The only good thing is that Marek’s disease is NOT transmitted vertically.
But once infected, there is no treatment.
Some infected chickens may not show obvious symptoms but are Marek’s disease carriers.
– Gameness til the End
Disease can be directly transmitted in two ways:
- Horizontal disease transmission – from one individual to another in the same generation (peers in the same age group). Horizontal transmission can occur by either direct contact (licking, touching, biting), or indirect contact air – cough or sneeze (vectors or fomites that allow the transmission of disease without physical contact).
- Vertical disease transmission – passing a disease causing agent vertically from parent to offspring, such as perinatal transmission.
According to University of New Hampshire PDF download below (near the bottom), there are 4 different forms of Marek’s:
- Cutaneous (skin form)
- Neural (nerve form)
- Ocular (eye form)
- Visceral (internal-organ form)
Marek’s disease is a highly contagious viral neoplastic disease in chickens. It is named after József Marek, a Hungarian veterinarian. Occasionally misdiagnosed as an abtissue pathology it is caused by an alphaherpesvirus known as ‘Marek’s disease virus’ (MDV) or Gallid herpesvirus 2 (GaHV-2). The disease is characterized by the presence of T cell lymphoma as well as infiltration of nerves and organs by lymphocytes. Viruses related to MDV appear to be benign and can be used as vaccine strains to prevent Marek’s disease. For example, the related Herpesvirus of Turkeys (HVT), causes no apparent disease in turkeys and continues to be used as a vaccine strain for prevention of Marek’s disease (see below). Birds infected with GaHV-2 can be carriers and shedders of the virus for life. Newborn chicks are protected by maternal antibodies for a few weeks. After infection, microscopic lesions are present after one to two weeks, and gross lesions are present after three to four weeks. The virus is spread in dander from feather follicles and transmitted by inhalation.
There are six syndromes known to occur after infection with Marek’s disease. These syndromes may overlap.
- Classical Marek’s disease or neurolymphomatosis causes asymmetric paralysis of one or more limbs. With vagus nerve involvement, difficulty breathing or dilation of the crop may occur. Besides lesions in the peripheral nerves, there are frequently lymphomatous infiltration/tumours in the skin, skeletal muscle, visceral organs. Organs that are commonly affected include the ovary, spleen, liver, kidneys, lungs, heart, proventriculus and adrenals.
- Acute Marek’s disease is an epidemic in a previously uninfected or unvaccinated flock, causing depression, paralysis, and death in a large number of birds (up to 80 percent). The age of onset is much earlier than the classic form; birds are four to eight weeks old when affected. Infiltration into multiple organs/tissue is observed.
- Ocular lymphomatosis causes lymphocyte infiltration of the iris (making the iris turn grey), unequal size of the pupils, and blindness.
- Cutaneous Marek’s disease causes round, firm lesions at the feather follicles.
- Atherosclerosis is induced in experimentally infected chickens.
- Immunosuppression – Impairment of the T-lymphocytes prevent competent immunological response against pathogenic challenge and the affected birds become more susceptible to disease conditions such as coccidiosis and “Escherichia coli” infection . Furthermore, without stimulation by cell-mediated immunity, the humoral immunity conferred by the B-cell lines from the Bursa of Fabricius also shuts down, thus resulting in birds that are totally immunocompromised.
Diagnosis of lymphoid tumors in poultry is complicated due to multiple etiological agents capable of causing very similar tumors. It is not uncommon that more than one avian tumor virus can be present in a chicken, thus one must consider both the diagnosis of the disease/tumors (pathological diagnosis) and of the virus (etiological diagnosis). A step-wise process has been proposed for diagnosis of Marek’s disease which includes (1) history, epidemiology, clinical observations and gross necropsy, (2) characteristics of the tumor cell, and (3) virological characteristics
The demonstration of peripheral nerve enlargement along with suggestive clinical signs in a bird that is around three to four months old (with or without visceral tumors) is highly suggestive of Marek’s Disease. Histological examination of nerves reveals infiltration of pleomorphic neoplastic and inflammatory lymphocytes. Peripheral neuropathy should also be considered as a principal rule out in young chickens with paralysis and nerve enlargement without visceral tumors, especially in nerves with interneuritic edema and infiltration of plasma cells.
The presence of nodules on the internal organs may also suggest Marek’s disease but further testing is required for confirmation. This is done through histological demonstration of lymphomatous infiltration into the affected tissue. A range of leukocytes can be involved, including lymphocytic cell lines such as large lymphocyte, lymphoblast, primitive reticular cells and occasional plasma cells as well as macrophage and plasma cells. The T-cells are involved in the malignancy, showing neoplastic changes with evidence of mitosis. The lymphomatous infiltrates need to be differentiated from other conditions that affect poultry including Lymphoid Leukosis and Reticuloendotheliosis, as well as an inflammatory event associated with hyperplastic changes of the affected tissue.
Key clinical signs as well as gross and microscopic features that are most useful for differentiating Marek’s disease from Lymphoid Leukosis and Reticuloendotheliosis include (1) Age: MD can affect birds at any age, including <16 weeks of age; (2) Clinical signs: Frequent wing and leg paralysis; (3) Incidence: >5% in unvaccinated flocks; (4) Potential nerve enlargement; (5) Interfollicular tumors in the Bursa of Fabricius; (6) CNS involvement; (7) Lymphoid proliferation in skin and feather follicles; (8) Pleomorphic lymphoid cells in nerves and tumors; (9) T-cell lymphomas.
