The bright side Tapeworm in fox poop that will slowly destroy your organs is on the rise The worm indefinitely proliferates into cystic masses in organs, mimicking cancer. Beth Mole – Apr 23, 2025 5:46 pm | 7 This is a portrait taken of a red fox kit in Lake Clark National Park, Alaska Credit: Getty | Vincent Balsamo This is a portrait taken of a red fox kit in Lake Clark National Park, Alaska Credit: Getty | Vincent Balsamo Story text Size Small Standard Large Width * Standard Wide Links Standard Orange * Subscribers only   Learn more No matter how bad things might seem, at least you haven't accidentally eaten fox poop and developed an insidious tapeworm infection that masquerades as a cancerous liver tumor while it slowly destroys your organs and eventually kills you—or, you probably haven't done that. What's more, according to a newly published study in Emerging Infectious Diseases, even if you have somehow feasted on fox feces and acquired this nightmare parasite, it's looking less likely that doctors will need to hack out chunks of your organs to try to stop it. That's the good news from the new study. The bad news is that, while this infection is fairly rare, it appears to be increasing. And, if you do get it, you might have a shorter lifespan than the uninfected and may be sicker in general. Meet the fox tapeworm The new study is a retrospective one, in which a group of doctors in Switzerland examined medical records of 334 patients who developed the disease alveolar echinococcosis (AE) over a 50-year span (1973–2022). AE is an understudied, life-threatening infection caused by the fox tapeworm, Echinococcus multilocularis. The parasite is not common, but can be found throughout the Northern Hemisphere, particularly regions of China and Russia, and countries in continental Europe and North America. In the parasite's intended lifecycle, adult intestinal worms release eggs into the feces of their primary host—foxes, or sometimes coyotes, dogs, or other canids. The eggs then get ingested by an intermediate host, such as voles. There, eggs develop into a spherical embryo with six hooks that pierce through the intestinal wall to migrate to the animal's organs, primarily the liver. Once nestled into an organ, the parasites develop into multi-chambered, thin-walled cysts—a proliferative life stage that lasts indefinitely. As more cysts develop, the mass looks and acts like cancer, forming necrotic cavities and sometimes metastasizing to other organs, such as the lungs and brain. The parasite remains in these cancerous-like masses, waiting for a fox to eat the cyst-riddled organs of its host. Back in a fox, the worms attach to the intestines and grow into adults. Humans crash this vile cycle by accidentally eating the eggs excreted by infected foxes or other primary hosts. This generally happens by a delightful "hand-to-mouth" transfer or contamination of food. In humans, the parasites invade organs much like they do in voles, forming cancer-like masses in organs. In the liver, the infection closely resembles liver cancer and cirrhosis. The tumor-like parasites can also spread to the lungs, brain, heart, bone, and other organs. In humans, the infection is insidious, with an asymptomatic incubation period of between 5 and 15 years. Once the disease develops, about 90 percent of people will die within 10 years if they are not treated. The most common treatment in the past has been surgically removing sections of organs where the cysts are endlessly proliferating, which doesn't always catch all the parasites. However, modern treatment has turned more toward using benzimidazole drugs that fight parasitic worms, namely albendazole or mebendazole. Insights from Zurich Of the 334 patients with AE in the Swiss study—who were all treated at the University Hospital of Zurich between 1973 and 2022—the median age at diagnosis was 57.5 years. Of the 334 patients, 151 had some type of surgery to remove the parasites, and 315 received benzimidazole drug therapy. Over the 50-year study period, 90 patients died, but most of the deaths were from causes other than the parasitic infection. Only 13 deaths were caused by AE. Survival analyses showed that those with AE had lower survival rates compared with the general population five years after diagnosis, especially those who were diagnosed with AE later in life. But, AE did not appear to be the main driver of their shortened life expectancy. The reasons for this aren't entirely clear, but the authors speculate that "the gradual decline of relative survival 5 years after diagnosis could reflect a generally sicker population." Further, those who had curative surgery did not have a statistically significant boost in survival compared with infected patients who didn't have curative surgery. The authors attributed this finding to the "excellent disease control with benzimidazole drug therapy." They recommend that clinicians rethink the optimal treatment for AE. "Today, treatment decisions should be made on the basis of the patient’s expected remaining years with the disease and the potential complications and cost-effectiveness of either a surgical or conservative approach," they write. "Although younger patients will most likely benefit from radical resection, older patients may not." Like other previous studies, the Swiss analysis found a jump in infections starting around 2000. It's unclear what's causing this, but researchers have speculated that habitat expansion of primary host populations, an increased use of imaging in health care, and a more susceptible population may be possible explanations. In the current study, the increase in the number of cases was linked to a "substantial" increase in incidental findings of AE—that is, asymptomatic parasitic cysts were detected inadvertently during medical care. That points to increased imaging. But, in 2021, researchers in Canada reported AE as an emerging disease in Alberta, which they partly attributed to the growing urbanization of coyotes. Beth Mole Senior Health Reporter Beth Mole Senior Health Reporter Beth is Ars Technica’s Senior Health Reporter. Beth has a Ph.D. in microbiology from the University of North Carolina at Chapel Hill and attended the Science Communication program at the University of California, Santa Cruz. She specializes in covering infectious diseases, public health, and microbes. 7 Comments