Marek's disease in poultry; cause, symptom, prevention and control

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Marek's disease in poultry; cause, symptom, prevention and control Marek disease is a highly contagious viral disease of poultry characterized by T-cell lymphomas and peripheral nerve enlargement. Although no treatme

Standard criteria used for diagnosis include history, clinical signs, gross necropsy, and histopathology. Although no treatment is available, current vaccines are highly protective. Chickens are the most important natural host for Marek disease virus (MDV), a highly cell-associated but readily transmitted alphaherpesvirus with lymphotropic properties of gammaherpesviruses. Quail can be naturally i

nfected, and turkeys can be infected experimentally. However, severe clinical outbreaks of Marek disease in commercial turkey flocks, with mortality from tumors reaching 40%–80% between 8 and 17 weeks 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 disease virus that is commonly used as a Marek disease vaccine in chickens. Other birds and mammals appear to be refractory to the disease or infection. Marek 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. Etiology of Marek Disease in Poultry
Marek 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 disease virus. Gallid alphaherpesvirus 2 (MDV serotype 1) represents all virulent Marek disease virus strains and is further divided into pathotypes, designated as mild (m), virulent (v), very virulent (vv), and very virulent plus (vv+). Gallid alphaherpesvirus 3 (MDV serotype 2) and Meleagrid alphaherpesvirus 1 (turkey herpesvirus, MDV serotype 3) represent avirulent virus strains isolated from chickens and turkeys, respectively, and are commonly used as vaccines against Marek disease. Transmission and Etiology of Marek Disease in Poultry
Marek 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 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 disease virus strains vary greatly in their transmissibility among chickens; the most highly attenuated are not transmitted. Marek disease virus is not vertically transmitted. Pathogenesis of Marek Disease in Poultry
Currently, four phases of infection with Marek disease in vivo are recognized:
Early cytolytic infection (productive-restrictive)
Latent infection
Second phase of cytolytic, productive-restrictive infection coincident with permanent immunosuppression
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 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 cocultivation with susceptible cells in tissue cultures. Some T cells, latently infected with oncogenic Marek 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. Clinical Findings of Marek Disease in Poultry
Marek disease, leg paresis, chicken
Marek disease, leg paresis, chicken
COURTESY OF DR. JEAN SANDER. The incidence of Marek 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
several environmental factors, including stress
In addition to lymphoid neoplasms, Marek disease virus can also induce other clinically distinct disease syndromes, including:
transient paralysis
early mortality syndrome
cytolytic infection
atherosclerosis
persistent neurologic disease
Typically, affected birds show only depression before death, but a transient paralysis syndrome has been associated with Marek 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. Lesions
Marek disease, peripheral nerve enlargement, chicken
Marek disease, peripheral nerve enlargement, chicken
COURTESY OF DR. JOHN DUNN. Marek disease, skin involvement, chicken
Marek disease, skin involvement, chicken
COURTESY OF DR. JEAN SANDER. Marek disease, eye involvement, chicken
Marek disease, eye involvement, chicken
COURTESY OF DR. JEAN SANDER. 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, go**ds, 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. Diagnosis of Marek Disease in Poultry
Standard criteria: history and clinical signs, gross pathology, and histopathology
Advanced criteria: immunohistochemistry, standard and quantitative PCR, virus isolation, serology
For the diagnosis of Marek disease, it is critical to diagnose the tumors and not the infection because Marek 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, although the presence of bursal tumors does not exclude Marek disease. Marek disease can develop in chickens as young as 3 weeks old, whereas lymphoid leukosis typically is seen in chickens >14 weeks old. Reticuloendotheliosis, although rare, can easily be confused with Marek disease, because both diseases can feature enlarged nerves and T-cell lymphomas in visceral organs. Standard criteria are often sufficient for a presumptive diagnosis, but advanced criteria are needed for a definitive diagnosis. Immunohistochemistry can be used to confirm tumors are composed of predominant T-cell populations or expressing specific MDV antigens. There is a quantitative association between viral load and Marek 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 disease. Control of Marek Disease in Poultry
There is no effective treatment for Marek disease
Prevention methods include vaccination, biosecurity, and genetic resistance
Vaccination is the central strategy for the prevention and control of Marek disease, along with strict sanitation to reduce or delay exposure and by breeding for genetic resistance. The most widely used vaccines include:
Turkey herpesvirus (HVT, naturally avirulent Meleagrid alphaherpesvirus 1)
SB-1 or 301B/1 (naturally avirulent Gallid alphaherpesvirus 3)
CVI988/Rispens (attenuated Gallid alphaherpesvirus 2)
HVT vaccine has seen rapidly increased use as a backbone in recombinant vaccines featuring the insertion of genes from other poultry viruses, such as Newcastle disease virus, infectious bursal disease virus, or infectious laryngotracheitis virus. These recombinant vaccines offer protection against both Marek disease virus and the inserted virus. Bivalent vaccines consisting of HVT and either the SB-1 or 301B/1 strains of Gallid alphaherpesvirus 3 have been used to provide additional protection against challenge with virulent Marek disease virus isolates. The most protective commercial vaccine currently available appears to be CVI988/Rispens, an attenuated Marek disease virus strain that is also commonly mixed with HVT at vaccination.

