David C. Rostal,1 Janice S. Grumbles,1 and Valentine A. Lance2
1Department of Biology, Georgia Southern University, Statesboro, GA 30460
2Bel-Rea Institute of Animal Technology, Denver, CO
3Center for Reproduction of Endangered Species, P.O. Box 120551, San Diego, CA 92112
In 1992, an outbreak of URTD was observed in our research animals maintained at the Desert Tortoise Conservation Center (DTCC). Our initial results showed that tortoises that had antibodies to the mycoplasma and had mild signs of URTD were able to reproduce, but that mycoplasma positive animals that had severe signs had lower hormone levels than healthy animals and failed to reproduce.
Today, eight years later, 28 of the original 30 female tortoises and 16 of the original 20 male tortoises are surviving at the DTCC. Equal numbers of URTD positive and negative animals have died or disappeared over the past 8 years. Of these 28 animals, 18 are mycoplasma antibody positive (URTD positive) and 10 are mycoplasma antibody negative (URTD negative). This is the identical ratio of positive to negative animals verified in May 1993 (following the outbreak in 1992). During the summer of 2000, 16 of the 18 URTD positive and nine of the ten URTD negative females produced eggs. Furthermore, nine of the 18 URTD positive females and six of the ten URTD negative females produced second clutches of eggs. Several females that had stopped reproducing during the outbreak of the disease have now recovered and are reproducing again. Many (70%) of the URTD positive animals never showed signs of URTD or exhibited signs only upon initial emergence from hibernation. Many URTD positive tortoises could not be distinguished from URTD negative tortoises based on signs during late summer and fall 2000. This may indicate an increased immune response as indicated by seasonally increased white blood cell numbers that correlate with increased hormone levels. This increase in hormone levels occurs during the late summer and fall as fall mating season approaches. Hatching success (>90%) was similar for eggs produced by URTD positive and negative females. Hatchling size was also similar for hatchlings produced from eggs or URTD positive and negative females.
These data support our conclusions that (1) tortoises with persistent titers to Mycoplasma agassizii are capable of reproduction over extended time periods, (2) that URTD positive tortoises maintained with adequate nutrition can produce similar size clutches to free-ranging tortoises and to captive tortoises that have not been exposed to the mycoplasma, and (3) that URTD positive tortoises produce hatchlings that are free of signs of the disease and are indistinguishable from hatchlings from URTD negative animals. Given these results from captive tortoises, understanding how URTD impacts wild populations is critical.