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Lyme Page 19

by Mary Beth Pfeiffer


  That’s when Auerbach, a savvy, indignant survivor—sick though she was—began a decades-long quest against ticks, personal and public, to limit the damage that was coming. She hatched a plan. She would get Horowitz together over dinner with Rick Ostfeld, a scientist at the Cary Institute of Ecosystem Studies in nearby Millbrook. Here were two men who were on their way to becoming world-class Lyme disease experts. The reason: they lived and worked in a beautiful but forbidding place, where Frederick Church landscapes were swathed in pathogen-packed ticks. By the end of the dinner in 1998, Ostfeld had agreed to pack up thirty tubes, each containing one adult tick in a solution of 70 percent ethanol, for delivery to a testing laboratory. Separately, Horowitz would send 192 blood specimens for analysis. The results showed B. microti DNA in Ostfeld’s ticks—though he was skeptical of what seemed an inflated infection rate—and in Horowitz’s blood samples. “This report constitutes the first evidence of coinfection among Ixodid ticks with Babesiosis in upstate NY,” Horowitz wrote in a conference abstract presented in April 1999.

  In 1992, a twenty-five-year-old woman named Lia McCabe was earning her MBA and working for an investment banking company in New York City when things went terribly wrong. She became confused, forgetful, and immensely tired. She had migraines and would stumble when walking. She went to at least fifteen doctors and was told she had multiple sclerosis and chronic fatigue syndrome before she was ultimately diagnosed with Lyme disease. Unable to walk or care for herself, she recalls the day when she was twenty-seven and a hospital administrator said to her, “You have to decide what nursing home you want to go to.” McCabe, who told her story at a New York State hearing on Lyme disease in November 2001, was unbelieving at the turn her life had taken. At one point, her mother came to her bedside, and McCabe could neither speak nor move. “I felt like I was in a coffin and couldn’t get out,” she said. Her mother walked out, thinking she was asleep.

  Like many patients with advanced tick-borne disease, McCabe’s life was both a struggle to get well and a battle to get care. Her insurer balked at paying for intravenous antibiotics, so her parents did. The drugs helped her improve but she backslid when she went off of them. Then in 1999, seven years after she became ill, she went to see Horowitz. He diagnosed her with babesiosis on top of Lyme. A month into treatment, she felt her legs again. “My drenching night sweats disappeared, my need for sleep decreased, and my energy level improved,” she told the lawmakers. “After six years of being trapped in my wheelchair, I’ve packed it away and removed the ramp. I’m living a life I didn’t think was possible.” If she had participated in the Klempner study that decreed long-time antibiotics have no value she said, “I’d still be in a wheelchair today.”

  But it wasn’t antibiotics alone that turned McCabe’s life around; it was the diagnosis of babesiosis and treatment with both antibiotic and antimalarial drugs. Horowitz likes to say, definitively and often, “Babesiosis makes Lyme disease three times worse.” Indeed, a 1996 study led by Peter Krause, a foremost Babesia researcher, found that people with both infections had more symptoms and longer illnesses than patients with either infection alone. Of great concern, about one in ten Lyme disease patients in southern New England, Krause found, were also infected with babesiosis in areas where local mammals harbored both infections. And that, Horowitz knew from the patients he saw, was a bit of geography that was growing. Three years before the babesiosis bulletin, he had reported the results of his own treatment study of 120 patients who had been unresponsive to antibiotic treatment for Lyme disease, or had relapsed after it, and who later tested positive for antibodies to Babesia. He found significant improvement after they were treated both with an antibiotic and antimalarial drug.

  Jill Auerbach’s effort to bring recognition to babesiosis involved researchers from institutions in New York and Rhode Island, led to the collection and testing of scores of ticks and blood samples, and prompted formation of a county tick force to pay for it. She wrote dozens of letters, made endless phone calls, and lobbied legislators and health officials. This was not government leading the way. This was government being led, as it is, with mixed success, in many places around the world. It was not until March of 2002 that New York State health officials issued a warning to doctors about babesiosis. That was a decade after Lia McCabe was infected and eight years after Jill Auerbach. It was also three years after Horowitz’s conference presentation and his warning that babesiosis wasn’t just coming. It was already there.

