Infection with Mycoplasma synoviae (Avian mycoplasmosis)

Many infections are silent. In the synovitis form, birds show pale or bluish combs, lameness, reluctance to stand, stunted growth and swollen hocks, footpads and joints, sometimes with breast blisters from lying down; droppings are often greenish with excess urates. Respiratory infection is usually mild, with occasional rales. In laying hens a newer form causes shells with rough, thin, translucent areas at the apex, more breakage and a drop in lay. At necropsy, creamy to grey viscous exudate fills hock and wing joints and tendon sheaths, with enlarged liver and spleen and swollen, mottled kidneys.

Avian mycoplasmosis of this type is caused by Mycoplasma synoviae, a wall-less bacterium of the class Mollicutes, family Mycoplasmataceae. Strains differ markedly in virulence and in which tissues they favour. In the joint form the organism adheres to and invades the cells lining tendon sheaths; the infected cells switch on inflammatory cytokines and chemokines (including IL-1 beta, IL-6 and IL-8) that draw macrophages and other leukocytes into the synovial layer, producing synovitis with viscous exudate. In the respiratory tract it causes mild tracheitis, sinusitis and airsacculitis, worsened by co-infection with other respiratory agents. In laying hens some strains are associated with eggshell apex abnormality: thin, translucent, rough shell at the egg tip.

Chickens and turkeys are the main hosts, and ducks, geese, guinea fowl, quail and pheasants can also be infected; the infection occurs worldwide. It passes vertically through the egg and horizontally within a flock, spreading rapidly by aerosol and respiratory secretions once introduced by carrier birds, people or fomites; the organism can survive for days on synthetic fibres. Infected birds carry it for life. A Chinese serological survey from 2010-2015 found about 41% of samples positive. There are no reports of human infection. It is a WOAH-listed disease, and flocks are monitored by serological surveillance.

Lameness must be separated from skeletal abnormalities and trauma, viral tenosynovitis, and staphylococcal or other bacterial joint infections; respiratory signs from Newcastle disease, infectious bronchitis and Mycoplasma gallisepticum, which produces more pronounced coryza, sinusitis and conjunctivitis than M. synoviae. Because lesions overlap, confirmation relies on isolating the organism or detecting its DNA by PCR, with serology (rapid agglutination, ELISA, haemagglutination inhibition) used for flock screening rather than individual birds.

Joints and tendon sheaths (hock, wing, footpad), sternal bursa, trachea, infraorbital sinuses, air sacs, oviduct and eggshell, liver, spleen, kidneys

Buy stock from M. synoviae-free breeder flocks, keep strict biosecurity and serological surveillance. Live vaccines (MS-H, MS1) are licensed in several countries and must precede field challenge; inactivated vaccines are little used.

Morbidity is usually low to moderate and mortality about 1-10%. Antimicrobials may help prevent disease but are not effective in established cases, and recovered birds stay infected for life.