Emerging Diseases

From Chronic Fatigue to Lyme: Medically Unexplained No More

Pamela Weintraub — Sat, 10 Oct 2009 02:05:28 +0000

Over the past year, forces at the highest reaches of medicine have made ever stronger efforts to burden the chronically ill with psychiatric labels, consigning them to often mind-numbing psych meds and untreated infection, immune dysfunction, and pain. Some critics see this as psychiatric abuse at the hands of non-psychiatrists --since it is rarely the psychiatrist, but rather, those in other specialities who step outside the circle of their training to impose these crude diagnoses on patients with medical ills.

On the Lyme disease front, one acronym of choice for the patients who fail the "standard" treatment --10 days to a month of antibiotic-- is MUS, for Medically Unexplained Symptoms; another favorite is CMI, for Chronic Multisymptom Illness. These acronyms join MBP, for Munchausen Syndrome by Proxy, a blame-the-mother theory of illness without credence in the psychiatric world --in all, an alphabet soup of invented diagnoses butressed by controversial disease definitions and unsupported by blinded, controlled studies in the peer review.

Taking one disease and muddying the water so much you render diagnosis this vague --well, that's hubris. Taking a host of different infections and syndromes, and wrapping them ALL up in the same psychiatric ribbon without proof --as these non-psychiatrists do-- is reckless, indeed.

For a window onto the phenom, just roll back the clock to summer, when the Infectious Diseases Society of America convened a meeting in Washington, D.C. to review its controversial Lyme disease guidelines after panelists were charged with conflicts of interest by the attorney general of Connecticut. The attorney general felt the panelists could be profiting from the guidelines they had set. The IDSA denied this was true.

The original guidelines recommended only short-term treatment for patients, leaving many of the sickest and longest-infected out on the cold. Yet scientists supporting the short-course standard (many of them members of the unseated panel) could hardly hide their disdain at the D.C. meeting, consistently attaching psych labels to the patients who failed the treatment they were there to defend.

"I believe that clinical and scientific studies of these patients in the context of a functional somatic syndrome will be more likely to shed light on its pathophysiology and appropriate treatment," said Arthur Weinstein, MD Professor of Medicine, Georgetown University Medical Center Chief, Rheumatology Division, Washington Hospital Center. The "concept of narrow specialty-based diagnoses of patients with unexplained somatic symptoms - fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, atypical facial pain -TMJ syndrome, noncardiac chest pain syndrome - needs revision. These syndromes have more in common than their apparent differences would suggest and may be best considered under the rubric of a functional or more accurately, dysfunctional, somatic syndrome," he said at the IDSA review in July 2009.

Non-psychiatrists like Weinstein have been given free reign in the peer review, where those with like attitudes may tend the gates. "Psychiatric comorbidity and other psychological factors distinguished [chronic Lyme disease] patients from other patients commonly seen in Lyme disease referral centers, and were related to poor functional outcomes," wrote Leonard Sigal, an academic rheumatologist who previously ran a Lyme clinic but now works for Big Pharma, in the journal Arthritis and Rheumatism in 2008.

Other doctors without psychiatric training have stigmatized women with psych labels for their physical disease --contending that chronic fatigue syndrome, chronic Lyme disease, and depression in females, in particular, may really be one and the same. Gary Wormser and Eugene Shapiro, an infectious diseases doctor and a pediatrician respectively published the proposal in the Journal of Women's Health in 2009, despite lacking psychiatric training themselves.

When it comes to stigmatizing the sick, why let science interfere?

This past week the American Association for the Advancement of Science reported in its prestigious journal, Science, that 68% of chronic fatigue syndrome patients were infected with a new retrovirus, called xenotropic murine leukemia virus-related virus, or XMRV. A follow-up study, also reported in Science, raised the number of CFS patients infected with the retrovirus to 98%, in all. (Just 3.7% of healthy people are infected. More studies are needed to prove the virus causative of CFS, for sure. )

News of the retrovirus has circulated among scientists researching CFS for months, but that didn't stop Sigal and colleagues --including psychologists but not a single psychiatrist-- from hitting the peer review in September 2009 with the acronym du jour, CMI. That didn't stop them from sweeping chronic fatigue patients up in their psychiatric theory-of-everything-under-the-Sun. "Conditions including, but not limited to, fibromyalgia, chronic fatigue syndrome, and Gulf War syndrome can be considered collectively as Chronic Multisymptom Illness," the team wrote.

An actual psychiatrist, Brian Fallon of Columbia University, has this to say about so many diseases presenting in similar ways: "Those who say that the patients with MUS have a purely psychological illness are missing the point about the commonality of these syndromes," he states. "The key element is that these illnesses share symptom profiles because these symptoms represent an abnormally perpetuated physiologic response. For example, it is well known that elevated proinflammatory cytokines produce these symptoms; also well known is the fact that depression can be a by-product of such an elevation because certain cytokines reduce the conversion of tryptophan to serotonin in the body."

What might be at the root? In Lyme patients, some doctors believe it is untreated infection with the Lyme spirochete, Borrelia burgdorferi; others point to nerve damage or immune dysfunction triggered by borrelial proteins after infection is gone. Medical research into disease pathogenesis, they say, might yeild cures on these fronts. "When it comes to understanding neuropsychiatric manifestations of Lyme disease, I would suggest investigating post-infectious autoimmune factors triggered by antigens of Borrelia burgdorferi in the central nervous system. Such forthcoming investigations will be provence of medical neuroimmunology, not psychiatry," says David Younger, a neurologist researching Lyme disease at NYU.

Rheumatologist Sigal veers, expressing not neurology, not even uncertainty, but psychiatry, dishing out diagnoses like "Major Depressive Disorder" and "Generalized Anxiety Disorder" to the folks he says never had Lyme. (Of course, with Lyme disease diagnosis itself the subject of so much controversy, his restrictive diagnostic standards serve merely to highlight the fuzz.) Only if you read the fine print in the American Journal of Medicine do you get to this concession: "Depression and poor affect could be the result of living with chronic symptoms instead of being predisposing factors." So true. (But no mention that the Lyme spirochete, like the syphilis spirochete, may itself infect the brain, causing infection-triggered neuropsychiatric disease.)

And then there's the big news from Science, the top peer-reviewed journal for research in the world: A new retrovirus in 98% of chronic fatigue syndrome patients --a group also labeled "MUS" and "CMI" by Weinstein, Sigal and crew. Oops. No need for proponents of CMI to acknowledge XMRV. A little retrovirus won't stop some flat-earthers from labeling sick patients psychiatric and consigning them to lives of untreated physical disease.

Despite the effort to keep patients running on empty, science is moving on. “I think this establishes what had always been considered a psychiatric disease as an infectious disease,”Judy Mikovits, the scientist leading the retrovirus work at the Whittemore Peterson Institute in Reno, said this week in the New York Times.

Hillary Johnson, the author of Osler's Web: Inside the Labyrinth of the Chronic Fatigue Sydrome Epidemic, has said it best in her blog:

"A nova has appeared in the constellation. We knew it would appear some day-but in our lifetimes? Many of us, having given up on recovery, had merely hoped we might live long enough to understand the scientific basis of our suffering. Thousands, perhaps hundreds of thousands, of us didn't make it, or simply gave up. Between the time Dr. Judy Mikovits of the Whittemore Peterson Institute and her collaborators at the National Cancer Institute and the Cleveland Clinic submitted their paper to Science and today, we know at least one woman, the British citizen Pamela Weston, chose assisted suicide rather than go on; in the note she left behind she wrote that she hoped her choice would, in some part, move the UK medical research forward. Might Weston have hung on had she known about XMRV? We grieve for those who couldn't wait, couldn't hang on, and acknowledge their bravery. For the rest of us, this is a day to celebrate"

I urge everyone to read this as well as Johnson's prior post, a copy of a speech she recently gave in London in May 2009.

Pamela Weintraub is a senior editor at Discover Magazine and author of Cure Unknown: Inside the Lyme Epidemic, first place winner of the American Medical Writers Association book award, 2009. A revised, updated PAPERBACK version of Cure Unknown will be published October 13, 2009. The update covers the topic here, and is available on Amazon for a little over $10.

