28th Annual Meeting and Symposium of the
Desert Tortoise Council, February 21-23, 2003
Abstracts

The History of Upper Respiratory Tract Disease in the Eastern Mojave Desert Tortoise: Observations from the Desert Tortoise Conservation Center, Las Vegas, Nevada

David C. Rostal¹ and Valentine A. Lance^2
1Department of Biology, Georgia Southern University, Statesboro, Georgia
²Center for Reproduction of Endangered Species, San Diego, California

Upper Respiratory Tract Disease (URTD) in the desert tortoise (Gopherus agassizii) continues to be a major factor affecting health and survival in wild populations. Mycoplasma agassizii is one causative agent of URTD. Other pathogens as well as other strains of Mycoplasma may also cause URTD or similar symptoms. The objective of this talk is to provide some history on what we have learned at the Desert Tortoise Conservation Center (DTCC) and put this into perspective. URTD was first identified in desert tortoises in the Mojave Desert in the late 1980's. Since its identification, it has been detected in a variety of other tortoise species including the gopher tortoises (Gopherus polyphemus) from the SE United States. The desert tortoise was listed as a Threatened species under the Endangered Species Act by USFWS due to recent declines in populations throughout the Mojave Desert. Studies funded in 1991 to provide basic information on the biology of desert tortoise were confounded by outbreaks of URTD in animals maintained under semi-natural conditions at the DTCC. These animals were healthy appearing animals which had been collected off development sites throughout the Las Vegas Valley. All animals underwent a 30 day visual quarantine for signs of URTD. At the time, there were no tests available to determine if an animal had been exposed to Mycoplasma or carried the organism in its upper respiratory tract. We have now learned that this organism is probably transmitted via direct contact, is highly contagious and has an apparent acute phase followed by a chronic phase. Reproduction was observed to drop off in sick animals during the acute phase however there appears to be a potential for recovery following the acute phase if the animal is relatively healthy when it is exposed. There also appears to be a low probability that the organism is transmitted vertically from mother to egg. Current methods for testing for the organisms include an ELISA that detect antibodies to the organism and a Culture/PCR technique that allows for the detection of Mycoplasma DNA in nasal flushes. It should be noted that animals collected during the early period of these studies but not incorporated in study groups but were instead left alone in pens without the stress of interacting with other individuals were rarely observed to break with signs of URTD. As well, offspring produced from mothers during the acute phase of URTD in 1992/1993 have been raised for ten years with no signs of URTD. Several hypotheses have been presented as to how URTD was spread in the desert tortoise including the release of sick captive animals back into wild populations. This is a possible and probably now continues to be a factor however this is also confounded by the fact that the gopher tortoise in the southeastern USA has been shown to also harbor Mycoplasma sp. and are associated with URTD outbreaks in many wild populations in Florida. It is important to note that gopher tortoises have not been kept as pets but were a food source up until recent times and in some areas continue to be. Other factors related to increased development may be involved and must be investigated.