Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide


Marek's disease



Marek's disease


  • Last modified
  • 20 November 2019
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • Marek's disease
  • Overview
  • Marek’s disease (MD), named after the Hungarian pathologist Jozsef Marek, is a lymphoproliferative and neuropathic disease of domestic chickens, and less commonly, turkeys and quails, caused by a highly contagious, ce...

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Fowl with Marek's disease showing signs of paralysis.
CaptionFowl with Marek's disease showing signs of paralysis.
CopyrightK. Venugopal
Fowl with Marek's disease showing signs of paralysis.
SymptomsFowl with Marek's disease showing signs of paralysis.K. Venugopal
Characteristic enlarged sciatic plexus in Marek's disease.
TitlePathology; symptoms
CaptionCharacteristic enlarged sciatic plexus in Marek's disease.
CopyrightK. Venugopal
Characteristic enlarged sciatic plexus in Marek's disease.
Pathology; symptomsCharacteristic enlarged sciatic plexus in Marek's disease. K. Venugopal
Nerve showing mononuclear infiltration in Marek's Disease.
TitleMononuclear infiltration
CaptionNerve showing mononuclear infiltration in Marek's Disease.
CopyrightK. Venugopal
Nerve showing mononuclear infiltration in Marek's Disease.
Mononuclear infiltrationNerve showing mononuclear infiltration in Marek's Disease. K. Venugopal
Marek's disease affected visceral organs, including ovarium.|Marek's disease-affected visceral organs, including ovarium.
CaptionMarek's disease affected visceral organs, including ovarium.|Marek's disease-affected visceral organs, including ovarium.
CopyrightSri Poernomo
Marek's disease affected visceral organs, including ovarium.|Marek's disease-affected visceral organs, including ovarium.
PathologyMarek's disease affected visceral organs, including ovarium.|Marek's disease-affected visceral organs, including ovarium.Sri Poernomo
Feather follicle epithelium showing Marek's Disease viral genome by in situ hybridisation.
TitleViral genome
CaptionFeather follicle epithelium showing Marek's Disease viral genome by in situ hybridisation.
CopyrightK. Venugopal
Feather follicle epithelium showing Marek's Disease viral genome by in situ hybridisation.
Viral genomeFeather follicle epithelium showing Marek's Disease viral genome by in situ hybridisation. K. Venugopal


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Preferred Scientific Name

  • Marek's disease

International Common Names

  • English: fowl paralysis; gray-eye; grey-eye; Mareks disease; marek's disease, herpesvirus lymphoma, in chickens; marek's disease, herpesvirus lymphoma, in chickens and turkeys; MDV infection; ocular leukosis; paralysis, fowl; range paralysis; skin leukosis; visceral leukosis

English acronym

  • MD


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Marek’s disease (MD), named after the Hungarian pathologist Jozsef Marek, is a lymphoproliferative and neuropathic disease of domestic chickens, and less commonly, turkeys and quails, caused by a highly contagious, cell-associated herpesvirus. MD virus (MDV) is one of the most oncogenic herpesviruses known and remains the only neoplastic disease for which an effective vaccine has been widely used successfully (Payne and Venugopal, 2000). A summary on the immune response to Marek's disease virus infection was compiled by Schat and Markowski-Grimsrud, 2001.

Host Animals

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Animal nameContextLife stageSystem
CoturnixDomesticated hostPoultry: Not known
Coturnix japonica (Japanese quail)Domesticated hostPoultry: Not known
GallusDomesticated hostPoultry: Day-old chick|Poultry/Young poultry|Poultry/Mature female|Poultry/Cockerel|Poultry/Mature male
Gallus gallus domesticus (chickens)Domesticated hostPoultry: Day-old chick|Poultry/Young poultry|Poultry/Mature female|Poultry/Cockerel|Poultry/Mature male
MeleagrisDomesticated hostPoultry: Young poultry|Poultry/Mature female|Poultry/Mature male
Meleagris gallopavo (turkey)Domesticated hostPoultry: Young poultry|Poultry/Mature female|Poultry/Mature male

Hosts/Species Affected

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Infection mainly occurs in domestic chickens, although the disease can occur in other species of poultry such as turkeys and quails. The rate of the spread of MD within a flock can vary greatly and depends on, among several factors, the level of initial exposure and the concentration of susceptible birds. A number of stress factors, including those from handling, change of housing, and vaccination can increase disease incidence. The existence of genetic resistance against MD among chickens has long been recognized and the genetic constitution of the flock influences the outcome of MDV infection. There is also a sex influence on the disease, as females are usually more susceptible to the development of tumours.

