diagnosis

It is based on following consideration:

Clinical signs – Paralytic syndrome.
Gross pathologic changes – Generalised neoplastic growth. Bursa atrophic, brachial sciatic and other visceral nerves are greyish, thickened, oedematous with loss of striations, skin appears reddish, nodules noticed in pectoral, brachial and feather tract.
Histopathological changes: Proliferation of lymphoblastic cells which are pleomorphic in nature. Nucleus is small and impact with no prominent nucleolus. Mitotic figure is absent.

Laboratory tests

Demonstration of tumour associated surface antigen on some individual cells by immunofluorescence.
Isolation of virus by chick embryo inoculation (Yolk sac route).
Transmission test in young chicks.
Intradermal test.
Agar gel precipitation test with feather follicle antigen.
Virus neutralization test.
Fluorescent antibody test on sections of feather follicles.
Indirect fluorescent antibody test.
Haemagglutination test with inactivated tannic acid treated erythrocytes.
Modified direct complement fixation test.
Indirect Haemagglutination test.
Immunoperoxidase test.

Treatment

There is no effective method of available treatment. Symptomatic treatment for paralysis may be adopted.

Control

Management and hygeinic measures are the important ways of control of this disease.

Attempt should be made to rear the chicks in strictly isolated manner.
Sophisticated method of rearing by using filtered air positive pressure as used in other countries may be made, if possible.
The farm should be disinfected with formalin and the house should be kept vacant for about a month following outbreak.
All in and all out method of rearing should be followed.
Insecticides should be used to prevent insect load in the farm since virus may be transmitted through insects and insects may act as reservoirs.
Attempt should be made to evolve a MD resistant stock by careful breeding and repeated testing. Genetic resistance stock should be made by making markers for resistance such as B21 blood group allele.

Vaccine: Three types of Marek’s disease vaccines are commonly n use e.g. attenuated MDV, avirulent MDV and turkey herpes virus (HVT). Out of the three, HVT vaccine is widely used.

Commercial vaccines:

(a) Marek’s disease vaccine (cell associated)

Living, HVT, FC-126. It contains FC-126 strain of turkey herpes virus grown on cell culture derived from SPF eggs.

Used in grand parents and parents and in pure line breeder flocks.

Dose: inject 0.2 ml subcutaneously in the back of neck with 3/4 or 1/2 needle in 20-24 gauge.

(b) Marek’s disease vaccine (cell associated)

Living SB-1 strains.

SB-1 strain of Marek’s disease of serotype-2 grown on cell cultures derived from SPF eggs.

Used to prevent Marek’s disease. Used in parents and grand parent and in pure line breeder flock especially where there are high level of Marek’s disease maternal antibodies are present in day old chicks.

Used against late Marek’s disease and very virulent Marek’s disease.

Dose: inject 0.2ml subcutaneously in the back of the neck.

(c) Marek’s disease vaccine (Freeze dried)

FC-126 strain of turkey herpes virus grown on cell cuture derived fro SPF eggs and then released from cell by cell rupture (cell free virus) and freeze dried.

Prevents from Marek’s disease. Day old healthy flocks to be vaccinated.