Zoonotic diseases associated with free-roaming cats.

Free-roaming cat populations have been identified as a significant public health threat and are a source for several zoonotic diseases including rabies, toxoplasmosis, cutaneous larval migrans because of various nematode parasites, plague, tularemia and murine typhus. Several of these diseases are reported to cause mortality in humans and can cause other important health issues including abortion, blindness, pruritic skin rashes and other various symptoms. A recent case of rabies in a young girl from California that likely was transmitted by a free-roaming cat underscores that free-roaming cats can be a source of zoonotic diseases. Increased attention has been placed on trap-neuter-release (TNR) programmes as a viable tool to manage cat populations. However, some studies have shown that TNR leads to increased immigration of unneutered cats into neutered populations as well as increased kitten survival in neutered groups. These compensatory mechanisms in neutered groups leading to increased kitten survival and immigration would confound rabies vaccination campaigns and produce naïve populations of cats that can serve as source of zoonotic disease agents owing to lack of immunity. This manuscript is a review of the various diseases of free-roaming cats and the public health implications associated with the cat populations.

Ultrastructural and molecular confirmation of the development of Sarcocystis neurona tissue cysts in the central nervous system of southern sea otters (Enhydra lutris nereis).

In 2004, three wild sea otters were diagnosed with putative Sarcocystis neurona-associated meningoencephalitis by histopathology and immunohistochemistry. Schizonts, free merozoites and tissue cysts were observed in the brains of all three infected animals. Tissue cysts walls from sea otter 1 (SO1) stained positively using anti-S. neurona polyclonal antiserum. However, positive staining does not preclude infection by closely related or cross-reactive tissue cyst-forming coccidian parasites. Two immature tissue cysts in the brain of SO1 were examined using transmission electron microscopy. Ultrastructural features included cyst walls with thin villous projections up to 1 microm long with tapered ends and a distinctive, electron-dense outer lining layer composed of linearly-arranged, semi-circular structures with a "hobnailed" surface contour. Small numbers of microtubules extended down through the villi into the underlying granular layer. Metrocytes were short and plump with an anterior apical complex, 22 sub-pellicular microtubules, numerous free ribosomes and no rhoptries. Some metrocytes appeared to be dividing, with two adjacent nuclear profiles. Collectively these ultrastructural features were compatible with developing protozoal cysts and were similar to prior descriptions of S. neurona tissue cysts. Panspecific 18S rDNA primers were utilized to identify protozoa infecting the brains of these otters and DNA amplification and additional sequencing at the ITS1 locus confirmed that all three otters were infected with S. neurona. No other Sarcocystis spp. were detected in the brains or skeletal muscles of these animals by immunohistochemistry or PCR. We believe this is the first ultrastructural and molecular confirmation of the development of S. neurona tissue cysts in the CNS of any animal.

Type X Toxoplasma gondii in a wild mussel and terrestrial carnivores from coastal California: new linkages between terrestrial mammals, runoff and toxoplasmosis of sea otters.

Sea otters in California are commonly infected with Toxoplasma gondii. A unique Type X strain is responsible for 72% of otter infections, but its prevalence in terrestrial animals and marine invertebrates inhabiting the same area was unknown. Between 2000 and 2005, 45 terrestrial carnivores (lions, bobcats, domestic cats and foxes) and 1396 invertebrates (mussels, clams and worms) were screened for T. gondii using PCR and DNA sequencing to determine the phylogeographic distribution of T. gondii archetypal I, II, III and Type X genotypes. Marine bivalves have been shown to concentrate T. gondii oocysts in the laboratory, but a comprehensive survey of wild invertebrates has not been reported. A California mussel from an estuary draining into Monterey Bay was confirmed positive for Type X T. gondii by multilocus PCR and DNA sequencing at the B1 and SAG1 loci. This mussel was collected from nearshore marine waters just after the first significant rainfall event in the fall of 2002. Of 45 carnivores tested at the B1, SAG1, and GRA6 typing loci, 15 had PCR-confirmed T. gondii infection; 11 possessed alleles consistent with infection by archetypal Type I, II or III strains and 4 possessed alleles consistent with Type X T. gondii infection. No non-canonical alleles were identified. The four T. gondii strains with Type X alleles were identified from two mountain lions, a bobcat and a fox residing in coastal watersheds adjacent to sea otter habitat near Monterey Bay and Estero Bay. Confirmation of Type X T. gondii in coastal-dwelling felids, canids, a marine bivalve and nearshore-dwelling sea otters supports the hypotheses that feline faecal contamination is flowing from land to sea through surface runoff, and that otters can be infected with T. gondii via consumption of filter-feeding marine invertebrates.