Systems Affected

Top of page blood and circulatory system diseases of poultry
digestive diseases of poultry
multisystemic diseases of poultry
nervous system diseases of poultry
skin and ocular diseases of poultry


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MDV infection mainly occurs in domestic chickens and is ubiquitous among poultry populations throughout the world. Losses from the disease are especially high in areas where broiler production is very intensive.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Last updated: 10 Jan 2020
Continent/Country/Region Distribution Last Reported Origin First Reported Invasive Reference Notes


AlgeriaAbsent, No presence record(s)OIE (2009)
BotswanaAbsent, No presence record(s)OIE (2009)
Cabo VerdePresentOIE Handistatus (2005)
CameroonPresentOIE Handistatus (2005)
Central African RepublicAbsent, No presence record(s)OIE Handistatus (2005)
Côte d'IvoirePresentOIE Handistatus (2005)
DjiboutiAbsent, No presence record(s)OIE (2009)
EgyptAbsent, No presence record(s)OIE (2009)
EswatiniAbsent, No presence record(s)OIE (2009)
GabonAbsent, No presence record(s)OIE (2009)
GhanaAbsent, No presence record(s)OIE (2009)
KenyaAbsent, No presence record(s)OIE (2009)
LesothoAbsent, No presence record(s)OIE (2009)
LibyaPresentOIE Handistatus (2005)
MadagascarPresentOIE (2009)
MalawiPresentOIE (2009)
MauritiusAbsent, No presence record(s)OIE (2009)
MozambiqueAbsent, No presence record(s)OIE (2009)
NamibiaPresentOIE (2009)
NigeriaPresentOIE (2009)
RwandaPresentOIE (2009)
São Tomé and PríncipePresent, Serological evidence and/or isolation of the agentOIE Handistatus (2005)
SeychellesPresentOIE Handistatus (2005)
South AfricaAbsent, No presence record(s)OIE (2009)
SudanAbsent, No presence record(s)OIE (2009)
TanzaniaAbsent, No presence record(s)OIE (2009)
TunisiaPresentOIE (2009)
ZimbabwePresentOIE (2009)


ArmeniaAbsent, No presence record(s)OIE (2009)
AzerbaijanAbsent, No presence record(s)OIE (2009)
BahrainAbsent, No presence record(s)OIE (2009)
BangladeshPresentOIE (2009)
BhutanAbsent, No presence record(s)OIE (2009)
ChinaPresent, LocalizedOIE (2009)
Hong KongAbsent, No presence record(s)OIE (2009)
IndiaAbsent, No presence record(s)OIE (2009)
IranAbsent, No presence record(s)OIE (2009)
IraqPresentOIE (2009)
IsraelAbsent, No presence record(s)OIE (2009)
JapanPresentOIE (2009)
JordanPresentOIE (2009)
KazakhstanAbsent, No presence record(s)OIE (2009)
KuwaitAbsent, No presence record(s)OIE (2009)
KyrgyzstanAbsent, No presence record(s)OIE (2009)
LaosAbsent, No presence record(s)OIE (2009)
LebanonAbsent, Unconfirmed presence record(s)OIE (2009)
MalaysiaPresentOIE (2009)
-Peninsular MalaysiaPresent, Serological evidence and/or isolation of the agentOIE Handistatus (2005)
-SarawakPresentOIE Handistatus (2005)
MyanmarPresentOIE (2009)
NepalPresentOIE (2009)
OmanPresentOIE (2009)
PakistanPresentOIE (2009)
SingaporeAbsent, No presence record(s)OIE (2009)
South KoreaPresentOIE (2009)
Sri LankaPresentOIE (2009)
TaiwanPresentOIE Handistatus (2005)
TajikistanAbsent, No presence record(s)OIE (2009)
ThailandPresentOIE (2009)