In addition to gross pathology and histology, other advanced procedures used for a definitive diagnosis of Marek’s disease include immunohistochemistry to identify cell type and virus-specific antigens, standard and quantitative PCR for identification of the virus, virus isolation to confirm infections and serology to confirm/exclude infections.
The World Organisation for Animal Health (OIE) reference laboratories for Marek’s disease include the Institute for Animal Health, Compton Laboratory, UK and the USDA Avian Disease and Oncology Laboratory, USA.
Vaccination is the only known method to prevent the development of tumors when chickens are infected with the virus. However, administration of vaccines does not prevent transmission of the virus, i.e., the vaccine is non-sterilizing. However, it does reduce the amount of virus shed in the dander and hence reduce horizontal spread of the disease. Marek’s Disease does not spread vertically. The vaccine was introduced in 1970 and the scientist credited with its development is Dr. Ben Roy Burmester. Before that, Marek’s disease caused substantial revenue loss in the poultry industries of the United States and the United Kingdom. The vaccine can be administered to one day old chicks through sub-cutaneous inoculation or by in-ovo vaccination when the eggs are transferred from the incubator to the hatcher. In-ovo vaccination is the preferred method, as it does not require handling of the chicks and can be done rapidly by automated methods. Immunity develops within two weeks.
The vaccine originally contained the antigenically similar turkey herpesvirus, which is serotype 3 of MDV. However, because vaccination does not prevent infection with the virus, the Marek’s Disease virus has evolved increased virulence and resistance to this vaccine. As a result, current vaccines use a combination of vaccines consisting of HVT and gallid herpesvirus type 3 or an attenuated MDV strain, CVI988-Rispens (ATCvet code: QI01AD03).
Chickens are the most important natural host for Marek’s disease virus, a highly cell-associated but readily transmitted alphaherpesvirus with lymphotropic properties of gammaherpesviruses. Quail can be naturally infected, and turkeys can be infected experimentally. However, severe clinical outbreaks of Marek’s disease in commercial turkey flocks, with mortality from tumors reaching 40%–80% between 8 and 17 wk of age, were reported in France, Israel, and Germany. In some of these cases, the affected turkey flocks were raised in proximity to broilers. Turkeys are also commonly infected with turkey herpesvirus (HVT), an avirulent strain related to Marek’s disease virus that is commonly used as a Marek’s disease vaccine in chickens. Other birds and mammals appear to be refractory to the disease or infection.
Marek’s disease is one of the most ubiquitous avian infections; it is identified in chicken flocks worldwide. Every flock, except for those maintained under strict pathogen-free conditions, is presumed to be infected. Although clinical disease is not always apparent in infected flocks, a subclinical decrease in growth rate and egg production may be economically important.
Marek’s disease virus is a member of the genus Mardivirus within the subfamily Alphaherpesvirinae. Within the genus Mardivirus are three closely related species previously designated as three serotypes of Marek’s disease virus. Gallid herpesvirus 2 (MDV-1) represents all virulent Marek’s disease virus strains and is further divided into pathotypes, designated as mild (m), virulent (v), very virulent (vv), and very virulent plus (vv+). Gallid herpesvirus 3 (MDV-2) and Meleagrid herpesvirus 1 (turkey herpesvirus, MDV-3) represent avirulent virus strains isolated from chickens and turkeys, respectively, and are commonly used as vaccines against Marek’s disease.
Transmission and Epidemiology
The disease is highly contagious and readily transmitted among chickens. The virus matures into a fully infective, enveloped form in the epithelium of the feather follicle, from which it is released into the environment. It may survive for months in poultry house litter or dust. Dust or dander from infected chickens is particularly effective in transmission. Once the virus is introduced into a chicken flock, regardless of vaccination status, infection spreads quickly from bird to bird. Infected chickens continue to be carriers for long periods and act as sources of infectious virus. Shedding of infectious virus can be reduced, but not prevented, by prior vaccination. Unlike virulent strains of Marek’s disease virus, which are highly contagious, turkey herpesvirus is not readily transmissible among chickens (although it is easily transmitted among turkeys, its natural host). Attenuated Marek’s disease virus strains vary greatly in their transmissibility among chickens; the most highly attenuated are not transmitted. Marek’s disease virus is not vertically transmitted.
Currently, four phases of infection in vivo are recognized: 1) early productive-restrictive virus infection causing primarily degenerative changes, 2) latent infection, 3) a second phase of cytolytic, productive-restrictive infection coincident with permanent immunosuppression, and 4) a proliferative phase involving nonproductively infected lymphoid cells that may or may not progress to the point of lymphoma formation. Productive infection may occur transiently in B lymphocytes within a few days after infection with virulent Marek’s disease virus strains and is characterized by antigen production, which leads to cell death. Because few if any virions are produced, this has also been termed a restrictive-productive infection. Productive infection also occurs in the feather follicle epithelium, in which enveloped virions are produced. Latent infection of activated T cells is responsible for the longterm carrier state. No antigens are expressed, but virus can be recovered from such lymphocytes by co-cultivation with susceptible cells in tissue cultures. Some T cells, latently infected with oncogenicMarek’s disease virus strains, undergo neoplastic transformation. These transformed cells, provided they escape the immune system of the host, may multiply to form characteristic lymphoid neoplasms. Cell-mediated and humoral immune responses are both directed against viral antigens, with cell-mediated immunity probably being the most important.
