Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide


Marek's disease



Marek's disease


  • Last modified
  • 06 May 2021
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • Marek's disease
  • Overview
  • Marek’s disease (MD), caused by Marek’s disease virus (MDV), is a multifaceted disease, which can be characterized based on neoplastic transformation of T lymphocytes, immunosuppression and neurological disorders in domestic chickens. Less frequen...

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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.
CaptionMarek's disease affected visceral organs, including ovarium.
Copyright©Sri Poernomo
Marek's disease affected visceral organs, including ovarium.
PathologyMarek'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), caused by Marek’s disease virus (MDV), is a multifaceted disease, which can be characterized based on neoplastic transformation of T lymphocytes, immunosuppression and neurological disorders in domestic chickens. Less frequently, MD can also be found in turkeys, quails, common pheasant, ducks, and white footed geese. MDV is spread via the respiratory system after inhalation of cell-free MDV particles within the contaminated dust; otherwise the virus exists only as cell-associated form in the infected host. MDV vaccines are widely used and can protect chickens against MD but they fail to provide sterile immunity and vaccinated chickens can be infected and spread MDV into the environment (Boodhoo et al., 2016). Different clinical forms of the disease in domestic chickens include the classical form, acute form, transient paralysis syndrome and acute cytolytic form.

Host Animals

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

Hosts/Species Affected

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Infection mainly occurs in domestic chickens, although the disease can occasionally occur in other species of birds such as turkeys, quails, common pheasant, common buzzard, sparrow hawk, mallard, mute swan, little owl, eagle owl and domestic geese. The causative agent of MD, MDV, spreads through direct or indirect contact with contaminated dust and dander, which stays infectious in the environment for several months, from infected birds. The shedding of MDV occurs 2-4 weeks post infection and will continue through the life of the span of the infected bird. A minor role has been described for indirect transmission by darkling beetles (Alphitobius diaperinus). The rate of spread of MD within a flock can vary greatly and depends on several factors, including the level of initial exposure and the susceptibility of the birds based on their genetic background (Boodhoo et al., 2016), and females tend to develop more visceral lesions. 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

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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. MD is prevalent wherever poultry industry is located, however, losses from the disease are especially high in areas where broiler production is very intensive. More virulent strains of MDV are continuously emerging, and these highly virulent pathotypes reduce the effectiveness of current MDV vaccines.

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)
BotswanaAbsent, No presence record(s)
Cabo VerdePresent
Central African RepublicAbsent, No presence record(s)
Côte d'IvoirePresent
DjiboutiAbsent, No presence record(s)
EgyptAbsent, No presence record(s)
EswatiniAbsent, No presence record(s)
GabonAbsent, No presence record(s)
GhanaAbsent, No presence record(s)
KenyaAbsent, No presence record(s)
LesothoAbsent, No presence record(s)
MauritiusAbsent, No presence record(s)
MozambiqueAbsent, No presence record(s)
São Tomé and PríncipePresent, Serological evidence and/or isolation of the agent
South AfricaAbsent, No presence record(s)
SudanAbsent, No presence record(s)
TanzaniaAbsent, No presence record(s)


ArmeniaAbsent, No presence record(s)
AzerbaijanAbsent, No presence record(s)
BahrainAbsent, No presence record(s)
BhutanAbsent, No presence record(s)
ChinaPresent, Localized
Hong KongAbsent, No presence record(s)
IndiaAbsent, No presence record(s)
IranAbsent, No presence record(s)
IsraelAbsent, No presence record(s)
KazakhstanAbsent, No presence record(s)
KuwaitAbsent, No presence record(s)
KyrgyzstanAbsent, No presence record(s)
LaosAbsent, No presence record(s)
LebanonAbsent, Unconfirmed presence record(s)
-Peninsular MalaysiaPresent, Serological evidence and/or isolation of the agent
SingaporeAbsent, No presence record(s)
South KoreaPresent
Sri LankaPresent
TajikistanAbsent, No presence record(s)


AndorraAbsent, No presence record(s)
BelarusAbsent, No presence record(s)
BelgiumAbsent, No presence record(s)
Bosnia and HerzegovinaAbsent, No presence record(s)
BulgariaAbsent, No presence record(s)
CroatiaAbsent, No presence record(s)
CyprusAbsent, No presence record(s)
CzechiaAbsent, No presence record(s)
EstoniaAbsent, No presence record(s)
FinlandAbsent, No presence record(s)
GreeceAbsent, No presence record(s)
HungaryAbsent, No presence record(s)
IcelandAbsent, No presence record(s)
JerseyAbsent, No presence record(s)
LatviaAbsent, No presence record(s)
LiechtensteinAbsent, No presence record(s)
LithuaniaAbsent, No presence record(s)
LuxembourgAbsent, No presence record(s)
MaltaAbsent, No presence record(s)
MontenegroAbsent, No presence record(s)
North MacedoniaAbsent, Unconfirmed presence record(s)
NorwayAbsent, No presence record(s)
PortugalAbsent, No presence record(s)
RomaniaAbsent, No presence record(s)
SerbiaAbsent, No presence record(s)
Serbia and MontenegroAbsent, No presence record(s)
SlovakiaAbsent, No presence record(s)
SloveniaAbsent, No presence record(s)
SpainPresent, Localized
SwedenAbsent, No presence record(s)
SwitzerlandAbsent, No presence record(s)
UkraineAbsent, No presence record(s)
United KingdomPresent
-Northern IrelandPresent

