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Institute of Medicine (US) Committee on Lyme Disease and Other Tick-Borne Diseases: The State of the Science. Critical Needs and Gaps in Understanding Prevention, Amelioration, and Resolution of Lyme and Other Tick-Borne Diseases: The Short-Term and Long-Term Outcomes: Workshop Report. Washington (DC): National Academies Press (US); 2011.

Cover of Critical Needs and Gaps in Understanding Prevention, Amelioration, and Resolution of Lyme and Other Tick-Borne Diseases

Critical Needs and Gaps in Understanding Prevention, Amelioration, and Resolution of Lyme and Other Tick-Borne Diseases: The Short-Term and Long-Term Outcomes: Workshop Report.

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3The Social Construction and Human Face of Tick-Borne Disease


Robert A. Aronowitz, M.D., University of Pennsylvania

The apparent consensus about a treatable disease caused by a spirochete found in New England in the mid-1970s turned out to be anything but a simple story. The American definition and diagnosis of Lyme disease has generated considerable controversy. Disease definitions are often negotiated balances between two ways of understanding illness: as a specific disease or as an individual idiosyncrasy. Although biological processes place limits on how diseases can be defined, what counts as a (new) disease often depends on values, interests, and contingent historical events. As the history of Lyme disease suggests, the definition of a disease often results in winners and losers, and controversy among the stakeholders is apt to follow.1

To place the discovery of Lyme disease in the United States in context, it is helpful to review earlier events in Europe. As early as 1910, European clinicians described a rash they called erythema chronicum migrans following a tick bite. In the 1930s, the disease was connected to meningitis, and people had strong suspicions that it was bacterial in origin, pointing to Rickettsia in particular. There was even speculation that spirochetes might be involved, although the evidence seemed weak. After World War II, European clinicians used penicillin to fight the illness, and it generally was thought to work. At the same time, different groups, primarily dermatologists and syphilologists, linked different syndromes, such as acrodermatitis chronica atrophicans and Bannwarth’s syndrome, that are now considered part of the Lyme disease complex. These Europeans were already viewing the illness that Americans would later call Lyme disease as a systemic disease.

The first U.S. case report of erythema migrans appeared in Wisconsin in the 1970s. In 1976, physicians at the naval base in Groton, Connecticut, reported the first cluster of erythema migrans cases in the Journal of the American Medical Association (Mast and Burrows, 1976). Although this report received little attention, a Danish doctor participating in dermatology grand rounds at Yale connected the cases to erythema chronicum migrans in Europe. A prospective study was mounted in 1976 that identified erythema migrans in new cases.

During this same period, Yale rheumatologists had begun investigating undiagnosed illnesses among children and adults in and around Lyme, Connecticut, focusing especially on an apparent clustering of joint and other problems in children. These clinicians suspected some kind of juvenile rheumatoid arthritis, but that illness was not known to cluster geographically. About 25 percent of the patients had a history of a rash, but that sign did not appear prominently in these early case descriptions. By 1976 the Yale researchers had postulated a new condition, which they first called “Lyme disease arthritis” (Medical News, 1976; Steere et al., 1977), now known as Lyme disease.

The Yale rheumatologists considered Lyme disease to be a new rheumatological condition because it was unlike any previously described condition, and swollen joints were one of the most prominent signs. In addition, referral patterns reinforced the rheumatological identity of the disease. Later the fact that Lyme disease represented a new synthesis of previously separate diseases provided another rationale for declaring it a new illness, reinforced by the accompanying professional rewards and media and medical interest. Some observers noted that changing ecological conditions in and around the Northeast may also be associated with the occurrence of Lyme disease.

Framing Lyme disease as new disease rather than an American variant of an existing one had consequences. Early investigations focused on viruses as the prime etiological suspect. Thereforth, many cases were not treated with antibiotics, as was common in Europe.2 Newness brought fear, uncertainty, and controversy over the proper definition, diagnosis, and treatment of Lyme disease, as did various biological and sociological factors. The timing of the disease’s emergence coincided with the evolution of the AIDS epidemic. There was geographical risk of contracting the disease, as well as an apparent tendency for it to disproportionately affect certain populations, such as residents, especially children, of suburban areas. Diagnosis came primarily from clinical criteria, due to the imprecision of laboratory tests. Finally, because of the emergence of this new disease and the associated clinical manifestations, patients were concerned and frightened.

