MAREK’S DISEASE

MAREK’S DISEASE MD is a common and important neoplastic disease of chickens caused by serotype 1 herpes virus (MDV). These are related antigenically to non-oncogenic herpes virus of chickens (serotype 2) and turkeys (serotype 3), also known as turkey herpes virus (HVT). Within serotype 1, MDV four pathotypes are recognized: (mild (m), virulent (v), very virulent (vv) and recently, very virulent + (vv+). All pathotypes of serotype 1 cause disease but serotype 1 isolates can be attenuated by serial passage in cell cultures. This disease occurs after 2 months (2-4 months). Virus strains: MD has been recognized in chickens for over 80 years. Even after a decade of research and development and the use of several effective vaccines MD continues to be a contributing cause of mortality in almost every commercial flock today. Epidemiology Loses experienced by the layer industry during the past 5 years confirm that this disease is still a major threat to profitability. Continued use of a single vaccine in areas of a high poultry density and with genetic susceptibility of stock and multiage placement programs, field MD strains with enhanced pathogenicity emerge. Close proximity of rearing and laying houses on same units provide the opportunity for airborne transmission of MDV from older flocks to newly placed, vaccinated pullets under 2 weeks of age. Outbreaks of vv+ MD are characterized by mortality, which ranges from 20-50 % commencing during the terminal month of the growth period and extending for at least 15 weeks into the early laying period. Deficiencies in biosecurity involving uncontrolled movement of personal and contaminate equipment may contribute to infections. Field experience confirms that vaccination alone cannot be regarded as totally effective in protecting the flocks. It is imperative to place started pullets in thoroughly decontaminated single age units and to maintain high levels of biosecurity to prevent introduction of MDV during the first 8 weeks of rearing Feather and dander acts as the source of infection or contamination to the environment. Morbidity and mortality equals, mortality : 25 -30%. An infected dropping from the infected bird is the source. Morbidity and morality are due to the development of tumors in various internal organs and paralysis resulting form infiltration of the nerves by lymphocytes. MD does not come from the breeder, and spreads horizontally form birds to birds. Pathogenesis • Virus is widespread and hardy, all flocks and all chickens are infected with the virus and are the source of infection. • Four phases of infections in vivo: 1. Early productive restrictive virus infection causing primary degenerative changes. 2. Latent infection. 3. A second phase of cytolytic infection coincident with permanent immunosuppression. 4. A proliferative phase: involving non-productively infected lymphoid cells that may or may not progress to the point of lymphoma formation. • Virus gains entrance via the respiratory tract where it is picked up by the phagocytic cells. • Thereafter, cytolytic infection can be detected in the spleen, bursa of fabricious and thymus peaking at 3-6 days. • A hyperplastic response in the spleen can follow at about 7 days and a transient immunosuppression may occur due to the presence of suppressor macrophages. Ultimately, there can be atrophy of the bursa or thymus • At about 6-7 days, the infection switches to latency coincident with the development of immune responses. The latent infection is persistent and can last for the lifetime of the bird. • Susceptible birds develop a second wave of cytolytic infection after 2 or 3 weeks coincident with permanent immunosuppression. Foci of infection in visceral organs i.e. kidney, pancreas, adrenal gland, proventriculus etc. Focal necrosis and inflammatory reaction develop around affected areas. • The cause of inflammatory CNS lesion associated with MDV induced transient paralysis is not clear but it is known that the syndrome is under the control of genes of MHC and that is cells are required for its induction. Clinical Signs 1. Asymmetric progressive paresis and later complete paralysis of one or more of the extremities. Since any one or several nerves may be affected, signs vary from bird to bird. 2. Wing involvement is characterized by dropping of the wings and limbs. 3. If nerves controlling neck muscles are affected, the head may be held low and there may be some torticollis. 4. Vagal involvement can result in paralysis and dilation of the crop and / or gasping. 5. Incoordination or stilted gait may be the observed sign. Bird has one leg stretched forward and other back as a result of unilateral paralysis of the leg. 6. Severe depression, ataxia, unilateral or bilateral paralysis, emaciation, dehydration and comatose. 7. Blindness may result from the involvement of iris. 8. Nonspecific signs such as weight loss, paleness, anorexia and diarrhoea may be observed especially in birds in which the course is prolonged. Diagnosis • Isolation of virus from the skin, dander or feather tips. • By serological tests – AGPT, ELISA, HA, VNT, FAT • By PM findings • Nerve lesions – celiac, cranial mesenteric, brachial and sciatic plexus and splanchnic nerves. • Plexuses of the sciatic and brachial nerves are more enlarged than respective trunks. • Lymphoid tumors may occur in the gonads especially the ovary but lymphomatous lesions can also be found in lung, heart, mesentry, kidney, liver, spleen, bursa, thymus, adrenal gland, pancreas, proventriculus, intestine, iris, skeletal muscle and skin. PM lesion • Diffuse infiltration of liver cause loss of normal lobulation and giving a coarse granular appearance. • Proventriculus becomes thickened and firm as a result of small to large leukotic areas within and between the glands. • Affected hearts are pale from diffuse infiltration or have single or multiple nodular tumors in the myocardium. • Atrophy of bursa of fabricious. Differential Diagnosis Avian Leucosis Complex • Caused by RNA or Oncovirus type C. • Older birds 3-8 months of age are affected. • CNS less commonly affected. • Ocular lesion – not common. • Neoplastic origin. • Not airborne transmission, i.e. vertically transmitted. • No peripheral nerve involvement. • Tumor of bursa of Fabricious and hypertrophy of bursa. Reticuloendotheliosis • Occurs in 2-6 months • Paralysis and gross lesion on skin is rare • Bursa atrophy is common Prevention Cleaning and disinfection of the house (biosecurity) • Clean the floor, sides, ceiling, fan etc. • Washing the building with detergents. • Disinfection with iodine and formaldehyde (5%) • Dust also can be carried into the brooder house on clothing of hair or slippers. Restrict the visitors in the farm • Fumigation Vaccination • Dose can vary 5,000 to 10,000 pfu. The ovo-vaccination is now applied in 80% of the eggs in developed countries. • Early challenge : Chicks placed on multi aged farms or in contaminated housings exposed to virulent vvMD before the onset of vaccine stimulated the immunity. • Increased Virulence of MDV: • Mutation of MDV has resulted higher levels of virulence. • Vaccine alone cannot suppress MDV infection. • An integrated strategy i.e. minimizing early exposure, enhancing genetic resistance and introduction of noble vaccines are recommended. Infections influencing MD immunity • Chicken anaemia and IBD viruses are known to have a negative influence on the immunity for MD. • Therefore, by hygienic measures or by proper vaccinations is required. • Breeding for MD resistance flocks are important in these days Cooperations • Laboratory – proper diagnosis & isolation of virus • Vaccine industry – Development of new vaccines • Hatchery - Proper storage of vaccines and proper vaccination procedure • Farmers – Prevention of early MD exposure • Breeding organization – Development of more resistant strains