The incidence of Marek’s disease is quite variable in commercial flocks and depends on strain and dose of virus, age at exposure, maternal antibody, host gender and genetics, strain and dose of vaccine virus, and several environmental factors, including stress. In addition to lymphoid neoplasms, Marek’s disease virus can also induce other clinically distinct disease syndromes, including transient paralysis, early mortality syndrome, cytolytic infection, atherosclerosis, and persistent neurologic disease. Typically, affected birds show only depression before death, but a transient paralysis syndrome has been associated with Marek’s disease; chickens become ataxic for periods of several days and then recover. This syndrome is rare in immunized birds. Death is usually the result of paralysis, rendering the birds unable to reach food and water.
Enlarged nerves are one of the most consistent gross lesions in affected birds. Various peripheral nerves, but particularly the vagus, brachial, and sciatic, become enlarged and lose their striations. Diffuse or nodular lymphoid tumors may be seen in various organs, particularly the liver, spleen, gonads, heart, lung, kidney, muscle, and proventriculus. Enlarged feather follicles (commonly termed skin leukosis) may be noted in broilers after defeathering during processing and are a cause for condemnation. The bursa is only rarely tumorous and more frequently is atrophic. Histologically, the lesions consist of a mixed population of small, medium, and large lymphoid cells plus plasma cells and large anaplastic lymphoblasts. These cell populations undoubtedly include tumor cells and reactive inflammatory cells. When the bursa is involved, the tumor cells typically appear in interfollicular areas.
For the diagnosis of Marek’s disease, it is critical to diagnose the tumors and not the infection because Marek’s disease is considered ubiquitous within commercial poultry flocks. Usually, diagnosis is based on enlarged nerves and lymphoid tumors in various viscera. The absence of bursal tumors helps distinguish this disease from lymphoid leukosis (see Neoplasms: Lymphoid Leukosis in Poultry), although the presence of bursal tumors does not exclude Marek’s disease. Marek’s disease can develop in chickens as young as 3 wk old, whereas lymphoid leukosis typically is seen in chickens >14 wk old. Reticuloendotheliosis, although rare, can easily be confused with Marek’s disease, because both diseases feature enlarged nerves and T-cell lymphomas in visceral organs. A diagnosis based on typical gross lesions may be confirmed histologically, or preferably by demonstration of predominant T-cell populations and Marek’s viral DNA in lymphomas by histochemistry and PCR, respectively. There is a quantitative association between viral load and Marek’s disease tumors; most tumor-bearing chickens have high viremia titers and are usually PCR positive. Thus, the demonstration of high quantities of virus, viral DNA, or viral antigens in tumor cells and the exclusion of other relevant tumor viruses should be sufficient for a specific diagnosis of Marek’s disease. Furthermore, Marek’s disease lymphomas usually lack evidence of clonally integrated avian retroviruses or alteration of the cellular oncogene c-myc.
Vaccination is the central strategy for the prevention and control of Marek’s disease. The efficacy of vaccines can be improved, however, by strict sanitation to reduce or delay exposure and by breeding for genetic resistance. Probably the most widely used vaccine consists of turkey herpesvirus (HVT), which has seen rapidly increased use in recent years as a backbone in recombinant vaccines featuring the insertion of genes from other poultry viruses, such as Newcastle disease virus (see Newcastle Disease and Other Paramyxovirus Infections), infectious bursal disease virus (see Infectious Bursal Disease), or infectious laryngotracheitis virus (see Infectious Laryngotracheitis). These recombinant vaccines offer protection against both Marek’s disease virus and the inserted virus. Bivalent vaccines consisting of HVT and either the SB-1 or 301B/1 strains of Gallid herpesvirus 3 have been used to provide additional protection against challenge with virulent Marek’s disease virus isolates. The most protective commercial vaccine currently available appears to be CVI988/Rispens, an attenuated Marek’s disease virus strain that is also commonly mixed with HVT at vaccination. Because vaccines are administered at hatching and require 1–2 wk to produce an effective immunity, exposure of chickens to virus should be minimized during the first few days after hatching.
Vaccines are also effective when administered to embryos at the 18th day of incubation. In ovo vaccination is now performed by automated technology and is widely used for vaccination of commercial broiler chickens, mainly because of reduced labor costs and greater precision of vaccine administration.
Proper handling of vaccine during thawing and reconstitution is crucial to ensure that adequate doses are administered. Cell-associated vaccines are generally more effective than cell-free vaccines, because they are neutralized less by maternal antibodies. Under typical conditions, vaccine efficacy is usually >90%. Since the advent of vaccination, losses from Marek’s disease have been reduced dramatically in broiler and layer flocks. However, disease may become a serious problem in individual flocks or in selected geographic areas (eg, the Delmarva broiler industry). Of the many causes proposed for these excessive losses, early exposure to very virulent virus strains appears to be among the most important.
