TBDWG December 11 and 12, 2017 - Written Public Comment
All Tick-Borne Disease Working Group (TBDWG) meetings dedicate time for public comments. The Working Group invited public comment on issues related to the Working Group's charge. Verbal comments were provided in-person during the meeting. Written comments were submitted via email to the TBDWG inbox. Below are the written comments submitted by individuals for the December 11 and 12, 2017, meetings.
I appreciate your looking further into Lyme disease. I believe I was bitten by a tick in the summer of 2012 when I spent some time out at a park. Later that week I had what looked like a pimple on my hip. I thought it was strange, but worry too much about it. By the end of that year, in 2012, I noticed that during meetings, I was unable to focus and hear what people were saying. By January or February I was too weak to make it up stairs, I was too tired to perform normal tasks and my joints would ache. I have not recovered now in the year 2017. But, I am one of the fortunate ones because many thousands of others end up permanently disabled and suffer from secondary issues such as cancer or heart issues. I still suffer. I still have days that I cannot think straight, that I have severe anxiety for no reason, and I am in pain every day. My quality of life is greatly diminished as are thousands of others who remain undiagnosed and untreated.
I have always tested negative for Lyme disease while at my regular physicians and specialists. I was told, there is nothing wrong with me, even after a spinal tap and an MRI. It was not until a friend of a friend stated that what I had sounded like Lyme disease and I was given the name and number of an ILAD’s doctor that I was able to get some answers. After that I explored natural path doctors and Chinese medicine doctors. Some of my symptoms are relieved from time to time, but at great expense.
It is my understanding that the rules for testing/diagnosing for Lyme changed a few decades ago, and many who have chronic Lyme or post treatment symptoms will remain undiagnosed and untreated due to the decision to change the criteria to meet the Lyme diagnosis. Who would do this? Why would someone deliberately change this so that many would not be diagnosed, who previously were. If you really want to make a difference, look into the time that the criteria was changed. Ask yourselves why. Was it greed? Was it ignorance? Thousands, perhaps millions of people are relying on you to make a choice for them, for their lives and livelihood. Please consider carefully.
Gary Wormser from the ALDF is part of your panel, from my understanding. He is aware that the testing for Lyme from back in 1994 was only 15% accurate. Ask him about this fact. Ask him why thousands of people, perhaps millions by now would fake a horrible disease. He doesn’t deserve to be on this panel, as he falsified results and has no interest in helping those already with this terrible disease.
Pat Smith from TBDRP has a long history of knowing about the problems with OspA. OspA alone can cause disease, initially from the vaccine that was stopped after patients developed ongoing issues, the same issues that many with Chronic Lyme disease have-which is not being treated for thousands, or millions of people by now.
Again, I am not a professional in the field, but a victim of this crisis. How many more people have to die or suffer to get your team to decide that this is a national crisis? Do you really want a few more decades of not doing anything? Your names will be marred as being on the wrong side of history. The side that did nothing for the millions who are suffering right now.
Fix this, Now! For those who already have Lyme disease! For God’s sake, do it for the future generations! How many mothers will be unable to give their children the type of care that they need because they cannot take care of themselves? How many children suffer and are unable to function normally in society because they are unable to learn when Lyme infections start early? Where is your conscience? Your common decency and desire for health for all?
If you cannot help, who will?
Sincerely, thank you for your time,
Beth (Radiant Eagle Lyme Warrior)
August 29, 2017
WRITTEN TESTIMONY TO NYS SENATE TBD TASK FORCE AND HEALTH COMMITTEE
A Critical Reappraisal of the Science and Bioethics of Lyme Disease Medicine
Holly Ahern, Associate Professor of Microbiology, SUNY Adirondack; Michael C. Brannigan, Pfaff Endowed Chair in Ethics and Moral Values, The College of St. Rose
The Centers for Disease Control and Prevention (CDC) holds as its mission the protection of U.S. citizens from disease regardless of whether the disease threat is “chronic or acute, curable or preventable, human error or deliberate attack.” The CDC includes in its “Pledge to the American People” that all public health decisions will be based on the highest quality scientific data that is derived openly and objectively; to place the benefits to society above the benefits to the institution; and to treat all persons with dignity, honesty, and respect (1).
However, in the case of Lyme disease, the CDC is not fulfilling its mission or its pledge to protect the American public from a disease this governmental agency readily acknowledges it has been underestimating for years (2).
Based on epidemiological reports of notifiable diseases maintained by the CDC, Lyme disease is overall one of the top three notifiable infectious diseases in the United States. Although commonly referred to as the leading vector-borne disease in the United States, a review of CDC surveillance data on all infectious diseases on the “Nationally Notifiable” list of diseases, shows that Lyme disease is second only to Chlamydia (a sexually transmitted disease) in terms of overall number of new cases annually.
The public health response to this high incidence infectious disease is not commensurate with the significant disease burden experienced by people who acquire the infection, nor to a society which must support those left sick and disabled by Lyme disease symptoms. This disease burden stems directly from fundamental misconceptions about the nature of the bacteria, the biology of the infection they cause, and the symptoms patients experience as a result.
Seminal research studies created and perpetuated Lyme disease misconceptions
In 1977, Steere et al. (3) published the first description of an “epidemic” of arthritis occurring in patients clustered in the vicinity of Lyme, Connecticut. By 1982, Wilhelm Burgdorfer, a research scientist employed by the Epidemiology Branch of the National Institute of Allergy and Infectious Diseases (NIAID), had identified a spiral-shaped bacterium in the genus Borrelia as the agent responsible for the disease symptom (4). The bacterium was named for him shortly thereafter, and Borrelia burgdorferi was firmly established as “the cause” of Lyme disease.
In epidemiology research, it is common practice to seek a unique characteristic (a clinical “sign”) that can be used to definitively distinguish one condition from all others. In his search for the perfect clinical “sign,” Steere noted that a small proportion (25%) of his original group of patients had developed a very unusual rash resembling a target or “bulls-eye.” Steere focused on this rash, medically referred to as an “erythema migrans” or “EM” rash, because he presumed it to be the tell-tale sign he was seeking. His errant presumption has influenced scientific research related to tick-borne disease ever since.
All subsequent studies on the clinical aspects of Lyme disease in human subjects included a recruitment process heavily skewed toward the population of patients who developed an EM rash as a sign of “early” infection with Borrelia burgdorferi. While we now know that only a minority of patients with Lyme disease develop the EM rash, this fundamental study design flaw introduced a strong and pervasive bias into later studies on the clinical manifestations of Lyme disease. This is readily evidenced in a second paper published in 1977, which focused on patients with the EM rash and arthritis with joint swelling as the primary indicators of infection. Not surprisingly, by the time the second study was published, the purported incidence of the EM rash in Lyme disease patients had been increased to 70% (5).