AndorraAbsent, No presence record(s)OIE Handistatus (2005)
BelarusAbsent, No presence record(s)OIE (2009)
BelgiumAbsent, No presence record(s)OIE (2009)
Bosnia and HerzegovinaAbsent, No presence record(s)OIE Handistatus (2005)
BulgariaAbsent, No presence record(s)OIE (2009)
CroatiaAbsent, No presence record(s)OIE (2009)
CyprusAbsent, No presence record(s)OIE (2009)
CzechiaAbsent, No presence record(s)OIE (2009)
DenmarkPresentOIE (2009)
EstoniaAbsent, No presence record(s)OIE (2009)
FinlandAbsent, No presence record(s)OIE (2009)
GermanyPresentOIE (2009)
GreeceAbsent, No presence record(s)OIE (2009)
HungaryAbsent, No presence record(s)OIE (2009)
IcelandAbsent, No presence record(s)OIE (2009)
JerseyAbsent, No presence record(s)OIE Handistatus (2005)
LatviaAbsent, No presence record(s)OIE (2009)
LiechtensteinAbsent, No presence record(s)OIE (2009)
LithuaniaAbsent, No presence record(s)OIE (2009)
LuxembourgAbsent, No presence record(s)OIE (2009)
MaltaAbsent, No presence record(s)OIE (2009)
MontenegroAbsent, No presence record(s)OIE (2009)
NetherlandsPresentOIE (2009)
North MacedoniaAbsent, Unconfirmed presence record(s)OIE (2009)
NorwayAbsent, No presence record(s)OIE (2009)
PolandPresentOIE (2009)
PortugalAbsent, No presence record(s)OIE (2009)
RomaniaAbsent, No presence record(s)OIE (2009)
RussiaPresentOIE (2009)
SerbiaAbsent, No presence record(s)OIE (2009)
Serbia and MontenegroAbsent, No presence record(s)OIE Handistatus (2005)
SlovakiaAbsent, No presence record(s)OIE (2009)
SloveniaAbsent, No presence record(s)OIE (2009)
SpainPresent, LocalizedOIE (2009)
SwedenAbsent, No presence record(s)OIE (2009)
SwitzerlandAbsent, No presence record(s)OIE (2009)
UkraineAbsent, No presence record(s)OIE (2009)
United KingdomPresentOIE (2009)
-Northern IrelandPresentOIE Handistatus (2005)

North America

BarbadosPresentOIE Handistatus (2005)
BelizeAbsent, No presence record(s)OIE (2009)
BermudaAbsent, No presence record(s)OIE Handistatus (2005)
British Virgin IslandsAbsent, No presence record(s)OIE Handistatus (2005)
CanadaPresentOIE (2009)
Cayman IslandsAbsent, No presence record(s)OIE Handistatus (2005)
Costa RicaPresentOIE (2009)
CubaPresentOIE (2009)
CuraçaoAbsent, No presence record(s)OIE Handistatus (2005)
DominicaAbsent, No presence record(s)OIE Handistatus (2005)
Dominican RepublicPresentOIE (2009)
GreenlandAbsent, No presence record(s)OIE (2009)
GuatemalaAbsent, No presence record(s)OIE (2009)
HondurasAbsent, No presence record(s)OIE (2009)
JamaicaAbsent, No presence record(s)OIE (2009)
MartiniquePresentOIE (2009)
MexicoPresentOIE (2009)
Saint Vincent and the GrenadinesAbsent, No presence record(s)OIE Handistatus (2005)
Trinidad and TobagoPresentOIE Handistatus (2005)
United StatesPresentOIE (2009)


