Proceedings: Conservation, Restoration, and Management of Tortoises and
Turtles—An International Conference, pp. 91–99
© 1997 by the New York Turtle and Tortoise Society.
Demographic Consequences of Disease
in Two Desert Tortoise Populations in California, USA
KRISTIN H. BERRY
U.S. Department of the Interior, Bureau of Land Management,
6221 Box Springs Blvd., Riverside, CA 92507-0714, USA
Current Agency: U.S. Geological Survey, Biological Resources Division (same address)
ABSTRACT: Disease is a causal factor in declines of desert tortoise,
Gopherus agassizii, populations at two locations in California. In the interior of the
Desert Tortoise Research Natural Area (DTNA), population densities of all sizes of tortoises
declined 76% from 75/km² in 1979 to 18/km² in 1992. Densities of adults followed the same
pattern and declined 90% from 61/km² in 1979 to 6/km² in 1992. Declines of adult tortoises
are attributed primarily to an upper respiratory tract disease (URTD) caused by the pathogen
Mycoplasma agassizii. Additional disease-related mortalities are expected to occur,
because 25–38% of four samples of adult tortoises from an adjacent site within the DTNA
tested positive for antibodies to M. agassizii in 1992. This disease may have been
introduced to the DTNA through release of ill captive tortoises.
A second disease, cutaneous dyskeratosis, is present at another reserve, the
Chuckwalla Bench Area of Critical Environmental Concern, and is linked to population
declines. Between 1982 and 1988 the incidence of cutaneous dyskeratosis increased and
lesions became more severe. Between 1982 and 1992 the total tortoise population (all size
classes) declined 54% from 153 tortoises/km² to 70 tortoises/km². The adult population
declined 61% from 87 tortoises/km² to 34 tortoises/km². The cause(s) of cutaneous
dyskeratosis remain uncertain, but possibilities include deficiency diseases or
environmental toxicosis.
Diseases, especially if introduced to a native population or if environmentally
caused, can have serious consequences for threatened chelonians and will complicate
conservation and recovery efforts. Of the two diseases, URTD is of the greatest immediate
concern because of its potential to harm tortoise populations on a global scale.
Desert tortoise, Gopherus agassizii, populations have declined
substantially in the past two decades due to a wide variety of causes, including collecting,
vandalism, predation, and habitat loss and deterioration (U.S. Fish and Wildlife Service
[USFWS], 1994). Declines became so precipitous that in August 1989, the USFWS listed the
species as “Endangered” under the emergency provisions of the Endangered Species Act of 1973,
as amended. Disease was a factor in the emergency listing. Subsequently, in April 1990 the
USFWS permanently listed the desert tortoise as “Threatened.”
Disease was first implicated as having a significant role in mortality of wild desert
tortoises in the 1980s, when remains of tortoises from the Beaver Dam Slope of Arizona and Utah
were found to have osteopenia, indicative of malnutrition (Jacobson, 1994). Disease was
documented as the major cause of mortality in a wild desert tortoise population in 1988, when
ill tortoises with upper respiratory disease were observed by field-workers at a long-term
permanent study plot in the interior of the Desert Tortoise Research Natural Area (DTNA) in the
western Mojave Desert of California (Berry, 1990; Jacobson et al., 1991). Further research in
1989 and 1990 (e.g., Knowles, 1989; Berry, 1990) confirmed that many tortoises at the DTNA were
ill, dying, or had recently died. The signs of disease (nasal discharge, lassitude, cachexia)
were similar to signs observed in an often fatal upper respiratory disease of captive desert
tortoises throughout southern California (W. Rosskopf, DVM, pers. comm.). Prior to 1988 upper
respiratory disease had not been observed in wild, free-living tortoises at the DTNA (Berry and
Nicholson, 1984; Berry et al., 1986).