Transmission of Toxoplasma: clues from the study of sea otters as sentinels of Toxoplasma gondii flow into the marine environment.

Toxoplasma gondii affects a wide variety of hosts including threatened southern sea otters (Enhydra lutris nereis) which serve as sentinels for the detection of the parasite's transmission into marine ecosystems. Toxoplasmosis is a major cause of mortality and contributor to the slow rate of population recovery for southern sea otters in California. An updated seroprevalence analysis showed that 52% of 305 freshly dead, beachcast sea otters and 38% of 257 live sea otters sampled along the California coast from 1998 to 2004 were infected with T. gondii. Areas with high T. gondii exposure were predominantly sandy bays near urban centres with freshwater runoff. Genotypic characterisation of 15 new T. gondii isolates obtained from otters in 2004 identified only X alleles at B1 and SAG1. A total of 38/50 or 72% of all otter isolates so far examined have been infected with a Type X strain. Type X isolates were also obtained from a Pacific harbor seal (Phoca vitulina) and California sea lion (Zalophus californianus). Molecular analysis using the C8 RAPD marker showed that the X isolates were more genetically heterogeneous than archetypal Type I, II and III genotypes of T. gondii. The origin and transmission of the Type X T. gondii genotype are not yet clear. Sea otters do not prey on known intermediate hosts for T. gondii and vertical transmission appears to play a minor role in maintaining infection in the populations. Therefore, the most likely source of infection is by infectious, environmentally resistant oocysts that are shed in the feces of felids and transported via freshwater runoff into the marine ecosystem. As nearshore predators, otters serve as sentinels of protozoal pathogen flow into the marine environment since they share the same environment and consume some of the same foods as humans. Investigation into the processes promoting T. gondii infections in sea otters will provide a better understanding of terrestrial parasite flow and the emergence of disease at the interface between wildlife, domestic animals and humans.

An unusual genotype of Toxoplasma gondii is common in California sea otters (Enhydra lutris nereis) and is a cause of mortality.

Toxoplasma gondii-associated meningoencephalitis is a significant disease of California sea otters (Enhydra lutris nereis), responsible for 16% of total mortality in fresh, beachcast carcasses. Toxoplasma gondii isolates were obtained from 35 California otters necropsied between 1998 and 2002. Based on multi-locus PCR-restriction fragment length polymorphism and DNA sequencing at conserved genes (18S rDNA, ITS-1) and polymorphic genes (B1, SAG1, SAG3 and GRA6), two distinct genotypes were identified: type II and a novel genotype, here called type x, that possessed distinct alleles at three of the four polymorphic loci sequenced. The majority (60%) of sea otter T. gondii infections were of genotype x, with the remaining 40% being of genotype II. No type I or III genotypes were identified. Epidemiological methods were used to examine the relationship between isolated T. gondii genotype(s) and spatial and demographic risk factors, such as otter stranding location and sex, as well as specific outcomes related to pathogenicity, such as severity of brain inflammation on histopathology and T. gondii-associated mortality. Differences were identified with respect to T. gondii genotype and sea otter sex and stranding location along the California coast. Localised spatial clustering was detected for both type II (centred within Monterey Bay) and x (centred near Morro Bay)-infected otters. The Morro Bay cluster of type x-infected otters overlaps previously reported high-risk areas for sea otter infection and mortality due to T. gondii. Nine of the 12 otters that had T. gondii-associated meningoencephalitis as a primary cause of death were infected with type x parasites.

Patterns of mortality in southern sea otters (Enhydra lutris nereis) from 1998-2001.