Disputes about the definition and diagnosis of Lyme disease helped spawn the debate about chronic Lyme disease that continues today. The controversy also spurred dispute about the benefits and risks of a vaccine against the disease that was developed during the 1990s and early 2000s. This dispute partly concerned the vaccine’s benefits and risks; however, the core issue remained the legitimacy of chronic Lyme disease as a sequela of infection with Borrelia. In particular, some people contested the diagnostic criteria employed during clinical trials for the vaccine, seeing them as much too narrow and reminiscent of the orthodox view of Lyme disease as an acute, treatable, and self-limited disease rather than a disease that could become chronic.

The decision by vaccine developers to opt for a narrow-case definition seemed perfectly sensible from one perspective: Such a definition increased the power of clinical trials to detect a positive effect from the vaccine. However, vaccine promoters failed to understand and anticipate what was at stake in the controversy over Lyme disease. To patient advocates, evidence of the efficacy of the vaccine simply reinforced the fallacy inherent in narrowly defining the disease. This dispute played out when investigators of two clinical trials, who published the results in the New England Journal of Medicine, found very little, if any, asymptomatic seroconversion among people vaccinated during the trials (Steere et al., 1997; Sigal et al., 1998). To promoters of the vaccine, this was evidence of its efficacy over and above the 75–85 percent reduction in clinical cases of Lyme disease seen during the trials. The fact that asymptomatic seroconverters were not subject to clinician and patient bias during referral and diagnosis underscored this finding.

However, critics who thought the trial was designed to reinforce the orthodox view of Lyme disease argued that no asymptomatic seroconversion occurred because the vaccine induced everyone who was asymptomatic to become symptomatic. No data could reconcile these two points of view: They were simply incommensurate. Indeed, regulatory hearings on the vaccine suggested that its promoters and critics inhabited different universes.

Immediately after winning regulatory approval for the vaccine, the manufacturers launched an extensive advertising campaign built largely on provoking fear of the disease and raising awareness of the vaccine among consumers. In so doing, the manufacturers again misjudged what was at stake in the Lyme disease controversy: not solely or perhaps even primarily fear of the disease, but rather fear among those favoring a broader definition of Lyme disease that the vaccine could cause a chronic Lyme disease-like syndrome and evidence of vaccine efficacy could be understood to delegitimize chronic Lyme disease. In addition, Lyme disease does not reflect the typical characteristics of a disease against which to vaccinate. Many vaccines are developed for diseases that are communicable and potentially severe and are designed to reduce or prevent the spread of the disease through herd immunity. Because Lyme disease is not contagious, the vaccine would not generate herd immunity; it would prevent infection only in vaccinated individuals. Furthermore, the perception by a few that Lyme disease was an acute, self-limiting condition tended to reduce the impetus to vaccinate widely. In different ways, both those who adhere to an orthodox view of Lyme disease and those who advocate for inclusion of the experience of chronic, persistent symptoms within the diagnostic umbrella had reservations about widespread use of the vaccine.

Interestingly, people on both sides of the debate seemed to share the assumption that suffering is legitimate only if linked to a “real” disease. The controversy arises partially over who determines whether the suffering among patients with chronic, persistent symptoms is legitimate, and perhaps more generally a societal concern over the reach of medical authority.

In conclusion, Aronowitz noted that the history and sociology of Lyme disease suggest several lessons:

  • Recognizing a new disease has no hard-and-fast rules: what counts often depends on historical events and participants’ interests and values.
  • Participants in such controversies need to tone down efforts to amplify fear of a disease, while avoiding overly optimistic pronouncements about it—a difficult balance to achieve.
  • Clinicians and researchers need to accept the diversity of diagnostic names and possible natural histories of a disease and to decouple disease naming and diagnosis from treatment decisions.


Pamela Weintraub

Pamela Weintraub is the features editor at Discover magazine and author of the book Cure Unknown: Inside the Lyme Epidemic. Her presentation is not intended to reflect the views of all patients, but rather to draw on her personal experiences with Lyme disease, and her interviews with both Lyme disease patients and researchers to provide a commentary and a basis for discussion of how research takes place in a context of human experience. What follows is a first-person narrative.

Lyme disease entered my life in 1993, when my husband, Mark, our two sons, and I moved to Westchester County, New York. Our lovely property abutted a spruce forest, and we reveled in our new contact with nature, which included squirrels, raccoons, mice, and other animals and birds.