In the earliest epidemiological investigations of Lyme disease in New York (6) and Minnesota (7), the EM rash was used as the primary defining criteria for a “case” of Lyme disease. To assess the risk and burden of Lyme disease in these states, physicians were “urged” to report patients presenting to them with a “case” of Lyme disease, which for the purpose of both studies was defined as a person with Lyme disease symptoms who had the “presence of erythema chronica migrans (EM) rash,” or secondarily, systemic symptoms of meningitis, facial palsy, or large joint arthritis, appearing during the months of May, June, or July (6, 7).
By using this study design, investigators biased the data toward those persons who presented to physicians with an EM rash during the summer months. Consequently the data appeared to show a relative increase (to nearly 80%) in the proportion of Lyme disease cases associated with an EM rash. These investigations also gave rise to another misconception, which is that new Lyme disease cases occur in only a few regions of the United States (particularly the northeast), during the months of May, June and July. These months coincide with the feeding activity of the second life stage (called a nymph) of Ixodes scapularis ticks.
The enzootic cycle of Borrelia burgdorferi requires an infected host animal to serve as a “reservoir” that maintains the bacteria in nature, and a tick to serve as the “vector” that transmits the bacteria from the reservoir to other animals, including humans. Ticks have three life stages (larvae, nymph, and adult), each requiring a blood meal to fuel transition to the next stage. Entomological research indicates that nymph ticks feeding on an infected reservoir host (such as mice and migratory birds) is central to perpetuating the enzootic cycle (8).
Although all three stages of Ixodes spp. can feed on humans, past and present entomological and ecological studies on Lyme disease transmission have focused almost exclusively on the feeding activities of the nymph stage tick on mice. To date, there have been no studies done to determine which tick life stage is most involved in transmission of Borrelia or any other tick-borne pathogen to humans. According to disease ecologists, this is because humans are considered “dead end” hosts in the enzootic cycle of the disease-causing agent.
The overreliance on the EM rash as a clinical sign and the presumption that nymph ticks are the primary vector in human cases of Lyme disease has biased scientific thought on this topic for many years. For example, in an investigation of the efficacy of a single dose of doxycycline administered shortly after a tick bite as a preventative treatment for Lyme disease, the “primary end point” for defining a case of Lyme disease “was the development of erythema migrans at the site of the tick bite” (9).
This study, published in the influential New England Journal of Medicine in 2001, is notable for two reasons. Although the authors concluded that a “single 200 mg dose of doxycycline administered within 72 hours” of a tick bite prevented Lyme disease, the study design excluded persons who did not develop an EM rash as evidence of Lyme disease. Therefore, the data shows only that treatment prevented the development of an EM rash. Additionally, the entomological data presented in the paper showed that an EM rash appeared at the tick bite site only when the person had been bitten by the nymph stage tick. Therefore only patients bitten by nymph ticks met the inclusion criteria for the secondary determination of whether the prophylactic treatment was a success.
A more probable scenario that can be derived from the data is that persons bitten by an adult tick do not develop an EM rash. These people were excluded from the rest of the study, but may have still developed Lyme disease. An alternative hypothesis that can be derived from the data is there may be as yet unexplored differences between the nymph and adult tick life stages in terms of the mechanics of the biting process and possibly the range of pathogens and/or interactions among pathogens carried by each. The role of adult ticks in the transmission cycle of Lyme disease in humans is therefore still unknown.
To date, this study has never been repeated, and all other studies on tick bites and disease transmission have involved animal models and nymph stage ticks. Although completed over 15 years ago, there has been no followup assessment of the efficacy of administering a single dose of doxycycline at the time of a tick bite to prevent the development of other Lyme disease symptoms, or if this approach would work to prevent Lyme disease if a person is bitten by an adult stage tick. Because it was published in an influential journal, however, this single study is the only “evidence” that can be cited to support the recommendation to physicians that treating a patient with a tick bite with a single prophylactic dose of doxycycline will prevent them from developing Lyme disease.
Other published clinical studies have provided conclusive evidence that in clinical practice, the EM rash is present in only a minority of Lyme disease cases (10), and that the EM is only weakly associated with any Lyme disease symptom other than arthritis. Despite this, the EM rash continues to be used as a diagnostic standard and a treatment end point, with the CDC standing behind its oft-repeated public health recommendation that an EM rash will be the primary sign of Lyme disease 60-80% of the time.
Little scientific evidence to support “Post-treatment Lyme disease syndrome”
Since their discovery and development as drugs in the 1950s, antibiotics have been thought of as a “magic bullet” capable of curing infectious diseases caused by bacteria. Antibiotics had been used so successfully against bacterial diseases that Dr. William H. Stewart, the U.S. Surgeon General from 1965–1969, has been quoted as having said, “It is time to close the book on infectious diseases, and declare the war against pestilence won.” In 1982, this was still a strongly held belief.
Once a bacterium was determined to be the cause of the epidemic of “Lyme arthritis” in the early 1980s, the next step was to determine which antibiotics should be used for treatment. The first investigation of the efficacy of antibiotic treatments for Lyme disease was published in 1983
The data presented in this seminal study indicated that nearly 50% of antibiotic treated patients continued to experience debilitating symptoms post-treatment. However, the study authors surprisingly concluded that for patients with “early” Lyme disease, 10 – 14 days of tetracycline was an effective treatment. After reviewing the data, it should be asked how the researchers were able to reconcile data showing a high rate of treatment failure with their conclusion that 10 – 14 days of an antibiotic was an effective treatment for Lyme disease.
At the time this study was conducted, infectious diseases caused by bacteria were no longer considered to be a significant threat to human health. While that simplistic view has been shown over the past two decades to be false and short-sighted, in 1984 research that appeared to show an antibiotic failing to effectively treat a bacterial infection deeply conflicted with prevailing medical dogma.
Because the research findings did not support the precept that antibiotics never fail, the data was rearranged in such a way to create the artificial impression that the vast majority of Lyme disease patients recovered fully after completing a standard antibiotic regimen of 10-14 days.
Specifically, the data on patient outcomes was broken down into two groups – patients who experienced “Major” symptoms after the antibiotic treatment vs. those with “Minor” symptoms. “Major” symptoms were defined as those a physician would be trained to perceive as clinical “signs” of Lyme disease, including a recurrence of the EM rash and/or severe and potentially life threatening meningitis, carditis, or arthritis with noticeable swelling of the joint. Patients who experienced post-treatment “Major” symptoms were considered treatment failures. Few people in any of the treatment groups developed these “Major” conditions.
“Minor” symptoms were defined as those a physician would be trained to perceive as disease “symptoms” as opposed to a “sign.” In medical practice, symptoms are considered more “subjective” because they were based on a patient’s description of their personal experience. In the “Minor” symptoms group, patients showed symptoms of arthritis without apparent joint swelling, tachycardia, cranial nerve palsy, peripheral neuropathy, severe fatigue, headaches, and changes in mental function. While these symptoms greatly impaired the patients’ quality of life, they were interpreted as a treatment success, not antibiotic treatment failures.
