‘Brain-eating amoeba’ appears to love crawling into narrow spaces

19 Aug 2026 / 12:10 / By Isabella Backman

doi: 10.1126/science.z78ol5k

Naegleria fowleri is a harmless pond dweller—unless it ends up in the nose of a human swimmer. Once inside, the amoeba can crawl along nerve fibers in the nasal cavity and through little openings in the skull until it reaches the brain. Once there, it can cause an infection that is almost universally fatal, earning it the frightening moniker the “brain-eating amoeba.”

Exactly why N. fowleri, which normally feeds on bacteria, exhibits this behavior has long been unclear. But a study posted last month on the preprint server bioRxiv suggests a possible reason: The parasite loves to seek out tight spaces. This “claustrophilic” behavior may help it find its prey—and explain why it occasionally ends up deep in the human brain.

“A lot of the research done on Naegleria is focused on drug discovery and not the fundamental reasons behind pathogenesis,” says Ashley Moseman, an immunologist at Duke University who studies the body’s immune response to N. fowleri but who was not involved with the new work. A better understanding of the pathogen’s basic biology could help pave the way for specific drugs against it, which currently don’t exist.

N. fowleri, which lives in warm freshwater and soil around the world, can cause a disease called primary amoebic meningoencephalitis (PAM) that starts with a headache, fever, and nausea, quickly followed by confusion, a stiff neck, seizures, hallucinations, and coma. PAM is exceedingly rare, with fewer than 500 reported cases globally since 1962, but it has a fatality rate of about 95%. Doctors have saved some patients using a combination of drugs, including antifungal medications and miltefosine, which is used primarily to treat a parasitic disease named leishmaniasis.

But because PAM is so rare and its early symptoms are similar to those of other diseases, the diagnosis often comes after patients have died.

N. fowleri infections are biological accidents; they don’t help the species spread, says Katrina Velle, a cell biologist at the University of Massachusetts Dartmouth. “We’re not a part of its life cycle.” So why does the amoeba go after us in the first place?

Working with N. fowleri requires strict and cumbersome biosafety measures, so Velle and her colleagues used its nonpathogenic relative, N. gruberi, whose behavior is generally similar. (The study was supported in part by a nonprofit set up in honor of Aven Bruce Moffat, a boy who died from PAM at age 6 after he got infected in a pond on his family’s property in North Carolina in 2021.)

The scientists pipetted N. gruberi into a dish containing small parallel channels between 2 and 8 micrometers wide and tracked their movements using a microscope. The amoebae tended to move away from open spaces and enter the channels, they found, even though there wasn’t anything enticing inside. Amoebae in the 8-micrometer channel crawled twice as fast as those on the outside—at a rate of about 40 micrometers per minute. The amoebae were too big to enter the narrowest passages, but the team watched them piling up around the opening. “We saw these frustrated attempts to enter these channels,” Velle says. 

Researchers discovered Naegleria gruberi was drawn to—and entered—microscopic channels in a dish. The amoebae were too big for the narrowest channels, which were 2 micrometers wide, but researchers watched them pile up around the opening. Katrina Vell

Once inside the channels, N. gruberi rarely turned around. This behavior contrasts with that of dendritic cells, specialized human immune cells that defend against pathogens, which are more prone to change direction in microchannels, Velle says. Previous research showed these immune cells travel much slower in confinement, between 5 and 10 micrometers per minute. If N. fowleri moves at similar speeds to N. gruberi, the ability to outrun our immune defenders could play a role in its pathogenicity, she suggests.

Studying Naegleria’s movements is important because its behavior plays a fundamental role in the amoeba’s ability to cause disease, Moseman says. But he wonders whether there is something different between the ways N. fowleri and N. gruberi move; after all, only the former infects the brain. “It’s reasonable to think that what N. gruberi is doing is similar to what N. fowleri does, but N. fowleri is the only one that’s pathogenic.”

Preliminary data from Velle’s laboratory suggest N. fowleri shows claustrophilic behavior as well, but her team plans to investigate this more thoroughly. There may be other reasons why this strain is infectious but N. gruberi is not, Velle says. N. gruberi can’t live at the temperature of the human body, for example, and certain enzymes used by N. fowleri may help it invade human tissues.

Naegleria’s claustrophilia would make sense from an evolutionary point of view. The bacteria it feeds on are sometimes found in crevices in the bottoms of ponds, so wiggling into narrow spaces may simply be how it finds food. “It’s really just an unfortunate circumstance when the amoebae get into your upper sinuses,” Velle says. “They’re just doing what they’ve evolved to do—looking for nooks and crannies where their bacteria should be.”