RuthHinWV
07-18-2007, 01:07 AM
Continued from previous post...
First my blood was tested on a Lyme ELISA (Enzyme-Linked Immunosorbent Assay). This test employs a plate coated with ruptured spirochetes. When an infected patient’s blood is washed over the plate, the antibodies generated against the spirochete will latch on & stick to the plate; the “stickier” the blood, presumably the worse the Lyme. As it happened, my Lyme ELISA was highly reactive, four times the level required for a positive. But this was only a first step, according to the doctor & the CDC. A positive ELISA would have to be confirmed by a Western blot, & there I was out of luck. Like Jason before me, I needed 5 of 10 bands for a positive, but I had only 4. Four specific bands combined with signs of disease in an area as infested as Chappaqua should have warranted treatment, some experts later told me. But with Lyme disease so controversial & doctors so cautious they stuck to the cookie-cutter guidelines. I landed outside the curve.
In the end, I sought treatment from a nurse practitioner with an office across the street from Chappaqua’s favorite watering hole, Starbucks, right on the mail road. Considered skilled by the Lyme patient community, she enjoyed a small clientele. These patients came from a handful of Westchester physicians who rejected restrictive views on Lyme disease but didn’t want to deal personally with the controversy. She was as natural to Chappaqua as its medical massage parlors, as native as Lyme disease itself.
I was lucky she took me on. Despite my equivocal test results, she understood that I was sick. It wasn’t just my residence at the heart of the epidemic in Chappaqua & my constant exposure to ticks that informed her but also my signs & symptoms. The Mount Kisco doctors had said my fatigue & migraine, my numbness & confusion had nothing to do with Lyme disease, but she vehemently disagreed.
At first she treated me with the common antibiotic, Amoxicillin. Since the buzzing, confusion, & headache indicated the infection was neurological, she prescribed a dose high enough to reach my brain. Initially, I got worse. It was the die-off of the spirochete flooding my system & causing what experts called a Herxheimer reactions, “an intensification of the symptoms,” the nurse practitioner said. My “Herx” was so severe that after a few days of the antibiotic I took to bed. Every joint ached, my left hand formed a claw that couldn’t unclench, & every nerve felt electrified to the root. The sensation of cotton seemed to push out of my extremities, especially my hands & my head. My migraine flared so much it felt like a drill in my brain, revving a tidal wave of nausea in my gut. I tried to stand up, but my muscles were too weak. It lasted days.
Then the illness subsided, & I floated back up. Slowly, the “cotton” thinned, & the drill in my brain quieted. The claw unclenched & the buzzing subsided. I could get out of bed & walk. Several weeks later I awoke with a lightness of being I could not at first pinpoint. One of my symptoms was missing: it was gone for the first time in years.
A week or so afterward, my 20/20 eyesight returned, allowed me to see into the distance & read the fine print in The New York Times. One day I picked up the neuro-science I’d been unable to comprehend & read it to the end. To be sure, I wasn’t entirely well. The headache would return. I was exhausted, & intermittently I still buzzed. But a layer of the illness was gone.
On the Trail of Nantucket Fever
Sometime after the New Year, I drove into town for a latte at Starbucks & an appointment with the nurse. She greeted me with a smile, waving lab results at me. A couple of weeks before, dissatisfied with a plateau in my recover, she’d drawn blood & sent it to Quest Lab to test for the presence of Babesia, a genus of tick-borne sporozoa known for causing fevers & sweats, as well as headache & malaise. “When Lyme disease patients don’t get well,” she told me, “coinfection with babesiosis can be the cause.” Now the results had come back. As with my Lyme ELISA, antibodies were sky-high, four times the cutoff for positive.
The pieces were falling into place; the babesiosis diagnosis certainly made sense for me. A decade earlier, in 1990, I’d spent a month as a science-writing fellow at the Marine Biological Laboratory at Woods Hole, Massachusetts, right across the water from Nantucket Island, where tropical medicine expert Andrew Spielman of the Harvard School of Public Health had charted human babesiosis for more than 15 years before.
