avian mycoplasmosis (Mycoplasma synoviae)

International Common Names

• English: avian mycoplasmosis; infectious sinusitis; infectious sinusitis of chickens; infectious synovitis; infectious synovitis of chickens; Mycoplasma induced arthritis; Mycoplasma induced upper respiratory tract infection; mycoplasma synoviae in chickens and turkeys; Mycoplasma synoviae infections

Mycoplasma synoviae was first isolated in the USA in 1954 (Olson et al., 1956). The importance of M.synoviae is almost certainly under reported as it is difficult to isolate and detect, even until relatively recently by serological techniques. This has been compounded by its close serological relationship with M. gallisepticum, a cause of chronic respiratory disease in poultry. Furthermore, large variations in the virulence and antigenic properties of strains have led to the view that M. synoviae is not economically important. However the experience of many workers indicates that M. synoviae can cause significant losses, particularly egg production losses. In parts of Europe, infection is endemic in laying flocks. Control measures are hampered by the ability of the mycoplasma to infect progeny through egg transmission and its increased resistance to antibiotics.

This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). For further information on this disease from OIE, see the website: www.oie.int.

Disease caused by M. synoviae in chickens is an acute generalised process characterised by air-sacculitis or arthritis. Arthritic lesions are characterized by a turbid to caseous exudate, infiltration with mononuclear cells and plasma cells, hyperplasia of the synovial linings and sometimes erosion of the articular cartilage. Synovitis occurring in the joints, keel bursae and tendons may also seen (Blaxland et al., 1982). Lesions of the respiratory tract are common in chickens but rare in turkeys. In some affected chicken flocks, spleens may be enlarged, livers and kidneys swollen and discoloured with atrophy of the bursa and thymus gland. In the first case of its kind, M. synoviae was isolated from the brains of 22-week-old commercial meat turkeys, showing severe synovitis and infrequent nervous system signs; protein profiles of isolates were markedly different from the type strain (Chin et al., 1991).

Aerosol infection of chicks with M. synoviae causes changes in the trachea, including oedema, deciliation and some desquammation of epithelia; the epithelia begin to regenerate 2 weeks after infection (Ross, 1993). An experimental infection in hens led to a drop in egg production after a week; a reduction of 18% after two weeks before returning to normal levels after a month (Olson, 1984).

The incubation period of disease may be relatively short; chicks can show infectious sinusitis at 6 days of age following egg transmission of M. synoviae. Following contact exposure, the incubation period is usually 11-21 days, with antibodies being detected before clinical signs are apparent. Birds are susceptible to most infection routes.

M. synoviae is introduced via infected hens or eggs and then spreads to other birds by direct and indirect contact as well as by egg transmission, in which the highest rates of transmission are seen in the first 4-6 weeks after infection (Stipkovits and Kempf, 1996). It is believed to spread more quickly than M. gallisepticum. Great variations occur among M. synoviae strains in terms of virulence and tissue tropisms, which lead to different forms of disease. Other agents such as those causing Newcastle disease, infectious bronchitis and influenza, as well as Escherichia coli and M. gallisepticum and M. meleagridis may exacerbate disease caused by M. synoviae.

Disease is believed to be under-reported because of the difficulties of isolating the mycoplasma. While mortality rates rarely exceed 5% in chickens, morbidity rates can vary from 2 to 75% with 5-15% being most usual (Olson, 1984). Stipkovits and Kempf (1996) reported a reduction of 5-10% in egg production and a 5-7% reduction in hatchability, with 5% mortality in the offspring in breeder flocks without obvious clinical signs.

In vitro tests have shown that M. synoviae isolates are sensitive to tilmicosin and tylosin (Jordan and Horrocks, 1996); enrofloxacin, sarfloxacin, and oxytetracyclines (Wang et al., 2001). However, Stipkovits (2000) has reported that M. synoviae strains are becoming more resistant to antibiotics than other avian mycoplasmas, which means it is more difficult to treat infected flocks successfully. The ability of the mycoplasma to spread via the egg makes control difficult. Some successes have been seen in reducing infection by:

• dipping warm fertile eggs in cold antibiotic solutions, usually chlortetracyclines, for 15-20 minutes which enables the drugs to attack the mycoplasmas within the egg.
  
• gradual heating of the eggs to 46-47°C over a period of 11-14 hours prior to incubation.

Losses in egg fertility of up to 10% may be seen as a result of these treatments, particularly with heat treatment. The same antibiotics are also usually included in the feed or in water for a limited period. Control programmes should also include the culling of all clinically affected birds and the maintenance of progeny flocks in small groups so that if infection is found following treatment only the infected group need be removed (Blaxland et al., 1982).