Rebel with a Cause: The Incredible Dr. Masters, Part IV (Conclusion)

Pamela Weintraub — Wed, 01 Jul 2009 02:31:24 +0000

It was July 2003 that I set out on a journey to Cape Girardeau, Missouri, to visit Edwin J. Masters, the doctor involved in hand-to-hand combat with the Centers for Disease Control and Prevention over the existence of Lyme disease in the southern United States. Working with a few intrepid colleagues, Dr. Masters managed to generate powerful evidence for Southern Lyme, though his evidence was continually undermined.

For two days straight I sat with Dr. Masters in his oversized basement, reviewing document after document showing how data had been cast to shed doubt on the disease. Ed Masters' story sheds light not only on Lyme disease but also the dangers we all face when medicine is politicized and studies skewed. His great persistence finally led to recognition of Masters' disease, the Lyme of the south.

The heroic Dr. Masters died on June 21 2009. In his honor, I'll spend several days retelling his sprawling, riveting, and most important tale.

PART I

PART II

PART III

PART IV (CONCLUSION):

By summer of 1994, Masters and Denny Donnell had resigned from the CDC effort and struck out on their own. Working night and day, the Missouri researchers were able to execute two preemptive strikes -- a detailed letter of objection to the Journal of Infectious Diseases, where the CDC would be submitting the manuscript, and an article of their own for the journal, Missouri Medicine.
    They were so efficient that their article in Missouri Medicine was actually published first. There, in July 1995, Masters and Donnell presented the results as they saw them: Missouri patients fulfilling the strict CDC surveillance definition for Lyme disease had been documented in significant number, and there was growing evidence that lone star ticks were infected with a a still-unidentified spirochete representing a new species of Borrelia.
    When the CDC article came out in the Journal of Infectious Diseases a month later, cooler heads had prevailed. Whether due to further reflection from the authors or pressure from the editor who had reviewed Ed Masters' critique, the final, published article conceded the possibility that some lone star ticks were infected with a new spirochete, but, the CDC emphasized, likelihood was low. Instead, said officials, the rashes in Missouri -which they called STARI (for Southern Tick-Associated Rash Illness) might be allergy to tick saliva. In the extensive acknowledgement section of the paper, in which dozens of physicians and scientists were thanked for help and guidance, Ed Masters wasn't mentioned at all.
     It would take a world class entomologist to put it all together, explaining the rationale for a southern version of the disease. That scientist was James. H. Oliver, Jr., Callaway Professor of Biology and Director of the Institute of Arthropology and Parasitology at Georgia Southern University. The first thing Oliver did was determine that mice through the Carolinas, Georgia, Florida, Alabama, and Mississippi tested positive for the Lyme disease spirochete, Borrelia burgdorferi, generating as many reactive antibodies as mice from Connecticut.
     Oliver later learned that southern Lyme is transmitted most often by the lonestar tick, which carries a spirochete that is still unknown. (Evidence is mounting that the unknown spirochete may be nothing more than an alternate strain of northern-style Lyme) But there's more. Oliver has ultimately found a range of new Southern ticks transmitting a pastiche of borreliae. And he's recently reported a unique Southern strain of B. burgdorferi with outer surface proteins so unusual they are undetectable on blood tests used up North.
     "When you consider Jim Oliver's findings," said Ed Masters, "comparing northern stuff to southern stuff is like comparing a pedigreed world champion poodle to a junkyard dog."

     Despite such differences, Masters held that "Lyme-like illness deserved Lyme-like treatment." And he warned northerners to beware: The term "Southern" in the CDC's name of Southern Rash-Associated Illness could be most misleading of all. The aggressive lone star tick has expanded its range relentlessly. Found up the East Coast as far north as Maine and throughout the Midwest, it carries Master's disease and a host of other illnesses -including the Southern versions of babesiosis and ehrlichiosis-- wherever it goes.
    The CDC, for its part, has finally agreed that the disease actually exists --and that it may well be caused by a spirochete, in fact, a Borrelia; that's a victory for Ed Masters, who fought hand-to-hand combat with the government over the reality of a Lyme-like illness in the South and southern Midwest for almost twenty years.
     But even as the protagonists agree on more facts, the philosophical divide remains vast. Where Masters saw "Missouri Lyme" as just one borreliosis on a spectrum, the CDC contends that STARI is a rash-only illness largely unrelated to Lyme. While Masters reported continued illness if treatment was delayed, the CDC insists, to this day, that its studies have ruled that out. While Masters recommended Lyme-like treatment, the old guard says that since no one has found a spirochete, antibiotics should be used sparingly, if they are used at all. In the end, Ed Masters sought a unified field theory of borreliosis that included that Southern patients, while the CDC divides the spectrum into smaller and smaller parts.

***
We were sitting in Ed Masters' basement, a room so long it had the feel of a football stadium. The length worked well: Ed Masters' full and varied life, starting from his earliest days, splashed in photographs and news stories across the walls. I saw Ed Masters, a strapping, athletic Dartmouth kid, holding a basketball." I always liked to run with that ball," he said.

Then there was the section devoted to his fight with the Congressman, the one he chased from office a quarter of a century back: Reading the news clips on Ed Masters' wall, you got the story straight: the initial dispute, the weekly editorials written on medical clinic stationery, and finally, a Congressman toppled from office, never to be heard from again. Masters noted how ironic life was, how everything that went around came around, in the end.

He was a tempting target: "With my data, nothing fit anymore --not the tick, not the microorganism, not the serology," Ed Masters said. "One person told me, ‘Masters, they were having a big old fine party, and you're the turd in the punchbowl. You spoiled it.'" And so he had. #THE END

Adapted from Cure Unknown, Inside the Lyme Epidemic.(St. Martins Press, 2008)

Rebel with a Cause: The Incredible Dr. Masters, Part III

Pamela Weintraub — Tue, 30 Jun 2009 00:45:19 +0000

It was July 2003 that I set out on a journey to Cape Girardeau, Missouri, to visit Edwin J. Masters, the doctor involved in hand-to-hand combat with the Centers for Disease Control and Prevention over the existence of Lyme disease in the Southern United States. Working with a few intrepid colleagues, Dr. Masters managed to generate powerful evidence for Southern Lyme, though his evidence was continually undermined.

The heroic Dr. Masters died on June 21 2009. In his honor, I'll spend several days retelling his sprawling, riveting, and most important tale.

