Echinococcus spp. Tapeworms in North America

Jacey Roche Cerda; Danielle Elise Buttke; Lora Rickard Ballweber

Disclosures

Emerging Infectious Diseases. 2018;24(2):230-235. 

In This Article

Echinococcus Spp. Tapeworms and Echinococcosis in Alaska and Canada

Even before advances in molecular genetics, researchers recognized the form of E. granulosus cycling between wild canids and their ungulate prey species in Alaska and Canada as distinct and referred to it as the northern biotype.[11] The northern biotype species is now recognized as E. canadensis. In the boreal regions of North America, E. canadensis are ubiquitous parasites of wild canids and ungulates from the western coast of Alaska through all territories and provinces of Canada, exclusive of its east coast.[11–13] Caribou (Rangifer tarandus), moose (Alces alces), and elk (Cervus canadensis) appear to be the most important intermediate hosts, although other ungulate species may become infected. Wolves (Canis lupus) and domestic dogs are the most important definitive hosts; however, coyotes (Canis latrans) are also competent.[11] Rausch's[11] comprehensive review of E. canadensis tapeworms provides extensive information regarding the strongly endemic cycles he and others observed from the 1950s to the late 1990s throughout Alaska, Canada, and other Arctic countries. Likewise, readers are directed to Schurer et al.'s[14,15] reviews of ungulate and wolf infections.

All 3 reviews indicate fairly stable E. canadensis cycles and transmission dynamics in the Arctic and sub-Arctic regions of North America. For example, Rausch reported that in a randomly collected sampling of 200 wild canids in the Brooks Range of Alaska, ≈30% were infected with E. canadensis tapeworms. This finding is similar to Schurer et al.'s[15] recent report indicating infections in 37% (71/191) of wolves sampled across Canada. Rausch[16] found 24% (24/101) of moose infected in an agricultural region of southern Alaska, and 4% (1/23) of moose infected in the Anchorage area. Schurer et al.'s[14] review of ungulate infections in Canada revealed prevalence of 0%–73% in elk, 1–21% in caribou, 11–38% in moose, and 0.3%–44% in white-tailed deer (Odocoileus virginianus), depending on sample location.

E. multilocularis tapeworms are similarly endemic in Alaska and Canada, spanning from the northern Arctic regions south into the rural and urban southern provinces of Canada, where urban coyotes and domestic dogs have been confirmed as both definitive and aberrant intermediate (dog) hosts.[7,13,17,18] As with E. canadensis, Rausch et al.[19] performed important work related to E. multilocularis in Alaska, with a particular focus on St. Lawrence Island. Their work revealed heavy infections in Arctic fox (Vulpes lagopus) and their small mammal prey species. The mean rate of infection for 1,579 fox examined was 77%, whereas infection in prey animals could range from 10% to 80%.[19] On St. Lawrence Island, dog necropsies also revealed a 12% prevalence of infection.[20]

Gesy et al.'s[21] recent review of E. multilocularis tapeworms across Canada demonstrated coyotes, red fox (Vulpes vulpes), wolves, and Arctic fox were all competent hosts, with prevalence differences related to sampling location. For example, their report indicated 37% (10/27) of coyotes and 17% (1/6) of red fox were infected in Quesnel, British Columbia.[21] Three dogs in Canada were also recently found to be infected with cysts.[7,13,17] The high prevalence in wild hosts along with the new intermediate infections in urban pet dogs has increased concern that the geographic reach of E. multilocularis tapeworms is expanding within Canada. As a result, Massolo et al.[22] suggest that much more research is necessary to understand potential public health risks associated with alveolar echinococcosis (AE) in North America.

Both AE and cystic echinococcosis (CE) have been reported in Alaska and Canada, with most infections occurring in Native American populations in Alaska. During 1940–1990, a total of 300 cases of CE were reported in Alaskan Native Americans, with only an additional 3 cases between 1990 and 1999.[23] Pathogenicity of CE in Native American patients appeared to be fairly benign, with smaller, asymptomatic cysts that often resolved without the need for surgery.[23] However, Castrodale et al.[23] reported 2 unusually severe cases of CE in Alaska in 1999, in a 51-year-old Caucasian woman and a 17-year-old Native Alaskan woman. The cysts from the latter patient were confirmed as belonging to the species E. canadensis (G8).[23] Most AE cases in Alaska also arose in Native American populations, with St. Lawrence Island as an infection hotspot. Jenkins et al.[13] reported 54 human cases during 1947–1986, none during 1986–2010, and potentially 5 during 2010–2014, although the latter infections were more likely to be CE.

Human AE and CE cases in Canada are much less prevalent than those in Alaska. Serosurveillance of indigenous populations in the Saskatchewan, Nunavut, Quebec, and the Northwest Territories of Canada indicated exposure to CE of 0%–48%.[20] CE infections in nonindigenous patients are rare and often only incidentally reported. AE cases in Canada are even more rare, with 1 autochthonous case reported before 2013.[20] Subsequent reviews have found 12–16 additional cases; however, Deplazes et al.[20] suggest these numbers are under representative, given the strongly endemic regions present in Canada.

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