From that point on we all became increasingly sick. First there were headaches, joint pains, and an inexplicable weariness. With time the symptoms intensified and multiplied. My knees became so painful that I had to sit down to descend stairs on my bottom one step at a time. I developed dysphasia (impaired speech and verbal comprehension). I had so much trouble swallowing that I choked on my food. I developed peripheral neuropathy: My arms and legs buzzed gently at first, and then increasingly painfully, until it felt like electricity was running through me. The headaches became relentless. My eyes were painfully sensitive to light. I spent hours each day in a darkened room in bed.

Meanwhile Mark, an avid tennis player, began stumbling and bumping into walls. An award-winning journalist, he began struggling with memory and groping for words. He was forced to leave his job after realizing that he had spent hours trying to read a single simple paragraph.

Our youngest son, David, began to sleep so much that he could not do his homework or see his friends, and eventually could not get to class. In the end he was sleeping 15 hours a day. Hardest hit was Jason, our oldest, who suffered profound fatigue and shooting pain starting at age 9, late in the summer of 1993. The doctors called these normal “growing pains,” so my son tried to keep going.

Then in 1998 he developed a huge erythema migrans rash over his torso. I called the doctor’s office and was told not to bring him in. Because the rash wasn’t in the shape of a bull’s eye, it wasn’t Lyme disease, they said. After that rash, Jason became increasingly ill and never seemed to get well. By 2000, at age 16, he was functionally disabled. He couldn’t think, walk, or tolerate sound and light. On medical leave from high school, he spent his days in the tub, drifting in a mental fog while hot water and steam eased his pain. A raft of specialists at New York City’s top teaching hospitals suggested diagnoses from migraine aura to parvovirus. Each diagnosis elicited a treatment, but none of them worked.

“What about Lyme disease?” I asked from time to time. “There are too many symptoms here and he is way too sick for Lyme disease,” responded the pediatrician, who told us he felt it was all psychological. Thankfully, the psychiatrist who we ultimately consulted, who literally wrote the book on child and adolescent psychiatry, disagreed. At his insistence the pediatrician drew 14 vials of blood testing for hormonal imbalance, mineral deficiency, anemia, and a host of infections, including one tick-borne disease: Lyme disease. A week later the pediatrician called to tell us that a Western immunoblot had come back positive for Lyme disease, with 8 of 10 bands highly lit.

Finally, the head of infectious disease at Northern Westchester Hospital weighed in with his opinion. Jason probably had been misdiagnosed for years, he said. I will never forget the way he phrased his grudging diagnosis: “I will give it to you,” he said, as if we had earned some coveted prize that others whose confusing array of multisystem ailments could be explained in some other way, would never get.

Unaware of the political turmoil surrounding this tick-borne disease, I didn’t yet understand how rare it was for a doctor like him to diagnose late-stage Lyme disease in New York State. However, when Jason didn’t get well after 8 weeks of intravenous Rocephin, the doctor consigned him back to psychiatry.

The situation would have stretched anyone’s credulity. Our formerly straight-A, basketball-playing son, after contracting Lyme disease, being misdiagnosed for years, and finally receiving antibiotic therapy for 2 months, had now developed a bizarre, unrelated psychiatric disorder whose symptoms were coincidentally exactly the same as those of Lyme disease. Perhaps it is possible to believe that kind of explanation when served up by experts talking about other people’s children, but it is the rare parent who would accept that decree for her own child, especially when her psychiatrist had never seen this form of psychiatric disease in his life.

Mark and I, by now both quite ill ourselves, faced a choice. Accept this unlikely story and give up on our son’s future, or find one of the Lyme disease doctors said to treat more aggressively, in opposition to the mainstream views we had followed for years to the current tragic state of affairs.

In the summer of 2000 we bundled our boy into the car and headed up to New Haven, Connecticut, and the practice of the embattled pediatrician Charles Ray Jones. Jones examined and tested Jason and told us he was so sick because he had contracted not only Lyme disease but two common coinfections: babesiosis and anaplasmosis. Epidemiologically it seemed like a reasonable call, given the many vacations we had taken on Martha’s Vineyard and Cape Cod, where babesiosis was ripe. Jones treated Jason with standard doses of doxycycline for anaplasmosis and Lyme disease, and Mepron and Zithromax for babesiosis.

Two weeks later, after years of free fall, our son got out of the bathtub and began throwing a basketball around the family room. Two years later he was playing varsity basketball for his high school, and today he holds a B.A. from Brown University and is a graduate student at Boston University earning his M.F.A. in film.