PART I // PART II

PART III

For two weeks in July 1991, CDC researchers occupied a space in Masters' office, interviewing his Lyme patients and reviewing their charts. Based on their interviews, the CDC scientists went to the areas the patients said they had been bitten and collected ticks. Masters provided the CDC with blood and biopsy samples taken from the patients during their illness. Finally, the CDC took the ticks, the samples, and the data back to Fort Collins to conduct their analysis and write their report.
     It was almost two years later in May of 1993 that the CDC sent a final draft to Masters for input, and he was alarmed. The first thing that stood out was the CDC assertion that, according to "unpublished data," Missouri rashes differed from real Lyme rashes on the basis of "coloration, degree of homogeneity, sharpness of borders, and shape." The CDC also contended that EM lesions in Missouri were smaller, on average, than those observed on Lyme disease patients in Wisconsin, based on a 12-patient study still in press.
     Masters was flabbergasted. After all, he had shown his rash photos throughout the world, and the most expert dermatologists on the planet, from Sweden and Germany to Long Island, had said he had a "ringer." As to lesion size, why, he wondered, had the CDC deferred to this small Wisconsin study over the work of dermatologist Bernard Berger, an internationally recognized Lyme disease expert who had done the seminal studies on the rash? Berger's widely cited report on 196 patients showed that the average rash size of confirmed Lyme cases and Missouri Lyme cases were exactly the same.
Could some of the confusion be traced to careless error? Comparing his patient charts to CDC data, Masters found inexplicable mistakes. One patient with a rash stretching across his back was reported with a lesion just a quarter inch in diameter. Two patients with obvious bull's-eye rashes were listed as having "no central clearing." And a patient whose chart contained a photograph of a rash across his abdomen had been reported as having no rash at all.
      "I called Fort Collins and a group of them were around the speaker phone. I went ballistic," Masters recalls. "I said, you are telling me that my rashes are visibly distinct from real Lyme, which means that you can tell by looking, that these are not real rashes? Then why are we doing the friggin' study? Hey if you can tell by looking, I demand that you hold a press conference to teach us dumb yokels out here in the boonies how to do it. I'm an author on this paper --and you say you have unpublished data? I have never seen it, I have never even heard of it, and if this data exists it is one of the most important keys to this puzzle. I want to see the data now."
    The CDC team was virtually silent. Then, three days later, Masters received a new version of the article, with the material he'd challenged removed. But as Masters and his colleague, Denny Donnell, read through what would be several more drafts of the CDC manuscript, they knew they could never sign on. As Masters saw it, the CDC had "skewed everything, and had literally tossed out data, to make what we found in Missouri look like a rash-only illness, and as different from Lyme disease as could be."
    Most misleading, he felt, were the arbitrary stop and start dates the CDC had imposed on the study after collection of data was complete. In most such studies, each patient is studied for the same amount of time as all the other participants. Start-dates are based on the start of illness for each individual patient and end-dates are determined by adding a consistent amount of time --the same for each and every patient-- onto that. But in the Missouri study, the CDC decided to cut all patients off on the same date, no matter when the illness had begun. Thus, some patients were followed for a couple of years, others for a couple of weeks. The disturbing part was that the stop dates placed patients with the most objective signs of illness, including carditis (inflammation of the heart) and arthritis, outside the study period and thus, beyond the scope of the report. To wit: Even though patients in the study had developed serious, late-stage signs considered classic for Lyme disease, the CDC paper referred, without qualification, to the "absence of documented early neurologic, cardiac, and arthritic complications." (An analogy would be the situation in which scientists studying HIV infection cut their study off after two weeks and so conclude the virus is not a cause of AIDS.)
      Masters complained passionately about the cut-off dates to Phillip R. Lee, MD, Assistant Secretary for Health, who he hoped might intervene. One of the patients, he wrote to Lee, was a previously healthy young man who had developed carditis 14 days after appearance of his rash, but five days after the arbitrary end of the study period. There was no reason to cut him off, said Masters, because it took another year before the manuscript was ready to submit. Similarly, three cases of arthritis were excluded from the "study period," and from the report. One patient's rash occurred before the CDC start date, "and what a shame," said Masters, "because he also had a positive Western blot and documented joint swelling in his knee." Two other patients developed arthritis after the stop-point. "One of those arthritis patients had symptoms emerge 58 days after the onset of the rash, just 34 days after the study's arbitrarily determined end. Such omissions were "absurd," said Masters, given that onset of Lyme carditis occurs, on average, 4.8 weeks after the rash and Lyme arthritis may not develop for months.
    There was more: The CDC had dismissed laboratory work, a wide swath of it, that indicated some kind of borreliosis in play. For instance, the report did not put much stock in the finding, by CDC scientists, of "motile spirochetes" in nearly five percent of the lone star nymphal ticks observed by darkfield microscopy. Nor did the CDC report that when spirochetes from the ticks were inoculated into mice, they later cultured spirochetes from the animals' ears. "Having seen these spirochetes myself, I am not comfortable with the CDC's position that Missouri is the hole in the donut," Masters wrote to Lee, "and that somehow Missouri is a magical, ‘Lyme-free' zone and that these observed Missouri spirochetes have nothing to do with human disease."
    Finally, and this was the last straw to Masters, the CDC rejected dozens of positive blood tests performed at its own lab. While it was true that the CDC used more specific tests as years went on --methodologies unavailable when the study began-- Masters could not understand how so many positive and equivocal results over so many samples were not considered suggestive of another, similar organism, even if not Borrelia burgdorferi itself. Instead, positive results where no Lyme disease was possible --as in Missouri-- were just the sort of incentive the CDC had needed to tighten the valve. The CDC kept refining and re-testing because, as the results from Missouri showed, the bar for diagnosis had been too low.
    In a nutshell, the CDC insisted the illness in Missouri, whatever it was, had nothing to to with Lyme disease, while Masters insisted the evidence had been left on the cutting room floor. When it came to Masters' insistence, Duane Gubler, head of the Vector-Borne Disease Division out in Fort Collins, was especially clear: When you biopsied a Lyme rash in the northeast, you cultured Borrelia burgdorferi -not so with rashes from Missouri. If he couldn't culture Borrelia burgdorferi from the rashes, then it wasn't causing the illness. If the Missouri rashes weren't caused by B. burdorferi, then no amount of other evidence could convince Gubler to call the outbreak Lyme disease. Whatever data Masters felt had been left out, it could mean little compared to that.

READ PART IV

Adapted from Cure Unknown, Inside the Lyme Epidemic.(St. Martins Press, 2008)

Rebel with a Cause: The Incredible Dr. Masters, Part II

Pamela Weintraub — Sat, 27 Jun 2009 17:30:03 +0000

It was July 2003 that I set out on a journey to Cape Girardeau, Missouri, to visit Edwin J. Masters, the doctor involved in hand-to-hand combat with the Centers for Disease Control and Prevention over the existence of Lyme disease in the Southern United States. Working with a few intrepid colleagues, Dr. Masters managed to generate powerful evidence for Southern Lyme, though his evidence was continually undermined.

For two days straight I sat with Dr. Masters in his oversized basement, reviewing document after document showing how data had been filtered to shed doubt on the disease. Ed Masters' story sheds light not only on Lyme disease but also the dangers we all face when medicine is politicized and studies skewed. His great persistence finally led to recognition of Masters' disease, the Lyme of the south.

The heroic Dr. Masters died on June 21 2009. In his honor, I'll spend several days retelling his sprawling, riveting, and most important tale.

READ PART I HERE

By 1990, Ed Masters was regularly diagnosing Missouri patients with Lyme disease based on presentation with the EM rash (which CDC called diagnostic) and other objective signs.After sending his patients to specialists to rule out other health problems, he treated them with antibiotics, generally amoxicillin or doxycycline.

Masters knew the Yale scientists were reporting a treatment failure rate between 10 and 15 percent for early Lyme disease and “deemed that unacceptable. If I had an 85-90 percent success rate treating strep throat I would be drawn and quartered. So I treated patients at the longer end of the recommended scale --for about three or four weeks-- assuming that I would then be at the higher end of the success curve as well.” Intuitively he’d hit upon the treatment that scientists at Stony Brook would soon recommend for early Lyme disease, and his patients got well. “It was a new thing, but I was getting enough success that I was enormously encouraged,” Masters states.

Masters’ credibility was bolstered not just by the quantity of his data and his treatment success, but also by the work of the preeminent Missouri entomologist Dorothy Fier, a specialist in Rocky Mountain spotted fever at St. Louis University. Fier had visited Masters’ personal tree farm and collected samples of the common lone star tick (species name Amblyomma americanum) notable for the distinctive white dot, or “lone star,” on the backs of females, found not just in Missouri but throughout the Midwest, the Northeast all the way to Maine, and the South. A force to be reckoned with, the influential Fier found some kind of borrelia in two percent of the lone star ticks she sampled, and came out in support of Masters’ Missouri Lyme.

With the support of Fier and data on about 125 patients, 30 with well-documented erythema migrans rashes, Masters was publishing his findings and taking his show on the road. His reports garnered so much interest he was invited, in July 1990, to present his findings at the prestigious IV International Conference on Lyme Borreliosis in Stockholm, Sweden, where experts from the US and Europe, alike, studied his pictures and case histories and agreed they could see no difference between his patients and those with classic Lyme disease. Ben Luft of Stony Brook was so impressed he invited Masters to enter his patients in an upcoming NIH study on antibiotics.

By 1991, Masters had made such a stir that the New York Times was prompted to run a story about the “mystery” Lyme disease cases along the Mississippi River in Cape Girardeau. That’s when the CDC really took note. The CDC had long told doctors that the EM rash alone was diagnostic for the disease. Yet now they insisted the rule did not hold for Missouri, where neither Ixodes dammini (the specific tick northern scientists erroneously said was needed to transmit Lyme in the northeast and midwest) nor Ixodes pacificus (the Western tick found to transmit Lyme disease) could be found.