In an economic loss, Marek’s disease is a most important malady of chickens. It often causes severe death loss in pullet flocks and has been a major cause of condemnations at the broiler processing plant. Generally, chickens under 16 weeks of age are most often affected.
Caused by a herpesvirus, the disease is often characterized by abnormal cell growth in the peripheral nerves and central nervous system. Hence, the common name for one form of Marek’s: fowl paralysis. In addition to the nerves, however, the disease also may cause lesions on visceral organs and other tissues, including feather follicles of the skin. The most prominent lesions may be tumors on the liver, kidneys, testes, ova, spleen and lungs. In such cases, nerve swelling may not be involved.
How Marek’s Disease is Spread
Chicken “dander” from feather follicles spreads the disease. The virus also is excreted in the saliva, and the virus probably enters the body through the respiratory system. Transmission via the egg is not significant.
Some chickens die without any clinical signs of Marek’s disease. Most of the affected birds will have some degree of paralysis, although chickens with the acute form may not show this condition. Those with paralysis may die because they are unable to reach feed and water. The first indication of infection is a variation in the growth rate and degree of feathering.
Swelling of the peripheral nerves, particularly of the nerves of the leg and wing, is often noticeable. The visceral organs may contain tumors ranging from microscopic size to fairly large. Such tumor lesions may be confused with those of lymphoid leukosis without a qualified laboratory diagnosis.
Tumor formation from Marek’s disease can be prevented through vaccination. Salsbury MD-Vac, a vaccine of chick-embryo tissue culture, is recommended. Vaccination at one day of age usually protects birds through their lifetime. There is no treatment for Marek’s disease.
Marek’s disease (MD) is one of the most common lymphoproliferative diseases of chickens which causes mononuclear infiltration of one or more of the following cells: peripheral nerves, gonad, iris, muscle, viscera, and skin. MD has been called by several names including “range paralysis”, “neural lymphoma” and “skin leucosis”.
MD is caused by herpesvirus, which can be differentiated from other lymphoid neoplastic diseases. There are three serotypes of MDV which have many common antigens and are distinguished by serologic tests.
Viruses grow best in duck embryo fibroblast or chicken kidney cell
Viruses grow best in chicken embryo fibroblast
Viruses grow best in chicken embryo fibroblast.
Virus grows slowly
Virus grows slowly
Virus grows rapidly.
Produce small plaques
Produce medium plaques
Produce large plaques
Jordan and Pattison, Poultry Diseases, 4th ed.
Virulence and oncogenicity are associated only with serotype 1 MDV’s.
There are four phases of infection: 1) degenerative changes caused by early productive-restrictive virus infection, 2) latent infection, 3) another phase of cytolytic infection associated with permanent immunosuppression, and 4) nonproductive infected lymphoid cells that may or may not progress to lymphoma formation, a “proliferative” phase. The route of infection is inhalation. The virus then replicates in the lungs (in non-lymphoid cells). An acute phase of the disease can be seen within 72-96 hours where the lymphoid system, primarily bursa and thymus, undergoes cytolytic changes. Infected birds normally recover from the acute phase of the infection after 6-7 days and become latent. Infected lymphocytes carry the virus throughout the body, causing cell-associated viremia. Eventually, virus will be shed in the environment via feather debris and dander after the secondary cytolytic infection occurs in the feather follicle epithelium (~2 weeks post infection).
MDV can be transmitted by direct and indirect contact between birds. Transmission is primarily by airborne route as the virus is shed in epithelial cells of the feather follicle, dander, chicken house dust, feces and saliva. The virus has a long survival time in dander since viable virus has been isolated from houses that have been depopulated for many months. (Historically, prior to vaccine availability, control in broilers was based upon early brooding exposure to used broiler litter and dander, marketing survivors versus poorer results with the thoroughly cleaned and disinfected brooder houses). Transmission by egg has no significance (i.e., chicken hatched and reared in isolation will be free of MDV.
MD commonly affects pullets between 12-24 weeks of age, but can infect broilers as early as 6 weeks of age. The incubation period ranges from 3-4 weeks to several months. Signs may vary according to the nerve or nerves affected. Asymmetric progressive paralysis of one or more of the extremities can be seen. Wing involvement is characterized by drooping of the limb. Torticollis of nerves controlling the neck are affected. Vagal involvement will lead to dilatation of the crop and/or gasping. If the iris is involved, eyes will lose their ability to accommodate light intensity and blindness may occur (once called “grey eye”). Many birds die suddenly without symptoms. There are nonspecific signs such as weight loss, paleness, anorexia, and diarrhea.
Macroscopic lesions: Nerve lesions can be seen as grayish, edematous, two or three times the normal thickness, and loss of the normal striated white glistening appearance. Nerves commonly affected include the brachial and sciatic plexi, celiac plexus, abdominal vagus and intercostals nerves. Nerve enlargement may not always be seen in affected birds at necropsy, although characteristic lesions may be found histologically. Also, tumors such as lymphoma occur in the ovary along with the nerve lesions. Macroscopic appearance in affected viscera, with the exception of the bursa of Fabricius, are indistinguishable from leukotic lesions induced by other agents (e.g. lymphoid leucosis virus). Organs are enlarged with diffuse grayish discoloration.