Upper respiratory disease was considered a threat to wild populations of the desert
tortoise in the 1970s, long before the disease appeared. When the DTNA was established in 1972,
the author and the U.S. Bureau of Land Management (USBLM) expressed concerns about the
potentially infectious nature of the disease. We suspected wild populations may become infected
through release of ill captive tortoises, which were numerous throughout southern and central
California (St. Amant, 1977; Berry and Nicholson, 1984). Because of the potential threat, the
USBLM provided funds to Dr. Murray Fowler and his students to conduct research on the disease
(Fowler, 1977; Snipes and Biberstein, 1982). No specific bacterial organism was identified as
causing respiratory disease. Fowler (1977) concluded that the disease was not caused by a
single organism and was not infectious. Stress, especially from malnutrition, was considered
the prime predisposing factor.
By the mid-1970s the USBLM, the California Department of Fish and Game (CDFG), the
Desert Tortoise Preserve Committee, Inc., and the California Turtle & Tortoise Club distributed
literature and issued public statements warning that captive tortoises should not be released
to wild lands because of the potential for spreading disease, contaminating genetic stock, and
adversely affecting the behavior of wild resident populations (e.g., St. Amant, 1979, 1980;
Berry and Nicholson, 1984).
When several wild tortoises with respiratory disease were discovered at a long-term
permanent study plot in the DTNA interior in 1988, the CDFG and USBLM provided financial
support to initiate research on the pathogenesis of the disease. Within two years research
scientists at the University of Florida described the disease as an upper respiratory tract
disease (URTD) associated with a new and undescribed mycoplasma (Jacobson et al., 1991).
Shortly thereafter a transmission study demonstrated that a new mycoplasma, M. agassizii,
is a highly infectious pathogen and causes URTD (Brown et al., 1994). An enzyme-linked
immunosorbent assay (ELISA) test for M. agassizii was developed (Schumacher et al.,
1993) and was used to determine whether wild desert tortoises carried antibodies to the
pathogen (Brown et al., 1994b; Jacobson et al., 1995).
Within weeks of the time that ill tortoises were discovered at the DTNA in 1988,
tortoises at another long-term study site in the Chuckwalla Bench Area of Critical
Environmental Concern (ACEC), in the eastern Colorado Desert of Riverside County, were
discovered to have shell lesions. An abnormally high number of tortoises, many of which were
previously marked, were discovered dead (Berry, 1990). Research on the pathogenesis of shell
lesions was initiated by Jacobson et al. (1994).
In this paper, I describe the demographic consequences of disease on desert tortoises
at the long-term permanent study sites in the interior of the DTNA and on the Chuckwalla Bench,
and the evidence linking disease to deaths. I also review the status of the populations as of
1992, discuss the implications of the two diseases for chelonian populations, and outline
actions taken to cope with diseases within the two preserves and elsewhere.
METHODS
Description of the Two Long-Term Permanent Study Sites for Desert
Tortoise Populations
Desert Tortoise Research Natural Area (DTNA). The DTNA is a 100 km² reserve
established in 1972 in the western Mojave Desert to protect high-density tortoise populations
and their habitats (Figure 1) (USBLM and CDFG, 1988). Formally designated as a Research
Natural Area and Area of Critical Environmental Concern in 1980, the DTNA is protected from
recreational vehicle use and sheep grazing by a hog wire fence of which the lower edge is
approximately 25 cm above the ground (USBLM, 1980; USBLM and CDFG, 1988). The raised fence
permits wild animals to move into and out of the DTNA unimpeded. Since 1972 federal and state
governments and the Desert Tortoise Preserve Committee, Inc. have invested considerable effort
in establishing and securing habitat in the DTNA to create a viable reserve. To date, more
than 8,000 km² of private inholdings have been acquired. The USBLM took action to eliminate
all livestock grazing and hardrock mineral mining and also established long-term stewardship
and education programs.
Two research study sites on the DTNA were sources of information: (1) a long-term
study plot (2.8 km²), established in 1973 in the central interior to monitor changes in
populations and habitat (Berry, 1984, 1990); and (2) a short-term, adjacent study plot,
established in 1988 for research on health profiles (Christopher et al., 1993, this volume),
physiology (water balance and energy flow), and epidemiology of diseases (Brown, 1994b).