Without the expected tick, CDC scientists said, they wanted a higher level of evidence: Namely, Lyme spirochetes of the species Borrelia burgdorferi would need to be cultured from biopsies of human rashes, from ticks, or from animal hosts, and that had not been done.

“I was living in two worlds,” Masters said. “I would go to conferences and present to academic experts, and they would say, “Hmmm, that’s Lyme disease. Then I would go back home to Missouri and the people from the CDC would tell me I was misdiagnosing all these patients. Diagnosis of Lyme disease based on the erythema migrans rash was controversial only in Missouri, and nowhere else in the world.”

Through 1991, as Masters’ differences with the CDC became increasingly heated, he traveled to conferences equipped with a poster of his patients’ erythema migrans rashes and a quote from William Harvey, the 17th century physician and father of physiology, who had been ostracized for years for daring to suggest that blood circulated. “I appeal to your own eyes as my witness and judge,” William Harvey had said in 1651, just as Ed Masters appealed to his colleagues now.

The EM rashes on Masters’ poster were powerful visual evidence for some sort of borreliosis, Lyme disease proper or not. Missouri rashes had been found to contain spirochetes by the pathologists Paul Duray and J. DeKoning, widely recognized as the two top experts on such issues. Blood from Masters’ patients had by now tested positive for Lyme disease by ELISA at numerous labs, including the University of Connecticut, the University of Minnesota, and the CDC itself. Things came to a head during one of Masters’ presentations, when a CDC representative declared that none of it proved the phenomenon in question was Lyme disease.

“Why can’t you accept this,” Masters countered. “The evidence is overwhelming.”

“Because you haven’t proven it’s Borrelia burgdorferi,” the CDC official said.

“Excuse me!” Masters bellowed in front of a crowd. “You’re the CDC, the federally-funded, taxpayer-supported research institute that’s supposed to check this out, and you are telling me, a solo family physician finding these patients, that I haven’t proven it’s Borrelia burgdorferi? I think we need a little job clarification here. It’s not my job to prove it or disprove it, it’s yours!”

That’s when the CDC invited Masters and a few of his colleagues, including Dorothy Fier and Missouri state epidemiologist Denny Donnell, to apply for a grant to study the matter. The group wrote a proposal for studying Masters’ patients along with ticks captured in the vicinities where infection had likely occurred. Then Masters heard through the grapevine that the proposal had been rejected. Some time later the CDC called to say that while it lacked funds to outsource the study, they could conduct it with in-house researchers, in other words, scientists employed by the CDC itself. Masters could provide the patients and the ticks.

READ PART III HERE

To be continued, Adapted from Cure Unknown, Inside the Lyme Epidemic.(St. Martins Press, 2008)

Rebel with a Cause: The Incredible Dr. Masters, Part 1

Pamela Weintraub — Fri, 26 Jun 2009 03:12:16 +0000

The heroic Dr. Masters died on June 21 2009. In his honor, I'll spend several days retelling his sprawling, riveting, and most important tale.

***

Front and center in the debate over the existence of Lyme disease in the southern U.S. was the country doctor, Edwin J. Masters of Cape Girardeau, Missouri, who reveled in fighting for a cause.

It was near the start of his career, in 1979, that Masters wrote to his US Congressman, an ultra-liberal in a region of Midwest moderates, asking if he'd voted himself a raise. The Congressman, Bill Burlison, wrote back claiming he couldn't remember how he voted on his pay raise, but if the doctor wanted to know he could look it up himself.

Incensed at the rudeness, Masters' father-in-law alerted the media, and the exchange made TV news. Burlison retaliated by reporting Masters to the Federal Election Commission for writing a political missive on medical clinic stationery (an illegal tax deduction.) But Masters, a self-described "Eagle Scout and a stickler for every last detail," had proof in the form of cancelled checks that he'd paid for the stationery himself. Backed by the evidence (and the American Civil Liberties Union), Masters lashed back in anti-Burlison opinion pieces emblazoned on clinic letterhead and sent to newspapers throughout the State.

As election time neared, the drama increased: Whenever Burlison's opponent, conservative Republican Bill Emerson, couldn't attend a debate, Masters came in his stead. Once word got out, people crowded the debates not to see the candidates, but to watch the engaging Dr. Masters. A six-term incumbent, Burlison lost the election of 1980 --and Masters' new friend, the freshman Congressman Emerson, was swept in.

Despite his love of the brawl, Masters was your quintessential hail fellow well met --if you wanted a congenial sports buddy or a friend to confide in, Masters was your man. Tall, affable, and classically handsome, with a swath of thick hair and a wide, friendly grin, Ed Masters found himself front and center in a fight he never sought -- documenting a new Lyme-like illness or Lyme disease itself, often present in areas considered non-endemic by the CDC.

He entered the fray when, as an amateur forester, he was asked to give a talk on Lyme at a forestry meeting in 1988. Because he'd never seen a case of Lyme disease, he prepared exhaustively, even borrowing slides from health departments in Minnesota and throughout the East. "I spent a year working on the talk," Masters says.

The lecture went fine, but when he returned home to Missouri he started recognizing what seemed like Lyme disease in patients of his own. The first such patient was a farmer, age 55, who'd been the picture of health for years. One day he came in, emotionally overwrought and said, "I ache all over, knees and ankles, I can't think clearly and I need help getting out of the combine."

Masters knew his patient's hobby was fishing, and asked him whether, in the course of that activity, he'd ever been bitten by ticks. Of course he'd been bitten,the farmer responded, like anyone who fished. In possession of a good-sized collection of Lyme rash photos following the forestry talk, Masters took some out and asked the farmer to look at them. Had he ever noticed one of these?

"I had one of those last summer," the farmer said, explaining that he'd been going downhill ever since. First Masters tried to rule out any other cause for the illness. But when he could find nothing else the matter with the farmer, who was headed for disability, Masters treated with antibiotics. Not only did the farmer recover, but one year later he was so full of energy he expanded his operation by buying an adjacent farm.

Now that Masters knew what to look for, he started seeing Missouri Lyme in other patients, too. Not only did they have the typical erythema migrans rash,but also swollen joints, meningitis, neuropathy, and other specific hallmarks of the disease. Masters sent their blood into a lab, and many tested positive on the ELISA, the standard Lyme disease test of the day.

Thus validated, Masters reported his cases to the Missouri Department of Health, but his reports were ignored. If he'd read just a couple of articles on Lyme disease, he might have backed off, but after a year of prepping for his forestry talk he couldn't believe he had it wrong. So he started documenting the cases as precisely as he could. Every erythema migrans rash warranted an entire roll of film, and he made sure to photograph a rash and face together so he wouldn't be accused of recycling the same rash again and again. In preparation for the day that better tests would come, he obtained a special refrigerator for his office and began to store samples of patient rashes and blood.

READ PART II HERE

To be continued, Adapted from Cure Unknown, Inside the Lyme Epidemic.(St. Martins Press, 2008)

Dispassionate about swine flu

Pamela Weintraub — Sat, 02 May 2009 08:51:42 +0000

Maybe there's something wrong with me, but I've found it hard to get worked up over swine flu -now called H1N1-- the biggest looming pandemic since the great flu of 1918, when up to 50 million died. There haven't been many cases so far: A total of 144 in 21 states in the US to date, and one confirmed death --a baby from Mexico, where the infection began. While a number have died in Mexico, in the US the cases have been mild -more like bad colds.

At Discover Magazine, one of our staffers said the swine flu was one of the biggest science stories of the year, and everyone agreed, even me. Yet I had to point out: I came to work on the subway train. No one was coughing, no one was wearing a mask. The commuter population appeared blithely unconcerned.

Another staffer pointed out that the flu of 1918 started with a wimper, a mild illness in the Spring. Then it evolved, returning as killer in the Fall. "This flu has some genetic similariies to the 1918 flu," he said. "It could do that too."

Someone else explained the new flu could kill by provoking such a powerful immune response that our body's chemical onslaught against the organism would do us in as well. That meant that young, healthy adults in the prime of life might be most vulnerable of all.