Detailed postmortem examination of southern sea otters (Enhydra lutris nereis) found along the California (USA) coast has provided an exceptional opportunity to understand factors influencing survival in this threatened marine mammal species. In order to evaluate recent trends in causes of mortality, the demographic and geographic distribution of causes of death in freshly deceased beachcast sea otters necropsied from 1998-2001 were evaluated. Protozoal encephalitis, acanthocephalan-related disease, shark attack, and cardiac disease were identified as common causes of death in sea otters examined. While infection with acanthocephalan parasites was more likely to cause death in juvenile otters, Toxoplasma gondii encephalitis, shark attack, and cardiac disease were more common in prime-aged adult otters. Cardiac disease is a newly recognized cause of mortality in sea otters and T. gondii encephalitis was significantly associated with this condition. Otters with fatal shark bites were over three times more likely to have pre-existing T. gondii encephalitis suggesting that shark attack, which is a long-recognized source of mortality in otters, may be coupled with a recently recognized disease in otters. Spatial clusters of cause-specific mortality were detected for T. gondii encephalitis (in Estero Bay), acanthocephalan peritonitis (in southern Monterey Bay), and shark attack (from Santa Cruz to Point Año Nuevo). Diseases caused by parasites, bacteria, or fungi and diseases without a specified etiology were the primary cause of death in 63.8% of otters examined. Parasitic disease alone caused death in 38.1% of otters examined. This pattern of mortality, observed predominantly in juvenile and prime-aged adult southern sea otters, has negative implications for the overall health and recovery of this population.

Coastal freshwater runoff is a risk factor for Toxoplasma gondii infection of southern sea otters (Enhydra lutris nereis).

The association among anthropogenic environmental disturbance, pathogen pollution and the emergence of infectious diseases in wildlife has been postulated, but not always well supported by epidemiologic data. Specific evidence of coastal contamination of the marine ecosystem with the zoonotic protozoan parasite, Toxoplasma gondii, and extensive infection of southern sea otters (Enhydra lutris nereis) along the California coast was documented by this study. To investigate the extent of exposure and factors contributing to the apparent emergence of T. gondii in southern sea otters, we compiled environmental, demographic and serological data from 223 live and dead sea otters examined between 1997 and 2001. The T. gondii seroprevalence was 42% (49/116) for live otters, and 62% (66/107) for dead otters. Demographic and environmental data were examined for associations with T. gondii seropositivity, with the ultimate goal of identifying spatial clusters and demographic and environmental risk factors for T. gondii infection. Spatial analysis revealed clusters of T. gondii-seropositive sea otters at two locations along the coast, and one site with lower than expected T. gondii seroprevalence. Risk factors that were positively associated with T. gondii seropositivity in logistic regression analysis included male gender, older age and otters sampled from the Morro Bay region of California. Most importantly, otters sampled near areas of maximal freshwater runoff were approximately three times more likely to be seropositive to T. gondii than otters sampled in areas of low flow. No association was found between seropositivity to T. gondii and human population density or exposure to sewage. This study provides evidence implicating land-based surface runoff as a source of T. gondii infection for marine mammals, specifically sea otters, and provides a convincing illustration of pathogen pollution in the marine ecosystem.

Effects of petroleum on mink applied as a model for reproductive success in sea otters.

Ranch-reared mink (Mustela vison) were used as a model in an experimental trial to investigate the potential effects of exposure to two petroleum products on sea otters (Enhydra lutris). Mink were exposed either dermally on one occasion 60 days prior to breeding or via low level contamination of their diets daily from 60 days prior to breeding (January 1994) until weaning of kits (June 1994). For dermal exposure, we placed mink in either a slick of Alaskan North Slope crude oil (n = 24) or bunker C fuel oil (n = 24) on sea water or sea water alone (n = 10) for 1 min. For dietary exposure, we fed mink rations containing 500 ppm of either Alaskan North Slope crude oil (n = 24) or bunker C fuel oil (n = 24; control, n = 15). The number of liveborn kits did not differ significantly among mink exposed dermally (5.0 kits/female for crude oil and 6.5 kits/female for bunker C fuel oil) and unexposed controls (5.3 kits/female). However, only 2.3 and 0.7 kits were produced per female for those exposed through the diet to crude oil and bunker C fuel oil, respectively. Females with reduced reproductive success had no clinical signs of toxicosis or behavioral abnormalities. In addition, kits of females exposed through the diet had poor survival to weaning. Once mature, kits born to females exposed to bunker C fuel oil in the diet had significantly reduced reproductive success (3.4 kits/female) although their only exposure to the petroleum products was in utero or during nursing. Therefore, it is possible that sea otter populations consuming contaminated food sources or colonizing previously oiled habitats will have reduced reproductive success.