Habitats within the study plots are typical of diverse creosote bush ( Larrea tridentata)
scrub plant communities in the western Mojave Desert. Joshua trees ( Yucca brevifolia)
are widely scattered; creosote bushes are the predominant shrub; and more than three dozen
perennial species of shrubs and grasses are present in the understory, e.g., burrobush ( Ambrosia
dumosa), goldenhead ( Acamptopappus sphaerocephalus), cheesebush ( Hymenoclea
salsola), Anderson thornbush ( Lycium andersonii), Nevada joint fir ( Ephedra
nevadensis), desert needle grass ( Achnatherum speciosum), Indian rice grass ( A.
hymenoides), and one-sided blue grass ( Poa secunda ssp. secunda). Elevations
range from 853 to 914 m.
Chuckwalla Bench ACEC. In 1980 the USBLM established the Chuckwalla Bench ACEC
in the eastern Colorado Desert in recognition of unique wildlife and vegetation values,
including high densities of desert tortoises (Figure 1) (USBLM, 1980, 1986). The 371 km²
protected area is long (approx. 60 km) and narrow (2.4–12 km) and is a raised bench between
the Orocopia, Chocolate, and the Chuckwalla mountains. The bench drains into Milpitas Wash,
which has the largest known populations of ironwood, Olneya tesota. In 1980, 35% of the
ACEC was in numerous scattered privately owned parcels. Since that time, the USBLM has
acquired most of these inholdings (S. Eubanks, pers. comm.) through land acquisition and
mitigation programs.
The 2.8 km² long-term study plot (elev. 640 m) contains areas of desert pavement cut
by rocky gullies and microphyll woodland washes. The predominant vegetation on the pavements
and flat areas is diverse creosote bush scrub typical of the eastern Colorado Desert. It
contains burrobush, white rhatany ( Krameria grayi), California joint fir ( Ephedra
californica), cheesebush, ocotillo ( Fouquieria splendens ssp. splendens),
silver cholla ( Opuntia echinocarpa), and Mojave yucca ( Yucca schidigera). Washes
are dominated by blue palo verde ( Cercidium floridum), smoke tree ( Psorothamnus
spinosus), desert willow ( Chilopsis linearis ssp. arcuata), ironwood, and
catclaw ( Acacia greggii).
Collecting Data on Population Densities of Desert Tortoises
Data for estimates of densities were collected during 60 day spring surveys conducted
in 1979, 1982, 1988, and 1992 (Berry, 1984, 1990), according to the following procedure
established for these ongoing studies: Each study site was divided into a grid of quadrats,
each of which was 0.0259 km², and was permanently marked by rebar (iron reinforcing rods).
Between late March and early June, one or two field-workers walked transects on each quadrat
in search of tortoises. The plot was thoroughly and evenly covered twice, with each coverage
requiring about 30 person days of effort. Each coverage constituted a census, with a total of
two censuses conducted in each survey year. Surveys were conducted over a minimum of 45 and a
maximum of 90 calendar days to minimize the effects of immigration and emigration of
tortoises. For each tortoise located, the following data were collected for density estimates:
date, unique identification number assigned to each tortoise, size (carapace length at the
midline or MCL), sex, capture type (i.e., first capture of a previously unmarked tortoise,
first capture in a given year of a previously marked tortoise, second or subsequent capture of
a previously marked tortoise in a given year), location, and survey type (first or second
census).
Analyzing Data on Population Densities of Desert Tortoises
The Stratified Lincoln Index (Overton, 1971) was selected as the density estimator
because it satisfies two critical criteria for estimating densities of long-lived species such
as the tortoise: (1) the population data can be stratified into size classes based on
capturability, and (2) the equations allow for growth of individual tortoises and their shift
from a smaller to a larger size-age class between the first and second censuses (Berry, 1990).
The stratification is of particular importance, because larger tortoises are much easier to
find than smaller tortoises.