Although my book Cure Unknown is partly a memoir, it really focuses on what I found after I had dealt with my family’s health problems sufficiently for me to sit back and peer through the eyes of the skeptical, investigative science journalist I had been for decades before Lyme disease swept us away. From 2000 to 2008, I interviewed Lyme disease patients, Lyme disease doctors, and dozens of academic scientists, including most of those at the forefront of research, and many of those speaking at this forum. I met large numbers of patients with classic incontrovertible presentations of Lyme disease who, like Jason, would probably have been cured with early treatment, but who were instead diagnosed late—often very late—in the game.

Patients routinely reported going to their primary care doctors with the tick in hand and being told to throw it away and return only if symptoms emerged. Many patients told me of doctors who insisted that a Lyme disease rash had to look like a literal bull’s eye. Patients reported going to doctors with a tick bite, early flu-like symptoms, and sometimes even the erythema migrans rash, and being told to wait for a positive test before they could be treated. A significant percentage who had tested positive had been told they could still not be treated for Lyme disease until they developed gross, objective signs of disease, such as swollen knees or inflamed nerves—in other words, until they had advanced to the late stage of disease, when treatment was more likely to fail.

Other patients with known exposure and signs and symptoms of Lyme disease failed to test positive on their Western blots, according to criteria of the Centers for Disease Control and Prevention. Take me. I had a positive enzyme-linked immunosorbent assay (ELISA) test, and four positive bands on a Western blot, plus evidence of two additional Borrelia burgdorferi proteins—six bands in all. Yet I still had to step outside the bounds of the medical mainstream to find a practitioner who recognized this band pattern as Lyme disease.

Patients in the South with a trademark rash and other objective signs of disease would similarly be told there was no Lyme disease in their state and be turned away. Such patients in aggregate constitute what I think of as the chronic Lyme disease population. Instead of getting early treatment, these Lyme disease patients had been diagnosed months or years too late. They were eventually treated for late-stage Lyme disease in accordance with the guidelines of the Infectious Diseases Society of America, and they had failed that treatment.

Completing this community of patients are the coinfected: those with babesiosis, anaplasmosis, ehrlichiosis, or some other tick-borne infection. Surveys around the country report that ticks can transmit these well-known human diseases, yet primary care physicians almost never consider or test for them, even if they seriously consider Lyme disease. I think they need to determine the suite of possible diseases Lyme disease patients may be carrying because, like Jason, those patients can be very sick and resistant to treatment specifically because their illness isn’t just Lyme disease.

Mark Klempner of Boston University found that a cohort of chronic Lyme disease patients was as impaired as patients with congestive heart failure or osteoarthritis, and more impaired than those with Type 2 diabetes or a recent myocardial infarction. Brian Fallon of Columbia reported pain equivalent to post-surgical pain, and fatigue as severe as in multiple sclerosis.

Patients can suffer stabbing, boring, shooting pains in their arms and legs, or impaired vision and hearing from damaged nerves. They can suffer heart damage. Even more devastating are the cognitive and memory deficits. After testing hundreds of patients, Leo Shea, a neuropsychologist at New York University, found specific deficits in concentration, short-term memory, and processing speed.

Fallon has traced these impairments to blood flow and metabolism deficits in the brain. Some scientists have called the impact of these impairments mild, but that does not remotely capture the agony of falling behind in school or feeling perpetually foggy and confused. Many patients report getting lost while driving around their own neighborhood, and some patients told me they could no longer remember enough to perform the specific details of their jobs.

For me the fatigue was the worst symptom. During the years I had Lyme disease, I collapsed in a heap every afternoon while my children were in school, my exhaustion overwhelming and profound. Studies minimize these “subjective” symptoms as almost irrelevant. However, a lack of external evidence does not mean that such internal devastation cannot be reliably measured and shouldn’t be given weight as perhaps the most important outcome of all.

For parents, unresolved pediatric Lyme and tick-borne diseases are a nightmare, as they bear the heartache of watching their children suffer, along with helplessness and despair when the medical community all too quickly dismisses their complaints. After a child has been allowed to slip through the cracks of early diagnosis and treatment, the stage is set for isolation and alienation as she drops clubs, sports teams, friendships, and often even school.