A critical analysis of the data presented in this paper clearly shows that nearly half of the patients enrolled in this study were left with post-treatment symptoms. The study authors justified their conclusion that 10-14 days of an oral antibiotic was an effective treatment for Lyme disease by discounting the symptoms they quite subjectively and arbitrarily determined to be “Minor,” with no regard for th degree to which these symptoms impaired the patient’s quality of life.
Other studies have yielded similar results. In one such study titled “Failure of Tetracycline Therapy in Early Lyme Disease,” 100% of tetracycline-treated Lyme disease patients were left with the same painful and debilitating post-treatment symptoms deemed to be “Minor” (but not treatment failures) by Steere, et al. in 1983 (12). The authors of this study concluded that more research was needed to assess the true efficacy of the standard antibiotic treatment paradigm on Lyme disease patients. Yet, the CDC continues to support the recommendation that Lyme disease at any stage in the infection is curable by a short treatment with doxycycline.
An unfortunate but entirely avoidable outcome of the bias introduced and perpetuated in those early studies is that Lyme disease patients who continue to suffer debilitating joint pain, peripheral neuropathy, severe fatigue, tachycardia, and other symptoms after the recommended 10 – 14 days of antibiotic treatment, are now relegated to a nebulous medical state called “Post-treatment Lyme disease syndrome” (PTLDS), or sometimes just, “Medically Unexplained Symptoms.” This moniker establishes the baseless implication that the original infection was successfully treated, and that symptoms are due to some other cause. As there is diagnostic code among the International Classification of Diseases (ICD) medical coding system for this particular medical state, patients seeking medical help for their ongoing symptoms often must do so without insurance reimbursement.
Current competing hypotheses to explain so-called PTLDS include: 1.) continuing infection by bacteria that survive antibiotic treatment and precipitate chronic inflammation; 2.) the presence of remnants (including DNA) of dead bacteria in tissues precipitating chronic inflammation; 3.) an autoimmune type of reaction; or 4.) the overactive imaginations of people with nothing better to do than complain to their doctors about the pain of their daily lives (13).
The preponderance of the scientific evidence strongly points to persisting infection by antibiotic tolerant forms of several different Borrelia genospecies, along with comorbid infections caused by other tick-borne microorganisms, as the underlying cause of the chronic disease symptoms seen in both untreated and treated Lyme disease patients. Past and present research on the biology of Borrelia provides considerable insight into how these bacteria are able to cause chronic disease in humans.
The remarkable biology of Borrelia
Although the CDC insists the proportion of Lyme disease patients who have continuing disease after short term antibiotic treatment is in the range of 10-20%, the scientific evidence, including that which was presented in the earliest published studies, indicate this number to be significantly higher (30-50%). That many Lyme disease patients experience new onset or recurring symptoms after treatment
Is explainable within the context of the natural biology of infection by Borrelia and other tick-borne pathogens.
Borrelia are a type of bacterium called a spirochete, based on their appearance as a slender, twisted rod when observed under the microscope. Spirochetes are known to have a drill-like motility enabling easy movement through viscous solutions and penetration through collagen-rich tissues.
The biology of Borrelia is vastly different from other bacteria. They have an exceptionally complex genome. Because they evolved to be totally dependent on a host animal, Borrelia lack genes for many metabolic traits common in their free-living counterparts. Their reproductive strategies do not include rapid growth to large numbers, followed by a release of toxins to facilitate quick dispersal to new hosts. As such, they also lack genes for the known classic bacterial virulence factors, such as exotoxins and endotoxins (14). The pathogenicity of Borrelia is associated with slow growth and periods of no growth, which is more akin to the pathogenic approach taken by Mycobacterium tuberculosis, the cause of tuberculosis and a bacterium which is known to persistently infect as much as one-third of the world’s population, according to the World Health Organization.
The Borrelia genome evolves rapidly, with substantial genetic variation even within a single generation. There are hundreds of different genospecies of Borrelia, each known to prefer different host tissues (such as skin or joints, cardiac or nerve tissue), which may help explain the broad range of clinical symptoms observed in Lyme disease patients (14). For example, genospecies of Borrelia that localize to the skin (and produce an EM rash) may also localize to joint tissue due to the collagen-rich nature of these tissues, causing symptoms of arthritis. Other genospecies localize to regions of connective tissue associated with the membranous linings of the heart or nervous systems, leading to carditis or neuropathology.
In nature, Borrelia is at home as a “commensal” living in relative peace within small mammal hosts such as mice. Borrelia infection is permanent in their natural hosts, and although mice develop antibodies against the bacteria, the infection generally does not lead to disease. Ticks pick up the bacteria when they feed on infected mice or birds, and then transfer the bacteria to humans when they take their next blood meal (15).
Ecological relationship between the bacteria, ticks, and host are important considerations in Lyme disease for several reasons. To establish a permanent infection, the bacteria must communicate with their host to suppress the parts of the immune response that would lead to their destruction. In their natural host, this communication is largely successful and the bacteria are permitted to establish permanent residence and tap into host resources to survive (16).
Humans are not a natural host for Borrelia or other tick-borne microbes. As longer-lived animals, bacterial infections trigger a more complex immune response and attempts to establish a commensal relationship are not entirely successful. As a result, presence of the bacteria in a human host triggers inflammation and other “innate” responses (16). Baumgarth and others have provided conclusive evidence that Borrelia have the ability to disable the switch from the innate to the more specific “adaptive” immune responses, which includes the production of antibodies capable of sterilizing the infection (17, 18). The net result is a type of “frustrated commensalism” between Borrelia and a human host, one in which long term infection is established but accompanied by a waxing and waning state of immune system activation (16).
The inherent ability of Borrelia to suppress the production of antibodies in humans is highly significant. In the U.S., the most widely used blood tests for Lyme disease diagnosis are the ELISA and the Western blot. These are assays that detect antibodies produced by a human host to neutralize specific proteins (called antigens) located on the surface of Borrelia burgdorferi spirochetes. The inherent design flaw in a test that relies on an infected human producing sufficient quantities of specific antibodies, when the bacteria suppress antibody production, is obvious.
The specificity of the interaction between the antigens used in development of Lyme disease blood tests and the antibodies detected in those tests, presents an additional problem. Different genotypes of Borrelia capable of causing disease symptoms in humans do not all have the same surface antigens as Borrelia burgdorferi. Even within the same generation, individual cells of Borrelia have the genetic ability to vary expression of surface antigens to further thwart antibody production (19). These biological characteristics provide an additional reason why Lyme disease tests based on detecting high levels of specific antibodies against Borrelia burgdorferi in a person’s blood are simply inadequate as a diagnostic tool.
One additional factor is the biological ability of Borrelia to take different cellular forms. Best known and commonly portrayed in the spirochete form, Borrelia also develop rounded forms called “round bodies” or RBs, which have been observed in studies dating back several decades. Recently it has been shown that the surfaces of the spirochete and RB forms of Borrelia are different (20). The existing diagnostic tests for Lyme disease find antibodies in blood produced against cell surface antigens found on the spirochete form of the cell, only.
