2. DEFINATION
An infectious, highly contagious lympho-
proliferative viral disease of chicken
Caused by herpes virus
Characterized by
– Mononuclear cellular infiltration (lymphocytes) of
one or more of peripheral nerves & to lesser
extent in skin, muscles, iris & internal organs.
• Frequently there at tumors in the lymph
nodes, skeletal muscle, visceral organs.
3. HISTORY
1907 ----- Firstly reported by Jozsef Marek,
a Hungarian veterinarian
Herpes virus first isolated in 1968
4. ETIOLOGY
Marek’s disease virus
Characteristics:
Double stranded DNA virus
Highly cell-associated
Commonly seen in nucleus
Virus in dander(skin flakes), litter & feathers
remained viable for 4-8 months at room temperature
& for at least 10 years at 4 C
Inactivated by common chemical disinfectants
5. Serotypes: 3 times
Serotype 1: Pathogenic MDV
Serotype 2: Naturally apathogenic MDV
Serotype 3: Apathogenic & antigenically related
herpes virus of turkey (HVT)
HOSTS
Chickens are most important natural host but quails,
turkeys and pheasants are also susceptible
Common in birds of 12-24 weeks old
6. TRANSMISSION
Infectious virus is present in
Oral, nasal and tracheal secretions
Feather follicle epithelium
Horizontal
Airborne route, inhalation of infective particles
Epithelial cells in the keratinizing layer of the feather follicle slough off
& act as a source of contamination to the environment
Darkling beetles & fomites positively carry the virus but insects could
not be associated with transmission
Vertical
Not reported
Transmission due to external egg contamination is unlikely due to poor
virus survival at incubation temperature & humidity
7. FACTORS INFLUENCING
SUSCEPTIBILITY
Virus
Strain
Dosage
Route of exposure
Host
Age: Common in birds 12-24 weeks of age
Sex: Female are more susceptible
Immune status
8. Incubation period :- impossible to determine
in the field
Experimental infection :- can be short as 4
weeks but may be much longer.
Clinical signs and gross lesions appear
between 3rd and 4th week post-inoculation.
9. PATHOGENESIS
Infection occur by inhalation
Virus is taken up by phagocytic cells & replicates in lungs
An acute phase of disease within 2-3 days characterized by cytolytic infection of
the lymphoid system especially bursa & thymus
Viral antigens & immature virus particles are produced in B-cells
T-cells are activated & become susceptible to infection & neoplastic
transformation
Infected birds recover from acute phase of disease and infection become latent after
6-7 days
Virus is spread throughout the body by infected lymphocytes
Persistent cell-associated viraemia occur
Infection spread to various visceral organs (liver, spleen, kidneys, bursa of
Fabricius, gonads especially ovary ) and skin
Infection spreads to feather follicles & infectious virus is formed
Shed into environment in feather debris & dander
Transformed T-cells proliferate in peripheral nerve & other tissues
10. CLINICAL SIGNS
– Asymmetric progressive paresis
– Later complete paralysis of one or more of extremities
– Signs vary from bird to bird as any one or several nerves
may be effected
– Incoordination & lameness
– Bird stretch one leg forward & other backward as a result of
paralysis of leg
– Drooping of limb in case of wing involvement
– Dilation of crop & gasping if vagal paralysis
– If nerves controlling neck muscles are affected, head may be
held low
– Sometimes, blindness with diffuse bluish fading to diffuse
grayish opacity of the iris
– Death often results from starvation and dehydration because
of inability to reach food & water or from trampling by pen
mates
– Mortality prior to use of vaccine was upto 25 % but less than
5 % now
11. GROSS LESIONS
– Localized or diffused enlargement of peripheral nerves (2-3
times)
– Affected nerves show loss of cross striations along with
gray or yellow discoloration
– Celiac, cranial, mesenteric, brachial & sciatic plexuses,
abdominal vagus and intercostal nerve are most commonly
affected
– Lesions are often unilateral, so slight changes may be
detected by comparison with opposite nerve
– Lymphoid tumors can be found in visceral organs. These are
especially found in more acute form of disease & may be
found in absence of gross nerve lesions
– Enlargement of visceral organs with diffuse grayish
discoloration
– Loss of pigmentation in iris & irregularity of the pupil- gray
eye
12. DIAGNOSIS
Symptoms of lameness or paralysis in birds around 3 months of age & presence of
nerve lesions grossly & histopathologically
Presence of tumors in integral organs, in sexually immature birds
Histopathological appearance of lesions in nerves & organs
Virus isolation & identification
Site for sample preparation
Blood & cellular suspension of spleen or tumor tissue
Serology
– AGP test
– Fluorescent antibody
– ELISA
– Virus neutralization
PCR
Demonstration of virus in body by serological tests do not confirm MD because
apathogenic MD viruses & nonclinical infection virulent MD viruses may be present
For a positive diagnosis of MD in a flock one must consider the history of the flock
and the presence of characteristic gross & microscopic lesions in clinically sick or
dead chickens
14. PREVENTION & CONTROL
Vaccination
Commercial vaccines are derived from all 3 serotypes, for use either
alone or in combination
Vaccine is administered at hatching as a single dose
Significant level of protective is achieved within a week & lasts
throughout life.
MDV vaccine protect against the disease but not against infection with
the virus. Upon exposure to MDV, vaccinated or unvaccinated chicken
become carriers of the virus & persistently shed MDV into the
environment, thus making eradication difficult.
Biosecurity
Strict biosecurity practices to limit the extent of early MDV exposure.