Microscopic lesions: There are two main types of lesions in peripheral nerves. Type A is interpreted as neoplastic in character, consisting of masses of proliferating lymphoblastic cells. Sometimes, demyelination and proliferation of Schwann cells are seen with these lesions. Type B is inflammatory in nature and is characterized by diffuse infiltration of lymphocytes and plasma cells, edema, and sometimes demyelination and Schwann cell proliferation. Lymphomatous lesions in visceral organs are more uniformly proliferative in nature. Deposition and diffuse proliferation of small to medium lymphocytes, lymphoblasts, and primitive reticulum cells are seen. Plasma cells are rarely present.
Skin lesions are mostly inflammatory and can also be lymphomatous. Inflammatory cells are localized around the infected feather follicle. With small lesions, the integrity of the skin is maintained, but disruption of the epidermis leading to ulcer formation may occur with massive proliferation.
Herpesviruses replicate in the bursa of Fabricius and the thymus which results in degenerative changes in these organs. Atrophy of the thymus can be severe and involve the cortex and medulla. In some cases, lymphoid proliferation in the thymus was seen. Arterial lesions may occur in the aorta, coronary, celiac, gastric and mesenteric arteries which may show fatty proliferative changes.
Since there is no truly pathognomonic gross lesions of MD and because MD lesions can closely resemble those of lymphoid leucosis (LL), the clinical diagnosis of MD has been considered difficult in practice. Infection of MDV, not necessarily accompanied by the clinical disease, can be detected by virus isolation or agar gel precipitation tests of viral antigen in feather tips or antibody in serum. These are useful features to differentiate Marek’s disease from lymphoid leucosis.
|Feature||Marek’s disease||Lymphoid leucosis|
|Age||6 weeks or older||16 weeks or older|
|Incidence||Frequently 5%+ in unvaccinated flocks||Rarely above 5%|
|-Bursa of Fabricius||-Diffuse enlargement or atrophy||-Nodular tumors|
|-Tumors in skin, muscle, proventriculus||-May be present||-Usually absent|
-Focal or diffuse
|-Liver tumors||-Diffuse||-Often focal|
|-Spleen||-Either atrophy of follicles or interfollicular tumor||-Intrafollicular tumors|
|-Bursa of Fabricius CNS||-Yes||-No|
|-Lymphoid prolifer-ation of skin and feather follicles||-Yes||-No|
|Cytology of tumors||Pleomorphic lymphoid cells including lymphoblasts, small, medium and large lymphocytes and reticulum cells. Rarely may only be lymphoblasts||Lymphoblasts|
|Category of neoplastic lymphoid cell||T cell||B cell|
(Jordan and Pattison, Poultry Diseases, 4th ed)
There is no effective practical treatment for MD.
Vaccination: Vaccines are extremely effective (90%+) in the prevention of Marek’s disease. There are three serotypes: Serotype 1 which is available commercially as attenuated virulent or attenuated mildly virulent, Serotype 2 vaccines which are naturally non-pathogenic strains of MDV, or Serotype 3 “Herpes Virus Turkey (HVT) which are effective against virulent MDV but less effective against very virulent MDV. HVT was standard for the poultry industry throughout the 1970s, starting at over $.05/dose to as low as $3.00/1000 doses in the late 70s. It was developed at the Regional Poultry Research Lab in East Lansing , MI, now known as the Poultry Disease and Oncology Lab. Progress in the USA is due largely to USDA scientists.
Bivalent and Trivalent Vaccines: Synergistic effect and good protection can be achieved by combining the serotype vaccines 1,2, or 3 as bivalent or trivalent vaccines. These have become standard for the layer chick hatcheries, administered subcutaneously at hatching. Broiler chicks are given vaccine in ovo at the time of egg transfer.
Genetic selection: MD resistant chicks are obtained.
FAPP (filtered air positive pressure) ventilation: Biological filters to keep out airborne viruses are used.
For the commercial chick (layer and broiler) today, Marek’s disease is not common due to vaccine use. For backyard operations, ease of vaccine handling and effective administration remains a challenge.
– by George Khalil, ECFVG Student
– edited by Dr. Tom Bryan, ADDL Poultry Diagnostician
- Diseases of Poultry, Calnek, B.W. ed., 9th and 10th editions
- Harrison and Harrison: Clinical Avian Medicine and Surgery.
- Jordan, FTW. Poultry Diseases, 4th ed.
- Poultry Health Handbook, Pennsylvania State University, 3rd ed.
- Boden E. Poultry practice.
Marek’s disease (MD or fowl paralysis) is a very common disease of chickens caused by a herpes virus. Marek’s disease affects both commercial and backyard poultry and may result in death or severe production loss. The disease causes changes in many of the nerves and may cause tumours in major internal organs.
Chickens are the main species affected. The disease occurs rarely in some other types of birds.
Young birds are most susceptible to infection. Most deaths from Marek’s disease occur between 8 and 20 weeks of age, although in some cases the disease may be seen in birds as young as 3-4 weeks of age or as old as one year of age.
Typically, Marek’s disease occurs as the nervous form, appearing as a progressive paralysis of one or more of the limbs or, less often, the neck or wings. The sciatic nerve (the main nerve to the leg) is commonly affected The birds are unable to stand, become paralysed, appear uncoordinated and slowly waste away from lack of food and water. In most cases the paralysis comes on quickly. In some cases the eyes may be affected, resulting in blindness.