It was during the early seventies, before Lyme was even recognized, that Spielman 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, & fever that local doctors could not explain. So she chartered a plane to Rutgers in New Jersey. Rutgers doctors examined her blood under a microscope, diagnosed her with malaria, & placed her on the standard treatment, chloroquine. When the treatment didn’t work, they grew alarmed because treatment-resistant 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, a cousin of Babesia spp., known to cause cattle epidemics that wiped out entire herds. With the identification of her infection, the woman was finally treated correctly & 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, & 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, & the second patient was treated & recovered 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 & spread from one mammal to the next through the bite of an Ixodes tick. Larva & nymphal (baby & adolescent) ticks fed off the mice, but adult ticks reproduced en masse only after taking a blood meal from large mammals like deer, ensuring the cycle would continue. The spirochete Borrelia burgdorferi was identified as the cause of Lyme disease in 1981, & Spielman proved shortly afterward that this newly discovered illness involved the swam tick & the same natural cycle.
But few Lyme disease patients had even heard of babesiosis; thought the two epidemics had been spawned in tqndem, could be e1ually debilitating, & were spreading at proportional rates along with migrating deer, few primary care doctors in endemic areas like Chappaqua ran the babesiosis test. “We don’t test for that,” our Mount Kisco 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 e a cause.
Yet in retrospect I believe that babesiosis 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 spacious rustic bacin in the woods. Way before my arrival, Babesia microti had begun its migration, first over Cape Cod & then down the Long Island Sound, fast on the heels of Lyme disease, toward Connecticut, Westchester, & points beyond. In 1990, still traveling incognito toward New York State, B.microti was already rife in the forested enclaves of Woods Hole.
It wasn’t just my exposure that fit with the Quest Lab results but also the mystery illness I’d suffered after returning from Cape Cod. I never understood the strange spikes of fever up to 105 degrees Fahrenheit that hit me in hallucinogenic waves for more than a week that August, or the gullies of sleep so black that, except for the nightmares, I thought I might be dead. When the fever broke & I noticed the sweating, it seemed just a consequence of summer-perhaps the air conditioner was on the fritz, but only I could tell. After the sweat leveled off, I felt rthe start of what would become, a decade hence, the headache without end. This was classic acute babesiosis. Without treatment, an acute infection may have flared & then smoldered. Later it may have acted synergistically with the Lyme.
My Chappaqua nurse had a treatment to push the babesiosis back: I now added Mepron (atovaquone) to my arsenal of antibiotics. The thick gold sludge, known for treating malaria, made me want to vomit. But I held it down. Some six weeks later the drill in my head stopped whirring, & the nausea & dizziness I’d lived with for years receded like a tide pulled back to sea. I still wasn’t well, not entirely, but the treatment had extinguished another set of disease symptoms.
First my blood was tested on a Lyme ELISA (Enzyme-Linked Immunosorbent Assay). This test employs a plate coated with ruptured spirochetes. When an infected patient’s blood is washed over the plate, the antibodies generated against the spirochete will latch on & stick to the plate; the “stickier” the blood, presumably the worse the Lyme. As it happened, my Lyme ELISA was highly reactive, four times the level required for a positive. But this was only a first step, according to the doctor & the CDC. A positive ELISA would have to be confirmed by a Western blot, & there I was out of luck. Like Jason before me, I needed 5 of 10 bands for a positive, but I had only 4. Four specific bands combined with signs of disease in an area as infested as Chappaqua should have warranted treatment, some experts later told me. But with Lyme disease so controversial & doctors so cautious they stuck to the cookie-cutter guidelines. I landed outside the curve.
In the end, I sought treatment from a nurse practitioner with an office across the street from Chappaqua’s favorite watering hole, Starbucks, right on the mail road. Considered skilled by the Lyme patient community, she enjoyed a small clientele. These patients came from a handful of Westchester physicians who rejected restrictive views on Lyme disease but didn’t want to deal personally with the controversy. She was as natural to Chappaqua as its medical massage parlors, as native as Lyme disease itself.
I was lucky she took me on. Despite my equivocal test results, she understood that I was sick. It wasn’t just my residence at the heart of the epidemic in Chappaqua & my constant exposure to ticks that informed her but also my signs & symptoms. The Mount Kisco doctors had said my fatigue & migraine, my numbness & confusion had nothing to do with Lyme disease, but she vehemently disagreed.
At first she treated me with the common antibiotic, Amoxicillin. Since the buzzing, confusion, & headache indicated the infection was neurological, she prescribed a dose high enough to reach my brain. Initially, I got worse. It was the die-off of the spirochete flooding my system & causing what experts called a Herxheimer reactions, “an intensification of the symptoms,” the nurse practitioner said. My “Herx” was so severe that after a few days of the antibiotic I took to bed. Every joint ached, my left hand formed a claw that couldn’t unclench, & every nerve felt electrified to the root. The sensation of cotton seemed to push out of my extremities, especially my hands & my head. My migraine flared so much it felt like a drill in my brain, revving a tidal wave of nausea in my gut. I tried to stand up, but my muscles were too weak. It lasted days.