In the wake of a child’s decline, schools often push psychiatric interpretations, forcing inappropriate labels and help. When a child doesn’t respond to wrong-headed strategies, the schools may accuse parents of poor skills or even Munchausen by proxy—a diagnosis that has fallen into disrepute among top psychologists and psychiatrists but that still manages to rear its head as an accusation where mothers and Lyme disease are concerned.

What a chasm I found between the patients I interviewed and some of the physicians at Northeast teaching hospitals. One well-known academic told me that virtually all Lyme disease patients are diagnosed early these days, and that treatment response is guaranteed for the rare patient who slips through the cracks to late-stage disease. If the patient doesn’t respond, he or she never had Lyme disease, the doctor said.

When during grand rounds or training sessions such doctors suggest that patients are malingerers, too wimpy to handle stress, middle-aged suburban women with somatoform disorder, or hypochondriacs in search of the disease du jour, they have poisoned the chance of timely diagnosis by predisposing primary care physicians to seek psychiatric explanations first. With early treatment off the table, such patients wander from family doctor to clinic to teaching hospital, from one specialist to the next, and then off the grid.

My family found our way to doctors who diagnosed infections clinically and treated empirically while providing symptomatic relief for chronic disease. These were the best of the Lyme disease doctors. They treated our babesiosis and addressed our Lyme disease relapses, and over the course of years brought us back to health. We found them compassionate and responsible. However, being the patient of such a doctor is stressful. He or she may be under investigation, and will rarely take insurance for fear of being profiled as an outlier and further stigmatized. That makes the patient’s financial stress extreme.

Other patients default to outright quackery: dangerous chemicals, lethal levels of heat applied to internal tissues, risky doses of salt. Some patients spend life savings on trips to India for a black-box therapy said to be based on stem cells. A diaspora of the desperate and broke, many of these patients have come to the end of the line.

Being sick is hard enough, but being so sick for so long and also being a suspect, having your physical pain, your integrity, and your very sanity called into question as you travel the medical landscape begging for help: That is a crushing course of events. No one suggests that the cancer patient is fictitious, or that the heart patient is a sociopath. But in the case of Lyme disease and other tick-borne diseases, the brutality of such rejection on top of real physical illness has traumatized the patient community. No wonder patients are in such turmoil.

The three largest patient advocacy organizations have boycotted this forum because they say it is biased against them. To quote their press release, they remain skeptical that it will lead to a true understanding of patients’ needs. The history of the patient experience has robbed them of faith that anyone in government will understand their pain or truly address their plight.

Nearly 35 years ago, Polly Murray reported the strange set of symptoms in her town of Lyme to the Connecticut Department of Health. Murray noted the loneliness of her journey back in 1976, but decades later new patients travel the same lonely path, as if Murray and many others had never paved the way. Too many of us still spend years seeking help for what was in the beginning incontrovertible, classic, and curable Lyme disease, only to reap the whirlwind of late diagnosis and failed treatment even in the most endemic areas of the United States.

In interviews with hundreds of these patients, I found that relapsing-remitting illness was the overriding experience. Antibiotics were overwhelmingly the strategy these patients preferred for fighting back. However, which drug might work for which patient was highly variable, suggesting an extremely complex scenario.

I had relapsing–remitting disease. I was infected for some 7 years before diagnosis. I would get better after antibiotic treatment but then relapse like clockwork after 2 to 3 months. I went through such draining cycles for 4 years before a recovery was sustained. Can we really dismiss this common experience as coincidence or a psychiatric disease?

I have heard it said that all Lyme disease patients want are more antibiotics, but that isn’t true. Patients just want to get well, and will embrace any therapy that cures them. No reasonable person would argue that the answer sought by science should be endless antibiotic treatment, even if infection remains chronic at a low level, as evidence suggests. To help these patients, medicine must acknowledge their pain, and science must deal with the complexity.

Anyone who follows bioscience knows that pioneer Leroy Hood is building the medicine of the future that any patient group this varied needs: data-driven “P4 medicine,” for predictive, preventive, personalized, and participatory. As Benjamin Luft of State University of New York–Stony Brook has suggested, only a systems-biology approach can target the full spectrum of strains, infections, and immune cascades for every patient with tick-borne disease. Academic scientists are embroiled in a dumbed-down fight with patients about the chronicity of infection even as a revolution in bioscience has reframed the questions we need to ask.

To paraphrase Tolstoy: Every early-stage Lyme disease patient is pretty much the same, while each chronic patient takes a singular journey of one. This discomforting fact has undermined the patient narrative. But with the advent of proteomics, genomics, epigenomics, and other 21st-century tools—with greater powers of vision—the story told by bioscience and the story told by patients can finally converge.


