by Vidya Krishnan
By the time Mercy Lena Brown was born, in 1872, her New England farming community was becoming a ghost town. Young farmers were leaving the barren, rocky soil for jobs in the city, and the people who remained were suffering an outbreak of consumption, which seemed to move through households with no clear pattern, causing one out of every four deaths in the area.
Of the nine members of the Brown family, Lena’s mother was the first to die of consumption, in 1883. Seven months later Lena’s sister Mary Olive, a twenty-year-old dressmaker, died too, becoming so pale and emaciated in the final days of her illness that she knew in advance to choose the hymn she wanted sung at her funeral.
Lena’s brother, Edwin, a store clerk, fell ill next. Desperate, he went west to Colorado Springs, following the prevailing medical wisdom of the time that dry air and sunshine could arrest the illness. They didn’t. He returned home after eighteen months, weaker than ever, and by then Lena, who had been well when he left, was gone too, her own consumption the “galloping” variety. Edwin’s dreams became even more fevered. “She haunts me!” he called out in his sleep.
After Lena’s death, in 1892, an article in The Providence Journal reported that neighbors “besieged” her father, George, insisting that Edwin’s symptoms were a sign of something otherworldly: some spirit must be sucking the life from his thinning body. Because he fell sick after his mother’s and Mary Olive’s deaths, and because he quickly worsened after Lena’s, the three Brown women were the chief suspects. The only way to save his life, the neighbors told his father, was a morbid practice that had caught on in New England in reaction to the gothic horrors of consumption: exhume the bodies of his mother and sisters before Edwin entirely wasted away.
Four local men dug up the remains of the three Brown women. By then Lena’s mother and sister had been dead for nine years, and only their skeletons remained. Lena had died in the winter, and her body had been left in a crypt until the spring thaw softened the frozen earth enough for burial. Her doctor was enlisted to perform an autopsy; her body was still largely undecomposed. From beneath Lena’s rib cage he removed her liver, the twin pink slabs of her lungs, and her heart. This he slit open with a scalpel to find that it was filled with dark clots of rotting blood.
To the neighbors, who had watched many of their own loved ones waste away of consumption, the heart seemed like proof: Lena had been feeding on the living, sapping their blood and leaving them wan and feeble. They burned her liver and heart to ash, which they mixed with water and administered to Edwin as an exorcism and cure. He died two months later. In the end, only George and one of his seven children survived the disease. Lena’s lungs, the doctor later told a local newspaper, had been filled with “diffuse tuberculous germs.”
Lena’s death and exhumation—and a cultural history of this tradition of disinterment, common throughout eighteenth- and nineteenth-century New England—are recounted in careful detail in the Rhode Island folklorist Michael Bell’s Food for the Dead (2011). Drawing on decades of census data, death records, newspaper clippings, and oral histories, Bell argues that this model of disease—consumption caused by a vampiric spirit—had an internal logic no different from the explanations of doctors and scientists at the time. The myth could explain why the disease clustered in certain houses, cursing entire families. And it accounted for the visceral horror of the affliction, the way it consumed each of the body’s vital organs in turn.
A decade before Lena’s death the German physician and microbiologist Robert Koch, informed by the nascent germ theory of disease, had discovered the bacterium—Mycobacterium tuberculosis—that causes consumption. But the first antibiotics were not discovered for another half-century, and the medical establishment, loath to attribute consumption to a pathogen that could not yet be treated, was slow to accept Koch’s explanation. Instead doctors clung to the older theory that consumption was caused by damp lungs, prescribing therapies—like Edwin’s sojourn in the West—intended to desiccate their patients’ failing bodies: “What cures and hope for recovery were medical practitioners offering their consumptive patients?” asks Bell.
If you judge by sheer number and kinds of treatments, they offered a great deal. But if you measure the effectiveness of these treatments, then, unfortunately, they were still groping in the dark.
Among these treatments were leeches and opium, warm sea air and cold baths, milk from the breasts of a pregnant woman, and dried seaweed placed beneath one’s pillow.
Therapies have changed, but tuberculosis remains the leading infectious cause of death worldwide.
Nearly a century and a half after Koch’s first attempts to devise an inoculation, we still have no effective vaccines. Globally, one in four people carries tuberculosis, though most are neither contagious nor symptomatic. In the United States, where the prevalence is closer to three in one hundred, the disease thrives primarily in the conditions created by social injustice: overcrowded prisons, for instance, or temporary shelters. Yet programs to curb the spread of TB are among those hit hardest by both the Trump administration’s closure of USAID and its assault on the National Institutes of Health, attacks that are projected to lead to millions of avoidable TB deaths over the coming decade.