AustraliaPresentOIE (2009)
French PolynesiaPresentOIE (2009)
New CaledoniaPresentOIE (2009)
New ZealandPresentOIE (2009)
SamoaAbsent, No presence record(s)OIE Handistatus (2005)
VanuatuAbsent, No presence record(s)OIE Handistatus (2005)

South America

ArgentinaPresentOIE (2009)
BoliviaAbsent, No presence record(s)OIE (2009)
BrazilPresentOIE (2009)
ChilePresentOIE (2009)
ColombiaAbsent, No presence record(s)OIE (2009)
EcuadorAbsent, No presence record(s)OIE (2009)
Falkland IslandsAbsent, No presence record(s)OIE Handistatus (2005)
French GuianaAbsent, No presence record(s)OIE (2009)
GuyanaAbsent, No presence record(s)OIE Handistatus (2005)
ParaguayPresentOIE Handistatus (2005)
PeruAbsent, Unconfirmed presence record(s)OIE (2009)
UruguayPresentOIE (2009)
VenezuelaAbsent, No presence record(s)OIE (2009)


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Both gross pathological lesions and microscopic lesions characteristic of MD have been recognized in infected birds. In general, while gross appearance can provide indications of the nature of the disease, identification of microscopical lesions can provide a more accurate diagnosis. The most useful set of tissues for examination of microscopic lesions of MD are the liver, spleen, bursa of Fabricius, thymus, heart, proventriculus, kidney, gonads, kidney, nerves and skin, as well as tissues with gross tumours.

Classical form

The characteristic pathological lesion is the enlargement of one or more of the peripheral nerves. The most commonly affected nerves that are easily seen on post-mortem examination are the brachial and sciatic plexus and nerve trunks, celiac plexus, abdominal vagus and intercostal nerves. The affected nerves are grossly enlarged, and often two or three times their normal thickness. The normal cross-striated and glistening appearance of the nerves is lost; they have a greyish or yellowish appearance and are oedematous. Lymphomas are sometimes present in this form of the disease, most frequently as small, soft grey tumours in the ovary, kidney, heart, liver and other tissues.

Acute form

The typical lesion in this form of the disease is the widespread, diffuse lymphomatous involvement of visceral organs such as the liver, spleen, ovary, kidney, heart and proventriculus. Sometimes lymphomas are also seen in the skin around the feather follicles and in the skeletal muscles. Affected birds may also show involvement of the peripheral nerves similar to that seen in the classical form. The liver enlargement in younger birds is usually moderate compared to that in adult birds, where the liver is greatly enlarged and the gross appearance is very similar to that seen in lymphoid leukosis. Nerve lesions are less frequent in adult birds.

Nerve damage

The peripheral nerves in both forms of the disease are affected by proliferative, inflammatory or minor infiltrative changes that are termed A-, B- and C-type lesions, respectively. The A-type lesion consists of infiltration by proliferating lymphoblasts and large, medium and small lymphocytes, and macrophages, and appears to be neoplastic in nature. Nerves with B-type lesions show oedema and infiltration by small lymphocytes and plasma cells with Schwann cell proliferation, and the lesion appears to be inflammatory. The C-type lesion consists of mild scattering of small lymphocytes, often seen in birds that show no gross lesions or clinical signs, and is thought to be a regressive inflammatory lesion. Demyelination that is frequently seen in nerves showing A- and B-type lesions is thought to be mainly responsible for the paralytic symptoms.


Lymphomas seen in the visceral organs are similar cytologically to the lymphoproliferations in the nerve A-type lesions. The lymphoid cells are usually of the mixed type, with a preponderance of small and medium lymphocytes, but sometimes, especially in adult birds, large lymphocytes and lymphoblasts may predominate.


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Diagnostic procedures for MD include both pathological and virological methods. While pathological diagnosis based on the symptoms and lesions described in the Pathology section would identify the nature of the tumours, virological diagnosis is essential for establishment of the identity of the causative viruses present in the flock.

