The thing I cannot stop thinking about with Echinococcus multilocularis is that it does not behave like a tapeworm at all. When its eggs end up in a person, the larvae burrow into the liver and then start budding off new lobes the way a metastatic carcinoma would, slowly and silently, for five to fifteen years. By the time anything hurts, the radiologist is squinting at a scan that looks for all the world like cancer and reaching for the biopsy tray. The CDC’s clinical overview calls the lesion “tumor-like.” That is the polite version. The disease is alveolar echinococcosis, and untreated it kills more than nine out of ten patients within a decade or so of diagnosis.

So when I tell you that researchers at the University of Washington just published a survey of 100 coyotes around Puget Sound and 37 of them were carrying it, the question is not whether that is interesting. The question is why nobody was looking until now. When the team restricted the analysis to the 81 animals they could actually dissect, the rate climbed to 45.7 percent of that sub-sample. The carcasses came from Whidbey Island, Everett, Burlington, and other Puget Sound localities. Whatever the per-site number turns out to be, the regional signal is that the parasite is established in West Coast coyotes at a prevalence comparable to what you see in endemic European foci.

This is the first time E. multilocularis has been documented in a wild host along the contiguous U.S. Pacific seaboard. The work, led by Yasmine Hentati and just out in PLOS Neglected Tropical Diseases, was funded by the National Science Foundation and the University of Washington’s Hall Conservation Genetics Fund. The strain they sequenced is the punchline. It is not a North American haplotype that drifted west out of Alaska. It is a European one, mtG h28, sometimes called BC1, the same lineage that turned up in coyotes in British Columbia and across the prairie provinces over the last decade. It came from somewhere else, and it is settling in.

I want you to sit with the lifecycle for a second, because the lifecycle is elegant in the way evil things sometimes are. Adult worms live in the gut of a coyote or fox or domestic dog and shed microscopic eggs in their feces. Those eggs end up on grass, in gardens, on the fur of a dog that rolled in something it should not have. A vole eats them. The larvae cyst up in the vole’s liver. A coyote eats the vole, the worm matures, and the cycle closes. Humans are not part of this loop. We get pulled into it by accident, by swallowing eggs from contaminated soil, produce, or, very often, the coat of a pet that hunts rodents. The vole’s liver and our liver look close enough to the parasite that it does not notice the mistake.

So how does a European strain end up west of the Rockies? The paper is candid that the introduction route is not nailed down, but the candidate list is short and uncomfortable. Red foxes imported from Europe for hunting starting in the 1700s. Foxes that escaped from fur farms. Wolves moved across the continent for reintroduction programs. And, most pointedly, the international movement of pet dogs that have not been dewormed before crossing the border. The Hentati paper explicitly flags the absence of any U.S. or Canadian requirement to deworm imported dogs as a “policy gap” that allows undetected introductions. The European-strain expansion across western Canada has been documented in the wildlife-disease literature since the early 2010s. Nothing in U.S. or Canadian import policy has moved.

What the official framing of “first detection” papers over is that this was almost certainly here for years before anyone went looking. The same group documents seven recent diagnoses in domestic dogs spread across Washington, Oregon, Idaho, and southern British Columbia since 2023, including one Washington dog with full-blown alveolar echinococcosis. That is a regional warning siren, and it has been going off for two years. Washington did not make human echinococcosis a notifiable condition until December 2024. Before that, a doctor who diagnosed it was not required to tell the state. Surveillance is not a passive activity. You do not find what you do not look for, and on this we mostly were not looking.

The treatment story is the other half of why this matters. If a surgeon can resect the lesion completely while it is still localized, follow with at least two years of albendazole, and watch the patient for a decade, modern series report long-term survival approaching the general population. That is extraordinary for a parasitic disease. The catch is that complete resection only stays possible if the disease is caught early, and “early” in a condition with a five-to-fifteen-year silent phase means catching it before the patient knows anything is wrong. Inoperable cases on albendazole monotherapy do much better than they used to, with ten-year survival pushed from around 10 percent up past 80 percent, but the drug is parasitostatic, not parasitocidal. You take it indefinitely, and the cysts wait.

Hentati’s co-author Guilherme Verocai, at Texas A&M, gave the public-facing guidance plainly: do not let your dog hunt or scavenge rodents, deworm with praziquantel on a schedule your vet sets, and wash produce from your garden. Those are the small, real things a person in King or Snohomish County can do this week. The bigger thing, the policy thing, is the one I would actually push my representatives on. We require rabies certificates for dogs crossing the border. Norway, the United Kingdom, Ireland, Malta, and Finland all require a documented dose of praziquantel administered by a vet 24 to 120 hours before an imported dog arrives, specifically to keep E. multilocularis from setting up in their wildlife. The drug is cheap. The protocol is settled. Other countries with intact public-health agencies have considered it obvious for years. The U.S. and Canada have not.

What I keep coming back to is the biology, though, because the biology is what makes this worth taking seriously instead of shrugging at. A worm that has learned to grow like a tumor in the wrong host. A European haplotype that arrived in North America by some combination of fur-farm escapees, wolf reintroductions, and the steady international traffic of unscreened pets, and that is now cycling through the rodents in a temperate rainforest. A surveillance gap that turned a one-third-of-coyotes infestation into news only because a graduate student decided to look. The next time someone tells you the public health system is keeping watch, remember who actually went out and counted: a doctoral student with an NSF grant and a freezer full of coyote intestines, doing the work the agencies were supposed to do, and finding what nobody wanted to find.

If I lived in Whidbey or Burlington with a dog that likes to hunt voles, I would call my vet on Monday and add a praziquantel dose to the schedule, wash the lettuce twice, and write a short, specific note to my member of Congress asking why imported dogs still cross the northern border without one. The biology is doing what biology does. The policy is what is supposed to be ours.

Sources

  1. Hentati et al., PLOS Neglected Tropical Diseases, “Detection of Echinococcus multilocularis in coyotes in Washington State, USA highlights need for increased global wildlife surveillance” (June 2026)
  2. University of Washington News, “Parasitic tapeworm, a risk to domestic dogs and humans, found in Washington coyotes” (April 6, 2026)
  3. CDC, “About Alveolar Echinococcosis (AE)”
  4. Joliat et al., “Alveolar Echinococcosis: A Challenging Task for the Hepatobiliary Surgeon,” Pathogens (2022)
  5. Norwegian Food Safety Authority, “Mandatory treatment for echinococcosis for dogs imported to Norway”