Tuberculosis can seem inscrutable, a protean disease that can settle in virtually any organ in the body. In the lungs it causes the bloody cough and gasping breath that ravaged the Brown family; in the lymphatic system it causes swollen masses that can press on the soft muscles of the vocal cords, robbing victims of their voices; in the guts it causes raw, bleeding ulcers and obstructed bowels. The disease is airborne: colonies of bacteria are exhaled from the lungs of a person with pulmonary TB in a fine mist of particles that can linger suspended in the air for hours. How long the bacteria survive in the air depends on the surrounding conditions; in spaces with poor ventilation—an enclosed car, for instance, or a windowless room—they can last hours or even days.
Our lungs are a strange paradox: they are protected by the hard carapace of our ribs but also tremendously exposed to airborne bacteria, which can slip in with a single breath. To prevent infections, the labyrinthine passages that make up each lung are lined with white blood cells. But Mycobacteria tuberculosis are impenetrable. Each cell is surrounded by a thick barricade made of fats and proteins. In the lungs they are consumed by white blood cells but not digested, surviving undisturbed as more white blood cells arrive to wall off the infection, forming scarred balls called tubercles. Here the bacteria can live for decades or even a lifetime, forming a latent infection and replicating slowly within an unwitting host, undetected until they take advantage of an aging or suppressed immune system to explode into full-blown consumption. A multitude of factors can determine whether a person living with latent TB is likely to develop the active disease, as Lena, her mother, and her siblings did, or whether they will survive into old age with an infection that remains latent, as her father probably did. Malnutrition, pollution, and illnesses like HIV and diabetes can all contribute to TB activation.
Fossils show the marks tuberculosis leaves on bones, tiny holes that resemble the work of termites, the result of the human immune system’s futile attempts to ferret out islands of bacteria lodged in the hard tissue. In hips or wrists, the disease knits joints together into an immobile mass. In spinal vertebrae, which are particularly prone to tuberculosis because they are traversed by innumerable tiny arteries that can deposit the bacteria deep into each bone, the holes cause successive vertebrae to collapse into one another until the spine contorts into a painful curve. The telltale hunched back of spinal TB is immortalized in ancient Egyptian tomb paintings, ivory carvings, and the bodies of unearthed mummies.
The earliest evidence of tuberculosis comes from the Natural Trap Cave, in northern Wyoming’s Bighorn Mountains. The cave lies along an ancient game trail that connects the mountains with lower-lying grazing lands. Shaped like an iceberg—the small opening is about the length of a compact car, while the floor, nearly a hundred feet below, is as wide as a cruise ship—the cave is nearly invisible from the snow-covered ground above it. Its unusual shape has made it particularly interesting to paleontologists: the steep fall caused the deaths of innumerable animals, and the temperature at its floor never rises above forty-two degrees Fahrenheit, preserving their remains. Among the animals that have died there since the last ice age—dire wolves and woolly mammoths, American cheetahs and an ancient species of camel that once wandered the American West—are a multitude of Pleistocene bovids, from bighorn sheep to long-horned bison, with the eroding bones and genetic traces of tuberculosis.
We once thought tuberculosis arrived in humans with the advent of agriculture, acquired from cattle as hunters and gatherers became settled farmers during the Neolithic revolution. The bovine form of the disease—caused by the closely related Mycobacterium bovis—can jump the species barrier to humans through unpasteurized milk, causing an infection that is clinically indistinguishable from one caused by the human variant.
But more recent studies suggest that Mycobacterium tuberculosis and Mycobacterium bovis evolved separately, from an even more ancient common ancestor long before the Neolithic Period. As far back as we can imagine, TB has been a human disease.
I practice neurology at a so-called safety-net hospital—a designation unique to the deeply flawed and segregated American health care system—where the many inequities that drive tuberculosis infection rates are evident. “Safety net” is a euphemism for hospitals that care for people who, because of their health insurance or lack thereof, their citizenship status, or their bank balance, are denied care everywhere else. Nearly all my patients are in some way displaced, and more than half recently arrived in the United States. My hospital includes centers for refugee health, the treatment of addiction, and the treatment of trauma.
Roughly once a year I care for someone whose tuberculosis has entered their brain, resulting in a vicious meningitis that can clot the arteries and cause strokes, dangerous swelling, and inflamed tuberculous abscesses of the brain that often look at first glance like tumors. Still, I have always felt removed from TB, as though it were a curious relic of medical history rather than a contemporary plague.