  Poison Blood

  With symptoms like air hunger, in which patients cannot seem to catch their breath, babesiosis can be a devastating illness. But its implications are as disturbing for people who are infected but who do not get sick. Their robust immune systems apparently keep the infection in check. But lacking any sign of illness, it does not stop them from the altruistic act of donating blood, which in turn goes to the sickest and least able to fight the infection.

  In the United States, Babesia-tainted blood has been transfused into a forty-four-day-old baby with malformed lungs, an eleven-year-old boy on chemotherapy for a brain tumor, a fifty-four-year-old heart transplant recipient, and three premature infants. Those patients survived. But at least eight people in the United States have died, and twenty-five worldwide, after contracting transfusion-related babesiosis, the leading cause of transfusion-related microbial infection deaths in the nation. Among the deaths were two babies under twelve months, among nineteen infected. But these reported cases—162 in the United States through 2009—may be woefully misleading, representing what an article in the Annals of Internal Medicine in 2011 termed “a fraction of those that occurred.” At the same time, tests and procedures to keep Babesia out of the blood supply and out of donated organs are still in the experimental stage. “Babesiosis is killing people, and it’s contaminating the blood supply,” Dr. Raymond Dattwyler, an author of the Lyme disease guidelines, told me. “You gotta have an appropriate way to screen for it,” he said, something that, for now at least, is “cost prohibitive.”

  In the scheme of things, the babesiosis numbers may be low. But trends are important in tick-borne disease, and all the indicators point up: the number of reported cases, the number of places from which those cases emerge, and the prevalence of the organism in the wild. Lyme disease grew from a smattering of cases on the US East Coast in the 1980s to 38,000 nationwide in 2015, which represents a tenth of the true caseload. Will babesiosis follow suit? From 2001 to 2008, cases rose twentyfold in the Lower Hudson Valley, from 6 to 119, sickening patients with AIDs, cancer, and splenectomy, conditions that made them susceptible to the pathogen; one patient died. Cases in the United States rose from 900 in 2012 to 2,100 in 2015, a 133 percent increase. As with Lyme disease, a great many cases are thought to go unreported and undiagnosed.

  Just as that public health warning about babesiosis in Dutchess County came nearly a decade after Lia McCabe’s infection, other countries are playing catch-up in a race in which the organism leads. In China, the pathogen had been detected in ticks and mice in nine provinces and Taiwan. Researchers in 2014 were able to count twenty-seven human cases in five broadly spaced provinces, in the country’s far north, south, east, and west. They included one babesiosis patient who, before taking ill, had received a transfusion of potentially tainted blood, according to an article in the journal Parasites & Vectors. “If this was the case, screening of blood donors in this region is urgently needed,” the authors wrote. “Human babesiosis may have previously been overlooked in P.R. [the People’s Republic of] China due to a lack of medical awareness and the limitation of clinical diagnostic methods.”

  China is not alone. Babesia strains have been detected in human blood from Germany, Switzerland, and France. The organism has been detected in ticks in the Netherlands, though human cases have not been found, yet. Cases have been diagnosed in Australia, Great Britain, and Austria, where the first human babesiosis case was reported in 2003 in a hunter who became ill two weeks after a tick bite. Five ye
ars later, 441 of 864 ticks, or half, were found to be infected with the pathogen. In Canada—where scientists have documented an unmistakable northward migration of Ixodes ticks—the first human babesiosis case was diagnosed in the summer of 2013 in a seven-year-old Manitoba boy weakened by congenital deformities.

  By the early 2010s, researchers were trying to unravel the forces that led to ticks becoming infected with both the Lyme pathogen, Borrelia burgdorferi, and Babesia microti in the coastal Northeast. They tried putting uninfected ticks on mice that carried both infections—and discovered a new dynamic, reported in 2014 in PLoS One: “Coinfection in mice increases the frequency of B. microti infected ticks.” In other words, ticks picked up the infection for Babesia more readily when mice were also infected with Lyme disease. Three of the researchers explained the dynamic in a review in Trends in Parasitology in 2016. On its own, Babesia is an organism of “low ecological fitness” that struggles to survive. But with Borrelia’s help, Babesia apparently could evade the mouse immune system, “removing one of several of the ecological bottlenecks” that would otherwise keep this bug in check and, rather, promoting its circulation in nature. “The Lyme agent somehow was helping increase the amount of Babesia in the mice,” Krause, the babesiosis researcher, told me.

