Mycoplasma iowae infection of turkey breeder hens has been most commonly associated with late embryo mortality and reduced hatchability and occasionally with a low prevalence of leg abnormalities in their young progeny. M iowae requires enriched media with cholesterol, similar to those used for other avian mycoplasmas for culture and isolation, but is resistant to bile salts because it has a predilection to the intestinal tract.
M iowae is egg transmitted (transovarian) in turkeys, and horizontal transmission with slow spread within a flock may occur. Antigenicity and virulence vary considerably among M iowae strains. Infection rates in turkey flocks in Europe and North America have been reduced by intensive eradication efforts in certain primary breeding stocks, but M iowae is not currently included in the National Poultry Improvement Plan. It is a relatively uncommon infection of chickens and has been reported in geese. However, from time to time, outbreaks occur and are generally limited to poults coming out of specific parent flocks.
Chickens and turkeys experimentally inoculated have shown airsacculitis, stunting, poor feathering, and leg lesions. These effects are rarely recognized in the field, except for some outbreaks in young turkeys with skeletal lesions.
Turkey breeder flocks with Mycoplasma iowae infection show no clinical signs other than reduced hatchability (usually 2%–5%) due to embryo mortality in the last 10 days of incubation. In many flocks, the hatchability returns to normal after 1–2 months.
Dead turkey embryos are edematous, congested, and stunted; they may have "clubbed down." Poults experimentally challenged in ovo or at 1 day of age developed various skeletal deformities such as rotated tibia, deviated toes, chondrodystrophy, or erosion of the articular cartilage of the hock joint. Chicks experimentally challenged at 1 day of age developed tenosynovitis and ruptured tendons.
Natural infections in several young commercial turkey flocks were associated with skeletal lesions consistent with chondrodystrophy, characterized by leg and vertebral deformities. Microscopic skeletal lesions were characterized by excess cartilage matrix and disorganization of chondrocytes, features of osteochondrosis.
In turkeys, M iowae infection should be considered in cases of late embryo mortality and decreased hatchability and in young turkeys with leg and vertebral chondrodystrophy. M meleagridis and nutrient deficiencies are the top differential diagnoses for these conditions, respectively.
Turkeys develop only a weak antibody response to M iowae, and no reliable serologic test is available. Diagnosis relies on culture, isolation, and identification of the organism, or on detection of M iowae DNA by real-time PCR and can be performed directly on clinical swabs taken from infected sites (yolk sacs from dead, in-shell embryos, airsacs, and joints of young poults), or isolates can be appropriate samples for molecular diagnostics. Sequence typing by targeting and amplifying specific sequences allows for identification of MI isolates, and outbreaks and can be particularly useful for epidemiologic investigations and to identify the source parent flock.
The best method of control and prevention for Mycoplasma iowae infection is to establish and maintain turkey breeder flocks free of M iowae. Surveillance is challenging because serology is unreliable, but flock monitoring by real-time PCR and strict biosecurity should help.