The remarkable biology of Borrelia contributes greatly to the inadequacy of antibody-based tests as a diagnostic tool for Lyme disease. The experimentally determined sensitivity (probability of detecting a disease) of the ELISA test, applied as a “screening” or “first tier” test that must be positive before the more specific Western blot is even done, is less than 50% (21). Due to test unreliability, Virginia (Va. Code Ann. § 54.1-2963.2) and Maryland (Md. Code Ann., Health Law § 20–1701) have passed laws stipulating that physicians must inform their patients that a negative result on a blood test does not mean they do not have Lyme disease.
As previously mentioned, Borrelia responds to adverse environmental changes (such as when exposed to antibiotics) by changing from motile spirochete form into RB forms. RBs are dormant with little or no metabolic activity, such as protein synthesis or DNA replication. Antibiotics work by disrupting cell metabolism, and therefore the dormant RBs are antibiotic tolerant “persister” cells. As the name implies, RBs persist in their dormant state but are capable of reactivation when conditions improve, leading to resurgence in bacterial numbers and disease symptoms (22).
Notably, a significant recent research finding shows that antibiotic tolerance due to Borrelia persisters is actually induced by exposure to the antibiotics routinely used as front-line treatment approaches for Lyme disease (23).
An additional biological factor that contributes to antibiotic tolerance in Borrelia is biofilm growth. Biofilms are sessile communities of bacteria, and biofilm-based bacterial cells are biologically different from the “planktonic” (motile and metabolically active) forms.
Biofilms of Borrelia have been directly observed in studies conducted on culture-grown bacteria, and now also have been shown to form in human tissues (24). Borrelia is known to preferentially localize to collagen containing tissues – skin, the joints, the linings of the heart, and the membranes of both the central nervous system (from where they sometimes spill into the highly protected interior and cause meningitis) and peripheral nervous system. Biofilms of Borrelia in these protected tissue sites may serve as a source of the bacteria detected during resurgence events.
Persistent infection by Borrelia, relying on biofilm growth and persistent round body forms, is the rule in nature and not the exception for all of the genospecies of this bacteria discovered to date. This has been repeatedly, and conclusively, shown in numerous studies conducted on animal models (mice, hamsters, dogs, and non-human primates) and recently, in humans (25).
Combined, these research results provide an explanation for why a few weeks of antibiotics does not always result in complete resolution of disease symptoms, or prevent a recurrence of disease symptoms weeks, months, or years after the initial infection occurred.
The sizeable body of research on the microbiology of Borrelia, the disease as it occurs in animal models, (particularly non-human primates which are excellent models of human disease), and the variability of the clinical disease manifestations in humans reveals the false dichotomy exhibited by defenders of the current Lyme disease status quo who proclaim there is “No Evidence” in support of the hypothesis that 10-14 days of an antibiotic is not a curative treatment. This false and circular argument is an “appeal to ignorance” that attempts to shift the burden of proof in the contentious debate over whether differing treatment approaches (longer therapy, pulsed dosing, different antimicrobial agents) would provide better patient outcomes in Lyme disease.
There is abundant scientific evidence supporting the hypothesis that persisting infection by antibiotic tolerant forms of Borrelia, and/or comorbid tick-borne infections may be the underlying cause of the chronic inflammation that precipitates persisting, recurring, or post-treatment Lyme disease symptoms. A lack of research, or over-reliance on evidence derived from poorly designed studies that have been interpreted with extreme bias, are not the same as “No Evidence.”
The medical construct of Lyme disease must be revised to match the science
The current medical construct of Lyme disease, rooted in the earliest published studies from 1977, describes a disease that is entirely inconsistent with the disease as it is experienced by patients. Clinically, the current medical construct for Lyme disease describes an infectious disease caused by one single genospecies of a specific bacterium (Borrelia burgdorferi), in which the initial infection leaves behind a tell-tale EM rash as a clear objective sign, for which there is a reliable, antibody-based blood test. Lyme disease is additionally considered to be easily and fully treatable with routine doses of antibiotics.
A complete and unbiased review of the scientific literature shows clearly that the above Lyme disease construct is only one manifestation of a complex, systemic disease. In actuality, the disease rarely begins with an EM rash, and nearly 50% of the time evolves into a disabling chronic disease with a myriad of disabling symptoms. The current “gold standard” blood tests for Lyme disease are only effective when high levels of specific antibodies are produced, but Borrelia employ immune evasive strategies to skew or suppress antibody production. In addition, conclusive scientific evidence shows that B. burgdorferi is only one of many disease-causing genospecies of Borrelia, that Borrelia cells can exist in nearly “invisible” forms, and that Lyme disease may involve other comorbid infections, none of which are directly detected by the existing diagnostic blood tests for Lyme disease (26).
While the patient narrative for Lyme disease matches the existing medical construct about half the time, the other 50% of patients describe a completely different disease process. With nearly 400,000 new cases of Lyme disease diagnosed each year, the number of people in the U.S. with long term debilitating symptoms and chronic disease precipitated by a tick-borne infection can be estimated at over 150,000 people per year. Compounded over many years, there are millions of people in the U.S. with chronic disease stemming from diagnosed and undiagnosed Lyme disease. Studies show that people with chronic Lyme disease symptoms have significantly lower life functioning ability (27), and this comes at considerable cost to the U.S. healthcare system (28).
Existing and emerging research shows that in nature, most genospecies of Borrelia cause persistent infections in animals, including humans. This same body of science also strongly implicates coinfections with other tick-borne microbes as the cause of many of the problems associated with Lyme disease diagnosis and treatment (29, 30).
From the meager scientific data accumulated from studies done with human subjects treated with antibiotics, the only conclusion that can be legitimately reached is that short-term antibiotic treatment makes an EM skin rash subside. There is currently no existing published research studies done with human subjects that addresses the efficacy of antibiotic therapy on any other manifestation of Lyme disease, particularly those in which patient complaints are not considered “signs” in the medical sense. The so-called “subjective” symptom – heart issues, joint and muscle pain, overwhelming fatigue, and cognitive disruptions -- significantly impair the quality of life for Lyme disease patients. More research on treatment approaches for all forms of the disease are desperately needed.
Lack of leadership on the part of the NIH and CDC has left a void in the knowledge needed to successfully lessen the disease burden on millions of past, present and future Lyme disease victims. Because of a recent influx of funding from private philanthropic individuals and groups, microbiological and clinical research that should have taken place 30 years ago is currently underway at several leading research universities across the country. There is hope that this research will lead the way to a better understanding of the microbiology and pathology of Lyme disease, along with a broader recognition of the health burden Lyme disease places on both individuals and society. With this knowledge must come a long overdue commitment of publically funded initiatives to address the public health disaster that Lyme disease has been allowed to become.
