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Human alveolar echinococcosis (AE) is a zoonotic cestode infection which is usually fatal in the absence of treatment. Treatment involves major surgery or indefinite antiparasitic therapy. The incidence is rising in Europe and Asia, with an increased risk observed in immunocompromised individuals. Previously, AE acquisition in North America was extremely rare, except for one remote Alaskan Island. Recent studies have demonstrated a new European-like strain of Echinococcus multilocularis (Em) in wildlife and in human AE in western Canada. We report the experience of all AE patients diagnosed in Alberta. Each was diagnosed by histopathology, serology, and PCR-confirmed by a reference laboratory. Seventeen cases of human AE, aged 19-78 years, nine females, were diagnosed between 2013 and 2020: all definitely or probably acquired in Alberta. Six lived in urban areas, and 14 had kept dogs. In eight, the lesions were found incidentally on abdominal imaging performed for other indications. Six were immunocompromised to varying degrees. Six were first diagnosed at surgery. All have been recommended benzimidazole therapy. One died of surgical complications. Clinicians should be aware of this diagnostic possibility in patients presenting with focal nonmalignant hepatic mass lesions. Greater urbanization of coyotes, the predominant definitive host of Em in Alberta, and growing numbers of immune suppressed individuals in the human population may lead to increasing recognition of AE in North America.

Alveolar echinococcosis is the most serious helminthic zoonosis of the northern hemisphere affecting humans. The causative agent, Echinococcus multilocularis, occurs in geographically distinct strains that can be distinguished based on sequence variations of mitochondrial genes and nuclear microsatellite targets. This report finds that the human case of Alveolar echinococcosis occurring in Minnesota in 1977 was caused by the N2 haplotype described previously; the N2 haplotype is distinct from European and Asian isolates of the parasite and is restricted to the central region of North America., (© The American Society of Tropical Medicine and Hygiene.)

To investigate echinococcosis in co-endemic regions, three polymerase chain reaction (PCR) assays based on the amplification of a fragment within the NADH dehydrogenase subunit 1 (ND1) mitochondrial gene were optimized for the detection of Echinococcus shiquicus, Echinococcus granulosus G1, and Echinococcus multilocularis DNA derived from parasite tissue or canid fecal samples. Specificity using parasite tissue-derived DNA was found to be 100% except for E. shiquicus primers that faintly detected E. equinus DNA. Sensitivity of the three assays for DNA detection was between 2 and 10 pg. Ethanol precipitation of negative PCR fecal samples was used to eliminate false negatives and served to increase sensitivity as exemplified by an increase in detection from 0% to 89% of E. shiquicus coproDNA using necropsy-positive fox samples.

To date, only a single proven case of autochthonous human alveolar echinococcosis has been recorded in Minnesota in 1977. At that time, echinococcal lesions removed from the patient were experimentally inoculated into voles, and the parasite materials obtained from the voles were preserved as histopathologic specimens for 30 years. In this study, retrospective genetic analysis of larval Echinococcus multilocularis originating in the human case was performed using the histopathologic specimens. DNA was extracted from the hematoxylin and eosin-stained specimens, and mitochondrial cytochrome c oxidase subunit 1 gene (cox1) was amplified by polymerase chain reaction. Subsequently, 20 small fragments (100-216 bp) covering almost the entire sequences (97%) of the cox1 were successfully amplified, and the nucleotide sequence analysis showed that the E. multilocularis isolate from Minnesota was almost identical to an isolate from South Dakota rather than isolates from contiguous Alaska.