Upper respiratory tract disease in the gopher tortoise is caused by Mycoplasma agassizii

Upper respiratory tract disease (URTD) has been observed in a number of tor toise species, including the desert tortoise (Gopherus agassizii) and the g opher tortoise (Gopherus polyphemus). Clinical signs of URTD in gopher tort oises are similar to those in desert tortoises and include serous, mucoid, or purulent discharge from the nares, excessive tearing to purulent ocular discharge, conjunctivitis, and edema of the eyelids and ocular glands. The objectives of the present study were to determine if Mycoplasma agassizii w as an etiologic agent of URTD in the gopher tortoise and to determine the c linical course of the experimental infection in a dose-response infection s tudy. Tortoises were inoculated intranasally with 0.5 ml (0.25 ml/nostril) of either sterile SP4 broth (control group; n = 10) or 10(8) color-changing units (CCU) (total dose) of M. agassizii 723 (experimental infection group ; n = 9). M. agassizii caused clinical signs compatible with those observed in tortoises with natural infections, Clinical signs of URTD were evident in seven of nine experimentally infected tortoises by 4 weeks postinfection (p.i.) and in eight of nine experimentally infected tortoises by 8 weeks p .i. In the dose-response experiments, tortoises were inoculated intranasall y with a low (10(1) CCU; n = 6), medium (10(3) CCU; n = 6), or high (10(5) CCU; n = 5) dose of M. agassizii 723 or with sterile SP4 broth (n = 10). At all time points p.i. in both experiments, M. agassizii could be isolated f rom the nares of at least 50% of the tortoises. All of the experimentally i nfected tortoises seroconverted, and levels of antibody were statistically higher in infected animals than in control animals for all time points of > 4 weeks p.i. (P < 0.0001). Control tortoises in both experiments did not sh ow clinical signs, did not seroconvert, and did not have detectable M. agas sizii by either culture or PCR at any point in the study. Histological lesi ons were compatible with those observed in tortoises with natural infection s. The numbers of M. agassizii 723 did not influence the clinical expressio n of URTD or the antibody response, suggesting that the strain chosen for t hese studies was highly virulent. On the basis of the results of the transm ission studies, we conclude that M. agassizii is an etiologic agent of URTD in the gopher tortoise.