An ethics construct
Ethical concerns in Lyme disease medicine are glaring, particularly regarding both evident bias in the prevailing guidelines and issues surrounding informed consent. These are certainly pertinent in the broader context of patient beneficence and autonomy. As for the moral principle of non-maleficence, the other side of beneficence, its relevance was recently addressed in Jariwala et al. (31). The time-honored principle of beneficence requires that physicians act in their patients’ best interests. Patients’ well-being overrides any interests of others – physicians, institution, insurance, etc. The modern notion of autonomy insists that patients are the primary decision-makers regarding their healthcare. Autonomy has become a cornerstone in medical ethics due to the recognition that patients are persons in the full moral sense, that is, by virtue of being persons they possess moral status and therefore certain inviolable moral rights, principally the right of self-determination. These principles incorporate the moral rule of informed consent. Failure to properly inform patients by not acknowledging the clear controversy surrounding Lyme disease diagnosis and treatment and excluding viable treatment options violates both beneficence and autonomy.
As the start, none of this suggests that science and politics must never mix. Indeed, they do. Good science and ethics drives morally sound policy. However, policy grounded on skewed science is bad policy. Consider the issue of undue bias. Increasingly evident is the deliberate selectivity of data to fashion policy that sustains the orthodox paradigm regarding Lyme disease, a paradigm squarely outdated when considering accumulating scientific evidence as to the biology of infection caused by Borrelia and downplaying numerous patients’ symptoms affecting their qualities of life.
There are clearly dissenting positions regarding diagnosing and treating Lyme disease. Yet guideline panels appear to have stacked the deck rather than pursuing the imperative to seriously examine the evidence. While knowledgeable and respected scientists represent the orthodox position regarding Lyme disease diagnosis and treatment, there are equally competent and experienced scientists as well as clinicians on the front lines with first-hand clinical exposure to patients suffering from symptoms of Lyme disease and familiar with patients’ histories and symptom trajectories. These clinicians hold positions at odds with the official dogma. Yet their voices are quelled when not allowed at the table in addressing guidelines. Eliminating dissent shows little respect for acknowledging diverse positions. In the process, it short-circuits the reasonably sufficient information patients need in order to consent to treatment.
This explains why, in November 2006, Connecticut Attorney General Richard Blumenthal launched an anti-trust investigation into the influential Infectious Diseases Society of America (IDSA) guidelines that established the medical standard of care regarding Lyme disease diagnosis and treatment. This was the first instance of antitrust inquiry into treatment guidelines’ process (32). The power that IDSA wields is apparent on multiple levels. Not only do its members act as peer reviewers for various medical journals, but the organization itself publishes The Journal of Infectious Diseases and Clinical Infectious Disease, both considered preeminent journals specializing in infectious diseases.
In their 2010 analysis, attorney Lorraine Johnson, JD, MBA, and hematologist Raphael Stricker, MD carefully lay out specific problems with those guidelines (33). Since both authors are affiliated with societies opposing the guidelines, notably the International Lyme and Associated Diseases Society (ILADS), their study itself is not without bias. Nonetheless, they cite how Blumenthal’s office noted problems regarding conflicts of interest, particularly financial, over-dependency on certain expert opinion already favoring the official status, false appearance of unanimity, and others. But the most striking flaw in the guidelines lies in the non-acknowledgement of the fact of clear controversy, thereby minimizing any efficacy to alternative treatment. As described later, this limitation impairs the legitimacy of informed consent.
Spurred by Blumenthal’s anti-trust inquiry and after close review of the IDSA guidelines and hearing arguments supporting and opposing them, an ISDA review panel issued a final report in April 2010. In fairness to IDSA, bear in mind that not all its members support the official line. Some who opposed requested seats on the review panel. Their requests, however, were refused on the tenuous reason that seating was already filled, even though panel membership later increased (32). Moreover, two months prior to the final report, Blumenthal’s office expressed concern over the review panel’s voting procedures. Nonetheless, the concluding report, chaired by former IDSA president Carol Baker, upheld the earlier guidelines with a nearly unanimous vote. The decision strongly rested its case on the argument that there was no solid evidence indicating absence of benefit to Lyme disease patients from standard antibiotic treatment after one month. In the face of counter arguments from ILADS, this conclusion is a classic example of the fallacy of appeal to ignorance, the wrongheaded argument that lack of evidence to the contrary claim constitutes evidence, thus begging the question regarding the diagnosis of Lyme disease.
Clustered together, biases described earlier -- that the EM rash and arthritis with joint swelling are clear “signs” of Lyme disease, that the disease is regionally limited to the northeast and only during summer months, and that it is inflicted by ticks in lymph stage -- seem to indicate a more serious underlying disposition, referred to as “confirmation bias.” Confirmation bias arises when professionals with pre-established premises and conclusions and, particularly if sitting on committees or panels to design clinical practice guidelines, with obvious or subtle conflicts of interest, examine and interpret data in ways that strengthen and support their own presuppositions. Surely, human bias is natural, but clearly hazardous when it determines standards of medical care, thereby influencing public opinion, determining insurance coverage, and, in turn, impacting patients’ health and well-being, breaching patient beneficence.
Confirmation bias is more than simply the “inattentional blindness” that can beset us when we assume we’ll notice what stands out from the ordinary, the unexpected “gorilla” on the basketball court (34). Confirmation bias is tainted with a certain quality of deliberateness and intention, perhaps unconscious, to behold and fashion evidence in ways that confirm our strongly held beliefs. It is this disposition to see what one seeks that reflects confirmation bias, a process counter to scientifically sound research that demands examining evidence as impartially as possible. The science on the biology of Borrelia infection and intricacies of symptoms described earlier offers an up-to-date scientific base that offers more solid ground for policy.
Controversy in the Lyme debate fundamentally revolves around whether or not the disease persists after standard treatment to become chronic Lyme disease. That is, does chronic Lyme disease exist? It appears that the weight of scientific studies supports that it does. Why then are other treatment approaches not alluded to or explained when informing patients of treatment options? If these are excluded from discussion, there are insufficient grounds for properly informed consent.
Issues regarding informed consent, the cornerstone of modern healthcare ethics in reflecting the vital moral principle of patient autonomy, typically arise in the context of patients about to undergo a specific procedure, often radical or invasive. Nonetheless, it applies more generally to diagnosis and proposed treatment. Lyme disease is no exception. Hence, the central concern lies in whether sufficient grounds for informed consent exist when the informing process excludes competing views of the condition and accompanying treatment options. The notion of informed consent therefore needs further unpacking.
Genuine informed consent is more than merely fulfilling the institutional requirement of signing a consent form. It is a complex process that entails a rich communicative dynamic requiring that patients be sufficiently informed before they can offer consent, both voluntarily and competently. In the case of Lyme disease, the first ingredient of being sufficiently informed is directly relevant.