Samples were sorted for analysis by study site, year, and census period (Berry, 1990).
For each census within a year, each tortoise was assigned to one of five strata based on MCL:
juveniles 1 and 2 (<100 mm MCL), immature 1 (100–139 mm MCL), immature 2 (140–179 mm MCL),
small or young adults (180–208 mm MCL), and adult (>208 mm MCL). Tortoises were placed in
three groups based on time of capture: (1) tortoises captured during the first census, (2)
tortoises captured during the second census, and (3) tortoises captured during both the first
and second censuses. Capture-recapture data were arranged in matrices to allow for growth of
individual tortoises from one size group to another between censuses. The 95% Confidence
Interval (CI) was used to establish level of significance for changes in population densities.
An additional source of data was the number of individual tortoises encountered and marked
during the 60-day survey for each sample year. If CIs did not overlap from one survey year to
the next, the changes in the density estimates were considered statistically significant.
Evaluating Effects of Diseases on the Populations
Data on health status was gathered in detail on the two plots in 1992, including
information on presence or absence and type of nasal discharge, patency of the nares,
appearance of eyelids and eyes, condition of chin glands, presence or absence of ocular
discharge, presence of active or healed injuries, presence and extent of lesions on the shell
and limbs, and other signs of disease. In all survey years, 35 mm slide transparencies were
taken of the plastron and carapace of most tortoises (Berry, 1984, 1990). These slides
document the presence and extent of shell lesions.
Data were also available from necropsies of ill and dying tortoises salvaged from or
adjacent to the plots (Jacobson et al., 1991, 1994; J. Klaassen, pers. comm.) from the ELISA
tests of tortoises in the research program on epidemiology of URTD at the DTNA (Brown et al.,
1994b) and from mortality rates of tortoises in the health profile research program at the
DTNA (Christopher et al., 1993). The latter program began in May 1989 with ten adult males and
ten adult female tortoises, each fitted with radio transmitters. The tortoises were monitored
four times annually (Christopher et al., 1993). Over the next 35 months—through March 1992—as
tortoises died, new individuals were added to the program.
RESULTS
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The DTNA
In the 13 years between 1979 and 1992, both the total population and the adult
component of the tortoise population experienced statistically significant declines in
densities (Figure 2). The total population density, which included all sizes of tortoises,
steadily decreased 76%, from a high of 149 tortoises/km² (95% CI = 115–195) in 1979 to a low
of 18 tortoises/km² (95% CI = 8–44) in 1992. The pattern of decline of adults differed. First,
the adult population component rose in density from 59 tortoises/km² (95% CI = 43–78) in 1979
to 92 tortoises/km² (95% CI = 71–119) in 1982 as a result of recruitment of immature tortoises
into the adult size class (Berry, 1990). However, the adult component then steadily declined
to 61 tortoises/km² (95% CI = 47–79) in 1988 and thence to 6 adults/km² (95% CI = 2–15) in
1992. The 13-year decline resulted in a 90% loss of adults, during which the total of number
of tortoises registered per survey year declined from 189 to 25 individuals.
The deaths of tortoises and the population declines are attributable to several causes
(Berry, 1990), including predation by common ravens on the juvenile and small immature size
classes. However, between 1988 and 1992 the declines of adults are clearly attributable to
URTD caused by M. agassizii. The evidence is from several sources. Prior to 1988 wild,
free-ranging tortoises at the DTNA and other long-term tortoise study plots in California were
not observed with signs of URTD, and very few were observed with signs of illness or in a
dying state (Berry and Nicholson, 1984; Berry et al., 1986). In contrast, many ill, dying, and
dead tortoises (remains of animals dead <2 years), most of which were previously marked during
censuses, were found on the DTNA plot in 1988, 1989, and 1990, and many dead animals were
discovered in 1992 (Berry, unpubl. data). Ill tortoises showed classic signs of URTD (Jacobson
et al., 1991; Brown et al., 1994a). In May 1989, 12 tortoises (11 males and 1 female), all of
which showed signs of advanced and chronic URTD, were removed from the DTNA for observation
and necropsies during the initial research on URTD (Jacobson et al., 1991). The tortoises had
chronic inflammatory changes in the upper respiratory tract. A mycoplasma-like organism was
seen on the surfaces of the macroepithelial cells (Jacobson et al., 1991). Subsequently, a
transmission research program demonstrated that M. agassizii was the causative pathogen
(Brown et al., 1994a).