13/10/2022

Marek’s disease virus, a herpesvirus that is the causative agent of Marek’s disease, is a worldwide economic burden on poultry farming. However, little is known about the prevalence and dynamics of this virus in the field. Commercial poultry farming is highly structured, and so important questions are, how does virus prevalence differ across this structure, and how does virus prevalence change within a single level of this structure over time? To answer these questions, virus prevalence across farms in Pennsylvania for three years was surveyed. This involved collecting dust samples from chicken houses and using a qPCR (quantitative polymerase chain reaction) assay specific for non-vaccine Marek’s disease virus to assess the virus’s concentration in the dust.
In total, 4448 samples were collected across 15 operations, and 106 farms. These data were analyzed with generalized linear mixed effects models fit using Bayesian methods. Virus prevalence varied considerably in the collected data. Substantial amounts of variation were attributable to between operation, between grower, and between flock effects. A smaller magnitude of variation was attributable to between house effects and between sample effects. Also, significant effects of cohort age and seasonality were identified. Researchers were unable to identify a significant effect of production type, but it is unclear whether this was due to a lack of biological importance or due to sampling constraints. Examining the data from within farms over time confirmed many of the patterns discovered by the mixed effect modeling. These data also revealed apparent patterns of virus disappearance and reemergence, where the virus concentration dropped to below detectable levels only to reappear in later samples. Whether this was due to repeated extinction and reintroduction events, or due to virus population dynamics that occurred below the qPCR limit of detection is still an open question.

21/09/2022
The most protective commercial vaccine currently available appears to be CVI988/Rispens, an attenuated Marek's disease v...
21/09/2022

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.
Vaccines are administered at hatch or in ovo to embryos at the 18th day of incubation.

The Infected ChickenOnce a chicken catches this disease it would be best to separate it from its flock as soon as possib...
21/09/2022

The Infected Chicken
Once a chicken catches this disease it would be best to separate it from its flock as soon as possible. Many would suggest putting down the sick bird too.

How Does Marek’s Disease Spread?On a bigger scale, one infected chicken is enough to cause other chickens to get sick. A...
21/09/2022

How Does Marek’s Disease Spread?
On a bigger scale, one infected chicken is enough to cause other chickens to get sick. As we have said earlier, this disease is easy to pass from one chicken to another. The infected chicken does not even have to be there to do this.
An infected chicken can spread this disease by simply living. For one, it will unconsciously shed its dander (skin flakes) where it goes. These flakes could then be a means of infecting other chickens.

Causes of Marek’s DiseaseThe cause of Marek’s disease is a virus. Specifically, one linked to those that bring about her...
21/09/2022

Causes of Marek’s Disease
The cause of Marek’s disease is a virus. Specifically, one linked to those that bring about herpes in humans. You do not need to worry. This one will not make you sick.

23/08/2022

Morbidity is 10-50% and mortality up to 100%. Mortality in an affected flock typically continues at a moderate or high rate for quite a few weeks. In 'late' Marek's the mortality can extend to 40 weeks of age. Affected birds are more susceptible to other diseases, both parasitic and bacterial.
The route of infection is usually respiratory and the disease is highly contagious being spread by infective feather-follicle dander, fomites, etc. Infected birds remain viraemic for life. Vertical transmission is not considered to be important.
The virus survives at ambient temperature for a long time (65 weeks) when cell associated and is resistant to some disinfectants (quaternary ammonium and phenol). It is inactivated rapidly when frozen and thawed.
Signs
Paralysis of legs, wings and neck.
Loss of weight.
Grey iris or irregular pupil.
Vision impairment.
Skin around feather follicles raised and roughened.
Post-mortem lesions
Grey-white foci of neoplastic tissue in liver, spleen, kidney, lung, go**ds, heart, and skeletal muscle.
Thickening of nerve trunks and loss of striation.
Microscopically - lymphoid infiltration is polymorphic.
Diagnosis
History, clinical signs, distribution of lesions, age affected, histopathology.
Differentiate from Lymphoid leukosis, botulism, deficiency of thiamine, deficiency of Ca/Phosphorus/Vitamin D, especially at the start of lay.

Treatment
None.

Prevention
Hygiene, all-in/all-out production, resistant strains, vaccination generally with 1500 PFU of HVT at day old (but increasingly by in-ovo application at transfer), association with other strains (SB1 Sero-type 2) and Rispen's.
It is common practice to use combinations of the different vaccine types in an effort to broaden the protection achieved. Genetics can help by increasing the frequency of the B21 gene that confers increased resistance to Marek's disease challenge.
Latest information
In 2018, Aviagen published their comprehensive brief "Marek's disease control in broilers birds" on The Poultry Site. It includes details of transmission, diagnosis, vaccinations, vaccine administration and causes of the disease.

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