But early in my first pregnancy, when I felt it only in the wave of nausea that woke me every morning, my own blood tested positive for TB. That week doctors X-rayed my lungs to be sure I wasn’t contagious, a lead vest laid over my belly to protect the baby. My lungs were clear, my infection was latent, and my baby was unscathed—the spongy layer of placenta that funnels nutrients from pregnant bodies into a fetus also keeps many infections at bay—but if I ever require chemotherapy or another immunosuppressive medication, I will need to be treated to make sure my tuberculosis does not become active.
The treatment regimen for an active tuberculosis infection is crude: months of toxic antibiotics that have the potential to harm nearly every part of the body. One of the treatments can strip the nerves and leave patients’ feet numb and tingling, while another turns both tears and sweat orange—patients are advised not to wear white T-shirts when taking the drug. Both medications can damage the liver. The treatment can take anywhere from three to nine months depending on the drug combination, and once it has begun, a patient cannot miss a dose. The first-line drugs we use to treat TB were all developed decades ago—one more than a century ago—and many of our second-line treatments for drug-resistant TB were originally developed to combat other infections before they were repurposed for the burgeoning plague of consumption.
How the world treats—or fails to treat—tuberculosis has everything to do with where the disease takes its greatest toll. In his new book Everything Is Tuberculosis: The History and Persistence of Our Deadliest Infection, John Green writes, “TB doesn’t just flow through the meandering river of injustice; TB broadens and deepens that river.”
Green, an unlikely source for an instructive book on TB, is perhaps best known as the author of The Fault in Our Stars, among other young adult best sellers. Online he is the cohost of the Vlogbrothers, a wide-ranging YouTube channel that, since 2007, has featured spots on everything from Harry Potter to microfinance. Green’s interest in twenty-first-century TB came about by accident, he writes, on a visit to Sierra Leone as part of a philanthropic program focused on the global maternal mortality crisis. In the coastal town of Lakka, he spent time at a tuberculosis hospital and met a teenager with a drug-resistant strain whose painful experience forms the central story of the book. Everything Is Tuberculosis, Green told The New York Times, is intended to foster awareness among American readers who would otherwise remain entirely ignorant of the communities ravaged by the disease.
Green uses the disease as a way to see more clearly the many injustices that have shaped our world. In Sierra Leone, where it is epidemic, TB is a product of centuries of British colonial rule. One Sierra Leonean physician tells Green to look at a map of the railroads if he wants to understand why the country is so impoverished. By extension, Green seems to imply, there is nothing inevitable about the ravages of tuberculosis; rather, it was fertilized by the devastation that colonialism left behind: housing insecurity, malnutrition, and poverty.
At times Everything Is Tuberculosis feels thin, a litany of historical and cultural anecdotes from New Mexico’s statehood to the Stetson cowboy hat, both born of the same “travel cure” that sent Lena’s brother, Edwin, west in search of open air. (Green notes that California became known as the “land of new lungs.”) The book never does the messier work of reporting and research to explain how colonization or development might propel an epidemic—why a country’s colonial-era train system or overcrowded cities are just as implicated in the spread of TB as any feature of the bacteria itself. Among the book’s greatest strengths is its bibliography, which includes a reference to Vidya Krishnan’s heftier Phantom Plague: How Tuberculosis Shaped History.
Phantom Plague tells the story of tuberculosis in India, where roughly a quarter of the world’s tuberculosis cases are found and where Krishnan has spent more than a decade reporting on the ways that antibiotic overuse, housing policy, casteism, and patent law have collided to create an epidemic of drug resistance, including TB strains that one Mumbai doctor calls “totally drug resistant”—TDR–TB. “The global battle against tuberculosis…will be won, or more likely lost, in India,” writes Krishnan.
Krishnan calls her book a “biography of the bacteria,” but it often reads more like a history of medical science itself, the story of tuberculosis bound up with that of germ theory. Krishnan traces Koch’s intellectual lineage from Ignaz Semmelweis, the unlucky Hungarian obstetrician who was ostracized from the medical establishment for suggesting that invisible “cadaverous particles” carried on doctors’ unwashed hands might be responsible for a devastating infection killing the women under his care, to Joseph Lister, the English surgeon who first said that surgical instruments ought to be sterilized.
The book includes fascinating digressions. Spittoons were counterintuitively introduced to curb the spread of tuberculosis and other infectious diseases once germ theory was widely accepted. And Sir Arthur Conan Doyle, who supplemented his floundering medical practice with popular writing, wrote a scathing rebuke, after being turned away from one of Koch’s lectures, of his earliest attempts to devise a remedy for tuberculosis.
But Phantom Plague is strongest when it shifts to our own time, examining policies that, Krishnan argues, have driven the long-lasting crisis:
One bad decision at a time, the global TB epidemic has been socially constructed by us—humans who are reliably small-minded, casteist, and racist every time we face a pathogen that is highly unpredictable, mutating, and thriving.