Laboratory Diagnosis

Isolation of MDV

MDV infection in a flock can be detected by isolating the virus from the infected tissues. Materials commonly used for the isolation of the virus are buffy coat cells from heparinised blood samples, or suspensions of lymphoma and spleen cells. As MDV is highly cell-associated, it is essential that the suspensions contain viable cells. These cell suspensions are inoculated into monolayer cultures of chick kidney cells and duck or chicken embryo fibroblasts. Less commonly, feather tips, from which cell-free MDV can be extracted, are also used for virus isolation. MDV replication in the culture can be seen as plaques that appear in 3-4 days.

Characterization of MDV serotypes

The MDV serotypes isolated in culture can be differentiated on the basis of the time of appearance, rate of development and morphology of the plaques. HVT plaques usually appear earlier and are larger than serotype 1 plaques, whereas serotype 2 plaques appear later, and are smaller than the serotype 1 plaques. The serotype specificity of the plaques can also be confirmed by using specific antibodies in immunological tests. Increasingly the polymerase chain reaction is used to detect the presence of MDV (Baigent et al., 2007; Cortes et al., 2011), and to differentiate serotypes directly (Barfoed et al., 2010), in addition to gene sequencing.

Detection of virus infection in tissues

The viral antigens can be detected in the infected tissues by immunofluorescence and immunohistochemistry using polyclonal and monoclonal antibodies. In situ hybridisation using MDV-specific nucleic acid probes can also be used for detecting virus in various tissues including the feather follicle epithelium.

Serological tests

The presence of antibodies to MDV in birds from about 4 weeks of age is an indication of infection. Antibodies detected in birds before that age are likely to represent maternally derived antibodies and are not considered evidence of active infection. Although there are no prescribed serological tests for detection of MDV-specific antibodies, the agar gel immunodiffusion (AGID) test is employed most commonly for this purpose. The antigen used in the test is either disrupted MDV-infected tissue culture cells, extract of the feather tips or skin containing feather tracts from infected chickens. A modification of the AGID test to detect MDV antigen in the feather tips by reactivity with MDV hyperimmune serum is also used. Other serological tests such as the indirect immunofluorescence test, ELISA and virus neutralisation have been described, but are used mostly for research purposes rather than for routine diagnosis.

List of Symptoms/Signs

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SignLife StagesType
General Signs / Abnormal proprioceptive positioning, knuckling Sign
General Signs / Ataxia, incoordination, staggering, falling Sign
General Signs / Generalized weakness, paresis, paralysis Sign
General Signs / Increased mortality in flocks of birds Sign
General Signs / Neck weakness, paresis, paralysis, limp, ventroflexion Sign
General Signs / Pale mucous membranes or skin, anemia Sign
General Signs / Swelling skin or subcutaneous, mass, lump, nodule Sign
General Signs / Weakness, paresis, paralysis of the legs, limbs in birds Sign
General Signs / Weakness, paresis, paralysis, drooping, of the wings Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Sign
Ophthalmology Signs / Blindness Sign
Ophthalmology Signs / Cataract, lens opacity Sign
Ophthalmology Signs / Corneal edema, opacity Sign
Ophthalmology Signs / Hypopyon, lipid, or fibrin, flare, of anterior chamber Sign
Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Sign
Skin / Integumentary Signs / Ruffled, ruffling of the feathers Sign

Disease Course

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Although clinical disease associated with MD can occur in chickens from 4 weeks of age, the signs are most frequently seen between 12 and 24 weeks of age and sometimes even later. The incubation period is also highly variable, between a few days in disease caused by very virulent pathotypes, to several weeks in disease induced by classical strains. Generally, four different clinical forms of the disease are recognised in MDV-infected flocks.

Classical or neural MD

The classical or neural form involves a large proportion of the birds showing signs of paresis or paralysis involving the legs and wings. These cases, also referred to as ‘fowl paralysis’ or ‘range paralysis’, are usually seen in birds of 2-12 months of age.

The acute form, a more virulent form of the disease where lymphomatous lesions of various organs develop and high mortalities in the affected flocks occur. Birds as young as 6-weeks-old can be affected, with losses commonly occurring between 3 and 6 months. Involvement of the eyes and nerves as well as lymphomatous lesion of the skin may also be evident in some cases. Visceral and skin lesions due to MD are important causes of carcass condemnation in slaughterhouses.