Tortoises with signs of URTD were not confined to a single part of the DTNA but were
present throughout the DTNA and in adjacent areas of the Fremont Valley and Rand Mountains
(Knowles, 1989; Berry, unpubl. data). In spring 1989, 13 sample plots (1.3–2.6 km² each) were
established in the 100 km² DTNA and in adjacent lands within the Fremont Valley and Rand
Mountains to determine distribution and frequency of ill tortoises (Knowles, 1989). The sample
plots totaled 31.2 km². Four hundred sixty-eight live tortoises were found, of which 202 (43%)
showed signs of URTD. From 9.4% to 66.7% of tortoises on 12 of the 13 sample plots showed
signs of URTD.
The DTNA experienced a catastrophic epidemic that is not yet over. In 1992 from 12 to
14 adult tortoises in the research program for epidemiology of URTD were tested for antibodies
to M. agassizii (Brown et al., 1994b) using the ELISA test (Schumacher et al., 1993).
The tortoises were tested during late winter, spring, summer, and fall and were in a study
area immediately adjacent to the long-term plot. From 25 to 38 percent of the tortoises in the
four seasonal samples tested positive for M. agassizii, indicating that the tortoises
had been exposed to the pathogen, or were currently ill, or had been ill and were recovered.
Between 1993 and 1995, from 7 to 62% of the tortoises in the four samples taken each year have
produced positive ELISA tests, indicating that the population is in a chronic disease state
(M. B. Brown et al., pers. comm.)
Of the 27 tortoises in the health profile research program between May 1989 and March
1992, six died between late 1989 and mid-1991. An additional 11 tortoises disappeared and have
not been found as of October 1995. The death rate for adults is abnormally high, compared to
approximately 2% per year in stable populations (Turner et al., 1987). The disappearance rate
is also high and unusual for tortoises fitted with radio transmitters. Many of the missing
animals should be considered dead.
 |
Chuckwalla Bench ACEC
Between 1979 and 1992 both the total population and the adult component of the
tortoise population exhibited statistically significant declines (Figure 3). The total
population density, which included all sizes of tortoises, steadily decreased from a high of
223 tortoises/km² (95% CI = 177–283) in 1979 to a low of 64 tortoises/km² (95% CI = 46–92) in
1988 (Berry, 1990). The 1992 census figures were slightly higher but not significantly
different from the figures recorded for 1988: 70 tortoises/km² (95% CI = 48–102). The pattern
of decline of adults was similar. There were no statistically significant differences in the
adult population component in the 1979 and 1982 censuses; in 1979 density estimates were 75
tortoises/km² (95% CI = 56–98), whereas in 1982 estimates were 87 tortoises/km² (95% CI =
68–112). By 1988 census figures showed statistically significant declines with 42
tortoises/km² (95% CI = 29–62). The 1992 estimates were lower still, 33 adults/km² (95% CI =
22–49), but not significantly different from the 1988 figures.
During the 13-year time frame, the total number of tortoises registered per survey
year on the study site also declined, from 265 individuals in 1979 and 262 in 1982 (Berry,
1990) to 107 individuals in 1992 (Berry, unpubl. data). Of considerable concern is the
differential loss of adult females. In 1979, 74 adult females and 79 adult males were
registered. The numbers of registered tortoises increased to 98 adult females and 80 adult
males in 1982 and then declined to 42 adult females and 44 adult males in 1988. By 1992 female
numbers had further declined to 26 individuals, while male numbers remained similar at 42. As
of mid-1992 (the end of the 1992 field survey season), deaths of adults continued to occur at
a rate higher than the 2% annualized death rate estimated for stable populations in the Mojave
Desert (Turner et al., 1987). The remains of 20 adults, all of which had been captured in
previous years, were found during the 1992 survey. Of the 20, eight had died within the last
year and ten had died within the last one to two years. Of the 20 adults, 15 were females.