One chapter examines housing policy in Mumbai, particularly the construction of “vertical slums,” airless high-rises designed to crowd the impoverished as close together as possible, well away from the city’s fabulous wealth but still within “serving distance.” “No city in the world had segregated the rich from the poor, the lower caste from the upper castes, as efficiently as Mumbai,” Krishnan writes. The buildings are perfect breeding grounds for tuberculosis. As one young woman living with drug-resistant TB tells Krishnan, you can get it “just by breathing” in certain parts of the city.
Despite more than a century of scientific advancement and the development of countless antibiotics, when it comes to TB twenty-first-century medicine is not unlike the New England townspeople digging up graves in search of a ravenous spirit. Krishnan blames the epidemic of drug resistance on doctors who dose antibiotics incorrectly or prescribe drug regimens without testing their patients to find out what their disease is likely to respond to. Among her most agonizing examples are the stories of two young women who were treated for months with a toxic drug that had no effect on their tuberculosis but rendered them profoundly deaf.
Worse still are the pharmaceutical companies that have produced remedies for the drug-resistant strains but have made them inaccessible where they are most needed, offering meager donations of medications in lieu of a sustainable pricing model, and arguing that people in India and other TB-endemic areas lack the health literacy to take them correctly. (Krishnan makes analogies to the early rationing of antiretroviral therapy for those with HIV, which was withheld from much of the world for racist reasons, including the presumption that people living with HIV in Africa couldn’t tell time and would not remember to take a twice-daily pill.) “Inherent in that argument,” one American scientist tells Krishnan, “is the fact that infectious diseases that affect poor people could someday affect rich people—or white people…. We, the rich and the white, want to save these medications for us, for later.”
While Green hopes to close the sympathy gap by bringing the stories of tuberculosis to readers oceans away, Krishnan is more direct. Her book, she writes, “has one intended audience: readers who have the good fortune to have remained ignorant of TB but can ill afford to be so any longer.” To imagine that Black and brown people, incarcerated people, and poor and unhoused people are somehow uniquely vulnerable is to be ignorant of TB’s long history, forever linked with our own. “No one is safe,” she writes, “until everyone is.”
Iwas born in the United States, but I spent my first four years in the urban India that Krishnan writes about, and stories of tuberculosis are enshrined in my family mythology. One great-aunt nearly lost her hands to a childhood TB infection that ravaged her joints, yet she learned to write despite her pained, frozen fingers. In what was then British-occupied India, where nearly all Indian women married young and bore children without ever learning to read, she studied economics and became the principal of a college. In the US my latent disease makes me an anomaly, but it also makes me feel part of a larger, ancient lineage.
Yet, even though I am a doctor, even though I am not contagious, I have kept my condition a secret until now, afraid of some nebulous stigma.
The autumn I was diagnosed, I left work early on a Thursday afternoon and drove an hour south from my hospital in Boston to visit the Rhode Island grave of Mercy Lena Brown*. More than a century after her burial, Lena’s grave has become something of a pilgrimage site. When I visited, the headstone was piled with offerings—some acorns and pennies, a freshly cut pumpkin, a bouquet of zinnias. The stone itself has been stolen so many times that it is bolted to the ground with an iron strap. Nearby is the crypt from which Lena’s body was exhumed. The cemetery is tidy, but the crypt, shaded by an overgrown swamp oak, is wild, its wooden door hanging loose from its hinges, and its stone walls blooming with starbursts of lichen.
Over the years, souvenir hunters have chipped away at Lena’s gravestone, stealing bits of marble as eerie mementos, but her epitaph remains: “Mercy L., daughter of George T. and Mary E. Brown, died January 17, 1892, aged 19 years.”
Neither a vampire nor a martyr, just a girl who suffered before she died, one of an uncountable number.
Pria Anand is a neurologist and the author of The Mind Electric: A Neurologist on the Strangeness and Wonder of Our Brains. She teaches at Boston University and practices at Boston Medical Center. (December 2025)
*Mercy Lena Brown's grave is in the Chestnut Hill Baptist Church Cemetery in Exeter, Rhode Island, marked by a headstone secured with metal to prevent theft, where visitors leave offerings for the famed "New England Vampire". Her plot is near a cedar tree, and a triangular stone structure, the crypt where she was first stored, is nearby in the cemetery, a site known for folklore about consumption victims believed to be vampires.
About the case of Mercy Lena Brown, a 19-year-old resident of the town of Exeter, was the last known instance in the state of Rhode Island of a large group of otherwise sensible folks exhuming, mutilating, immolating, and cannibalizing a corpse to kill a vampire.
