On the MRI, Lenine’s brain appeared luminous, pale with patches of inflammation and peppered with innumerable silvery rings like the halos of so many deadly angels. The largest rings were as big as marbles while the smallest were as tiny as the point of a pencil — glowing dots speckling the gray expanse of his brain.
The halos, doctors would discover, were worms: the larval form of the pork tapeworm, Taenia solium, endemic to much of South and Southeast Asia, South and Central America, and sub-Saharan Africa, including Cape Verde, where Lenine lived prior to moving to New Bedford a year before his symptoms began.
In some infected people, Taenia solium is silent, its larvae lodging in the brain without ever causing symptoms; in others, it lies dormant for decades before announcing itself. Because of this long lifespan, it’s difficult to know exactly how many people are infected, but the World Health Organization estimates that between 2 million and 8 million people worldwide are living with neurocysticercosis — the brain infection caused by Taenia solium.
In the lexicon of public health, neurocysticercosis is considered a “neglected tropical disease.” The disease rarely surfaces in the American public consciousness — in a notable exception, The New York Times reported in May that then-presidential candidate Robert F. Kennedy Jr. might have had neurocysticercosis. It’s still relatively rare in the United States — one study found that over one 10-year period, just under 20,000 people were treated in US hospitals for complications of neurocysticercosis. But in an increasingly globalized world, it isn’t just a tropical disease.
Massachusetts does not track statewide reports of neurocysticercosis, but at Boston Medical Center, the busy safety-net hospital where I practice as a neurologist specializing in infections of the brain, roughly 200 people have been treated for neurocysticercosis in the past 10 years. This number, which excludes the many who show no symptoms, likely underestimates the true prevalence of the disease.
In some ways, Taenia solium seems utterly alien. Every tapeworm is less a single individual than a chain of organisms, connected, one to the next, by ropy lateral nerves. The adult tapeworm has the appearance of the tape measure for which it is named, a long, flat ribbon that one parasitologist described as resembling “in every way a plate of pasta without the marinara sauce,” except if the worm is still alive, “the dish of pasta slowly undulates and writhes.”
Tapeworms have no brains, no hearts, no mouths, and no guts; they absorb nutrients through their pale skin. In a tapeworm chain, one end will become the “head,” growing specialized structures — suckers and hooks, like the beckoning arm of a phantasmagoric sea creature — designed to anchor it within the gut of an infected person. The other end will form a series of egg sacs able to separate from the chain and rupture, spilling eggs into the host organism’s stool.
To hatch, the eggs must be swallowed by a second host, either a person or one of the pigs for which the pork tapeworm is named. In the gut of a new host, these eggs hatch into tiny embryos that immediately bore through the intestinal wall and go into the bloodstream, spreading throughout the body and eventually swelling into fluid-filled tapeworm larvae roughly the size and shape of green peas. Sometimes, these larvae land in muscles, registering as a hard nodule beneath the skin that can be felt with the fingertips. When infected pork is eaten by a human, these muscle cysts come to life in the person’s gut, growing into an adult tapeworm, shedding eggs, and beginning the cycle anew. Sometimes, though, in either pigs or humans, the larvae land in other parts of the body — the eyes, or even the rubbery tissues of the brain, forming a tough capsule that can remain silent for decades.
While they are alive, the larvae skillfully evade detection by the human immune system. They begin to cause symptoms only in death, when they lose their ability to remain hidden. Paradoxically, the first signs of neurocysticercosis are caused not by the cyst itself, but by our own immune systems, which mount an inflammatory response to the sudden revelation of an alien invader. On an MRI, this inflammation is revealed by tell-tale silver rings such as those in Lenine’s brain.
These inflamed cysts can cause a spectrum of symptoms, ranging from headaches to brain swelling so severe it can be fatal. The most common symptoms, experienced by 70 percent to 90 percent of sufferers, are seizures, like the spells of confusion that brought Lenine to the hospital.
The World Health Organization estimates that around 1 in 100 people worldwide have epilepsy requiring treatment. Eighty percent of those people live in low- and middle-income countries like Cape Verde. By some estimates, neurocysticercosis is the most common cause of preventable epilepsy worldwide — a treatable condition with potentially devastating consequences.
Half a world away from the bustling metropolis of Praia, Cape Verde, where Lenine was raised, is the remote island of New Guinea. The island was flung from the Pacific by geological unrest, and the scars of its birth are still evident in the mountainous Highlands region. The Highlands travel the island from east to west in jagged peaks like a bony spinal column and are scattered with villages populated by members of the indigenous Ekari tribe.