Whether the patient is sufficiently informed pertains to the what, the how, and who of a proposed medical procedure. Surely this does not necessitate conveying all information – this is not possible – but information directly germane to the patient’s decision-making is required. Moreover, it is vitally important to bear in mind that properly informing a patient of the procedure, rationale, risks, benefits, and reasonable options means that the informing is not simply content-driven. In their illuminating Rethinking Informed Consent in Bioethics, philosophers Neil Manson and Onora O’Neill underscore the original meaning behind “to inform” -- to give form and shape, as in sculpting (35). Informing, therefore, is not merely a matter of transmitting content, but unavoidably involves process and context. The authors carefully discuss how information solely as content rests upon a strict mathematical, misguided model of information and communication, and this conduit model of the physician simply delivering information as data is incomplete.
Disclosure as strictly content distorts both information and communication since it obscures context, assumed norms, claims, and inferences. Manson and O’Neill examine the process of disclosure linguistically as consisting in speech acts, more especially truth claims. In applying all this to Lyme disease, consider treating patients bitten by a tick and possibly having the disease. Examples of truth claims would be “You may have Lyme disease,” “One sure sign of the disease is a small circle with a bulls-eye,” “Our standard way of treating the disease is to give you a 10-14 day regimen of antibiotics,” “This should be enough to prevent the disease from spreading.”
Here is where context is crucial. For the patient, and each patient is unique, truth claims like these are meaningful within the framework of his or her desires, beliefs, values, and expectations. To properly inform the patient, the claims in themselves must be both true (accurate) and truthful (honest). And being honest demands that one avoids being evasive. Even if the information is accurate, information can still be evasive, therefore dishonest.
To repeat, truth claims in the disclosure process must be both accurate and honest. If not, then there are no legitimate grounds for consent, since informed consent only makes sense if one is so informed. All this revives ways of re-examining the complex interactive dynamic of informed consent. Regarding Lyme disease, informing patients of the standard diagnosis and treatment protocol without acknowledging the unmistakable controversy over diagnosis and treatment and precluding any information as to alternative treatments offers accurate information to a degree, but remains evasive, untruthful, and therefore constitutes no ground for consent.
The patient is the center of moral concern in healthcare. Shifting the center of interest to other stakeholders violates patient’s personhood, dignity, well-being, and autonomy. Consider three fundamental questions when patients seek treatment. First, what is wrong? What is the condition from which the patient suffers? Next, what can be done about it? Third, what should be done about it? This latter reflects the patient’s own value systems and moral priorities. It ought to be the patient herself who decides this. As for the first two questions, they remain in the realm of medical expertise, and it is the physician who must address them. Given the clear controversy surrounding Lyme disease, it is imperative that physicians be honest with their patients to convey the complexity as well as possible and reasonable treatment options. Anything short violates the sacred covenantal relation between doctor and patient.
1. Mission, Role and Pledge| About | CDC. Cdcgov. 2017. Available at: https://www.cdc.gov/about/organization/mission.htm. Accessed August 21, 2017.
2. CDC Online Newsroom | Press Release | CDC provides estimate of Americans diagnosed with Lyme disease each year. Cdcgov. 2017. Available at: https://www.cdc.gov/media/releases/2013/p0819-lyme-disease.html. Accessed August 21, 2017.
3. Steere A, Malawista S, Snydman D et al. An epidemic of oligoarticular arthritis in children and adults in three connecticut communities. Arthritis & Rheumatism. 1977;20(1):7-17. doi:10.1002/art.1780200102.
4. Barbour A. Lyme disease: A tick-borne spirochetosis. Clinical Microbiology Newsletter. 1983;5(16):110-111. doi:10.1016/s0196-4399(83)80061-0.
5. Steere A. Erythema Chronicum Migrans and Lyme Arthritis. Annals of Internal Medicine. 1977;86(6):685. doi:10.7326/0003-4819-86-6-685.
6. Hanrahan J, Benach J, Coleman J, Bosler E, Grabau J, Morse D. Epidemiologic Features of Lyme Disease in New York. Yale J Biol Med. 1984;57(4):643-650. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2590009/pdf/yjbm00100-0190.pdf.
7. Osterholm M, Forfang J, White K, Kuritsky J. Lyme Disease in Minnesota: Epidemiologic and Serologic Findings. Yale J Biol Med. 1984;57(4):677-683. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2589986/pdf/yjbm00100-0222.pdf.
8. Radolf J, Caimano M, Stevenson B, Hu L. Of ticks, mice and men: understanding the dual-host lifestyle of Lyme disease spirochaetes. Nature Reviews Microbiology. 2012. doi:10.1038/nrmicro2714.
9. Nadelman R, Nowakowski J, Fish D et al. Prophylaxis with Single-Dose Doxycycline for the Prevention of Lyme Disease after an Ixodes scapularis Tick Bite. New England Journal of Medicine. 2001;345(2):79-84. doi:10.1056/nejm200107123450201.
10. Stonehouse A, Studdiford J, Henry C. An Update on the Diagnosis and Treatment of Early Lyme Disease: “Focusing on the Bull's Eye, You May Miss the Mark”. The Journal of Emergency Medicine. 2010;39(5):e147-e151. doi:10.1016/j.jemermed.2007.06.007.
11. Steere A. Treatment of the Early Manifestations of Lyme Disease. Annals of Internal Medicine. 1983;99(1):22. doi:10.7326/0003-4819-99-1-22.
12. Dattwyler R, Halperin J. Failure of tetracycline therapy in early lyme disease. Arthritis & Rheumatism. 1987;30(4):448-450. doi:10.1002/art.1780300414.
13. Sigal L, Hassett A. Contributions of Societal and Geographical Environments to "Chronic Lyme Disease": The Psychopathogenesis and Aporology of a New "Medically Unexplained Symptoms" Syndrome. Environmental Health Perspectives. 2002;110(s4):607-611. doi:10.1289/ehp.02110s4607.
14. Tilly K, Rosa P, Stewart P. Biology of Infection with Borrelia burgdorferi. Infectious Disease Clinics of North America. 2008;22(2):217-234. doi:10.1016/j.idc.2007.12.013.
15. Brisson D, Drecktrah D, Eggers C, Samuels D. Genetics of Borrelia burgdorferi. Annual Review of Genetics. 2012;46(1):515-536. doi:10.1146/annurev-genet-011112-112140.
16. Nussbaum J, Locksley R. Infectious (Non)tolerance--Frustrated Commensalism Gone Awry?. Cold Spring Harbor Perspectives in Biology. 2012;4(5):a007328-a007328. doi:10.1101/cshperspect.a007328.
17. Elsner R, Hastey C, Olsen K, Baumgarth N. Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection. PLOS Pathogens. 2015;11(7):e1004976. doi:10.1371/journal.ppat.1004976.
18. Berndtson K. Review of evidence for immune evasion and persistent infection in Lyme disease. International Journal of General Medicine. 2013:291. doi:10.2147/ijgm.s44114.