Evaluation of changes in hematologic and clinical biochemical values after exposure to petroleum products in mink (Mustela vison) as a model for assessment of sea otters (Enhydra lutris).

OBJECTIVE: To determine the effects of petroleum exposure on hematologic and clinical biochemical results of mink and to identify variables that may be useful for making management decisions involving sea otters (Enhydra lutris) that have been exposed to oil in their environment. ANIMALS: 122 American mink (Mustela vison). PROCEDURES: Mink were exposed once to a slick of oil (Alaskan North Slope crude oil or bunker C fuel oil) on seawater or via low-level contamination of their daily rations. RESULTS: In the acute phase of exposure, petroleum directly affected RBC, WBC, neutrophil, and lymphocyte counts, fibrinogen, sodium, calcium, creatinine, total protein, and cholesterol concentrations, and alanine transaminase, creatine kinase, alkaline phosphatase, and gamma-glutamyltransferase activities. Aspartate transaminase, alkaline phosphatase, gamma-glutamyltransferase, and lactate dehydrogenase activities and cholesterol concentration also varied as a result of chronic low-level contamination of feed. CONCLUSIONS AND CLINICAL RELEVANCE: Our results are in agreement with reports that attribute increased alanine transaminase and alkaline phosphatase activities and decreased total protein concentration to petroleum exposure in sea otters during an oil spill. Sodium, calcium, creatinine, cholesterol, and lactate dehydrogenase may be valuable variables to assess for guidance during initial treatment of sea otters exposed to oil spills as well as for predicting which petroleum-exposed sea otters will reproduce following an oil spill. Measurement of these variables should aid wildlife professionals in making decisions regarding treatment of sea otters after oil spills.

Pathogen exposure patterns among sympatric populations of bighorn sheep, mule deer and cattle.

We sampled sympatric bighorn sheep (Ovis canadensis, n = 31), mule deer (Odocoileus hemionus, n = 38), and domestic cattle (n = 26) in the San Bernadino Mountains of southern California (USA) for the presence of Psoroptes spp. mites and for serologic evidence of exposure to bluetongue virus (BTV) and Babesia spp. From 1991 through 1994, Psoroptes spp. infestations were found on 12 (44%) of 27 bighorn sheep. No mites were found on mule deer or cattle. The BTV serum antibody prevalence in a cohort of 26 cattle ranged from 17 to 89%. There was no evidence of exposure to BTV in the bighorn sheep or mule deer. The cumulative serum antibody prevalence of Babesia spp. during the study was 35% in 26 bighorn sheep and 85% in 20 mule deer, while antibodies were not detected in a cohort of cattle when they were sampled in May (n = 23) and December (n = 22) of 1992. Based on these results, we concluded that infestation with Psoroptes spp. and exposure to BTV was limited to bighorn sheep and cattle, respectively. In contrast, Babesia spp. infections appeared to be common in both mule deer and bighorn sheep while there was no evidence of exposure in cattle.

The distribution of Dermacentor hunteri and Anaplasma sp. in desert bighorn sheep (Ovis canadensis).

The ixodid tick Dermacentor hunteri has been collected intermittently this century, primarily from desert bighorn sheep (Ovis canadensis). Anaplasma spp. are intraerythrocytic rickettsial parasites of ungulates and are vectored in the western United States by ticks of the genus Dermacentor. We tested the hypotheses that D. hunteri would be found infesting all populations of desert bighorn, and that all infested populations would be seropositive for Anaplasma sp. Dermacentor hunteri was found on desert bighorn throughout their range in the Mojave and Sonoran deserts of the southwestern United States and northern Mexico, but not in any portion of the Chihuahuan desert of New Mexico and eastern Arizona or in Baja California Sur, Mexico. Using an indirect immunofluorescence antibody test (IIF), 8 populations of desert bighorn in California with D. hunteri were seropositive for Anaplasma sp. (n = 160). Four populations of desert bighorn with D. hunteri in Arizona (n = 69), 1 in Nevada (n = 22), and I in Utah (n = 14) with D. hunteri were seronegative. Six populations of desert bighorn were uninfested with D. hunteri and were also seronegative. Of these populations, 1 was in California (n = 19), 2 were in New Mexico (n = 33), 2 were in Utah (n = 30), and 1 was in Baja California Sur (n = 14). We found no support for either of our original hypotheses and concluded that both D. hunteri and Anaplasma sp. are limited in their distribution among desert bighorn. We also suggest a cautionary approach to translocations of desert bighorn given the high prevalence of ticks and the unknown effects of Anaplasma sp. on free-ranging bighorn.

