Mycoplasma lack cell walls, have highly variable surface proteins and a distinctive plasma membrane, and are the smallest self-replicating prokaryotes.

This led to an increased awareness of the disease and health monitoring protocols in wild turkey restoration programs.

[5] In January 1994, the first house finches with symptoms of M. gallisepticum were observed in the Washington DC area, including part of Maryland and Virginia.

[4] In 1994, efforts were made across North America to collect data on the spread and prevalence of M. gallisepticum using the House Finch Disease Survey.

[6] A few years later the epidemic that started in the mid-Atlantic states spread to the entire eastern population of house finches.

It has been suggested that those house finches were less resistant to the disease because they were introduced beginning with a small population, and were subsequently highly inbred.

[9] Research using RFID tags to track a sample of wild finches found an individual bird's likelihood of acquiring or transmitting the infection to be positively correlated with time spent at feeders.

[10][11] Mycoplasma gallisepticum infection in house finches (Haemorhous mexicanus) causes conjunctivitis with the symptoms of periocular swelling, swollen eyelids, ocular and nasal discharge, impaired vision, depression, and weight loss.

Infected birds may be listless or seem disoriented, present with reckless or limited flight, and a timid reluctance to flee predators or humans.

[3] Some major clinical signs of M. gallisepticum in chickens include those of respiratory distress such as coughing, sneezing, slight to marked rales, and difficulty breathing.

"[15] Other avian species that have been affected by this disease are pigeons, chukar partridges, quail, ducks, geese, pheasants, psittacine birds, and peafowl.

[13] Some exotic birds infected by this disease include greater flamingos, wild peregrine falcons in Spain, and yellow-naped Amazon parrots.

Also, M. gallisepticum can be transmitted via infectious aerosols and through contamination of feed, water, and environment as well as human activity on fomites which can come from equipment and shoes.

When they are in a flock, transmission occurs by direct and indirect contact from the movement of the birds, people and fomites from infected species.

[13] The greatest success in isolating M. gallisepticum has been from tissue swabs from live trapped or newly dead birds.

It has been found that antibody responses change in the early and advanced stages of the disease and the results vary according to the test method.