Transient paralysis

Transient paralysis is an uncommon condition in MDV-infected flocks usually occurring between 5 and 18 weeks of age. It is an encephalitic expression of infection characterized by a sudden onset of paralytic symptoms that often only last for 24-48 hours, although in some instances death can occur.

Acute mortality syndrome

Acute mortality syndromeis a form of the disease observed more recently, where the affected birds die with an early acute cytolytic disease well before the onset of lymphomas. The affected birds show characteristic atrophy of the bursa of Fabricius and thymus. This form of the disease is thought to be due to infections with highly virulent pathotypes of the virus.


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In commercial chicken houses, where infection is widespread, virtually all birds become infected within the first few weeks of life, although on occasions this may be delayed. Because of the prevalence of serotype 1 viruses of varying pathogenicity and non-pathogenic serotype 2 in the poultry house environment, birds can be infected with more than one MDV strain. There is some evidence to suggest that with increasing age of the birds, the frequency of isolation of non-pathogenic viruses becomes higher.

The transmission of MDV occurs by direct contact, or indirect contact by the airborne route. The epithelial cells in the keratinizing layer of the feather follicle hold fully infectious virus particles, and serve as source of contamination to the environment. The shedding of the infective material occurs from about 10 days after infection, before the appearance of the clinical disease, and can continue throughout the life of the bird. The virus associated with feather debris and dander in the contaminated poultry house dust can remain infectious for several months. Although the inhalation of infected poultry house dust remains the commonest route of disease spread, other less common mechanisms of indirect transmission, such as those involving darkling beetles (Alphitobius diaperinus), could also play minor roles in transmission. There is no evidence for the vertical transmission of MDV through the egg.

Impact: Economic

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Before the introduction of vaccines in the early 1970s, MD was a major global disease. Although vaccination has reduced losses, the disease remains one of significant economic importance, mainly due to the periodic appearance of new strains of MDV against which existing vaccines provide only suboptimal protection. Estimates from 1984 showed that total worldwide economic losses from MD, including the costs of vaccination, were US $943 million (Purchase, 1985).

Zoonoses and Food Safety

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The high prevalence of MDV and the widespread use of live MD vaccines have caused concerns in some quarters that exposure to MDV from the environment or from consumption of poultry meat could be a cause of cancer in man. However, a large body of evidence in both avian and human virology, serology, pathology and epidemiology strongly supported the conclusion that no aetiologic relationship existed between avian herpesviruses and human cancer (Purchase and Witter, 1986). There has been speculation that MDV infection might be associated with multiple sclerosis (MS), mainly based on serological findings. However, in detailed studies using sensitive methods such as PCR, no MDV-related sequences could be detected in the DNA of patients, ruling out the involvement of MDV in MS (Hennig et al., 1998).

Prevention and Control

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Immunization and Vaccines

Vaccination represents, currently and at least for the near future, the main strategy for the prevention and control of MD. However, other approaches such as increasing the genetic resistance of birds and improved hygiene and biosecurity should form valuable adjuncts for control programmes.

Live virus vaccines, used since 1970, are still the cornerstones of disease control programmes. These are usually administered to day-old chicks at hatching to provide protection against the natural challenge the chicks are exposed to early in life from the infected poultry house environment. With the introduction of in ovo immunisation methods, an increasing number of birds are vaccinated by this route. MD vaccines are highly effective, often achieving over 90% protection under commercial conditions.

HVT continues to be widely used as a monovalent product in many countries, because of its low cost, availability as cell-free and cell-associated forms, and effectiveness when the field exposure is not severe. HVT (serotype 3) and SB-1 (serotype 2) strains comprised the first commercial bivalent vaccine based on the protective synergism demonstrated between serotypes 2 and 3 viruses. CVI988 strain Rispens vaccines and their modified versions (serotype 1) are widely used and appear to be effective against some of the vv+MDV pathotypes. HVT is used as the basis for vectored vaccines by at least two vaccine companies e.g. expressing protective antigens of Newcastle disease virus and infectious laryngotracheitis virus.