The population decline appears to be linked to the appearance of shell lesions on the
tortoises. In a retrospective analysis of the 35 mm slides taken during surveys conducted
between 1979 and 1990, the disease was evident in 1979 but affected only 56% of the tortoises
and was generally of limited extent (mild) on the shell (Jacobson et al., 1994). Between 1982
and 1988 the percentage of tortoises affected increased to 90%, and the severity of the
lesions on the shells likewise increased. The lesions, which were on the scutes of the
plastron and carapace and on the scales of the forelimbs, consisted of white-gray or sometimes
orange flaky areas. They appeared at the seams, spreading outward in irregular patterns onto
the scutes. In severe cases, bone was exposed. The lesions were described as cutaneous
dyskeratosis, but the exact cause could not be determined. The locations on the shell and body
and histology of the lesions were suggestive of either a deficiency disease or toxicosis. Both
deficiency diseases and environmental toxicants are known to affect keratin in other
vertebrates. A wide variety of toxicants are responsible for lesions in the epidermal hard
parts of domestic hoofstock, for example (Blood et al., 1989).
Subsequent to the study of the shell and limb lesions in tortoises at the Chuckwalla
Bench, 32 ill or damaged tortoises (including some with similar shell lesions) were salvaged
for necropsy from the Mojave and Colorado deserts of California and the Sonoran Desert of
Arizona (Homer et al., 1994, 1996a, 1996b). The salvaged tortoises with cutaneous dyskeratosis
had elevated concentrations of toxicants in the liver, kidney, or plasma (e.g., barium,
calcium, cadmium, chromium, magnesium, molybdenum, nickel, phthalates, and selenium in
plasma), and/or nutritional deficiencies (e.g., low copper, zinc, selenium, plasma vitamin A).
The toxicants and/or nutritional deficiencies may be the cause of the shell disease. Tortoises
with cutaneous dyskeratosis may be more vulnerable to bacterial and fungal infections, other
diseases, and predation because of the thin scutes and loss of laminae.
DISCUSSION
Desert tortoises are slow-maturing animals that require 15–20 years to reach
reproductive maturity (Woodbury and Hardy, 1948). Once reproductive maturity is reached, wild
females generally produce relatively small and few clutches of eggs (Turner et al., 1986,
1987; Henen, 1994). During a six-year study of egg production in the eastern Mojave Desert,
females produced from 0 to 3 clutches per year. Mean clutch sizes ranged from 3.53 ±0.26 to
5.15 ±0.34 eggs and clutch frequency from 1.06 ±0.06 to 1.89 ±0.11 per year. Eggs and
hatchlings are vulnerable to many predators and pre-adult mortality is generally high (Turner
et al., 1987). However, under normal conditions, adult survivorship is about 98% per year.
Populations cannot rapidly recover from catastrophic losses of adults, such as the 90%
decline experienced at the DTNA or the 50–60% losses at the Chuckwalla Bench because
recruitment of young adults requires so many years. These populations face serious threat of
extinction (USFWS, 1994). According to analyses prepared by the Desert Tortoise Recovery
Team, desert tortoise populations that have declined to 4 adults/km² would require three
doublings, or 210 years, to reach a density of 31 adults/km²—if the population is able to
grow at an average rate of 1% per year (USFWS, 1994). Using these projections, the adult
population at the DTNA would require 280 years to reach the 1979 level of 61 adults/km². One
of the more serious aspects of the population declines for the DTNA and the Chuckwalla Bench
is that the declines may not have reached the lowest point and recovery may not be underway.
Furthermore, the long-term effects of the two diseases on reproduction, viability of eggs,
and general health of young are not yet known.