Prevalence of antibody to malignant catarrhal fever virus in wild and domestic ruminants by competitive-inhibition ELISA.

A competitive-inhibition ELISA (CI-ELISA), based on a monoclonal antibody to an epitope conserved among malignant catarrhal fever virus (MCFV) strains of both wildebeest and sheep origin, was used to determine the prevalence of antibody to MCFV in selected domestic and wild ruminants, both free-ranging and captive, from the USA. We evaluated 2528 sera from 14 species between 1990 and 1995, including 80 pronghorn antelope (Antilocapra americana), 339 bighorn sheep (Ovis canadensis), 103 biston (Bison bison), 17 black-tailed deer (Odocoileus hemionus columbianus), 395 domestic cattle (Bos taurus), 291 domestic goats (Capra hircus), 680 domestic sheep (Ovis ammon), 323 elk (Cervus elaphus), 41 llamas (Lama glama), 21 mouflon sheep (Ovis musimon), 54 mountain goats (Oreamnos americanus), 101 mule deer (Odocoileus hemionus), 20 muskox (Ovibos moschatus), and 63 white-tailed deer (Odocoileus virginianus). A high seroprevalence (37 to 62%) was observed in domestic sheep, domestic goats, muskox, and some bighorn sheep populations. Seroprevalence in these species was generally age-related: a very low seroprevalence was present in these animals under one year of age. A low seroprevalence (2% to 13%) was found in clinically-susceptible species such as domestic cattle, deer, elk and bison, supporting the concept that significant numbers of non-lethal infections occur among clinically susceptible ruminants.

Seroprevalence of two Babesia spp. isolates in selected bighorn sheep (Ovis canadensis) and mule deer (Odocoileus hemionus) populations in California.

Sera from 111 bighorn sheep (Ovis canadensis) and 95 mule deer (Odocoileus hemionus) were tested using an indirect immunofluorescence assay for antibodies to two isolates of Babesia spp. recently obtained from these hosts in California (USA). The study populations were from six locations: three areas of real or potential sympatry of bighorn sheep and deer, one area with deer only, and two areas with bighorn sheep only. Antibody titers from seroreactive individuals were similar with both babesial isolate antigens (P < 0.05), and seroprevalence was highest in the areas of host sympatry. A moderate to high seroprevalence (> or = 30%) in some of the study populations was evidence that babesial parasites may be common in bighorn sheep and mule deer in some areas of California.

Blastogenesis and interleukin-2 receptor expression assays in the harbor seal (Phoca vitulina).

Two in vitro functional assays were developed to evaluate mitogen-induced responses of peripheral blood mononuclear leukocytes (PBML) from free-ranging harbor seals, Phoca vitulina. Lymphocyte proliferation was measured by a standard blastogenesis assay following optimization of culture conditions including mitogen concentration, cell density, and incubation time. These optimized parameters, with the exception of incubation time, were subsequently employed to measure lymphocyte activation by analytical flow cytometry using fluorochrome-based identification of cell surface interleukin-2 receptor (IL-2r) expression. Baseline values established for free-ranging harbor seals had extensive animal variability; there was evidence that the samples were derived from a group of animals with a normal distribution. Positive correlations were observed between blastogenesis assays, and between blastogenesis and activation assays, when using pokeweed or concanavalin A as the stimulus. However, no relationship was found in the expression of the IL-2r induced by these mitogens. This result supports the contention that the two mitogens stimulate different lymphocyte subpopulations. This was observed only with the IL-2r expression assay because of its unique ability to measure the number of T lymphocytes initially activated rather than the ultimate number of progeny cells identified by blastogenesis. Both assays, used concurrently, should provide a more comprehensive representation of lymphocyte competence and serve as a measure of animal health.

Geographic analysis of pathogen exposure in bighorn sheep (Ovis canadensis).