Although MD vaccines have been largely successful in controlling major losses from the disease, there have always been threats of vaccine failures. Challenge with virulent viruses before the development of vaccine-induced immunity, interference by the maternal antibodies, improper use of the vaccine, and the use of a non-protective vaccine strain are some of the causes for vaccine failures. Vaccinating alternate generations with different types of vaccines can reduce effects of interfering passive antibodies. Whilst attempts are being made to improve MD vaccines, improvement of the use of existing vaccines does lead to better protection (Baigent et al., 2006). Double vaccination i.e. two injections of MD vaccine on the same day, is being used increasingly to maximise flock protection. The reason for the success of this approach is not known with certainty; it may simply be that some birds are not vaccinated correctly at the first vaccination but do get an effective dose at the second vaccination.

Early exposure to MDV can significantly be prevented by improved hygiene and biosecurity measures. In spite of the success achieved by vaccines in controlling MD, the continuous evolution of MDV strains towards greater virulence is threatening to pose problems in the future.




Dosage, administration and withdrawal times

Life stages

MD HVT, serotype 3, live vaccines e.g. strain FC126

Amniotic cavity in embryos; sub-cutaneous or intra-muscular in chicks

Embryo (in ovo)/1-day-old birds; sometimes revaccination at 7-12 days

MD serotype 2 live vaccines e.g. strains SB1, 301B/1

Amniotic cavity in embryos; sub-cutaneous or intra-muscular in chicks

As above

MD serotype 1 live vaccines e.g. strains Rispens CVI988, RMIT, R2/23

Amniotic cavity in embryos; sub-cutaneous or intra-muscular in chicks

As above

MD HVT (serotype 3) with serotype 2 bivalent vaccines

Amniotic cavity in embryos; sub-cutaneous or intra-muscular in chicks

As above

MD HVT (serotype 3) with serotype 1 bivalent vaccines

Amniotic cavity in embryos; sub-cutaneous or intra-muscular in chicks

As above

Recombinant HVT live vaccines expressing antigens of NDV or ILT

Amniotic cavity in embryos; also, depending on the product, sub-cutaneous or intra-muscular in chicks

Embryo (in ovo)/1-day-old birds


Selection for genetic resistance

Genetic resistance to MD is well documented and susceptible and resistant lines can be developed by progeny testing, selection from survivors of MD challenge, or blood typing. Two distinct genetic loci that play a major role in controlling resistance have been identified. The best association is the one between the chicken major histocompatibility complex (MHC) and resistance to MD, the most notable being the association with the B21 allele. This association develops early in life and is accompanied by reduced numbers of infected T-cells. A second type of resistance associated with non-MHC genes is provided by the observation that RPL line 6 and 7 chickens, which are both homozygous for the same MHC allele, differ markedly in MD susceptibility (Chang et al., 2010). Mapping of genes associated with such resistance is in progress and there is evidence to show that the NK region within chromosome 1 contains a resistance gene, which has been designated MDV1 (Bumstead, 1998). As more such tools for selection for genetic resistance become available, there will be more opportunity for genetic selection against MD (Emara and Kim, 2003).

Farm-level Control

The use of vaccines should never be an excuse for poor management or lack of biosecurity measures. Dander, feathers and litter from infected flocks are infectious for MDV, which can remain infectious for many months at about 20°C. Removal of used litter and disinfection of buildings are important aspects of disease control, especially in view of the possibility of selection for pathogens with increased virulence. Furthermore, placing chicks in an environment heavily contaminated with virus, before they have developed a solid immunity, can lead to vaccination breaks. Strict biosecurity is also necessary to prevent the introduction of new MDV strains into a farm.


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Baigent SJ; Smith LP; Currie RJW; Nair VK, 2007. Correlation of Marek's disease herpesvirus vaccine virus genome load in feather tips with protection, using an experimental challenge model. Avian Pathology, 36(6):467-474.