One of the diseases, URTD, is highly infectious (Brown et al., 1994a) and has
demonstrated its potential for producing catastrophic impacts on populations at the DTNA.
Captive tortoises are implicated in the spread of this disease to wild populations of both
desert and gopher tortoises, G. polyphemus (Jacobson, 1993a; Jacobson et al., 1995).
In the last five years the number of desert tortoise populations with clinical signs of URTD
has increased and the disease appears to be spreading. Wild tortoises that have positive
ELISA tests and show clinical signs of disease have been identified throughout the Mojave
Desert in California (Brown et al., 1994b; Homer et al., 1994), Nevada (Jacobson et al.,
1995), northern Arizona (Dickinson et al., 1995), and Utah (Dickinson et al, 1995; Jacobson
et al., 1991).
In California, government agencies have taken measures to prevent release of captive
turtles and tortoises since the late 1970s (e.g., St. Amant, 1979, 1980). In 1993 more than
7,500 copies of a booklet with information about wild and captive desert tortoises, URTD, and
adoption programs for captives (Berry, 1993) were distributed to people perceived to be
authorities on management of wild and captive tortoises (government agencies, librarians,
humane societies, police departments and county sheriffs, and veterinarians). The booklet
focuses on why captive tortoises should not be released, what one should do when encountering
desert tortoises in wild settings, and whom to contact when a tortoise is found in a city or
town. A four-page brochure that addresses scientific and medical aspects of URTD, including
treatment and guidelines for care and husbandry of tortoises, (Jacobson, 1993b) was also
distributed with the booklet. These materials were prepared and distributed not only to
educate the public but also to protect the considerable investment by both government and the
Desert Tortoise Preserve Committee in existing reserves and legally designated Critical
Habitat (USFWS, 1994) for the desert tortoise.
Will education reduce the threat of captive releases and better protect the tortoise?
Education is likely to reduce but not entirely eliminate the threat. Data are available on
behavior of the general public from the monitoring reports of naturalists at the DTNA
(Howland, 1989; Ginn, 1990; Jennings, 1992; Ogg and Gallant, 1992; Kidd, 1993; Boland, 1994,
1995). Since spring 1989 the Desert Tortoise Preserve Committee and the USBLM have sponsored
naturalists at the DTNA. Naturalists, who are generally present five to seven days per week
for three months in spring at the Interpretive Center, a single site on the 57.5 km fenced
boundary of the reserve, have reported that visitors arrive from throughout the state with
the intention of releasing captives for various reasons. These reasons include the belief
that the DTNA is the appropriate place to release tortoises or that public officials have
told them to do so. Some of these captives showed signs of URTD. The naturalists also
reported that visitors bring wild tortoises from nearby areas to the DTNA, believing it to be
a place that is safe from the hazards of vehicles and other land uses. The 31 illegal
incidents summarized in Table 1 occurred at a rate of 2.4 incidents/1000
visitors over a seven-year period. The documented incidents are a minimum number; they
represent only incidents of which the naturalists were aware and only at a single point along
the DTNA boundary. Certainly, such illegal activities occur more widely in the Southwest
(USFWS, 1994).
The second disease, cutaneous dyskeratosis, is also widespread in desert tortoise
populations (Berry, unpubl. data; Homer et al., 1994, 1996a, 1996b), with some populations
more affected than others. Cutaneous dyskeratosis may have multiple causes and be associated
with the presence of environmental toxicants and/or nutritional deficiencies. Field-workers
and research scientists need to be taught to identify and describe the lesions. The sources
of the environmental toxicants need to be identified, and the link of toxicants to cutaneous
dyskeratosis and to the high mortality rates needs to be established. Ultimately, the
cause(s) of the disease must be identified and actions taken to reduce the deaths in wild
populations.