The H1N1 germ is a hybrid, with DNA part human flu, part bird flu , part swine. And whatever it is today, tomorrow it could evolve into the instrument of our demise. This comment came from me.

Around the country and the world, things are tense:

*Hundreds of guests and staff were under quarantine in China after one hotel guest contracted the H1N1 virus.

*Europeans are cancelling trips to America.

*Schools have been closed around the U.S., keeping a quarter of a million healthy children at home.

*In college dorms everywhere, a list of symptoms help students to recognize if they have the disease.

*A figure no less than our vice president advised us to avoid infection incubators like public transportation and planes.

Okay when you put it like this, the swine flu might be frightening -but still, not to me. There was a time, before my whole family got sick with Lyme disease, when H1N1 might have given me pause -caused me to think about antivirals, stockpile masks, or even avoid the train.

But there's something cleansing about dealing with a bad disease for a decade and then emerging intact: You don't want to think about other illnesses, you've OD'd on the sick thing, you're done. Isn't life hard enough without focusing on a disease you don't have?

There really are epidemics in this country -autism diagnoses are skyrocketing and the fight over the cause -genes or environment- angry and divisive and sad. Illnesses like chronic fatigue syndrome and fibromyalgia attract controversial explanations and hodge-podge treatments while patients stay lost. Lyme disease and its co-infections continue to go undiagnosed, untreated, uncured. Cancer has turned out to be complex, the war on cancer a bust. I have a friend sick with a mystery illness no one can diagnose -she gets sicker and sicker while diagnoses are deep-sixed and treatments fail. More and more, people I know lose faith in Western medicine and the answers it can't provide.

Then along comes H1N1. Despite its hybrid genome, it is conceptually simple: The infection, a flu bug, is known and can be tested for. Cases are definitive. If it doesn't kill you, you get well. Maybe tomorrow the swine flu will kill millions, but today it's a pansy -a whisper illness usually not much worse than the common cold.

If any disease is going to mobilize our national agencies it will be something like swine flu. Promoted to 5 on the epidemic alert system -highest you can go is 6- it is diagnosable, definite, and the opposite of vague. As for me well, I can't muster alarm -not yet. It's hard to get worked up over a "maybe," even with shades of disaster and infection run amuck. I've already done the disease circuit. I'm spent. Maybe I'll change my mind if anyone I know gets sick, or if I see folks with masks on the subways in New York.

Pamela Weintraub is a senior editor at Discover Magazine and author of Cure Unknown: Inside the Lyme Epidemic published in 2008 by St. Martin's Press.

Babesia: The malaria-like disease in your yard, part 1

Pamela Weintraub — Sun, 05 Apr 2009 00:09:58 +0000

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.

An infection can change your personality --there's plenty of proof

Pamela Weintraub — Mon, 30 Mar 2009 09:07:24 +0000

In the past couple of weeks I've posted about the debate over Lyme disease as a trigger for violence. Can microbes and immune reactions to them actually contribute to cognitive decline, degenerative neurological disease, developmental disabilities, mental illness, personality changes and, at the most extreme, even violent and criminal behavior?

Here to weigh in with some evidence is psychiatrist Robert Bransfield, an expert on the psychiatric manifestions of Lyme disease and founder of the mailing list, Microbes and Mental Illness, where the discussions on such topics are held.

"There are several thousand peer-reviewed references demonstrating the association between infections and mental symptoms and at least 65 different microbes have been recognized as causing mental symptoms," Bransfield writes. "Over two hundred peer-reviewed articles describe the causal association between Lyme/tick-borne diseases and mental symptoms, pathophysiology, morbidity and mortality. Attempted suicide and completed suicide associated with neuropsychiatric manifestations of Lyme disease and other tick-borne disease has been observed and reported by many other clinicians and myself."

Bransfield's work has focussed, in part, on infection and aggresion. "Although most patients with Lyme/tick-borne disease do not become violent, a small percent of patients who become infected develop a type of neurological dysfunction that can increase their risk of aggressiveness. In working with a number of patients with Lyme/tick-borne diseases it is apparent to many clinicians these conditions can cause reduced frustration tolerance, irritability, depression, cognitive impairments and mood swings, but more significantly, in a few patients, suicidal and aggressive tendencies."

For the doubters on the issue, Bransfield refers to his own website, Mental Health and Illness, and has provided peer-reviewed publications that offer not just theory but also nuance, complexity, and proof. With his permission, I list some of those, below.-- Pamela Weintraub (author of Cure Unknown: Inside the Lyme Epidemic and senior editor at Discover Magazine.)

