(Fig. points of 4 weeks p.i. ( 0.0001). Control tortoises in both experiments did not show clinical signs, did not seroconvert, and did not have detectable by either culture or PCR at any point in the study. Histological lesions were compatible with those observed in tortoises with natural infections. The numbers of 723 did not influence the clinical expression of GSK2606414 URTD or the antibody response, suggesting that the strain chosen for these studies was highly virulent. On the basis of the results of the transmission studies, we conclude that is an etiologic agent of URTD in the gopher tortoise. Gopher tortoises (proposed sp. novum (2, 4). Histologically, the lesions from experimentally infected desert tortoises were consistent with those seen in naturally infected tortoises (4, 16). In the desert tortoise, we have shown that the presence of clinical indicators of URTD was positively related to the presence of specific antibody to from your nasal passages of clinically ill gopher tortoises submitted to VMTH, UF. The similarity of the clinical indicators and histological lesions between experimentally infected and naturally infected tortoises and the isolation of from naturally huCdc7 infected gopher tortoises suggested that URTD in this species might also be of mycoplasmal origin. The objectives of this study were to determine if = 10) were sham inoculated intranasally with 0.5 ml (0.25 ml/nostril) of sterile SP4 broth. Tortoises in the experimental contamination group (= 9) were inoculated intranasally with 0.5 ml (0.25 ml/nostril; 108 color-changing models [CCU] [total dose]) of 723. Isolate 723 was obtained from a clinically ill tortoise from Sanibel Island, Lee County, Fla. 723 was produced in SP4 broth and was only two passages from the primary isolation. Aliquots of strain 723 were frozen at ?80C, and all infections were done with a common stock of caused URTD in the gopher tortoise, an experiment was designed to determine the effect of dose on clinical expression of disease and immune response. Tortoises were inoculated intranasally with a low (101 CCU; = 6), medium (103 CCU; = 6), or high (105 CCU; = 5) dose of = 10) were sham inoculated intranasally with 0.5 ml GSK2606414 (0.25 ml/nostril) of sterile SP4 broth. Monitoring and housing were identical to those in the initial experimental contamination study. Postinfection monitoring of tortoises. The tortoises were observed from 3 to 7 days each week, GSK2606414 with some days including GSK2606414 multiple observations. Because of individual behavior patterns, not every tortoise was observed at each daily observation time point. At specific time points (usually 2- to 4-week intervals, depending on the study), tortoises were captured by hand or with wire cage-type traps (Tomahawk Live Trap Organization, Tomahawk, Wis.) that were covered with brown paper to protect the animals from the weather. The traps were washed, sprayed with bleach answer, and allowed to air flow dry following each use. The paper was discarded, and GSK2606414 new paper was utilized for the next trapping effort. Each tortoise was placed in a plastic, lidded container (LEWISystems; Menasha Corporation, Watertown, Wis.) for transport and holding. Containers were bleached, scrubbed, and washed in an automatic cage washer before reuse. Tortoises were examined for clinical indicators of URTD: nasal and ocular discharge, palpebral edema, and conjunctivitis..