Echinococcus spp. Tapeworms in North America

Jacey Roche Cerda; Danielle Elise Buttke; Lora Rickard Ballweber


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

In This Article

Abstract and Introduction


Alveolar and cystic echinococcosis are emerging and reemerging in Europe, Africa, and Asia. The expansion of Echinococcus spp. tapeworms in wildlife host reservoirs appears to be driving this emergence in some areas. Recent studies suggest a similar phenomenon may be occurring in North America. We describe the context of Echinococcus spp. research in North America, with a specific focus on the contiguous United States. Although studies were conducted in the United States throughout the 1900s on various sylvatic and domestic Echinococcus spp. tapeworm cycles, data are lacking for the past ≈30 years. We review previous research, provide analysis of more recent focal studies, and suggest that Echinococcus spp. tapeworms, in particular E. canadensis, may be underrecognized. As a result, we suggest that additional research and surveillance be conducted for these tapeworms in wildlife host reservoirs across the United States.


Echinococcus spp. (family Taeniidae, class Cestoda) are zoonotic tapeworms currently infecting 2–3 million persons worldwide and causing US $200–$800 million in annual economic losses related to human infection.[1,2] Infection appears to be increasing, reemerging, and geographically expanding in multiple locations across Europe, Asia, Africa, and the Americas (primarily in Latin America), with >200,000 new cases/year.[3]Echinococcus spp. tapeworms have complex domestic and sylvatic life cycles that affect the health of >40 companion animal, livestock, and wildlife host species.[4,5]

The basic Echinococcus spp. life cycle involves 2 hosts, where carnivores (wild and domestic) are the definitive hosts and small mammals and ungulates (domestic and wild) are the intermediate hosts.[6] From within the small intestine of the definitive host, the mature tapeworm releases immediately infective eggs that are shed with the feces into the environment. Intermediate hosts ingest the eggs as they feed on contaminated vegetation. Once ingested, the oncosphere hatches and penetrates the small intestine to migrate to various organs and tissues, where it develops into one or more hydatid cysts.[6] Definitive hosts ingest the cysts when feeding on the viscera of infected intermediate hosts.[6] Humans are aberrant dead-end hosts that are infected from accidental ingestion of eggs, typically from interaction with domestic dogs, which act as bridge hosts between wildlife and the human environment. Contamination of the human environment may occur either directly (from feces) or indirectly (eggs carried on paws and fur).[7] Humans may also become infected through foodborne transmission, most often through eating inadequately washed fruits and vegetables.[8] Intermediate hosts and humans may develop alveolar, cystic, or polycystic echinococcosis, depending on the parasite species involved.[6]

Infection in livestock can cause substantial economic losses, including the condemnation of infected viscera; decreased meat, milk, and wool production; and delayed fecundity, growth, and performance.[4] Estimated global economic loss due to infection in production animals is US $1.5–$2 billion annually.[2] The global disease burden on wildlife species is unknown, as is the effect that echinococcosis may have on the overall fitness of wildlife animals and populations.

Throughout the early decades of the 1900s, only 1 species of Echinococcus, E. granulosus, was formally recognized in North America and across the world. Analysis of genetic and phenotypic data, host specificity and preference, and differences in human pathogenicity and tissue tropism has since revealed that E. granulosus sensu lato is actually composed of a complex of 10 specific genotypes, G1–10.[9] Subsequently, several of the genotypes or genotype complexes have been elevated to distinct species: E. granulosus sensu stricto (G1–G3), E. equinus (G4), E. ortleppi (G5), E. intermedius (G6–G7), and E. canadensis (G8–G10).[9,10] Genotypes 6–7 are still often grouped with E. canadensis; however, distinct host preferences and genetics demonstrate the proper elevation to their own species.[10] Additional recognized species of Echinococcus are E. shiquicus, E. vogeli, E. felidis, E. oligarthra, and E. multilocularis. E. granulosus sensu stricto and E. multilocularis tapeworms cause the 2 most pathogenic forms of disease in humans; E. multilocularis infections are the most deadly, given the metastatic nature of the cysts and the related difficulty of treatment.

Although well studied globally, the current presence, prevalence, and transmission dynamics of Echinococcus spp. tapeworms in the contiguous United States are currently unknown. Substantial research was conducted between the early 1930s and the 1980s; however, very little research has occurred in the past 3 decades. Given the documented expansion of these tapeworms across many regions of the world, including within Canada, a better understanding of the presence, prevalence, and disease ecology in the United States is needed, particularly because echinococcosis is not a reportable disease. Additional research will provide scientists, veterinary and human medical professionals, and other public health officials with a more complete picture of Echinococcus spp. cycles in the United States. Here we set the context for additional research through a synopsis of Echinococcus spp. and echinococcosis in humans in North America, with a focused discussion of endemic US Echinococcus spp. cycles from the early 1900s to the present. We conclude with recommendations for further research.