19. Norris S. The vls Antigenic Variation Systems of Lyme Disease Borrelia: Eluding Host Immunity through both Random, Segmental Gene Conversion and Framework Heterogeneity. Microbiology Spectrum. 2014;2(6). doi:10.1128/microbiolspec.mdna3-0038-2014.
20. Meriläinen L, Brander H, Herranen A, Schwarzbach A, Gilbert L. Pleomorphic forms of Borrelia burgdorferi induce distinct immune responses. Microbes and Infection. 2016;18(7-8):484-495. doi:10.1016/j.micinf.2016.04.002.
21. Coulter P, Lema C, Flayhart D et al. Two-Year Evaluation of Borrelia burgdorferi Culture and Supplemental Tests for Definitive Diagnosis of Lyme Disease. Journal of Clinical Microbiology. 2005;43(10):5080-5084. doi:10.1128/jcm.43.10.5080-5084.2005.
22. Hodzic E, Imai D, Feng S, Barthold S. Resurgence of Persisting Non-Cultivable Borrelia burgdorferi following Antibiotic Treatment in Mice. PLoS ONE. 2014;9(1):e86907. doi:10.1371/journal.pone.0086907.
23. Feng J, Shi W, Zhang S, Sullivan D, Auwaerter P, Zhang Y. A Drug Combination Screen Identifies Drugs Active against Amoxicillin-Induced Round Bodies of In Vitro Borrelia burgdorferi Persisters from an FDA Drug Library. Frontiers in Microbiology. 2016;7. doi:10.3389/fmicb.2016.00743.
24. Sapi E, Balasubramanian K, Poruri A et al. Evidence of in vivo existence of Borrelia biofilm in borrelial lymphocytomas. European Journal of Microbiology and Immunology. 2016;6(1):9-24. doi:10.1556/1886.2015.00049.
25. Marques A, Telford S, Turk S et al. Xenodiagnosis to Detect Borrelia burgdorferi Infection: A First-in-Human Study. Clinical Infectious Diseases. 2014;58(7):937-945. doi:10.1093/cid/cit939.
26. Molloy P, Telford S, Chowdri H et al. Borrelia miyamotoi Disease in the Northeastern United States. Annals of Internal Medicine. 2015;163(2):91. doi:10.7326/m15-0333.
27. Aucott J, Rebman A, Crowder L, Kortte K. Post-treatment Lyme disease syndrome symptomatology and the impact on life functioning: is there something here?. Quality of Life Research. 2012;22(1):75-84. doi:10.1007/s11136-012-0126-6.
28. Adrion E, Aucott J, Lemke K, Weiner J. Health Care Costs, Utilization and Patterns of Care following Lyme Disease. PLOS ONE. 2015;10(2):e0116767. doi:10.1371/journal.pone.0116767.
29. Swanson S, Neitzel D, Reed K, Belongia E. Coinfections Acquired from Ixodes Ticks. Clinical Microbiology Reviews. 2006;19(4):708-727. doi:10.1128/cmr.00011-06.
30. Moutailler S, Valiente Moro C, Vaumourin E et al. Co-infection of Ticks: The Rule Rather Than the Exception. PLOS Neglected Tropical Diseases. 2016;10(3):e0004539. doi:10.1371/journal.pntd.0004539.
31. Jariwala N, Ilyas E, Allen H. Lyme Disease: A Bioethical Morass. Journal of Clinical Research & Bioethics. 2016;07(05). doi:10.4172/2155-9627.1000288.
32. Weintraub P. Cure Unknown. New York: St. Martin's Press; 2008.
33. Johnson L, Stricker R. The Infectious Diseases Society of America Lyme guidelines: a cautionary tale about the development of clinical practice guidelines. Philosophy, Ethics, and Humanities in Medicine. 2010;5(1):9. doi:10.1186/1747-5341-5-9.
34. Simons D, Chabris C. Gorillas in our midst: sustained inattentional blindness for dynamic events. Perception. 1999;28(9):1059-1074. doi:10.1068/p2952. http://www.chabris.com/Simons1999.pdf. See Chabris C, Simons D. The Invisible Gorilla. New York: Crown; 2010.
35. Manson N, O'Neill O. Rethinking Informed Consent In Bioethics. Cambridge etc.: Cambridge University Press; 2008.
Since tick borne diseases (TBD) are often a matter of life and death for those who are exposed to a host of vectors and/or are currently suffering with chronic and often disabling symptoms, I respectfully request the following actions be taken:
- A strong recommendation to HHS and others by the TBD Working Group for the transfer or dismissal of those previously or currently involved in any federal TBD related activities. This action is absolutely necessary due to the disastrous way research, education and patient care has been handled for the past three decades by a select few.
- TBD Working Group members should engage in strict oversight and monitoring of federal agencies and their budgets related to TBD. This will ensure the agencies will discontinue abusing a system originally created to provide quality research findings and solid solutions to problems faced by millions of people both nationally and world wide.
- All future TBD and antibiotic related research grants be patient oriented, closely monitored and approved by all TBD Working Group members before funds are released.
- Designate that the majority of government funding for TBD related research be awarded to independent scientific researchers and experienced medical professionals with a history of successfully treating patients with early, late-stage and chronic Lyme and tick borne diseases.
Once these measures are implemented we can all move forward having faith that a much needed change will take place- one that is necessary before we can find a cure for Lyme and many other tick borne diseases. Thank you in advance for your efforts in addressing these concerns.
And don’t forget… do a tick check!
Lucy Barnes, Director
Lyme Disease Education & Support Groups of Maryland
My name is Michael Bauer. I am the Head of Household, father to four children, and husband to Kristina Bauer. I am a well-educated and licensed Professional Engineer, and have been married for 17 years.
My wife, Kristina, was formally diagnosed with Lyme Disease in 2012 and has since traced her contraction of the disease back to over 30 years ago, which puts her Lyme Disease in the “chronic” category. In addition, three of my four children have been diagnosed with Lyme Disease transmitted gestationally through birth. Looking back over nearly 2 decades of marriage, and now for the past 5 years dealing actively with treatment of Lyme Disease, I can personally attest to the significant impact and toll this disease has taken on my wife’s physical, neurological and mental health, as well has the heavy financial burden of treating this otherwise misrepresented and woefully under-recognized disease.
To date, except for the brave and educated medical practitioners that have taken this disease seriously, the general medical profession, the Center for Disease Control, the Infectious Disease Society of America (IDSA), and other governing bodies have done a disservice to those suffering from this disease. In the most egregious of offenses, it is apparent that the treatment guidelines established in the United States in 2000 by the IDSA are now proven to be significantly lacking and under-informed as how to effectively treat Lyme Disease. Further, there is substantial evidence of historical corruption and conflict(s) of interest between IDSA-affiliated Doctors and the insurance industry… but this is not the purpose of my writing today.