Then the illness subsided, & I floated back up. Slowly, the “cotton” thinned, & the drill in my brain quieted. The claw unclenched & the buzzing subsided. I could get out of bed & walk. Several weeks later I awoke with a lightness of being I could not at first pinpoint. One of my symptoms was missing: it was gone for the first time in years.
A week or so afterward, my 20/20 eyesight returned, allowed me to see into the distance & read the fine print in The New York Times. One day I picked up the neuro-science I’d been unable to comprehend & read it to the end. To be sure, I wasn’t entirely well. The headache would return. I was exhausted, & intermittently I still buzzed. But a layer of the illness was gone.
On the Trail of Nantucket Fever
Sometime after the New Year, I drove into town for a latte at Starbucks & an appointment with the nurse. She greeted me with a smile, waving lab results at me. A couple of weeks before, dissatisfied with a plateau in my recover, she’d drawn blood & sent it to Quest Lab to test for the presence of Babesia, a genus of tick-borne sporozoa known for causing fevers & sweats, as well as headache & malaise. “When Lyme disease patients don’t get well,” she told me, “coinfection with babesiosis can be the cause.” Now the results had come back. As with my Lyme ELISA, antibodies were sky-high, four times the cutoff for positive.
The pieces were falling into place; the babesiosis diagnosis certainly made sense for me. A decade earlier, in 1990, I’d spent a month as a science-writing fellow at the Marine Biological Laboratory at Woods Hole, Massachusetts, right across the water from Nantucket Island, where tropical medicine expert Andrew Spielman of the Harvard School of Public Health had charted human babesiosis for more than 15 years before.
It was during the early seventies, before Lyme was even recognized, that Spielman 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, & fever that local doctors could not explain. So she chartered a plane to Rutgers in New Jersey. Rutgers doctors examined her blood under a microscope, diagnosed her with malaria, & placed her on the standard treatment, chloroquine. When the treatment didn’t work, they grew alarmed because treatment-resistant 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, a cousin of Babesia spp., known to cause cattle epidemics that wiped out entire herds. With the identification of her infection, the woman was finally treated correctly & 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, & 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, & the second patient was treated & recovered 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 & spread from one mammal to the next through the bite of an Ixodes tick. Larva & nymphal (baby & adolescent) ticks fed off the mice, but adult ticks reproduced en masse only after taking a blood meal from large mammals like deer, ensuring the cycle would continue. The spirochete Borrelia burgdorferi was identified as the cause of Lyme disease in 1981, & Spielman proved shortly afterward that this newly discovered illness involved the swam tick & the same natural cycle.
But few Lyme disease patients had even heard of babesiosis; thought the two epidemics had been spawned in tqndem, could be e1ually debilitating, & were spreading at proportional rates along with migrating deer, few primary care doctors in endemic areas like Chappaqua ran the babesiosis test. “We don’t test for that,” our Mount Kisco 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 e a cause.
Yet in retrospect I believe that babesiosis 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 spacious rustic bacin in the woods. Way before my arrival, Babesia microti had begun its migration, first over Cape Cod & then down the Long Island Sound, fast on the heels of Lyme disease, toward Connecticut, Westchester, & points beyond. In 1990, still traveling incognito toward New York State, B.microti was already rife in the forested enclaves of Woods Hole.
It wasn’t just my exposure that fit with the Quest Lab results but also the mystery illness I’d suffered after returning from Cape Cod. I never understood the strange spikes of fever up to 105 degrees Fahrenheit that hit me in hallucinogenic waves for more than a week that August, or the gullies of sleep so black that, except for the nightmares, I thought I might be dead. When the fever broke & I noticed the sweating, it seemed just a consequence of summer-perhaps the air conditioner was on the fritz, but only I could tell. After the sweat leveled off, I felt rthe start of what would become, a decade hence, the headache without end. This was classic acute babesiosis. Without treatment, an acute infection may have flared & then smoldered. Later it may have acted synergistically with the Lyme.
My Chappaqua nurse had a treatment to push the babesiosis back: I now added Mepron (atovaquone) to my arsenal of antibiotics. The thick gold sludge, known for treating malaria, made me want to vomit. But I held it down. Some six weeks later the drill in my head stopped whirring, & the nausea & dizziness I’d lived with for years receded like a tide pulled back to sea. I still wasn’t well, not entirely, but the treatment had extinguished another set of disease symptoms.