Microbes and mental illness: The evidence in black and white

Acute disseminated encephalomyelitis [letter] AUTHORS: Fallon BA, Nields JA.
SOURCE: J Neuropsychiatry Clin Neurosci 1998 Summer;10(3):366-7
Acute and chronic neuroborreliosis with and without CNS involvement: a clinical, MRI, and HLA study of 27 cases. AUTHORS: Krüger H, Heim E, Schuknecht B, Scholz S. SOURCE: J Neurol. 1991 Aug;238(5):271-80.
Altered mental status, an unusual manifestation of early disseminated Lyme disease: A case report. AUTHORS: Chabria SB, Lawrason J. SOURCE: J Med Case Reports. 2007 Aug 9;1:62.
The association between tick-borne infections, Lyme borreliosis and autism spectrum disorders AUTHORS: Bransfield RC, Wulfman JS, Harvey WT, Usman AI.
SOURCE: Medical Hypotheses. 5 Nov 2007
Alzheimer's disease Braak Stage progressions: reexamined and redefined as Borrelia infection transmission through neural circuits. AUTHOR: MacDonald AB. SOURCE: Med Hypotheses. 2007;68(5):1059-64. Epub 2006 Nov 17.
Alzheimer's neuroborreliosis with trans-synaptic spread of infection and neurofibrillary tangles derived from intraneuronal spirochetes. AUTHOR: MacDonald AB. SOURCE: Med Hypotheses. 2007;68(4):822-5. Epub 2006 Oct 20.
Antibodies against OspA epitopes of Borrelia burgdorferi cross-react with neural tissue. AUTHORS: Alaedini A, Latov N. SOURCE: J Neuroimmunol. 2005 Feb;159(1-2):192-5. Epub 2004 Nov 26.
Audiologic manifestations of patients with post-treatment Lyme disease syndrome AUTHORS: Shotland LI, Mastrioanni MA, Choo DL, Szymko-Bennett YM, Dally LG, Pikus AT, Sledjeski K, Marques A SOURCE: Ear Hear. 2003 Dec;24(6):508-17
Bartonella sp. Bacteremia in Patients with Neurological and Neurocognitive Dysfunction. AUTHORS: Journal of Clinical Midrobiology. 46(9):2856–2861 SOURCE: Breitschwerdt EB. Maggi RG, Nicholson WL, Cherry NA, Woods CW.
The basic syndromes of neurological disorders in Lyme borreliosis: AUTHORS: Dekonenko EP, Umanskii KG, Virich IE, Kupriianova LV, Rudometov, IuP, Bagrov FI: SOURCE: Ter Arkh 1995; 67 (11) : 52-53
Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes. AUTHORS: Miklossy J, Kis A, Radenovic A, Miller L, Forro L, Martins R, Reiss K, Darbinian N, Darekar P, Mihaly L, Khalili K. SOURCE: Neurobiol Aging. 2006 Feb;27(2):228-36.
Bell’s Palsy of the Gut and other Manifestations of Lyme and Associated Diseases AUTHOR: Sherr VT SOURCE: Practical Gastroenterology April 2006
Bilateral dorsolateral thalamic lesions disrupts conscious recollection. AUTHORS: Edelstyn NM, Hunter B, Ellis SJ. SOURCE: Neuropsychologia. 2006;44(6):931-8. Epub 2005 Oct 25.
Borrelia burgdorferi in the central nervous system: experimental and clinical evidence for early invasion. AUTHORS: Garcia-Monco JC, Villar BF, Alen JC, Benach JL. SOURCE: J Infect Dis. 1990 Jun;161(6):1187-93.
Borrelia burgdorferi central nervous system infection presenting as an organic schizophrenialike disorder. AUTHORS: Hess A, Buchmann J, Zettl UK, Henschel S, Schlaefke D, Grau G, Benecke R. SOURCE: Biol Psychiatry 1999 Mar 15;45(6):795
Borrelia burgdorferi persists in the brain in chronic lyme neuroborreliosis and may be associated with Alzheimer disease. AUTHORS: Miklossy J, Khalili K, Gern L, Ericson RL, Darekar P, Bolle L, Hurlimann J, Paster BJ. SOURCE: J Alzheimers Dis. 2004 Dec;6(6):639-49; discussion 673-81.
Borrelia burgdorferi-seropositive chronic encephalomyelopathy: Lyme neuroborreliosis? An autopsied report. AUTHORS: Kobayashi K, Mizukoshi C, Aoki T, Muramori F, Hayashi M, Miyazu K, Koshino Y, Ohta M, Nakanishi I, Yamaguchi N. SOURCE: Dement Geriatr Cogn Disord. 1997 Nov-Dec;8(6):384-90.
[Borreliosis--simultaneous Lyme carditis and psychiatric disorders--case report] AUTHORS: Legatowicz-Koprowska M, Gziut AI, Walczak E, Gil RJ, Wagner T. SOURCE: Pol Merkur Lekarski. 2008 May;24(143):433-5. Polish.
Brain SPECT Imaging in Chronic Lyme Disease. AUTHORS: Plutchok JJ, Tikofsky RS, Liegner KB, Fallon BA, Van Heertum RL. SOURCE: Journal of Spirochetal and Tick Borne-Diseases, 1999; 6: 10-16.
Carbamazepine in the treatment of Lyme disease-induced hyperacusis.
AUTHORS: Nields JA, Fallon BA, Jastreboff PJ. SOURCE: J Neuropsychiatry Clin Neurosci 1999 Winter;11(1):97-9
Case report: Lyme disease and complex partial seizures. AUTHOR: Bransfield RC.SOURCE: Journal of Spirochetes and Tick-borne Diseases; Fall/Winter 1999, Vol 6, p123-125
Central nervous system manifestations of human ehrlichiosis.
AUTHORS: Ratnasamy N, Everett ED, Roland WE, McDonald G, Caldwell CW.
SOURCE: Clin Infect Dis 1996 Aug;23(2):314-9
Cerebral metabolic changes associated with Lyme disease AUTHORS: Newberg A, Hassan A, Alavi A. SOURCE: Nucl Med Commun 2002 August;23(8):773-777
Chronic Bacterial and Viral Infections in Neurodegenerative and Neurobehavioral Diseases. AUTHORS: Nicholson GL. SOURCE: Lab Medicine. 2008;39(5):291-9.
Chronic borrelia encephalomyeloradiculitis with severe mental disturbance: immunosuppressive versus antibiotic therapy. AUTHORS: Kollikowski HH, Schwendemann G, Schulz M, Wilhelm H, Lehmann HJ. SOURCE: J Neurol. 1988 Jan;235(3):140-2.
Chronic inflammation and amyloidogenesis in Alzheimer's disease -- role of Spirochetes. AUTHORS: Miklossy J. SOURCE: J Alzheimers Dis. 2008 May;13(4):381-91. Review.
Chronic neurologic manifestations of erythema migrans borreliosis.
AUTHORS: Ackermann R, Rehse-Kupper B, Gollmer E, Schmidt R.
SOURCE: Ann N Y Acad Sci. 1988;539:16-23.
Chronic neurologic manifestations of Lyme disease. AUTHORS: Logigian EL, Kaplan RF, Steere AC. SOURCE: N Engl J Med. 1990 Nov 22;323(21):1438-44.
Clinical and demographic characteristics of psychiatric patients seropositive for Borrelia burgdorferi. AUTHORS: Hájek T, Libiger J, Janovská D, Hájek P, Alda M, Höschl C. SOURCE: Eur Psychiatry. 2006 Mar;21(2):118-22.
[Clinical manifestations and epidemiological aspects leading to a diagnosis of Lyme borreliosis: neurological and psychiatric manifestations in the course of Lyme borreliosis] AUTHORS: Créange A. SOURCE: Med Mal Infect. 2007 Jul-Aug;37(7-8):532-9. Epub 2007 Mar 26. Review. French.
Co-existance of toxoplasmosis and neuroborreliosis - a case report.
AUTHORS: Gustaw K, Beltowska K, Dlugosz E. SOURCE: Ann Agric Environ Med. 2005;12(2):305-8.
Cognitive functioning in late Lyme borreliosis. AUTHORS: Krupp LB, Masur D, Schwartz J, Coyle PK, Langenbach LJ, Fernquist SK, Jandorf L, Halperin JJ. SOURCE: Arch Neurol. 1991 Nov;48(11):1125-9.
Cognitive Impairments after Tick-borne Encephalitis. AUTHORS: Gustaw-Rothenberg K. SOURCE: Dementia and Geriatric Cognitive Disorders. 2008;26:165-168.
Cognitive processing speed in Lyme disease. AUTHORS: Pollina DA, Sliwinski M, Squires NK, Krupp LB. SOURCE: Neuropsychiatry Neuropsychol Behav Neurol. 1999 Jan;12(1):72-8.
Complaints attributed to chronic Lyme disease: depression or fibromyalgia? AUTHORS: Berman DS, Wenglin BD. SOURCE: Am J Med. 1995 Oct;99(4):440.
Concurrent infection of the central nervous system by Borrelia burgdorferi and Bartonella henselae: evidence for a novel tick-borne disease complex. AUTHORS: Eskow E, Rao RV, Mordechai E. SOURCE: Arch Neurol. 2001 Sep;58(9):1357-63.
Concurrent medical conditions with pediatric bipolar disorder. AUTHORS: Scheffer RE, Linden S. SOURCE: Curr Opin Psychiatry. 2007 Jul;20(4):398-401. Review.