  This phenomenon is translating into growing Babesia rates in ticks in areas with Lyme disease. In Lyme-rife Dutchess County in 2001, infection rates for Babesia in ticks were reported at 3 to 9 percent. By 2014, 13 percent were infected. Babesiosis had once been considered a coastal problem. But here in this place, a hundred miles from the Atlantic Ocean, the human rate of that tick-borne illness was then the highest in New York State, eclipsed the following year by Columbia County, just to the north. These are all harbingers, and there are many more.

  Block Island is a magical, windswept place of cliffs and rocky meadows, nineteen miles from the nearest ferry at Port Judith on the shore of Rhode Island. In 1991, the island became a laboratory for the study of tick-borne disease, attractive for epidemiological study precisely because of its isolation as one of a string of islands off the Northeastern US coast that are vestiges of sediment left when the last great glaciers receded more than 10,000 years ago.

  Block Island is part Welsh countryside, part rugged Irish cliffs, except that it does not have the unflappable rain. What this island does have, however, are residents with strikingly high rates of tick-borne disease: 516 cases per 100,000 for babesiosis and 1,677 for Lyme disease, according to the results of a ten-year study published in 2003. Researchers chose to study the island in 1991 because of its isolation and its population, both of people and ticks. When they were finished scouring medical records, Peter Krause and his team concluded, in an article in the American Journal of Tropical Medicine that a tenth of the population showed exposure to the Babesia organism and the risk of contracting babesiosis and Lyme disease was, as they put it, “intense.” This is a word not often used in scientific studies. Moreover, the team had taken pains to be “inherently conservative” in computing the per capita rates, using only symptomatic cases of babesiosis. They also included only those who reported to the local medical center, effectively excluding the many cases of disease taken home in the blood of tourists, who visit by the thousands every summer season. “Babesiosis may be acutely debilitating,” Krause and company noted, “and mortality rates of 5 percent have been reported among patients with babesiosis.”

  As with Lyme disease, Babesia does not respect borders. In Ireland, a fifty-eight-year-old farmer in Galway, in the west of the country, received a blood transfusion after having his spleen removed. A year later, he became ill with babesiosis and died after twelve days in a hospital. When his death was reported in 1989, there had been just six babesiosis cases, four fatal, in all of Europe. By 2011, about forty cases had been reported in Europe, still low. But something unusual was noted then. Two people, a woman, thirty-seven, and a man, thirty-five, in the Alsace region of northeastern France, were diagnosed with babesiosis. It was the first report of healthy people infected with the parasite, and it had occurred in a known hotspot for Lyme disease. Like Jill Auerbach and Lia McCabe, other French patients were likely told they were suffering some other ailment because the bug was unknown and doctors, unschooled. “In Europe,” the authors of the French report warned, “babesiosis is probably underdiagnosed.”

  CHAPTER 9:

  Childhood Lost

  * * *

  Kara: “Nothing more we can do.”

  In October of 2016, I stood in front of a painting at the Metropolitan Museum of Art in New York City called Poppy Fields near Argenteuil, a small masterpiece painted in 1875 by Claude Monet. Within an ornate gilt frame, I saw the idealized countryside of an Impressionist pioneer: a meadow flecked with poppies and lavender, bordered on the left by two slender green trees and lit gently by a sky more cloud than blue. In this field stood a child, said to be Monet’s son, Jean, at the age of eight, legs obscured by the generous wild grasses of the French earth. I can no longer look at such pastoral loveliness without seeing what lurks within. I know what is there. Argenteuil is about eight miles from the heart of Paris, where twenty-first century parks have sprouted signs, necessary in a country with perhaps 30,000 Lyme disease cases a year. Attention aux tiques, they warn. Les tiques sont des parasites qui se nourrissent de sang et qui peuvent transmettre des maladies à l’homme, notamment la maladie de Lyme. Translated: “Beware of ticks. Ticks are parasites that feed on blood and can transmit diseases to humans, especially Lyme disease.”