North America

BelizeAbsent, No presence record(s)
BermudaAbsent, No presence record(s)
British Virgin IslandsAbsent, No presence record(s)
Cayman IslandsAbsent, No presence record(s)
Costa RicaPresent
CuraçaoAbsent, No presence record(s)
DominicaAbsent, No presence record(s)
Dominican RepublicPresent
GreenlandAbsent, No presence record(s)
GuatemalaAbsent, No presence record(s)
HondurasAbsent, No presence record(s)
JamaicaAbsent, No presence record(s)
Saint Vincent and the GrenadinesAbsent, No presence record(s)
Trinidad and TobagoPresent
United StatesPresent


French PolynesiaPresent
New CaledoniaPresent
New ZealandPresent
SamoaAbsent, No presence record(s)
VanuatuAbsent, No presence record(s)

South America

BoliviaAbsent, No presence record(s)
ColombiaAbsent, No presence record(s)
EcuadorAbsent, No presence record(s)
Falkland IslandsAbsent, No presence record(s)
French GuianaAbsent, No presence record(s)
GuyanaAbsent, No presence record(s)
PeruAbsent, Unconfirmed presence record(s)
VenezuelaAbsent, No presence record(s)


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Gross and microscopic pathological lesions are observed in MDV-infected birds showing clinical signs of MD. In general, gross pathological lesions of tumour tissues can provide indications of the nature of the disease, while identification of microscopical lesions, characterized by infiltration of CD4+ T cells, can provide a more accurate diagnosis. Microscopic examination of affected tissues with gross lesions such as liver, spleen, bursa of Fabricius, thymus, heart, proventriculus, kidney, gonads, nerves and skin are recommended.

Classical form

The classical form is characterized with neuronal lesions which causes partial or complete paralysis of the wings and legs. The characteristic gross pathological lesion is the enlargement of one or more of the peripheral nerves but particularly the sciatic, abdominal vagus, intercostal, and brachial 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 acute form is characterized by transformation of CD4+ T cells and formation of lymphoma lesions in visceral organs. 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 more frequent in younger 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 within 3-12 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. Quantitative real time PCR can also differentiate virulent and vaccine strain of serotype 1.

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. The detection of MDV antigen “Meq” using monoclonal antibodies against this antigen is suitable for diagnosis of MD lymphoma. 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.

Acute form

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 form of MD and it may occur in flocks 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. Microscopy pathological lesions demonstrate vasculitis and oedema which causes paralysis in the affected birds.

Acute mortality syndrome

Acute mortality syndrome is a form of the disease observed more recently with the emergence of more virulent MDV pathotypes, which causes an early acute cytolytic disease well before the onset of lymphomas. The acute cytolytic form is caused by highly virulent pathotypes of MDV, which causes severe atrophy of the bursa of Fabricius and thymus and high mortality in chickens between 10-14 weeks of age.


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In commercial chicken houses, where infection is widespread, virtually all birds become infected within the first few weeks of their 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 infected 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 protects chickens from MD; however, it fails to induce sterile immunity and even the vaccinated birds can become infected and shed the virus. Vaccination currently represents a 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.

Modified live virus vaccines, based on herpesvirus of turkey (HVT from serotype 3), were initially developed in 1970 which provided protection against low pathotypes. However, with emergence of more virulent virus, the need for development of more effective MD vaccines led to the development of MD vaccines based on serotype 1 and 2. These vaccines are still the cornerstones of disease control programmes and they are usually administered to day-old chicks after hatching. With the introduction of in ovo immunisation methods, an increasing number of broiler chickens are vaccinated by this route as this route reduces cost and improve reliability of vaccination programmes. 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 against less virulent pathotypes. HVT is also used as vectored vaccines expressing other viral antigens including Newcastle disease virus and infectious laryngotracheitis virus. Due to limited protection conferred by MD vaccine from serotype 2 against highly virulent MDV, HVT (serotype 3) and SB-1 (serotype 2) strains were combined comprised the first commercial bivalent vaccine based on the protective synergism effects (Witter and Lee, 1984). CVI988 strain Rispens vaccines and their modified versions (serotype 1), as a cell-associated form, are currently widely used and appear to be effective against some of the vv+MDV pathotypes.

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. (Witter, 1998; Baigent et al., 2006; Boodhoo et al., 2016). 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 (Boodhoo et al., 2016); 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 virus replication in the infected chickens. However, the mechanism involved in resistance to MD in chickens with B21 MHC haplotype is unclear. 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). Interestingly, infection with vv+MDV can still cause the disease in MD resistant chickens (Burgess et al., 2001). 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 contaminated with infectious MDV, which can remain infectious for many months. Removal and appropriate disposal of dead and infected birds, manure and litter along with 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 their immune system is matured and developed, can lead to vaccination failure. In addition, avoiding multi-age flocks and air management in the farm are recommended. 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.

Boodhoo, N., Gurung, A., Sharif, S., Behboudi, S., 2016. Marek's disease in chickens: a review with focus on immunology. Veterinary Research, 47(119), (28 November 2016).

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

Burgess, S. C., Basaran, B. H., Davison, T. F., 2001. Resistance to Marek's disease herpesvirus-induced lymphoma is multiphasic and dependent on host genotype. Veterinary Pathology, 38(2), 129-142. doi: 10.1354/vp.38-2-129

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.

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

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

Witter, R. L., 1998. Control strategies for Marek's disease: a perspective for the future. In: Poultry Science , 77(8) . 1197-1203. doi: 10.1093/ps/77.8.1197

Witter, R. L., Lee, L. F., 1984. Polyvalent Marek's disease vaccines: safety, efficacy and protective synergism in chickens with maternal antibodies. Avian Pathology, 13(1), 75-92. doi: 10.1080/03079458408418510

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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04/05/2021 Updated by:

Dr Shahriar Behboudi, The Pirbright Institute

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