West Mojave Plan FEIR/S - Desert Managers Group

(Jacobson et al. 1991, Brown et al. 1994a). Short-term droughts may temporarily reduceimmune reactions and increase susceptibility to URTD (Jacobson et al. 1991), although this isspeculative. Whereas animals may become debilitated by chronic immune stimulation, nobiochemical indicators of stress have been identified in diseased compared to non-diseasedturtles (Borysenko 1975, Grumbles 1993, Christopher et al 1993, 1997).Although evidence indicates a correlation between high rates of mortality and incidenceof URTD within populations (Berry 1997), there is little direct evidence that URTD is the causeof the high rates of loss. In two preliminary analyses (Avery and Berry 1993, Weinstein 1993),animals exhibiting clinical signs of or testing positively for URTD were no more likely to dieover a one year period in the western Mojave Desert than were those not exhibiting signs ortesting positive. This may be because factors other than disease caused much of the mortality ormany animals not showing clinical signs of disease in the field were still infected.A shell disease, cutaneous dyskeratosis (CD), has been identified in desert tortoisepopulations (Jacobson et al. 1994). CD consists of lesions along scute sutures of the plastron andto a lesser extent on the carapace. Over time, the lesions spread out onto the scutes. This diseasemay be caused by the toxic effect of chemicals in the environment, but evidence is lacking to testthis hypothesis. Naturally occurring or human-introduced toxins such as selenium, chlorinatedhydrocarbons, organophosphates, nitrogenous compounds, and alkaloids have all beenimplicated (Homer et al. 1998), but there are no data showing a direct link. The disease may alsobe caused by a nutritional deficiency (Jacobson et al. 1994). It is not known whether or not CDis caused by an infectious pathogen or if secondary pathogens act to enhance the lesions (Homeret al. 1998, Homer pers. comm.). It is unclear if the disease is actually lethal or responsible fordeclines in infected tortoise populations (Homer et al. 1998).If the shell diseases are toxicoses, toxic responses to environmental toxins (e.g., heavymetals, chlorinated hydrocarbons, organophosphates, and selenium), then there may be a directlink between these diseases and human activities unless the toxin is a natural component of thephysical environment. Chaffee et al. (1999) found no significant correlation between elevatedlevels of metals in organs of ill tortoises and in the soil where the tortoises came from.There is some recent, albeit weak, preliminary evidence linking heavy metals to diseasein tortoises. In necropsies of 31 mostly ill tortoises, Homer et al. (1994, 1996) found elevatedlevels of potentially toxic metals and minerals in the liver or kidney of one or more of theanimals. Since most of the animals were ill to begin with, an association was made between thepresence of the toxicants and presence of the disease. However, that study is strictly correlative,and fails to demonstrate a cause and effect relationship. Berry (1997) claims, “the salvagedtortoises with cutaneous dyskeratosis had elevated concentrations of toxicants in the liver,kidney, or plasma...and/or nutritional deficiencies.” Homer (pers. comm.) has foundsignificantly reduced levels of calcium in the livers of tortoises with CD, which suggests anutritional deficiency may be involved in the disease.Several other diseases and infections have been identified in desert tortoises (Homer et al.1998). These include a poorly known shell necrosis, which can result in sloughing of entirescutes; bacterial and fungal infections; and urolithiasis, a solid ball-like deposition of urateChapter 3 3-111