In the mid-1970s, two physicians at the regional hospital noticed a frightening trend: villager after villager — men, women, and children — had arrived at the hospital with severe burns blistering their entire bodies. Nearly all were third- or fourth-degree, penetrating the muscle and even bone, leaving flesh blackened and charred and sometimes requiring amputation.
Between 1973 and 1976, 157 people were admitted to the hospital with burns, 17 bad enough to require amputation. The burns were a curse of the night: at an altitude of 5,000 feet, the Highland air can be bitingly cold, and every village hut was heated by a central fire. Most of the sufferers, their families reported, had fallen into these fires as they slept, the result of nighttime seizures. In their muscles, the doctors found the tell-tale nodules of cysticercosis.
One such patient was a 35-year-old man admitted with severe burns on his left foot. When he awoke, he did not recall the fire; third- and fourth-degree burns are eerily painless because even the deepest nerves are ravaged by the heat. He survived just 18 hours. The doctors performing his autopsy found that his brain had been invaded by some 20 larval cysts, each hard, hollow swelling surrounded by the white blood cells of his own immune system.
Another was a 13-year-old girl who fell into a fire during her first seizure. The seizures never stopped; over months, she began to develop strange movements, as though her limbs were being pulled by a crazed puppeteer. Finally, she fell into a coma. Twelve months after her first seizure, she died. Her brain was sent to the US Armed Forces Institute of Pathology. It was filled with over 2,000 cysts, speckling all of its lobes.
Despite the fires, burns had been vanishingly rare among the Ekari before the ‘70s, mostly limited to toddlers who were injured while playing too close to the flames. Between 1968 and 1970, the doctors estimated, just four burn patients had found their way into the local hospital.
The burns were not the only way New Guinea had changed during those years. The Ekari people and their ancestors have lived on the island for tens of thousands of years, but the Dutch East Indies had claimed the western half — West Papua — in the early 1800s and clung to it until 1963, when they were finally forced out by an Indonesian military campaign. The new occupiers were equally unwelcome, and in 1969, an armed Ekari resistance met the Indonesian military in the central Highlands. The military invasion overcame the resistance with paratroopers and machine gun-armed aircraft, driving the villagers from their homes and into the mountainous jungle as refugees. But the Indonesian government tempered the military campaign with a gift: pigs imported from Bali.
Pigs are intimately entwined with Ekari culture, used as both gift and currency. They’re slaughtered to celebrate the birth of a child and to mourn the death of a parent, to ratify peace treaties and consecrate marriages. Ekari homes are raised on stilts to create a space for pigs to wallow below.
By 1971, Ekari villagers had begun to report strange nodules in the flesh of the Balinese pigs, and within months, the nodules had spread to their own livestock. The Ekari ate pork mostly at lavish feasts, in which the pigs were prepared over a fire. These bonfires cooked the pigs’ skins and rendered their fat, but left the cysts embedded in their muscles largely unscathed. The Veterinary Pathology Institute in Bogor, Indonesia, would later confirm that the imported pigs were infected with tapeworm larvae. By 1978, 1 in 4 Ekari adults and children were also infected.
The Ekari traded pigs with neighboring tribes, and Taenia solium spread first to the northern coast of the island and then to the south, where an Ekari teacher began to have seizures after he returned home to visit his family. It traveled in the bodies of infected pigs carried by airplane to the eastern edge of the Highlands, the border between Indonesian West Papua and sovereign Papua New Guinea. All of the pigs in the area were killed and their corpses burned with the hope of keeping the disease from spreading further, but by the mid-1980s, Taenia solium had crossed the border, harbored in the bodies of refugees fleeing the Indonesian occupation.
Taenia solium is ancient. Tapeworm eggs, which are coated in tough fibers that resist decay, have been found in the intestines of human corpses dating back to the Bronze Age, while a single whole cyst was found lodged in the stomach muscles of a Ptolemaic Egyptian mummy who was likely infected by eating pork cured in brine. Some historians have speculated that Julius Caesar’s epilepsy, which began one year after a visit to Egypt, resulted from neurocysticercosis, while others have suggested that biblical and Quranic taboos against pork consumption are fueled by a fear of the tapeworm.
Despite its long history, much about the life cycle of Taenia solium remained mysterious for millennia. Doctors didn’t realize that the ribbon-like tapeworm confined to the intestines and the cysts scattered through brain and muscle were the same species until a 19-century German pathologist proved the connection by feeding an incarcerated man, who was condemned to death, sausages and a noodle soup containing cysts from an infected pig. After the execution, the pathologist performed an autopsy and found 10 immature tapeworms in the man’s intestines.
In a heroic proof of concept, in 1934, a Japanese parasitologist spent months collecting fecal samples from four human subjects who had volunteered to be inoculated with cysts gathered from an infected pig. Three of the volunteers ended the experiment within a year, taking an antiparasitic medication to rid their bodies of the tapeworms. But the fourth — the parasitologist himself — continued for 451 days. When he finally took the treatment, he expelled a tapeworm that was over 7 feet long.