In the visceral form, Marek’s disease occurs as tumours in internal organs, including the ovaries, liver, spleen, kidney and heart. Sometimes the liver and spleen are swollen without distinct tumours being present. Birds may show signs of depression, paralysis, loss of appetite, loss of weight, anaemia (pale combs), dehydration (shrunken combs), and sometimes diarrhoea. Some birds die without any clinical signs being noticed.
Most birds that develop Marek’s disease usually die.
Veterinary examination is necessary to diagnose Marek’s disease. The clinical signs, combined with post-mortem findings, will confirm the diagnosis in most cases, and, most importantly, rule-out other diseases. Enlargement of nerves such as the sciatic nerve are commonly seen at post-mortem. Changes in one or more internal organs may also be observed.
A different viral disease known as lymphoid leucosis also causes tumours in organs, but does not cause paralysis. It is usually seen in birds over 16 weeks of age, whereas Marek’s disease is commonly seen in younger chickens.
Methods of Spread
Marek’s disease virus occurs commonly wherever chickens are raised and most chickens probably become infected. The virus is highly infectious and once introduced into a flock, it spreads rapidly to unvaccinated birds.
Infected chickens carry the virus for life whether they develop the disease or not, and continue to shed the virus for long periods. The virus is shed from the feather follicles and spreads readily in fluff and dust, gaining entry when the bird breathes infected dust particles. This material can also be carried by people and equipment.
The virus can survive in the environment for as long as several months at room temperature. It is not spread from the hen to the chicken through the egg.
There is no treatment for Marek’s disease.
Diseased birds should be promptly removed from the flock and humanely destroyed. Other birds in the flock are likely to be infected at this stage also, so close monitoring of all birds is important.
Although vaccines are commonly used in the commercial poultry industry, small numbers of doses cannot be purchased for use in backyard flocks.
For backyard flocks, the best protection against Marek’s disease is obtained by buying, from a commercial source, birds that have been correctly vaccinated.
Vaccination alone will not prevent Marek’s disease. Particularly for commercial flocks, it is important to have good biosecurity to ensure that vaccinated chicks will develop immunity before they are subjected to a severe challenge of virus. For example, chicks need to be reared separately so that they are free from the infected fluff and dust of older birds. Standard hygiene measures are also important, including a thorough clean-out and disinfection of sheds and equipment between batches of chicks with a disinfectant effective against viruses. Good nutrition and maintenance of freedom from other diseases and parasites are also very important. These practices will help maintain the flock’s health and to ensure that the birds have optimum resistance against Marek’s disease infection.
For general advice on biosecurity, see the biosecurity checklist for bird keepers.
The breeding of genetically resistant strains of chickens, combined with the use of vaccination and good hygiene, can also be used to help control Marek’s disease.
For flocks with a serious Marek’s disease problem, the only solution is to depopulate, clean and disinfect all sheds and equipment, and spell for several months. Vaccinated chicks from a reputable hatchery would then need to be sought as replacements.
DAHS Poultry Topics Feature Article, 28 August 2008
- Marek’s disease may not grab the headlines but it continues to negatively impact on flock health and economics
- Marek’s disease is a very stubborn virus
- Marek’s disease is capable of causing clinical disease and mortality
- Marek’s disease can also damage the immune system leading to poor performance, poor response to other diseases and their vaccinations
- The highly resistant virus is stable for 65 weeks in the un-cleaned environment surviving in poultry feathers, dust, and dander
- Vaccination programmes are challenging to implement
- Vaccination alone will NOT control the effects of this virus
- Keeping the viral challenge low for the new crop is key
- Highly effective, four stage Terminal cleaning and disinfection programmes using a proven virucidal disinfectant such as DuPont Virkon® S is recommended.
It is easy to get distracted by the headline grabbing poultry health issues of Avian Influenza, Newcastle disease and Salmonella. Whilst these may well be the most pressing disease problems for our industry, the danger is that concentrating all time and resources on them tends to ignore those diseases that may be having a chronic and significant impact on performance and profitability, day in and day out.
With outbreaks of Marek’s disease occurring in 2007 this article provides a timely reminder to producers that Marek’s disease is a hidden menace. It is caused by a very resistant and hence very persistent herpesvirus which causes infection in chickens and, to a lesser extent, turkeys1.
Control of Marek’s disease infection depends on a combination of effective vaccination and high quality cleansing and disinfection of poultry houses. Any deficiencies in either area can tip the balance in favour of the virus rather than the bird.
Marek’s disease was first described over 80 years ago as a condition causing paralysis of the legs and wings due to inflammation of the nerves. The condition was then known as fowl paralysis. In the 1920’s and 1930’s, an association with internal tumours in various organs such as liver, spleen, kidneys and lungs was made. The disease became a significant limitation to the success of the developing layer and broiler industries in the 1960’s due to some very high mortality rates of up to 80%!
The appearance of successful live vaccines in the late 1960’s was one of the most significant factors in enabling the poultry industry to develop to the extent that it has today.
Disease can manifest itself in a number of ways related to the type of bird, when the flock became infected, general hygiene and biosecurity on the rearing and laying farms, the presence of other diseases and the vaccines used or the strain of virus involved.
