avian mycoplasmosis (Mycoplasma synoviae)

Pictures

Picture	Title	Caption	Copyright
Title Histopathology Caption Histologic section of infected air sac (original x300 H&E stain) from young broiler. Immunologic response to Mycoplasma synoviae in air sac. The large. round, blue bundles of cells are lymphoid follicles. All the lymphocytes are clones of one lymphocyte. They are all programmed to produce plasma cells that secrete antibody to Mycoplasma synoviae. The large, blue cells scattered through the tissue are plasma cells containing Golgi bodies full of that antibody. Copyright Richard J. Julian	Histopathology	Histologic section of infected air sac (original x300 H&E stain) from young broiler. Immunologic response to Mycoplasma synoviae in air sac. The large. round, blue bundles of cells are lymphoid follicles. All the lymphocytes are clones of one lymphocyte. They are all programmed to produce plasma cells that secrete antibody to Mycoplasma synoviae. The large, blue cells scattered through the tissue are plasma cells containing Golgi bodies full of that antibody.	Richard J. Julian

Identity

Preferred Scientific Name

• 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

Overview

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.

Hosts/Species Affected

M. synoviae occurs mainly in chickens and turkeys, though the latter are less susceptible, and has also been isolated from guinea fowls, ducks, geese, pigeons, Japanese quail, house sparrows, red-legged partridge and pheasants (Stipkovits and Kempf, 1996). Its role in disease in game birds is unclear, as it has been isolated only from apparently healthy pheasants (Bradbury et al., 2001). Mycoplasmas similar to (or conspecific with) M. synoviae have also been isolated from ostriches (Cadman et al., 1994).

Distribution

Mycoplasma synoviae is probably distributed worldwide, but lack of diagnostic facilities in many countries and the difficulties in isolating the mycoplasma mean it is under-reported.

For current information on disease incidence, see OIE's WAHID Interface.

Distribution Table

The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Pathology

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).

Diagnosis

Clinical signs and lesions are not pathognomonic for M. synoviae, so laboratory diagnosis is necessary for accurate identification. Tracheal, oropharyngeal, eye, nasal or cloacal swabs from living birds are the preferred samples and should always be kept wet as this produces better survival rates for mycoplasmas (Bradbury, 1998). Isolation of M. synoviae from a dead bird is best achieved by aseptically taking fluids from the synovial fluids or tissue lesions from lungs or air sacs. Samples should be cultured onto media immediately, on the farm if possible, or cooled and dispatched rapidly to the laboratory. Serial dilutions of the tissues should be made to at least 10^-3 in medium containing thallium acetate and appropriate antibiotics. Aliquots of the homogenate should then be inoculated in broth and solid medium. A number of medium formulations including Sinovitis C medium and Frey’s Medium have been reported to support growth (Olson, 1984); nicotinamide adenine dinucleotide (NAD) and cystein are essential components of media. A commercial medium is also available from Mycoplasma Experience (Reigate, UK).

Identification of M. synoviae is best achieved by immunofluorescence using hyperimmune serum prepared in rabbits (Bradbury, 1998). Alternatively PCR tests are now available commercially (FlockChek, IDEXX Laboratories Inc, Portland, USA) for identification of mycoplasmas growing in vitro or directly in clinical material from affected birds (Bradbury et al., 2001). Salisch et al. (1998) concluded that the IDEXX PCR kit was specific and at least as sensitive as culture. Garcia et al. (1995) described a PCR using a single set of primers which amplifies DNA from M. synoviae, M. gallisepticum and M. iowae; the three mycoplasmas can be differentiated by restriction fragment length polymorphism with restriction enzymes HpaI, HpaII and MboI.

Successful detection of M. synoviae by culture and PCR from samples collected in the environment of experimentally infected chickens and turkeys, and under field conditions, was described by Marois et al. (2000); results showed that in an experimental infection, 10 of 96 and 46 of 96 samples of food, drinking water, feathers, droppings or dust were positive by culture and Mycoplasma-PCR, respectively. Under field conditions, the number of positive results for environmental samples were 7 of 28 and 17 of 28, respectively. These observations highlighted the high disseminating capacities of this mycoplasma and show the usefulness of the PCR method for epidemiological studies.

Serological detection of the presence of M. synoviae is not considered reliable because it does not induce a strong immune response in affected birds, particularly in turkeys. Indeed in one study, while mycoplasmas could be isolated from nearly 90% of experimentally infected turkeys, only 60% had seroconverted (Ortiz and Kleven, 1992). Traditionally, rapid slide tests (RST) have been used for antibody detection using stained antigens. Although they lack sensitivity and specificity, they are relatively robust and very easy to carry out, taking only 2 minutes to complete. They are most effectively used as flock tests on at least 60 birds per house. The haemagglutination inhibition test has been used in the past as a confirmatory test for the RST, but is not widely used because of the need to maintain actively growing cultures to produce antigen of the desired quality. ELISA tests have been available for many years and are slowly replacing RSTs. The more recently developed competitive ELISAs are more specific, show good sensitivity and have the added advantage that they can be used all avian species. One of major advantages of ELISAs is their ease of use in detecting antibodies in egg yolk; this provides a convenient indication of flock status.

List of Symptoms/Signs

Disease Course

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.

Epidemiology

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.

Impact: Economic

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.

Disease Treatment

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).

Prevention and Control

The economic effects of M. synoviae on the layer industry do not appear to justify the development and use of vaccines. However, this view may change, as its true prevalence becomes known with improved diagnostic tests, and with the likely failure of antibiotics to control disease in the future. A number of experimental vaccines have been reported and include the live avirulent MS-H strain which colonises the respiratory tract following eye-drop administration and stimulates serum antibody responses; clinical success and reduction in egg transmission was reported in a large field trial in broiler breeders in the USA (Whithear, 1996).

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Distribution Maps