In some ways, the term “pork tapeworm” is a misnomer. People can contract taeniasis, the mature intestinal tapeworm, by eating undercooked pork contaminated with larval cysts. Intestinal taeniasis is eminently treatable: a single dose of an antiparasitic medication kills the tapeworm.
But neurocysticercosis — the human brain infection caused by the larval cysts — comes instead from unwittingly eating tapeworm eggs, which easily pass from one person to another on skin, clothing, and food. The eggs spread best in places without indoor plumbing or underground sanitation, where they can survive in the soil. But they can also cling to the unlikeliest crevices — behind the ears, between the fingers, and beneath the fingernails — as they await a new host.
Cases of neurocysticercosis have been reported in people who have never consumed pork at all — from adherent Orthodox Jewish communities in Brooklyn, New York, to devout Muslim families across the Arabian peninsula — and in people who have never left the United States, who contract the disease from a family member or another close contact.
Although treating intestinal taeniasis is straightforward, treating neurocysticercosis can be more complicated. In people whose cysts have already died by the time they’re diagnosed, the treatment is purely symptomatic — antiepileptic medications if they struggle with seizures, for instance. In people diagnosed with still-living cysts, antiparasitic medications can help to kill the cysts. Because the brain swelling provoked by dying cysts can be dangerous or even fatal, these medications are prescribed alongside steroids to suppress inflammation. In some cases, the risk of swelling is so high a surgery is required to remove the cysts or reduce the pressure within the skull.
Lenine, now in his late 40s, is unsure how long his body harbored the cysts before they first began to cause symptoms, and wonders whether he contracted the disease in Cape Verde — where he worked as a driver for the Ministry of Health and often ate at roadside stands because he had no time to stop for meals — or after he arrived in Massachusetts, when he worked in the depths of a sewage treatment plant.
Lenine was discharged from the hospital 11 days after he was first admitted, armed with prescriptions for steroids, two antiparasitic medications, and an antiseizure drug. But when his family arrived at a pharmacy, the prescriptions were too expensive to fill — they would have cost over $20,000 out of pocket, his family recalls. Without the medications, the headaches returned, leaving Lenine speechless and reducing him to tears.
At Massachusetts General Hospital, where his family brought him soon after, an MRI showed the same glowing rings, rimmed with the pallor of inflammation: the hungry cells of Lenine’s own immune system, fighting the parasites.
Desperate to make sure Lenine’s infection was treated, his family reached out to his former employer, the Cape Verde Ministry of Health, to ask if medications could be shipped from Cape Verde to Boston. But before the pills were sent, MGH was able to fill Lenine’s prescriptions free of charge. He was finally treated, finishing a course of antiparasitics to kill the cysts. Yet, he returned to the hospital again and again — in June, with headaches that swelled as soon as he began to reduce his steroids, and in July, with a prickling sensation blanketing the right half of his body that seemed to come and go in waves. On MRI after MRI, the inflammation persisted, blooming and retreating around the cysts.
It has been nearly a decade since Lenine was first diagnosed and treated; the cysts in his brain have died, hardening with calcium and fading into pale scars. Still, the inflammation has never fully subsided. His headaches have been quieted by a series of progressively stronger anti-inflammatory medications but have never entirely disappeared. He can no longer work full time, occasionally picking up odd jobs painting or cleaning but struggling with a lingering weakness that fills the right half of his body. He has become forgetful, and his sister Monica often drives to Massachusetts from her home in New Hampshire to take Lenine to doctor’s appointments in Boston and make sure that he remembers to take his medications. When the rest of his family travels, Lenine stays home, afraid that his symptoms might flare. Some months, the inflammation leads to seizures. The seizures rob him of his speech, a loss his family now recognizes as a portent of the whole-body convulsions that will soon follow.
Despite our best scientific efforts, Taenia solium still harbors some mysteries, including the question of why in some people like Lenine, even long-dead, calcified cysts can still cause chronic inflammation, haunting sufferers with seizures and other intractable symptoms.
But millennia after Egyptian hieroglyphics first described the tapeworm, we understand now that Taenia solium still persists because of global disparities: unequal access to clean water, sanitation, and basic medical treatment. For all that remains inscrutable about neurocysticercosis, the greatest tragedy of the disease is an obvious one: It’s entirely preventable.
Dr. Pria Anand is a neurologist at Boston Medical Center who specializes in the diagnosis and treatment of neurologic infections. Her first book, The Mind Electric, will be out in June 2025. Send comments to magazine@globe.com.
