Mycoplasma synoviae was first recognized as an acute to chronic infection of chickens and turkeys that produced an exudative tendonitis and bursitis; it now occurs most frequently as a subclinical infection of the upper respiratory tract. Mycoplasma synoviae infection is also a complication of airsacculitis in association with Newcastle disease or infectious bronchitis. It occurs primarily in chickens and turkeys, but ducks, geese, guinea fowl, parrots, pheasants, and quail may also be susceptible. Serum (preferably swine serum) and nicotinamide adenine dinucleotide (NAD) are required for growth on artificial media.
Transmission, Epidemiology, and Pathogenesis: Mycoplasma synoviae is egg-transmitted, but the rate is low (probably <5%), and some hatches of progeny of infected flocks may be free of M synoviae . Egg transmission is greatest during the first 1-2 mo after infection of susceptible breeders. Lateral transmission is similar to that of M gallisepticum , but the rate of spread is generally more rapid.
Mycoplasma synoviae isolates vary widely in pathogenicity. Isolates from cases of airsacculitis are more apt to produce air sac lesions than isolates from synovial fluid or membranes. Some strains of M synoviae produce the typical clinical disease of synovitis. The paucity of natural outbreaks of clinical synovitis in chickens in recent years may be related to the adaptation of M synoviae to the respiratory tract; however, clinical synovitis in turkeys is still relatively common.
Clinical Findings: Although slight rales may be present in birds with respiratory infection, usually no signs are noticed. Younger birds, especially those under stress or suffering concurrent infections, are more likely to be affected. Outbreaks of infectious synovitis occur most commonly in chickens at 4-6 wk and in turkeys at 10-12 wk. Lame birds tend to sit. The more severely affected birds are depressed and are found around the feeders and waterers. Swellings of the hocks and foot pads are seen. Morbidity is 2-15% and mortality 1-10%. The effect on egg production is minimal, but instances of egg production losses have occurred.
Lesions: In the respiratory syndrome, airsacculitis occurs when the bird is stressed from Newcastle disease, infectious bronchitis, or improper ventilation. In many cases, air sac lesions resolve after 1-2 wk. Early in synovitis, the liver is enlarged and sometimes green. The spleen is enlarged, and the kidneys are enlarged and pale. A yellow to gray, viscid exudate is present in almost all synovial structures; it is most commonly seen in the keel bursa, hock, and wing joints. In chronic cases, this exudate may become inspissated and orange.
Diagnosis: A presumptive diagnosis can be based on the lesions and clinical signs, but laboratory confirmation is necessary. Skeletal abnormalities must be eliminated as the cause of lameness. The disease must be differentiated from viral tenosynovitis and from staphylococcal and other bacterial infections.
The serum plate agglutination or ELISA test is used to detect infected flocks, but cross-reactions with M gallisepticum and other nonspecific reactions may occur. Reactors are confirmed as positive by hemagglutination-inhibition or by isolation and identification of the organism. Polymerase chain reaction may be used to rapidly detect the organism in infected tissues. In turkeys, the agglutination test for M synoviae may not be reliable.
Treatment and Control: Serological testing and isolation similar to those for M gallisepticum have resulted in eradication of the infection in most primary breeder flocks of chickens and turkeys. Administration of a tetracycline antibiotic in the feed may be beneficial in treatment or prevention of synovitis. When airsacculitis is a problem, preventive antibiotic therapy during the time of respiratory reaction to Newcastle disease and infectious bronchitis vaccine may be helpful. Medication of breeder flocks is of little value in preventing egg transmission.
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