Marek’s Disease:

Syn: Range paralysis, Skin leukosis, Fowl paralysis, Polyneuritis

• It is highly contagious, lympho-proliferative disease of poultry.
• It is characterized by marked enlargement of nerves, liver, spleen and kidneys due to diffuse growth of certain cells (lymphoid cells).

Etiology:

• Alphaherpesvirus of Herpesviridae family
• Virus is enveloped, ds DNA, hexagonal in shape, size; 85-100µm
• 3 serotypes are recognized: serotype 1, 2 and 3
• Serotype-1; disease producing strain, serotype-2: non-disease producing strains, serotype-3: non-disease producing strain related to turkey
• Serotype-1 further classified as:
  • Mildly harmful (MMDV)
  • Harmful (vMDV)
  • Very harmful (vvMDV)
  • Very very harmful (vv+ MDV)
• It is strictly cell-associated virus, except in feather follicles, where cell-free virus is produced.

Epidemiology:

• Disease was first described by Hungarian Veterinarian Jozsef Marek in 1907.
• Outbreaks were reported in 1914 in USA, Netherlands, Great Britian and many other countries.
• It is distributed worldwide and has got economic importance.
• It usually occurs between 2-8 months of age; however, it has also been reported in egg producing birds.
• In 22 outbreaks in Haryana, average mortality was 32.4% and seroprevalence of 78.4%.
• It was a major threat to commercial poultry of Nepal during 1998-2002; 70% mortality and 40% drop in egg production was seen.
• Major outbreaks were reported from Chitwan, Nawalparasi, Kathmandu, Lalitpur, Bhaktapur, Kavre, Rupandehi, Syangja, Kaski and Nuwakot.

Transmission:

• Inhalation of infected material from the environment.
• Virus particle can persist for a considerable period of time in dandruff of feather follicles.
• Virus is also present in oral, nasal and tracheal secretions
• Darkling beetle (Alphitribus diaperinus) can carry the virus for several weeks.
• Virus is not transmitted through egg.

Pathogenesis:

• Chickens of 12-14 weeks of age are most susceptible to Marek’s disease.
• Generally, it doesnot occur in chickens below 6 weeks of age and older birds above 24 weeks of age.
• 3 phases of viral infection are present:
  • Productive-restrictive infection
  • Latent infection
  • Neoplastic transformation

• Virus enters through the respiratory tract, by inhalation.
• Virus grows within certain cells of the lungs.
• It is followed by cytolytic infection of lymphoid system, mostly in Bursa and Thymus. Lymphocytes are destructed mainly in Bursa of Fabricius, thymus and also spleen.
• After 6-7 days, infection becomes latent. Cell-mediated immunity has been shown to be important. Most latently infected cells are CD4+ T-cells, although CD-8+Tcells and B-cells.
• Virus is spread throughout body by infected lymphocytes and present in blood in a cell-associated form.
• Secondary destructive infection occurs in feather follicles 2 weeks after primary infection and cell-free virus is produced and shed into environment through feather debris and dander.
• Proliferation of lymphocytes is final response and progress to tumor formation. T-lymphocytes transform into tumor cells and proliferate in nerves and other tissues and organ.

Clinical Findings:

Disease appear in several forms:

a. Classical form or Neural form:

• Mostly noted at onset of sexual maturity, i.e. about 16 weeks and at time of peak laying, i.e. 30 weeks of age.
• Paralysis of legs, drooping of wings
• Birds are unable to stand.
• Legs and wings are stretched in either direction.
• Split leg stance is usual feature.
• If cervical nerves are affected, there may be torticollis.

b. Acute or Visceral form:

• Depression, droopiness, unthriftiness, dehydration
• Emaciation, anemia
• Mortality rate may go as high as 60%
• Chicks may die on all of sudden without any signs.

c. Transitional Paralytic form:

• It occurs in chicken at age of 5-18 weeks of age.
• Sudden development of paresis
• Paralysis of legs, wings and neck
• Sign usually disappear within 24-28 hours.

d. Ocular form:

• Blindness develops in the birds.
• Grey eye or pearl eye due to cell infiltration.

e. Skin or cutaneous form:

• Distinct white nodules are found on the skin.
• In extreme cases, it looks as brownish scales.

f. Muscular form:

• Muscles look lustreless, whitish grey.
• Tiny streaks to nodular tumors in skin.

Post-Mortem Findings:

• Marked enlargement of one or more nerves. Most commonly sciatic and brachial plexus; 2-3 times normal thickness.
• Striation and glistening appearance of nerve is lost.
• Nerve may appear greyish and sometimes edematous.
• Cauliflower like appearance of ovary due to growth of tumor.
• Lymphomas are sometimes seen in liver, heart, kidney and lungs.
• Marked enlargement of liver and spleen.
• Significant enlargement of proventriculus.
• Heart is pale, have single or nodular tumors in myocardium.
• Atherosclerosis, lipid accumulation in arteries.
• Degeneration of bone marrow.

Diagnosis:

• Based on clinical findings and PM findings
• Isolation of virus in chick embryo inoculation
• Demonstration of tumor-associated surface antigen (MATSA) on cells by immunofluorescence.
• Virus neutralization test (VNT), FAT, IFAT
• Immunoperoxidase test

Differential Diagnosis:

• In lymphoid leukosis, chickens usually have gross tumors in Bursa of Fabricius. Tumors are absent in Marek’s disease.

Treatment:

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

Control Measures:

• Isolation of growing chickens from source of infection.
• Farm should be disinfected with formalin and house should be kept vacant for about a month.
• All in and all out method of rearing should be adopted.
• Insecticides should be used to prevent insect load in the farm since virus may be transmitted through insects.
• Attempt should be made to evolve a MD resistant stock by careful breeding and repeated testing.
• Vaccination of flock; 3 types of vaccines are used; attenuated MDV, avirulent MDV and turkey herpesvirus (HVT). HVT is widely used.
• Living, HVT, FC-126 strain; 0.2 ml SC in back of neck in day-one old chick.