Consequences of treatment delay in Lyme disease. AUTHORS: Cameron DJ SOURCE: J Eval Clin Pract. 2007 Jun;13(3):470-2.
Constipation Heralding Neuroborreliosis AUTHORS: Shamim A, Shamim S; Liss G; Nylen E; Pincus J; Yepes M. SOURCE: Arch Neurol. 2005;62:671-673.
A Controlled Study of Cognitive Deficits in Children With Chronic Lyme Disease
AUTHORS: Tager FA, Fallon BA, Keilp J, Rissenberg M, Jones CR, Liebowitz MR.
SOURCE: J Neuropsychiatry Clin Neurosci 13:500-507, November 2001
FULL TEXT: http://www.lymediseaseassociation.org/Tager.pdf
Behavioral Consequences of Infections of the Central Nervous System: With Emphasis on Viral Infections AUTHORS: Tselis A, MD, Booss J. SOURCE: J Am Acad Psychiatry Law 31:289–98, 2003
Catatonic syndrome in acute severe encephalitis due to Borrelia burgdorferi infection. Pfister HW, Preac-Mursic V, Wilske B, Rieder G, Forderreuther S, Schmidt S, AUTHORS: Kapfhammer HP. SOURCE: Neurology. 1993 Feb;43(2):433-5.
Chronic neurologic manifestations of Lyme disease. AUTHORS: Logigian EL; Kaplan RF; Steere AC SOURCE: N Engl J Med 1990 Nov 22;323(21):1438- 44.
Delirium and Lyme disease. AUTHORS: Caliendo MV, Kushon DJ, Helz JW.
SOURCE: Psychosomatics. 1995 Jan-Feb;36(1):69-74.
Delusional disorders in the course of tick-born encephalitis and borreliosis in patients with hemophilia A and posttraumatic epilepsy--diagnostic and therapeutic difficulties] AUTHORS: Grzywa A, Karakuła H, Górecka J, Chuchra M. SOURCE: Pol Merkur Lekarski. 2004 Jan;16(91):60-3. Polish.
Demyelinating polyradiculitis in neuro borreliosis: AUTHORS: Corral I, Sanchis G, Garcia-Ribas G, Quereda C, Escudero R, de Blas G: SOURCE: Neurologia 1995 Feb; 10 (2) : 110-113
Detection of Bartonella henselae by polymerase chain reaction in brain tissue of an immunocompromised patient with multiple enhancing lesions. Case report and review of the literature. AUTHORS: George TI, Manley G, Koehler JE, Hung VS, McDermott M, Bollen A. SOURCE: J Neurosurg. 1998 Oct;89(4):640-4. Review.
The diagnosis of Lyme disease. AUTHOR: Bransfield RC. SOURCE: Hosp Pract (Minneap). 1996 Aug 15;31(8):35, 40.
Diagnosis, treatment, and prevention of Lyme disease. AUTHOR: Bransfield RC. SOURCE: JAMA. 1998 Sep 23-30;280(12):1049; author reply 1051.
Dementia associated with infectious diseases. AUTHOR: Almeida OP, Lautenschlager NT. SOURCE: Int Psychogeriatr. 2005;17 Suppl 1:S65-77. Review.
Differential Diagnosis and Treatment of Lyme Disease with Special Reference to Psychiatric Practice. AUTHORS: Nields JA, Fallon BA. SOURCE: Directions in Psychiatry, 1998, 18: 209-228.
A disease in disguise. Lyme can masquerade as migraine, or as madness.AUTHORS: Cowley G, Underwood A. SOURCE: Newsweek. 2004 Aug 23;144(8):62.
Do bartonella infections cause agitation, panic disorder, and treatment-resistant depression? AUTHORS: Schaller JL, Burkland GA, Langhoff PJ. SOURCE: MedGenMed. 2007 Sep 13;9(3):54.
Does process-specific slowing account for cognitive deficits in Lyme disease? AUTHORS: Pollina DA, Elkins LE, Squires NK, Scheffer SR, Krupp LB. SOURCE: Appl Neuropsychol. 1999;6(1):27-32.
Emerging infectious determinants of chronic diseases. AUTHORS: O'Connor SM, Taylor CE, Hughes JM. SOURCE: Emerg Infect Dis. 2006 Jul;12(7):1051-7.
Endogenous paranoid-hallucinatory syndrome caused by Borrelia encephalitis
AUTHORS: Barnett W, Sigmund D, Roelcke U, Mundt C.
SOURCE: Nervenarzt 1991 Jul;62(7):445-7 [German]
Epidemiologic, clinical, and laboratory findings of human ehrlichiosis in the United States, 1988. AUTHORS: Eng TR, Harkess JR, Fishbein DB, Dawson JE, Greene CN, Redus MA, Satalowich FT. SOURCE: JAMA 1990 Nov 7;264(17):2251-8
[Evaluation of cerebrospinal fluid serotonin (5-HT) concentration in patients with post-Lyme disease syndrome--preliminary study] AUTHORS: Kepa L, Oczko-Grzesik B, Badura-Glombik T. SOURCE: Przegl Epidemiol. 2008;62(4):793-800. Polish.
Evidence for Mycoplasma, ssp., Chalmydia pneumoniae, and Human Herpes-virus 6 Coinfections in Blood of patients with Autistic Spectrum Disorders. AUTHORS: Nicholson GL, Gann R, Nicholson NL, Haier J. SOURCE: Journal of Neuroscience Research 2007 85.
First-episode psychosis in a managed care setting: clinical management and research. AUTHORS: Jarskog LF, Mattioli MA, Perkins DO, Lieberman JA. SOURCE: Am J Psychiatry. 2000 Jun;157(6):878-84.
FLAIR and magnetization transfer imaging of patients with post-treatment Lyme disease syndrome. AUTHORS: Morgen K, Martin R, Stone RD, Grafman J, Kadom N, McFarland HF, Marques A. SOURCE: Neurology. 2001 Dec 11;57(11):1980-5.
Functional Brain Imaging and Neuropsychological Testing in Lyme Disease
AUTHORS: Fallon BA, Das S, Plutchok JJ, Tager F, Liegner K, Van Heertum R.
SOURCE: CID 1997; 25:S57-63 COMPLETE ARTICLE AT:
http://www.journals.uchicago.edu/CID/journal/issues/v25nS1/jy21_57/jy21_57.web.pdf
Geographical and seasonal correlation of multiple sclerosis to sporadic schizophrenia. AUTHOR: Fritzsche M. SOURCE: Int J Health Geogr. 2002 Dec 20;1(1):5.
Geographic correlation of schizophrenia to ticks and tick-borne encephalitis.
AUTHOR: Brown JS Jr. SOURCE: Schizophr Bull 1994;20(4):755-75
Geographic distribution of Lyme disease in Mudanjiang AUTHOR: Zhang Z.
SOURCE: Zhonghua Liu Xing Bing Xue Za Zhi. 1991 Jun;12(3):154-7. [Chinese]
Gestational Lyme borreliosis. Implications for the fetus. AUTHOR: MacDonald AB.SOURCE: Rheum Dis Clin North Am. 1989 Nov;15(4):657-77. Review.
Higher Prevalence of Antibodies to Borrelia Burgdorferi in Psychiatric Patients Than in Healthy Subjects AUTHORS: Hajek T, Paskova B, Janovska D, Bahbouh R, Hajek P, Libiger J, Hoschl C. SOURCE: Am J Psychiatry 159:297-301, February 2002 COMPLETE TEXT AT: http://ajp.psychiatryonline.org/cgi/reprint/159/2/297
Hypochondriasis and obsessive compulsive disorder: overlaps in diagnosis and treatment. AUTHORS: Fallon BA, Javitch JA, Hollander E, Liebowitz MR. SOURCE: Journal of Clinical Psychiatry. November 1991: 52(11):457-60.
Increased anti-streptococcal antibodies in patients with Tourette's syndrome. AUTHORS: Muller N, Riedel M, Straube A, Gunther W, Wilske B. SOURCE: Psychiatry Res. 2000 Apr 24;94(1):43-9.
Infectious Agents in Schizophrenia and Bipolar Disorder AUTHORS: Yolken RH, Torrey EF, SOURCE: 2006 June 43(7)
Inflammatory brain changes in Lyme Borreliosis. A report on three patients and review of literature; AUTHORS: Oksi J, Kalimo H, Marttila RJ, Marjarnaki M, Sonninen P, Nikoskelainen J, Viljanen MK: SOURCE: Brain, 1996 Dec; 119 (Pt 6) : 2143-2154
Invasion of human neuronal and glial cells by an infectious strain of Borrelia burgdorferi. AUTHORS: Livengood JA, Gilmore RD Jr. SOURCE: Microbes Infect. 2006 Nov-Dec;8(14-15):2832-40. Epub 2006 Sep 22.
Isolated monolateral neurosensory hearing loss as a rare sign of neuroborreliosis.AUTHORS: Iero I, Elia M, Cosentino FI, Lanuzza B, Spada RS, Toscano G, Tripodi M, Belfiore A, Ferri R. SOURCE: Neurol Sci. 2004 Apr;25(1):30-3.
Late-Stage Neuropsychiatric Lyme Borreliosis: Differential Diagnosis and Treatment AUTHORS: Fallon BA, Schwartzberg M, Bransfield R, Zimmerman B, Scotti A, Weber CA, Liebowitz MR. SOURCE: Psychosomatics 1995;36:295-300
COMPLETE TEXT AT:
http://www.wadhurst.demon.co.uk/lyme/lyme101.htm
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Pastor killing: Another act of violence attributed to Lyme disease

