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I have not heard of lameness as a sign of Mareks. Though .... I am inexperienced. I was thinking more of Mycoplasma Synoviae ????
Marek's Disease (Visceral Leukosis)
Marek's disease is characteristically a disease of young chickens but older birds can also be affected. In contrast to the lymphoid leukosis tumor response, Marek's disease may be observed in more diverse locations.
Marek's disease is caused by a virus belonging to the Herpes virus group. Much is known about the transmission of the virus; however, it appears that the virus is concentrated in the feather follicles and shed in the dander (sloughed skin and feather cells). The virus has a long survival time in dander since viable virus can be isolated from houses that have been depopulated for many months.
The usual mode of transmission is by aerosols containing infected dander and dust. Young birds are most susceptible to infection by Marek's disease; however, since the incubation period is short, clinical symptoms can appear much earlier than in the case with lymphoid leukosis.
Marek's disease may produce a variety of clinical responses, all lymphoid in character. These are acute visceral, neural, ocular, skin or combinations of the responses that can be seen.
Marek's of the visceral type is characterized by widespread involvement with lesions commonly seen in gonads, liver, spleen, kidney and occasionally heart, lungs and muscles. The disease is often acute, with apparently healthy birds dying very rapidly with massive internal tumors. The disease may appear in broiler-age birds but the most severe losses occur in replacement pullet flocks prior to onset of egg production.
The neural type of Marek's is typified by progressive paralysis of the wings, legs and neck. Loss of body weight, anemia, labored respiration and diarrhea are common symptom. If lesions are present, they are confined to the nerve trunks and plexes enervating the paralyzed extremities. Frequently no gross lesions can be observed.
Ocular (eye) leukosis or "gray-eye" is usually seen in early maturity. Morbidity and mortality are usually low but may approach twenty-five percent in some flocks. It is characterized by the spotty depigmentation or diffuse graying of the iris in the eye. The pupil develops an irregular shape and fails to react to light. Emaciation diarrhea and death follow.
Skin leukosis produces the most severe losses in broilers. The losses result from high condemnations at the processing plant. Enlargement of the feather follicles due to accumulations of lymphocytes is the typical lesion. This is the most infective virus since it is produced in the regions of the feather follicles and is shed with the skin dander.
Acute Marek's disease can be extremely rapid in its course, producing mortality in apparently healthy birds. However, in some cases the lesions may regress and clinically affected birds may make complete recoveries.
Diagnosis is based upon flock history and disease manifestations. Accurate diagnosis may depend on results of laboratory procedures. As is the case with lymphoid leukosis, there is no treatment for Marek's disease.
A vaccine is available that is extremely effective (90% +) in the prevention of Marek's disease. It is administered to day-old chickens as a subcutaneous injection while the birds are in the hatchery. Use of the vaccine requires strict accordance with manufacturer's recommendations in a sterile environment.
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Mycoplasma synoviae infection, M.s. Infectious Synovitis
Infection with Mycoplasma synoviae may be seen in chickens and turkeys in association with synovitis and/or airsacculitis. It occurs in most poultry-producing countries, especially in commercial layer flocks. Infection rates may be very high. Spread is generally rapid within and between houses on a farm, whilst illness is variable and mortality less than 10%.
Infection is via the conjunctiva or upper respiratory tract with a long incubation period, 11-21 days following contact exposure. Transmission may be transovarian, or lateral via respiratory aerosols and direct contact. Survival of the infectious agent outwith the bird is poor but fomite transmission between farms is important. Predisposing factors include stress and viral respiratory infections.
Signs
There may be no signs.
Depression.
Inappetance.
Ruffled feathers.
Lameness.
Swelling of hocks, shanks and feet (sometimes severe and bilaterally asymmetrical).
Faeces may be green in acute infections.
Effects on egg production appear to be minor under good management.
Post-mortem lesions
Joints and tendon sheaths have viscid grey to yellow exudate.
Some strains can lead to amyloidosis.
Swollen liver, spleen and kidney have been seen in the past but are not common now.
Green liver.
Exudate becomes caseous later.
Sternal bursitis.
Airsacculitis - usually in heavy broilers and associated with condemnations.
Diagnosis
Lesions, serology, isolation (difficult - requires NAD) and identification. Differentiate from viral arthritis, staphylococcal arthritis, Mycoplasma gallisepticum infections, Ornithobacterium rhinotracheale, viral respiratory disease with colibacillosis.
Serology: SAG used routinely, Elisa in some countries - PCR and/or culture used to confirm. False positives post inactivated vaccines are, if anything more common than in the case of M.g.
Treatment
Tilmicosin, chlortetracycline, oxytetracycline, tylosin.
Prevention
Eradication of this infection is also possible using similar techniques as described for Mycoplasma gallisepticum. These are based on purchase of uninfected chicks, all-in/all-out production, and biosecurity. Maintenance of Mycoplasma synoviae free status seems to be more difficult than for Mycoplasma gallisepticum. In some circumstances preventative medication of known infected flocks may be of benefit.
Vaccines are not widely used though they are available in some countries. Infected birds do develop some immunity to the effects of repeated inoculation.
