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Mycoplasma gallisepticum Infection in Poultry

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M gallisepticum is commonly involved in the polymicrobial "chronic respiratory disease" of chickens; in turkeys, it frequently results in swollen infraorbital sinues and is called "infectious sinusitis." These diseases affect chickens and turkeys worldwide, causing the most significant economic losses in large commercial operations, and are commonly seen in noncommercial flocks. Infection also occurs in pheasants, chukar partridges, peafowl, pigeons, quail, ducks, geese, and psittacine birds. Songbirds are generally resistant, although M gallisepticum causes conjunctivitis in wild house finches (and some similar species) in North America.

M gallisepticum is the most pathogenic avian mycoplasma; however, considerable strain variability is manifest in a range of host susceptibility, virulence, clinical presentation, and immunologic response. Integral membrane surface proteins (adhesins) that attach to receptors on host cells, allowing for colonization and infection, are important virulence factors involved in antigenic variation and immune evasion.

M gallisepticum is transmitted vertically within some eggs (transovarian) from infected breeders to progeny, and horizontally via infectious aerosols and through contamination of feed, water, and the environment, and by human activity on fomites (shoes, equipment, etc). Infection may be latent in some birds for days to months, but when birds are stressed horizontal transmission may occur rapidly via aerosols and the respiratory route, after which infection and clinical disease spread through the flock. Flock-to-flock transmission occurs readily by direct or indirect contact from the movement of birds, people, or fomites from infected to susceptible flocks. Some potential reservoirs of M gallisepticum in the USA are noncommercial (backyard) flocks, multiple-age layer flocks, and some free-ranging songbird species. Good management and biosecurity practices are necessary to ensure that M gallisepticum infections are not introduced to commercial poultry from these and other sources. In many outbreaks, the source of infection is unknown. Cold weather, poor air quality or crowding, concurrent infections, and some live virus vaccinations may facilitate infection, disease, and transmission.

Epithelium of the conjunctiva, nasal passages, sinuses, and trachea are most susceptible to initial colonization and infection; however, in severe, acute disease, infection may also involve the bronchi, air sacs, and occasionally lungs. Once infected, birds may remain carriers for life. There is a marked interaction (polymicrobial disease) between respiratory viruses, Escherichia coli, and M gallisepticum in the pathogenesis and severity of chronic respiratory disease.

In chickens, infection may be inapparent or result in varying degrees of respiratory distress, with slight to marked rales, difficulty breathing, coughing, and/or sneezing. Morbidity is high and mortality low in uncomplicated cases. Nasal discharge and conjunctivitis with frothiness about the eyes may be present. The disease is generally more severe in turkeys than in chickens, and swelling of the infraorbital sinuses is common. Feed efficiency and weight gains are reduced. Commercial broiler chickens and market turkeys may suffer high condemnations at processing due to airsacculitis. In laying flocks, birds may fail to reach peak egg production, and the overall production rate is lower than normal.

Uncomplicated M gallisepticum infections in chickens result in relatively mild catarrhal sinusitis, tracheitis, and airsacculitis. E coli infections are often concurrent and result in severe air sac thickening and turbidity, with exudative accumulations, adhesive pericarditis, and fibrinous perihepatitis. Turkeys develop severe mucopurulent sinusitis and varying degrees of tracheitis and airsacculitis. Microscopically, involved mucous membranes are thickened, hyperplastic, necrotic, and infiltrated with inflammatory cells. The mucosal lamina propria contains focal areas of lymphoid hypoplasia and germinal center formations.

History, clinical signs, and typical gross lesions may be suggestive of M gallisepticum. Serology by agglutination and ELISA methods are commonly used for surveillance. Hemagglutination-inhibition is used as a confirmatory test, because nonspecific false agglutination reactions may occur, especially after injection of inactivated oil-emulsion vaccines or infection with M synoviae. M gallisepticum should be confirmed by isolation from swab samples of infraorbital sinuses, nasal turbinates, choanal cleft, trachea, air sacs, lungs, or conjunctiva. Primary isolation is made in mycoplasma medium containing 10%–15% serum. Colonies on agar medium are used for species identification by immunofluorescence with species-specific antibodies. PCR can also be used for detection of M gallisepticum DNA using swabs taken directly from infected sites (choana, sinuses, trachea, air sacs) or after growth in culture.

Mycoplasma isolates must be identified by species, because birds may also be infected with nonpathogenic mycoplasmas. E coli infection, Newcastle disease, avian influenza, and other respiratory diseases (eg, infectious bronchitis in chickens) should be considered in the differential diagnosis and can act as inciting or contributing pathogens.

Most strains of M gallisepticum are sensitive to a number of broad-spectrum antibiotics, including tylosin, tetracyclines, and others but not to penicillins or those that act on the cell wall. Tylosin or tetracyclines have been commonly used to reduce egg transmission or as prophylactic treatment to prevent respiratory disease in broilers and turkeys. Antibiotics may alleviate the clinical signs and lesions but do not eliminate infection. Regulations on the use of antibiotics in food animals are rapidly evolving and should be consulted before use.

Prevention is based largely on obtaining chicks or poults from M gallisepticum–free breeder flocks. Eradication of M gallisepticum from chicken and turkey commercial breeding stock is well advanced in the USA because of control programs coordinated by the National Poultry Improvement Plan. The most effective control program is to establish M gallisepticum–free breeder flocks, managed and maintained under good biosecurity to prevent introductions, and monitored regularly with serology to continually confirm infection-free status. In valuable breeding stock, treatment of eggs with antibiotics or heat has been used to eliminate egg transmission to progeny. Medication is not a good long-term control method but has been of value in treating individual infected flocks.

Laying chickens free of M gallisepticum are desirable, but infection in commercial multiple-age egg farms where depopulation is not feasible is a problem. Inactivated, oil-emulsion bacterins are available and help prevent egg production losses but not infection. Three live vaccines (F-strain, ts-11, and 6/85) have been licensed in the USA for use during the growing phase to provide some protection during lay and may be used in some areas with permission of the state veterinarian. F-strain is of low virulence in chickens but is fully virulent for turkeys. Vaccinated chickens remain carriers of F-strain, and immunity lasts through the laying season. Vaccine strains ts-11 and 6/85 are less virulent, offer the advantage of improved safety for nontarget birds, and are widely used in commercial layers. A commercial recombinant fowlpox–M gallisepticum vaccine has been marketed.

Last full review/revision September 2013 by David H. Ley, DVM, PhD

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