Pamela Weintraub — Mon, 09 Mar 2009 13:30:12 +0000

Here's a quick post to supplement my story on the chimp attack in Connecticut, which some pundits attributed to a rage reaction caused by Lyme disease.

On the heels of the rage-filled chimp story comes a human version: This weekend a man opened fire on a pastor in a church in Maryville, Illinois, murdering him with a rain of gunfire. Here, too, the explanation for the attack has been given as psychiatric illness caused by Lyme disease. Infected by a tick on the family farm in the early 1990's, the young man was, his family said, left with lesions on his brain.

There's no question that Lyme disease is a neurological illness. It has been associated with neurological disease for decades in rigorous peer review in the top medical journals in the world

For a quick review of neurological Lyme disease and its psychiatric links, check out the blog posts:

part one, part two, part three, and a psychiatrist gets Lyme disease.

Lyme disease may certainly form brain lesions much like those seen in multiple scleroisis. These lesions are often reversible with antibiotic therapy, but are sometimes irreversible and seen in patient brain scans for life.

Can Lyme disease provoke rage? Many psychiatrists and doctors working in the trenches with some of the sickest patients say the answer is yes, as do reports in the peer review. But murderous violent crime is not the typical M.O. for a patient with Lyme. Mental illness exists apart from Lyme disease and even adverse reactions to antidepressants and other antipsychotic drugs could provoke outsized rage. Once psychiatric symptoms emerge from Lyme disease, outcomes may include everything from suicide due to physical pain and depression over the illness to severe adverse reactions to psychoactive drugs.

The most common signs and symptoms of neurological Lyme disease include neuropathies that involve buzzing and tingling, nerve pain, memory loss, confusion, and fatigue. Psychiatric problems like depression, anxiety, OCD, and ADD can be triggered by Lyme or other tick-borne infections, according to studies. Panic attacks, hallucinations, delusions, and extreme rage have all been reported in Lyme patients but compared to memory loss and confusion, these presentations are rare. A patient with severe neurological Lyme disease is far more likely to get lost on the road or have trouble reading than shoot up a Church.

While Lyme disease is not known for triggering killing sprees, the Infectious Diseases Society of America (IDSA) has issued a press release dismissing most presentations of neurological Lyme disease at all. "In some rare cases, people may have neurologic problems such as facial paralysis," the group concedes in its official statement on the situation, listing this single symptom and no others. The group cites a 95% cure rate for Lyme disease, failing to mention that the statistic refers only to early disease; that number has been called into question by some academic heavyweights due to new findings on Lyme strains. But more disturbing, the IDSA statement fails to mention the late-diagnosed Lyme cases --and due to flawed tests, these are plentiful-- that give rise to the lion's share of neurological forms of the disease.

What is especially misleading is that the IDSA statement fails to take note of the true mainstream authority on neurological Lyme disease, the American Academy of Neurology. That group, whose practice guidelines hold sway in mainstream circles on this painful and sometimes-devastating condition, says this:

If you or a family member have been told by a doctor that you have nervous system Lyme disease, regardless of age,age, your symptoms may include headache, facial nerve palsy (Bell’s palsy), and meningitis (swelling and pain in the membrane surrounding the brain). Rarely the brain or spinal cord may become inflamed, causing weakness or changes to the nerve impulses in parts of the body, or other symptoms. Patients with nervous system Lyme disease may also have one or more of these symptoms: radicular (sciatica-like nerve) pain, weakness or numbness due to nerve damage, or changes in cognitive function (thinking, reasoning, remembering, imagining).

Shame on you IDSA! In a situation where balance is required, extremism, including exaggeration or diminishment of a real situation, only muddies the waters and leaves everyone confused.

On Monday, March 9, the Associated Press reported that that attacker, Terry J. Sedlacek, 27, of Troy, was charged with two counts each of first-degree murder and aggravated battery, for gunning down the pastor and then stabbing himself and two worshippers who tried to tackle him down.

Pamela Weintraub is the author of Cure Unknown: Inside the Lyme Epidemic and senior editor at Discover Magazine.

Chimp attack: Can Lyme explain it? Forbes wants to know.

Pamela Weintraub — Sat, 07 Mar 2009 21:12:04 +0000

Sad news from the Cleveland Clinic that the woman attacked by a chimp in Stamford, Connecticut last month may have suffered not just disfigurement, but brain damage.

Some people have pointed to Lyme disease as a provocation for the chilling attack. Living in my old stomping ground, Stamford, CT, in a suburban family home, the chimp named Travis was diagnosed with Lyme disease. Given that Stamford is at ground zero for the disease, it's not a surprise.

One publication, Forbes.com, has questioned whether chimps could even get Lyme disease. Taking a snarky tone about the disease itself in a post called "The Chimp Attack-Lyme Disease Connection," the pub posed a question to the public on its website.

"One angle that didn't make that much sense was that the chimpanzee was supposedly being treated for Lyme Disease. Forbes has written about the over-diagnosis of Lyme Disease in humans.We'd like to know: Can an ape get Lyme Disease? Could the chimp's owner have been giving him medicine that contributed to the attack?"

Working in the Forbes.com building on the 11th floor of 90 Fifth Avenue in my role as senior editor for the award-winning science magazine, Discover, I was surprised when the snide post floated up from the bowels of the building below.

Disappointed patients, picking up on Forbe's condescension and history of skepticism toward them, responded online:

Said one poster:

I had Lyme Disease AND I ATTACKED TOO - out of pain, fatigue and frustration. My boyfriend, thankfully, understood and stuck by me anyway. He put up with a lot of things I never would have and deserves to be commended AS DO ALL OF US who know about, fight to educate others, and SUFFER through the horrors of this disease. How many genes do we have in common with chimps, again???

And another:

Of course apes can get Lyme disease. So can other animals and humans.

Were my colleagues at 90 Fifth laughing at this patient response? I hope not.

Can Lyme disease, a brain infection sometimes associated with anxiety and very rarely, rage reactions, explain the tragedy? In my opinion, the answer is probably not. Chimps are wild animals and male adolescent chimps, in particular, are known to defend their turf and impose their will violently.

In fact, responding to the situation, Richard Blumenthal, Attorney General of Connecticut, this week proposed a new law aimed at banning primates,alligators, kangaroos, wolverines and other types of wild and potentially dangerous animals from Connecticut private homes and yards. In announcing the bill, Blumenthal said, "We are playing Russian roulette in our homes because we have put dangerous animals in them." The story was carried in Connecticut newspapers on March 7.

There's no question that patients with neurological Lyme disease may commonly suffer numbness in extremities, memory loss and confusion. Fatigue is commonly reported in the group. Just read the scientific literature, and you will find that anxiety, depression, and OCD have all been triggered by Lyme. And yes, relatively rare violent reactions have been reported in the peer review.

But it would be wrong if the Connecticut chimp attack caused anyone to fear Lyme disease patients, or to think their infection might send them on killer rampages like the rage-infected zombies in Danny Boyle's post-apocalyptic thriller, 28 Days Later. Instead of looking to Lyme disease to explain these events, we would all be better served by exploring issues of animal rights: Especially the call for keeping wild animals where they belong, in the wild and out of our neighborhoods and homes.

As to whether a chimp can get Lyme disease, here's a shout-out from the science mag on 11 to my curious Forbes colleagues on the lower ten. Yes, you guessed it, I went not to the public but to some real scientists to help me out on this issue. Here's what they have to say:

"Borrelia [the Lyme spirochete] can infect chimps, but they would have to be bitten by an infected tick --their habitat does not overlap with that of the tick so very unlikely in the wild. Primates have been inoculated [with Borrelia] in studies in the lab." -- Eugene Davidson, Ph.D., former head of microbiology at Georgetown University for 15 years, who has studied Lyme disease in non-human primates,

"I don't know why a chimp couldn't get Lyme disease. Mario Phillip and Andy Pachner have infected other nonhuman primates. But those were experimentally induced. How would a chimp emcounter the ticks that transmit it? Was the chimp allowed to run free outside in an area with a risk of infected ticks?" --Alan Barbour, M.D., director of the Pacific-Southwest Regional Center of Excellence for Biodefense and Emerging Infectious Diseases at the University of California Irvine.

Note to the public: No need to fear Lyme patients. You're more likely find the sickest of them at home, too fatigued to get to work, in too much pain to care for their children or visit with friends. You might find them in bed.

All in all, it's not too cool to make a joke out of a tragedy: The tragedy of a women whose face was ripped off by a chimp and the tragedy of thousands of patients, often the butt of the kind of sarcasm found in Forbes --those with a disease diagnosed too late and treated too inadequately to achieve a total cure. Not PC to make fun of the sick and injured. Not funny Forbes, not funny at all. And while I am at it: not journalism.

Pamela Weintraub is the author of Cure Unknown: Inside the Lyme Epidemic and senior editor at Discover Magazine.