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It was sometime after the New Year when, feeling better but hardly well after initial treatment for Lyme disease, that I drove a mile down my hill for a latte at Starbucks and my appointment with my Lyme practitioner. She greeted me with a smile, waving a paper in my face. She seemed so pleased she was literally aglow.
A few weeks before, dissatisfied with a plateau in my treatment response, my returning migraines and fatigue, she'd drawn blood and sent it to Quest Lab for a babesia test. "When Lyme disease patients don't get well," she told me, "coinfection with babesiosis is often the cause." Now the results had come back, and as with my Lyme ELISA, antibodies were
four times the cutoff for positive-sky-high.
The pieces were falling into place. With my spiking headache and continued exhaustion, babesiosis certainly made sense for me. A decade earlier, in 1990, I'd spent a couple of weeks as a science-writing fellow at the Marine Biological Laboratory at Woods Hole, Massachusetts, right across the water from Nantucket lsland, where human babesiosis
had been studied more than fifteen years before.
It was during the early seventies, before Lyme was even recognized, that Andrew Spielman, a tropical medicine expert at the Harvard School of Public Health, was asked to investigate what locals called Nantucket fever. At the time, only two patients were known. The first was a wealthy Nantucket woman who came down with a disabling mystery illness marked by extreme anemia, fatigue, and fever that local doctors could not explain. So she chartered a plane to Rutgers, New Jersey.
Rutgers doctors examined her blood under a microscope, diagnosed her with malaria, and placed her on the standard treatment, chloroquine. When the treatment didn't work, they grew alarmed because drugresistant malaria is, after all, a threat to public health. A slide of blood was shipped off to the CDC, where experts identified not malaria but another similar agent that also inhabits red blood cells-Babesia microti, known to cause cattle epidemics that wiped out entire herds. With the identification of her infection, the woman was finally treated correctly and got well.
When a second case of babesiosis appeared on Nantucket Island a few years later, physicians again were stymied. But the second patient happened to be friends with the first, and finally, with doctors throwing up their hands, it fell to the first patient to diagnose the disease in the second. Her lay diagnosis was correct, and the second patient was
treated and recovered as well.
That's when Spielman entered the fray. Would he care to find the cause of these cases in the environment? Observing the cycles of infection year after year, he finally tracked babesia through the ecosystem, discovering that it lived in the blood of mice and spread from one mammal to the next through the bite of an Ixodes tick. Larva and nymphal (baby and adolescent) ticks ate by sucking the blood of mice and other small mammals like shrews and chipmunks. But adult ticks, far bigger in size, generally required larger mammals like deer for a blood meal. It was only in geographic areas with an abundance of large mammals that Ixodes ticks could mature to adulthood and reproduce substantially
enough for the disease to spread.
When the spirochete Borrelia burgdorferi was identified by Willy Burgdorfer as the cause of Lyme disease in 1981, Spielman realized that the newly discovered illness involved the same tick and same natural cycle he'd already charted for human babesiosis on Nantucket Island and beyond. For Spielman, the connection between the two infections-Lyme and babesiosis-was immediately clear. Every year since his first discoveries on Nantucket, after all, new babesia patients had been diagnosed.
And some of them had exhibited not just the malarialike headache and fever spikes typical of babesia, but also a confounding circular red rash and strange pains that migrated from joint to joint-symptoms classically associated not with babesiosis, but rather Lyme disease. "There was a woman who lived opposite our field station who had migratory arthritis and the expanding rash and-babesiosis. She obviously had Lyme as well, but no one had the organism, and restrictive case definitions came into play," Spielman recalled, "because in the beginning, the differential diagnosis for Lyme disease included a travel history to Lyme, Connecticut!"
Eventually the boundaries for both infections expanded at different but proportional rates, and with each infection requiring a treatment ineffective for the other, the coinfected patients of Nantucket Island provided important clues to the spectrum of disease. Sometimes physicians just needed to treat babesiosis for an intractably sick "Lyme" patient to get well. Even as babesiosis extended its range and came to rival Lyme disease as a cause of illness, the lessons of Nantucket's coinfected patients would fall on deaf ears.
Indeed, few Lyme disease patients were ever tested for, or had even heard of, babesiosis; and though the two epidemics had been spawned in tandem from the start and could be equally debilitating, few primary care doctors in endemic areas ran the babesiosis test. "We don't test for that," our Westchester county pediatrician explained at the time.
The internist who tried to treat my headaches-classic for babesiosis- never mentioned the possibility that infection, either Lyme or babesiosis, might be a cause.
Yet in retrospect I believe the Babesia diagnosis was my missing link. Most science-writing fellows at Woods Hole had stayed in residence halls near the lab, but with a family in tow I was given a gorgeous rustic cabin in the woods. Way before my arrival, Babesia microti had begun its migration west and south, first over Cape Cod and then down the Long Island Sound, fast on the heels of Lyme disease toward Connecticut, Westchester, and the points beyond. In 1990, still traveling incognito toward New York State, Babesia microti was already rife in the forested enclaves of Woods Hole.
It wasn't just my exposure that fit with the Quest results, but the mystery illness I'd suffered after returning from Cape Cod. Doctors could never explain the strange spikes of fever to 105 degrees Fahrenheit that hit me in hallucinogenic waves for more than a week that summer, or the gullies of sleep so black that, except for the nightmares, I thought I might be dead. When the fever broke and I noticed the sweating, it seemed just a consequence of summer. It was after the sweat leveled off that the headache-without-end licked its first noxious path through my brain.
This was classic acute babesiosis. Without treatment the acute infection had flared and apparently smoldered, my Lyme practitioner theoriezed. Then it had synergized in concert with the Lyme.
She had a treatment to push the babesia back: I now added Mepron to my arsenal of antibiotics. The thick gold sludge, known for treating malaria, made me retch and want to vomit. But I held it down. Some six weeks later, the drill in my head stopped whirring and the nausea and dizziness I'd lived with for years receded like a tide pulled back to sea. I still wasn't better, not entirely, but we had peeled another layer off the onion and extinguished another set of symptoms from my disease.
Pamela Weintraub is a Senior Editor at Discover Magazine. The post above is adapted from her book on Lyme disease and its coinfections, entitled Cure Unknown: Inside the Lyme Epidemic, published in 2008 by St. Martin's press.