  Kara Wilson grew up in a place with natural beauty that rivals Monet’s most breathtaking landscape. Wilson’s ancestors blazed the Oregon Trail with wagons and on horseback five generations before her, setting up a cattle ranch in Fossil, Oregon, a rural outpost on the Butte Creek east of the snow-capped Cascades. Nestled in the shadow of the brown and green foothills of the John Day River Basin, Fossil—population 473 in the 2010 census—has all the markings of American frontier: A broad main street lined with pickup trucks; a well-stocked mercantile, and a seventy-mile ride to the nearest chain supermarket. Life on the ranch, 9,000 acres family-owned, meant that Kara, born in 1976, began riding horseback early and often, first snugly linked to a parent’s chest at the age of six months, then at two, on her own horse. The Wilsons would take the kids, each in their own saddle, to move the ranch’s several hundred head of cattle on a big-sky afternoon, all of them returning dusty, achy, and exhausted at the end of the day.

  Kara was a week shy of seven years old in May of 1983 when, after one such foray, she and her siblings—a brother, four, and a sister, eight—jostled for first dibs in the bathtub, and all wound up in there together. That’s when Nancy, who had seen hundreds of ticks in her time, found one so deeply imbedded on the back of Kara’s leg that she had trouble pulling it off. The tick was noted in a visit to the health center that night, but no connection was made to it when Kara got sick. Not when she developed a spring flu shortly after. Not when she was wracked by fevers, had colds that wouldn’t quit, had pain that jumped from joint to joint. A photo from that time, taken against a white bed sheet, shows two stick-thin legs with knees swollen to the size of oranges. Doctors said the illness must be juvenile rheumatoid arthritis, but it came with an awful lot of symptoms—like raging nighttime fevers, vomiting, and rashes—that surely weren’t typical. It made the Wilsons wonder. They did not know then that a scientist by the name of Willy Burgdorfer, for whom the infamous Lyme spirochete was named, was on his way to collecting 715 western blacklegged ticks in southwestern Oregon. Two percent would test positive for Borrelia burgdorferi, he reported in 1985. Not much was known about Lyme disease in Oregon then or in the dark years that followed as the couple searched for a diagnosis and a treatment that fit. It is a road that many parents of Lyme know well, and the journey, for too many, is not so different today.

  In the months after Kara’s tick bite, Phil and Nancy Wilson watched their rodeo-loving cowgirl shrivel from 42 to 29 pounds, wh
ere she stayed for seven years. She left school in second grade and did not return until the 10th. She was diagnosed with assorted other diseases including leukemia, for which her parents refused treatment and were threatened with charges of medical neglect. They stood fast, aware of the death of a little boy who had been given chemotherapy against his parents’ wishes. In time, Kara lost her ability to walk and to see all but shadows. Her immune system was ravaged, making her prone, as is Lyme disease’s wont, to constant infection. At one awful point, in March of 1988, Kara, eleven, contracted spinal meningitis and was comatose for ten days. Phil and Nancy were each taken aside by a nurse they knew and told there was nothing more to be done. “Honey, you’ve got to let her go,” the nurse told Nancy. Kara nonetheless woke up, took 7-Up from a straw, and, because she could not speak, blew it into a doctor’s face. However mystifying and joyous that moment was, it was not the end of Kara’s trials. This is a doctor’s summary of her condition six months later and more than five years since she had become ill, after she was taken by ambulance to a Hermiston, Oregon, hospital:

  “PHYSICAL EXAMINATION: Reveals a girl of about 12 years old who looks not to be much larger than about 5 years of age. She is nonresponsive. Her jaws were clamped tight.…Her eyes deviated, one to the right and one to the left. Pupils were small but they did not react to the light.…CHEST: Thin. Ribs could easily be felt. BACK: Very thin. EXTREMITIES: So thin there is almost no muscle present. The joints are very knobby. It is difficult to tell whether they are just knobby because of the lack of tissue or whether they are actually swollen.”

 

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