The challenge of diagnosis of reported symptoms have been frustrating for patients and clinicians. Primary areas of discussion during the workshop included the polarization that has developed between some patients, particularly those experiencing chronic symptoms, and clinicians; the need to improve communication and understanding between clinicians and patients; and patients’ desire to focus greater discussion and research efforts on the care needs of those experiencing chronic symptoms.

Acknowledgment of patient experiences also may help keep barriers from forming between patients and clinicians or social institutions, such as schools, or break down existing ones. In response to a question about how best to support a teenager with debilitating symptoms, Weintraub observed that it helps teens to receive validation that they feel sick, as well as having the flexibility to make accommodations based on how they feel (e.g., deferring a test for a day if the student does not feel well).

In response to a participant’s comment about the apparent stigma attached to Lyme disease within the medical community, Ms. Weintraub noted that stigma and a bias against Lyme disease do exist and can result in delays in diagnosis and treatment, as reflected in her son being undiagnosed for years. In addition to the stigma, the vitriol of the fight gives many physicians pause. To avoid the angry atmosphere, they may wish to stay out of the fray, especially where long-untreated or late-diagnosed and complicated presentations of illness are concerned. However, she also noted that the multiple manifestations of the disease in many cases can contribute to the confusion surrounding it, likewise resulting in delays in diagnosis and initiation of treatment. As one family physician observed, patients with chronic symptoms tend to present as 1 sick person with 10 different diseases, whereas a patient with early or uncomplicated late-stage Lyme disease tends to present as an otherwise healthy person with 1 disease. Another participant noted the absence of an integrated model of care, resulting in the need for patients to obtain care from many different specialists. The result in any case can be mutual frustration on the part of patients and their clinicians at the failure to resolve or alleviate the symptoms experienced by the patients, as well as the difficulties patients experience in obtaining care. This frustration, perhaps combined with poor communication, in turn may lead to anger and polarization.

Weintraub observed that all this polarization is very destructive and perhaps a primary reason why little progress has been made in advancing the treatment of patients with chronic symptoms. With others, she pressed the need to move past the sound bites issued by the two extremes to appreciate and focus on the complexity and nuance of the work to be done. Many people with great expertise in the academic community are doing that and working to move the science of diagnosis and treatment forward, she noted. Two participants observed the need for substantial funding for research to help address some of the current knowledge gaps and to promote early diagnosis, as well as prevention and vaccine development.

Several participants, while noting the hope for future patients observed by Jacobs and others, emphasized the desire that focus also remain on or return to the quality of life of those individuals currently experiencing symptoms. One participant highlighted the current gap in communications, noting that how information is provided on the Internet can vary, with implications for how those to whom it is disseminated (e.g., schools, insurance companies) will respond to the disease. The same participant called for a centralized source of information on the latest research to facilitate patient/family efforts to obtain such information. Another participant called for better communication between patients and their physicians, noting the damaging effect of this disconnection between two groups who have worked together on other illnesses. By working together in creative ways, physicians and patients may help to advance the science and understanding of the disease processes and chronic manifestations to permit earlier diagnosis and better treatment outcomes.

Participants also expressed concern about the underuse of the current population of patients and families as a rich data source in terms of bioinformatics, and perhaps a biorepository, to advance research into tick-borne diseases and the efficacy of various treatments. Weintraub responded that retrospective assessment of patients would be informative, but that it is important to move forward as well. She noted the availability of new tools to advance the diagnosis of infection and understanding of the pathophysiology of the diseases. It is important to look at what clinicians treating Lyme disease are doing, but to do so in the context of the new technologies. The goal is to move toward a definitive diagnostic tool and targeted treatment. Weintraub counseled that if the diseases can be diagnosed definitively in their earliest stage and treated effectively, then the occurrence of chronic, persistent symptoms will be eliminated or greatly reduced.



The committee notes that other accounts of the history of Lyme disease exist, such as the book, Borrelia: Molecular Biology, Host Interaction and Pathogenesis Samuels and Radolf (2010), and the original research articles such as Steere et al., 1980b.


The committee notes that some reports from the 1980s demonstrate the effectiveness of antibiotic therapy (Steere et al., 1980b).

Copyright © 2011, National Academy of Sciences.
Bookshelf ID: NBK57014


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