Antibody responses were examined among 998 bighorn sheep (Ovis canadensis) in California (USA) to determine spatial patterns of pathogen exposure. Using a shifting frame analysis, a specific geographic region was delineated that contained bighorn sheep with higher (P < 0.05) levels of multiple exposure (antibodies detected against > or = two pathogens), as well as higher prevalence values for eight of ten individual pathogens. This region in southwestern California encompassed all of the peninsular populations of bighorn sheep recently proposed for listing as endangered by the U.S. Fish and Wildlife Service.

Antibody prevalence of eight ruminant infectious diseases in California mule and black-tailed deer (Odocoileus hemionus).

We tested 276 sera from 18 free-ranging black-tailed and mule deer (Odocoileus hemionus) herds in California (USA) collected from 1987 to 1991 in five biogeographical habitat types, for antibodies against eight infectious disease agents. Overall antibody prevalence was 56% for Anaplasma marginale, 31% for Borrelia burgdorferi, 16% for bluetongue virus serotype 17, 15% for epizootic hemorrhagic disease virus, 7% for Coxiella burnetii and Toxoplasma gondii, respectively, and 0% for bovine leukosis virus and caprine arthritis/encephalitis virus, respectively. Antibodies against Lyme borreliosis and anaplasmosis were found in deer throughout California, but antibodies against bluetongue and epizootic hemorrhagic disease were most prevalent in deer from southern California.

Serologic detection of bluetongue virus infection of black-tailed deer: comparison of serum neutralization, agar gel immunodiffusion, and competitive ELISA assays.

Three adult black-tailed deer (Odocoileus hemionus columbianus) and four fawns were inoculated with bluetongue virus (BTV) serotype 10 or 17, or epizootic hemorrhagic disease virus (EHDV) serotype 1. Animals were bled at irregular intervals thereafter and the presence of virus-specific antibodies in serum determined by agar gel immunodiffusion (AGID), serum neutralization (SN) and competitive enzyme-linked immunosorbent assay (C-ELISA) tests. Serum antibodies to BTV were detected in all three tests for 692 days after inoculation (DAI) of adult deer, but both the SN and AGID tests gave either erroneous or misleading results. Serum from one deer was negative by the AGID test at 409 DAI with BTV-10 but was positive at 248 and 692 DAI; also one adult and one fawn had antibodies by the SN test to serotypes of BTV with which they were not inoculated. The AGID test for EHDV had false positive results with some sera from animals inoculated only with BTV, and it consistently had false negative results with serum samples collected from an EHDV-inoculated deer at 140 DAI and thereafter. The C-ELISA was the most useful test for the detection of antibodies to BTV because it rapidly gave quantitative and accurate results.

A retrospective serologic survey for Anaplasma spp. infection in three bighorn sheep (Ovis canadensis) populations in California.

Using an indirect immunofluorescence assay, we determined the prevalence of Anaplasma-reactive antibody in three herds of bighorn sheep, each a different subspecies and occupying a different habitat in California (USA). Antibodies to Anaplasma spp. were identified in none of twenty California bighorn (Ovis canadensis californiana) sampled from the Mt. Baxter herd, 11 of 17 peninsular bighorn (O. canadensis cremnobates) sampled in the Santa Rosa Mountains, and all 20 desert bighorn (O. canadensis nelsoni) sampled at Old Dad Peak/Kelso Mountains. Based on an assay and an adsorption technique, the titers most likely were due to Anaplasma ovis. The presence and species of tick vectors in each of the habitats, and the presence or absence of deer or livestock were identified as factors potentially influencing seroprevalence of antibodies.

The isolation and partial characterization of a Babesia sp. from desert bighorn sheep (Ovis canadensis nelsoni).

A novel Babesia parasite of desert bighorn sheep was isolated. Its taxonomic description, host range, pathogenicity and antigenic relatedness were investigated. The parasite was infective for black-tailed and white-tailed deer, but with host-specific differences compared to that of bighorn sheep. A splenectomized calf and domestic sheep were refractory to infection. A comparative immunofluorescence assay detected antigens cross-reactive with Babesia odocoilei, B. divergens, B. equi and B. caballi, but not with B. bovis or B. bigemina. Babesia odocoilei was also infective for bighorn sheep, allowing comparison by a cross-challenge experiment, the results of which supported the conclusion that this parasite was not B. odocoilei. However, the bighorn sheep Babesia cannot currently be distinguished from B. capreoli described from roe deer in northern Germany. Data indicate that, while this parasite may not present a problem for domestic animals, it may cause disease in bighorn sheep and deer populations.