Recommendations
- Because our knowledge of infectious diseases in tortoises is limited (Jacobson, 1993a),
research scientists and government biologists should take precautions to prevent
transmission of known and unidentified diseases from one tortoise to another in the
laboratory and field. The field-worker should use a separate pair of disposable gloves for
each tortoise; sterilize equipment (e.g., calipers, scales) after use with each animal;
sterilize probes used to measure or view burrows after use at each burrow; and ensure that
the tortoise does not touch or contaminate the field worker’s clothing, day pack, or other
equipment. Equipment should be sterilized or properly disinfected between uses at different
sites. If the field-worker is visiting more than one study site, consideration should be
given to sterilizing clothing and shoes before traveling to the second site. Where an
infectious disease is known to occur in a population, protocols must be established to
prevent spread to unexposed populations (including cleaning field vehicles and camping
equipment). Sites where infectious diseases are known to occur should be visited last on
field trips.
- Field-workers should keep detailed records on the health of each wild tortoise in
research programs, including 35 mm slides of both healthy and ill individuals.
- Ill, dying, and recently dead (but not autolyzed) wild tortoises should be salvaged for
necropsies (especially if the tortoise is ill or is a victim of trauma from a vehicle or
predator). Where possible, necropsies should be performed by a licensed veterinary
pathologist, or a professional pathologist with expertise in reptile pathology. A complete
necropsy can provide invaluable information on diseases of tortoises.
- Legally designated “Natural Areas” and reserves can appear as attractive, natural, and
safe places for release of unwanted captive or illegally collected tortoises. Government
employees, research scientists, and the general public must be educated about the hazards of
releasing captive tortoises or translocating wild tortoises to a reserve. As a minimum
precautionary measure, Natural Areas and reserves should be posted with signs to reduce the
likelihood of release. Costs for patrols by recreation specialists and law enforcement
personnel should be included in management plans.
- Persons with unwanted captive tortoises must have ready access to facilities (e.g.,
adoption centers) or groups that will accept and properly care for the unwanted animals.
Such facilities and organizations serve as deterrents to illegal releases.
ACKNOWLEDGMENTS
C. Knowles, P. Knowles, and P. Gould contributed to the fieldwork at
the DTNA study site, and A. P. Woodman, J. Howland, and T. Shields made significant
contributions at the Chuckwalla Bench study site. The following people provided constructive
comments on the manuscript: B. Homer, M. Brown, V. Dickinson, E. R. Jacobson, and J.
Oldemeyer. The USBLM at Riverside, California supported all long-term research efforts on
desert tortoise study plots. Research on pathogenesis and epidemiology of URTD was supported
by USBLM contracts to E. R. Jacobson at the University of Florida (Contract No. CA-950-CT9-28)
and M. B. Brown (Contract No. B950-C2-0046), respectively. Research on cutaneous dyskeratosis
was supported through USBLM contracts to E. R. Jacobson and T. J. Wronski (No. CA951-CT0-046)
and to B. Homer and E. R. Jacobson (No. CA 950-C1-0062), as well as a National Biological
Service Research Work Order to B. Homer and E. R. Jacobson.
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| TABLE 1
Number of attempts to release captive and illegally translocated desert
tortoises at or adjacent to the Desert Tortoise Research Natural Area, eastern Kern
County, California, between 1989 and 1995. |
| |
Number of
incidents regarding tortoises: |
Number of illegal incidents |
|
| Year |
Captive releases |
Translocations |
per 1000 visitors |
Reference |
|
| 1989 |
5 |
0 |
2 |
Howland, 1989 |
| 1990 |
1 |
4 |
5 |
Ginn, 1990 |
| 1991 |
2 |
2 |
2 |
Jennings, 1992 |
| 1992 |
3 |
4 |
4 |
Ogg and Gallant, 1992 |
| 1993 |
0 |
3 |
1 |
Kidd, 1993 |
| 1994 |
2 |
2 |
2 |
Boland, 1994 |
| 1995 |
1 |
2 |
1 |
Boland, 1995 |
| Totals |
14 |
17 |
|
|
|
|
This article was reprinted with permission from the
New York Turtle and Tortoise Society
|
|