Signs and Symptoms
In laying stock, producers may suspect Marek’s disease if they identify paralysed birds; often with one leg trailing or wings dropped. In other cases, there may simply be higher than expected mortality or a number of birds wasting away.
In broilers, losses are mostly due to high condemnation rates at slaughter predominantly from the cutaneous (skin) form of Marek’s disease. In free range broilers or birds taken to heavier weights, mortality may result from internal tumours, predominantly of liver and spleen.
In turkeys, acute mortality can be associated with internal tumours of liver and spleen often where turkeys have been reared in the same accommodation as infected chickens.
Even where there is no acute mortality, the affects on internal organs can lead to significant damage to the immune system. This can be associated with suboptimal performance and clinical outbreaks of other diseases such as coccidiosis, heavy worm infestations or viral diseases such as Gumboro disease. The impaired immune system is also unable to respond to routine vaccinations and hence will leave flocks unable to resist a whole range of disease challenges which affect performance.
All this means that if the background challenge from Marek’s disease virus is allowed to build up, performance can suffer even without a specific diagnosis of clinical Marek’s disease being made.
This vicious circle continues and “silent infection” build-up can put pressure on any Marek’s disease virus vaccination programme. It is thought that this phenomenon has led to the regular emergence of more and more virulent pathotypes of Marek’s disease virus since vaccines first appeared in the 1970’s. Researchers then had to work hard to develop increasingly effective vaccines to keep ahead of the virus and prevent clinical outbreaks.
Vaccination is far from simple. Due to the persistence of the virus in the environment, vaccination is a race against time to get the bird to produce a protective response before it meets field infection. These requirements and the nature of the virus mean that protection can only be achieved by physically injecting chicks with live vaccine. This is done either at one day old by intramuscular injection into the leg or neck, or increasingly into the unhatched embryo by injecting hatching eggs at transfer.
The successful response to vaccination depends on choosing the correct vaccine strain, correct preparation of this delicate vaccine and its accurate administration to each and every chick. Even then, it is possible to overcome the protection offered by the vaccine by exposing vaccinated birds to field virus too early or in such large amounts that the vaccine response is overwhelmed.
To gain the benefit of all this hard work it is important to reduce the exposure of young birds to virulent field virus. Newly hatched chicks should be placed in thoroughly cleaned and disinfected houses that are well separated from houses with older chickens2. This can be achieved by using a structured biosecurity programme concentrating on terminal cleansing and disinfection using products of proven virucidal activity.
In infected birds, the virus is excreted in feather dander and dust and therefore environmental contamination of all surfaces and litter can be very high from infected flocks. Furthermore, since the virus survives at ambient temperature for a long time (65 weeks) when cell associated2 and is resistant to some disinfectants (quaternary ammonium and phenol) the selection of an appropriately virucidal disinfectant is important.
It is therefore essential that first stage cleaning is capable of removing all organic material from surfaces using good physical cleaning and degreasing agents to lift material from perches, nests and other wooden surfaces.
Terminal Biosecurity Programme
An effective Marek’s disease terminal biosecurity programme should comprise the following 4 specific stages, the objective of which is simple – to prevent the “carry-over” of pathogenic organisms, thus ensuring that each new crop gets a completely clean fresh start.
Stage 1: Removal of Equipment and Dry Cleaning
- Remove any residual food from the feeder system and silo.
- Remove all movable equipment.
- Blow or wash down all surfaces to remove dust from ceilings, ledges, water pipes, fan boxes and inlets.
- Remove all litter from the house using scrapers and blow or brush loose debris from the ceilings and floor.
- Load litter onto lorry ensuring that all outside areas such as concrete pads by doors and silos are cleared of old litter, dust etc.
- Make sure that the load is covered before transporting from site.
- Blow or wash down bulk feed bins before disinfecting.
Stage 2: Water System Clean and Disinfect
- Isolate header tank at mains inlet point, check that it is free from debris and then drain entire system from the drinker points farthest away. Clean as required.
- Fill the tank with the necessary volume of water to fill the entire drinking water system adding the appropriate amount of disinfectant concentrate to achieve the required dilution.
- Allow disinfectant solution to fill the system to the drinker points farthest away from the header tank. Leave for one hour.
- Thoroughly flush lines through with clean water. Repeat process if scale and biofilms remain.
- Refill the header tank with clean fresh water.
Stage 3: Cleaning Buildings and Equipment
Thorough washing of all surfaces and equipment is essential to soak and dislodge as much organic material as possible and achieve the best results from the subsequent disinfection stage.
Using a pressure washer apply an appropriate detergent solution (such as DuPont Biosolve® Plus) to all surfaces. Ensure inclusion of air inlets, fan boxes, partitions, feeders, drinkers and other equipment, including any removed from the house. Include any service/utility rooms in this cleaning procedure before rinsing all surfaces and equipment with clean water at high pressure.
- Externally, spray air inlets and built-up deposits from around fan boxes and loading areas with detergent solution. Ensure that all dirty areas such as concrete aprons around the houses and bulk bin pads are washed clean.
- Internally, soak all surfaces thoroughly with detergent solution applied at low pressure.
- Leave for 20-30 minutes, and then rinse at high pressure using clean water.
- Ensure all surfaces and equipment are visibly clean before moving on to the disinfection stage.