Baigent SJ; Smith LP; Nair VK; Currie RJW, 2006. Vaccinal control of Marek's disease: current challenges, and future strategies to maximize protection. Veterinary Immunology and Immunopathology, 112(1/2):78-86.

Barfoed AM; Østergaard E; Frandsen PL; Nielsen EB; Sandberg E; Rasmussen TB, 2010. Development of a primer-probe energy transfer based real-time PCR for detection of Marek's disease virus. Journal of Virological Methods, 165(1):21-26.

Becker Y; Asher Y; Tabor E; Davidson I; Malkinson M; Weisman Y, 1992. Polymerase chain reaction for differentiation between pathogenic and non-pathogenic serotype 1 Marek's disease viruses (MDV) and vaccine viruses of MDV-serotypes 2 and 3. Journal of Virological Methods, 40(3):307-322; 22 ref.

Bumstead N, 1998. Genomic mapping of resistance to Marek's disease. Avian Pathology, 27(Supp 1):S78-S81; 19 ref.

Chang S; Dunn JR; Heidari M; Lee LF; Song J; Ernst CW; Ding Z; Bacon LD; Zhang H, 2010. Genetics and vaccine efficacy: host genetic variation affecting Marek's disease vaccine efficacy in White Leghorn chickens. Poultry Science, 89(10):2083-2091.

Cortes AL; Montiel ER; Lemiere S; Gimeno IM, 2011. Comparison of blood and feather pulp samples for the diagnosis of Marek's disease and for monitoring Marek's disease vaccination by real time-PCR. Avian Diseases, 55(2):302-310.

Emara MG; Kim H, 2003. Genetic markers and their application in poultry breeding. Poultry Science [Ancillary symposium on Genetic technology related to poultry production in conjunction with the 91st Annual Poultry Science Meeting.], 82(6):952-957.

Hennig H; Wessel K; Sondermeijer P; Kirchner H; Wandinger KP, 1998. Lack of evidence for Marek's disease virus genomic sequences in leukocyte DNA from multiple sclerosis patients in Germany. Neuroscience Letters, 250:138-140.

Lee LF; Wu P; Sui D; Ren D; Kamil J; Kung HJ; Witter RL, 2000. The complete unique long sequence and the overall genomic organization of the GA strain of Marek's disease virus. Proceedings of the National Academy of Sciences USA, 97(11):6091-6096.

OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.

OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.

OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.

OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health.

Payne LN; Venugopal K, 2000. Neoplastic diseases: Marek's disease, avian leukosis and reticuloendotheliosis. In: Diseases of Poultry: World Trade and Public Health Implications. Office International Des Epizooties (OIE) Scientific and Technical Review, 19(2):544-564.

Purchase HG, 1985. Clinical disease and its economic impact. Marek's disease: scientific basis and methods of control, 17-42; [Developments in Veterinary Virology volume 1]; 31 ref.

Purchase HG; Witter RL, 1986. Public health concerns from human exposure to oncogenic avian herpesviruses. Journal of the American Veterinary Medical Association, 189(11):1430-1436; 42 ref.

Ross LJN, 1999. T cell transformation by Marek's disease virus. Trends in Microbiology, 7:22-29.

Schat KA; Markowski-Grimsrud CJ, 2001. Immune responses to Marek's disease virus infection. Current Top. Microb. Immun., 255:91-120.

Silva RF, 1992. Differentiation of pathogenic and non-pathogenic serotype 1 Marek's disease viruses (MDVs) by polymerase chain reaction amplification of the tandem direct repeats within the MDV genome. Avian Diseases, 36:521-528.

Tulman ER; Afonso CL; Lu Z; Zsak L; Rock DL; Kutish GF, 2000. The genome of a very virulent Marek's disease virus. Journal of Virology, 74(17):7980-7988.

Distribution References

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004)., Paris, France: Office International des Epizooties.

OIE, 2009. World Animal Health Information Database - Version: 1.4., Paris, France: World Organisation for Animal Health.

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