Stage 4: Disinfection
The level of disease-causing organisms present after the cleaning stage is high enough to present a serious disease challenge to a new crop of birds. Broad spectrum disinfectants such as DuPont Virkon® S are recommended. Tested at the Institute for Animal Health, Compton, UK on Marek’s disease virus strain HPRS16, using the DEFRA testing method at 4°C in a 5% yeast solution organic challenge, Virkon® S passed at all dilutions tested including the lowest test dilution of 1:200.
- Use either a knapsack sprayer or pressure washer on a low pressure setting (300psi) to disinfect all equipment removed from the building.
- Place the equipment back in the cleaned building prior to disinfecting the house itself.
- Using a pressure washer on a low pressure setting (300psi) or an orchard sprayer for larger premises apply the disinfectant solution evenly to all washed internal surfaces to achieve thorough wetting.
- Pay particular attention to corners, cracks and seams ensuring that all sides of supporting posts are covered.
- Spray into the apex of the roof and work down the walls to the floors.
- Working from one end of the building to the other, apply disinfectant solution to the floor of the building.
- Upon completion of the disinfectant process, close all doors and place disinfectant footdips at all entrances.
- To control organisms introduced to the house during the setting up procedure and to disinfect the air and other inaccessible areas of the building use either a fine mist sprayer or thermal fogging machine to apply a solution of Virkon® S evenly.
Marek’s is a virus disease that can cause significant economic damage to poultry production through a variety of direct and indirect effects. Vaccination alone will NOT control all these effects. This stubborn virus can survive in the environment for 65 weeks. Feather follicles in the skin are the site of viral replication resulting in feather, dander, dust and litter containing the virus which is then spread by the airborne route. Good hygiene practices which prevent “carry-over” of Marek’s organisms, thus ensuring that each new crop gets a completely clean fresh start in combination with effective vaccination are key to controlling the disease.
- The Economics of Marek’s Disease, University of Reading publication
- Control Strategies for Marek’s Disease: A Perspective for the Future. Author: R. L. WITTER 1998, Poultry Science 77: 1197-1203. USDA-Agricultural Research
- Service, Avian Disease and Oncology Laboratory, East Lansing, Michigan 48823 Immunosuppressive effects of Marek’s disease virus (MDV) and herpesvirus of turkeys (HVT) in broiler chickens and the protective effect of HVT vaccination against MDV challenge. Author: A. F. M. F. Islam et al 2002, Avian Pathology 31, 449-461
Stephen Lister BSc BVetMed CertPMP MRCVS
Crowshall Veterinary Services
Marek’s Disease Papers For Download
Marek’s Disease is a viral tumor-causing disease of chickens. Marek’s is distributed worldwide and is so common that if you have birds, they have been exposed to Marek’s, regardless of whether they show symptoms or not. There are 4 different forms of Marek’s:
- Cutaneous (skin form)
- Neural (nerve form)
- Ocular (eye form)
- Visceral (internal-organ form)
Marek’s Disease is caused by 6 different herpes viruses that primarily affect young birds. The virus concentrates in feather follicles and is shed in dander. Marek’s disease-causing virus particles can survive for months in chicken-house dust and litter.
Marek’s is highly contagious and spreads by bird-to-bird contact, by contact with infected dust and dander, and by darkling beetles and mealworms that live in the chicken house, although the virus has no affect on the beetles or mealworms.
Other organisms common to chicken houses such as free-living mites, mosquitoes and coccidia do not transmit the disease. Chickens are most commonly exposed to Marek’s by contact with residual dust and dander in previously infected houses, by aerosol (air) contamination from a nearby house, or by virus particles carried by personnel and equipment. The virus doesn’t survive the incubation process well and is not spread by hatching eggs. Immune transfer from the hen to the chick provides some protection to the chick for the first few days of life.
The signs and symptoms of Marek’s Disease vary depending on the form of disease present.
- Cutaneous form: Enlarged reddened feather follicles and white bumps on the skin that form brown crusty scabs.
- Neural form: Characterized by one, all, or none of the following symptoms –
- Progressive paralysis, usually of the leg or wing, a typical leg-paralysis victim will have one leg extended forward and one leg extended back. A swelling of the sciatic nerve is the cause.
- Weight loss
- Labored breathing
- Starvation and death due to an inability to reach feed and water and to trampling by penmates.
- Ocular form:
- Gray eye color
- Misshapen iris
- Weight loss
- Visceral Form: Tumors on internal organs including heart, ovary, liver and lung.
Morbidity and mortality
Morbidity (number affected) in unvaccinated flocks can reach 60 percent. Vaccinated flocks fare better with less than 5 percent affected. Mortality is high in affected birds reaching nearly 100 percent over a 10-week period. Pullets are more likely to be affected than cockerels.
Diagnosis is derived from the flock history, symptoms and necropsy findings.
• Breed for resistance.
• Good sanitation and ventilation.
• Brood chicks separately from adults until 5 months of age.
• Keep turkeys with chickens (this may help the chickens with Marek’s, but can lead to black
head disease in the turkeys).
• Vaccinate all chicks at 1 day old; keep chicks from exposure until immunity has developed, about 7 days.
None. Cull affected birds. Some birds develop temporary paralysis that disappears after 1-2 days. They appear to return to normal, but frequently die from internal tumors a short time later.