My writing to you today is to implore the TBD Working Group to focus on the moral and ethical obligation before you. I believe this obligation entails bringing together diverse and objective subject matter experts to set a course for thorough and aggressive treatment of Lyme Disease. Like other medical “rally-points” throughout recent history in the treatment of Cancer, HIV and even Zika, Lyme Disease warrants the best and brightest medical minds to eradicate this disease… without the burden of perverse financial interests, politics or institutionalized corruption. The citizens of the United States and the suffers of Lyme Disease deserve no less.
I don’t know where to begin to recite the burdens that my wife has carried in dealing with this disease; chronic pain, fatigue and exhaustion, neurological impacts, mental impacts, memory loss, digestive disorders… I could go on. I’ve watched, witnessed and attended-to an otherwise healthy and vibrant person suffer immensely over many years and long before a formal diagnosis. In addition, we are dealing with treatment of three of our four children.
I have spent no less than $100,000 of my hard-earned money in treating my family’s Lyme Disease and I do not see an end in sight. Although the financial requirements to try and treat this disease have taken a toll on my family’s way of life, I am fortunate to be able to provide for them in this manner… there are 10’s of thousands, if not 100’s of thousands, that are not so fortunate. I see this working group and being on the precipice of change; changing the future and outlook of those suffering from Acute and Chronic Lyme disease.
Decades of misdiagnosis, mismanagement and worse can be changed by the honorable conviction of this working group to do the right thing(s). If any of the TBD Working Group members question the validity of Chronic Lyme disease or the transmission of the disease gestationally, then I believe they do NOT belong in this working group. The debate on the existence of both has past and been proven in fact. Similarly, if any of the working group members have conflicts of interests with labs, insurers, or other commercial interests, then they should be removed and replaced by individuals with appropriate expertise and objectivity.
Living in the greatest country on earth, we are blessed with many great fortunes, including highly advanced technology and resources far beyond what other nations are blessed with. Yet, for myriad reasons, Lyme Disease patients have gone under-served for far too long. It’s time, long overdue, that the medical profession, it’s governing bodies, and the researchers and insurers (the Industry) join forces to aggressively address and eradicate this growing epidemic. The call to action is now, and the conduit for action (including funding) is provided for in the 21st Century Cures Act.
Michael J Bauer
I am wondering when the GLA test for the double stranded lambda bacteriophage will be recognized by the committee? I’d also like to know when the committee is going to inform the Lyme community of the truth regarding the amber lambda bacteriophages, especially the amber mutants and their connection to the superinfection of human E.coli? BBB01 - BBB32. I personally know that Pat Smith (one of the members of the committee and DoD) has in fact admitted to number of people within the community that this was a biological warfare agent. She also shared with LDO, Phyllis Marvin, some information regarding having had knowledge of the bacteriophages, to which I have in an email. This information according to Phyllis, has been known since the 1990’s. When will the community be told the truth? The scientific research shows that the ambers infect mast cells, T-cells, macrophages….why aren’t patients being told the truth? Why isn’t the science regarding the missing repressor genes/ stop codons being presented to medical community so they can try to help? Why hasn’t the Lyme community been informed of the cross-kingdom DNA and RNA that’s found in the ambers? Yes, many real advocates in the community are upset with those on the panel who claim to have been advocates, but hid this information from those that trusted them in the community. When will this committee tell the truth about the Cold Springs Harbor Lab experiments and the end results?
The Mayday Project
I'm a former member of the chronic Lyme cult who only got my health back by leaving the cult despite all the threats and intimidation about how I would never get better if I didn't continue to pay "Lyme-literate" physicians (read: modern day snake oil salesmen). I got banned from numerous support groups just for sharing my story about how I recovered and got my life back after a multi-year struggle because my experience doesn't fit the chronic Lyme propaganda. I feel I need to make sure my voice is heard, and some things about their advocacy that poses a danger to public health (not just those who have Lyme) are brought to your attention:
I am deeply concerned, troubled, scared, you name it, by what I have heard has transpired at your hearing the last two days. It pains me that I was unable to attend because I have a job and do not live in the DC area. Narratives are how ideas sell, and you are harming people by letting an antiscience movement that has been deemed a danger to public health spread its narrative instead of making it crystal clear to the public where the science actually stands in this.
Does it not raise major red flags to you how irrational and unhinged these suffering cult members are when they accuse infectious disease researchers of being like rapists? Why would anyone spend years in medical school with the intention of harming people? Does it not raise major red flags to you that most of the "chronic Lyme" community believes that AIDS, ALS, Alzheimer's, Parkinson's, MS, Syphilis and many more health conditions are *all* actually Lyme disease but all of our best scientists and microbiologists can't figure that out?
Are you aware that people are dying because they are told they have "chronic Lyme" when they actually have cancer that would have been treatable had they not been recruited into the chronic Lyme cult? Are you aware that these people are out there in dedicated droves telling patients with degenerative diseases and their family members that they should stop taking their medication that is saving/prolonging their life and spend tens if not hundreds of thousands of dollars treating a nonexistent chronic Lyme infection instead? How would you feel if you found out your mom or dad was dying from ALS and instructed by these people to stop taking their medication because it's poisoning them, and were sent to a "Lyme-literate" doctor who then treated them for chronic Lyme until they passed away? I could go on for hours and hours about things just like this and worse that I've seen, these are just some of the things I see happening so often it's expected and normal to me at this point.
These are not extreme cases these are things I see happening to people every day. Parents falsely believe all of their children have congenital Lyme and these kids grow up spending their entire childhood being told they have chronic Lyme and being treated at great cost for a disease that they don't actually have. It's not uncommon to see women claim that 4+ kids of theirs were all born with Lyme disease. These are not the type of people whose opinions should be taken into consideration when it comes to actual Lyme disease.
And why is it that almost all of the people pushing the "chronic Lyme" narrative are middle and upper-class, and in particular, white women. Why are other races and lower-class citizens seemingly immune from getting chronic Lyme? Shouldn't minorities be getting infected at the same rates as white people? What is the chronic Lyme cult's explanation for this disparity?
Why are you even entertaining this complete manufactroversy and ignoring the scientific evidence and giving a platform to a pseudoscientific cult-like community? You are allowing them to spread their narrative and falsely claim legitimacy when they have no credible scientific backing or evidence behind their claims. You need to change the narrative before they hurt countless more people.
I understand it is harsh to call them a cult, but having believed all of their propaganda and having been part of the cult myself that is the most accurate word to describe how these communities operate. To this day I am still threatened that I am delusional for thinking my health is better and I will regret believing I am better when it "comes out of remission" and I am more sick than ever. I'm constantly told that I am a paid shill for the CDC because it's impossible for people to get better without snake oil treatments like I did and other absurd reasons.
I honestly didn't know how to explain the experience until watching Leah Remini's show about Scientology, when I had an epiphany and suddenly realized for the first time that you could change out the name "Scientology" for "Chronic Lyme" and make it about exploiting sick people instead of a religion, and it would be essentially the same show.
Please listen to actual experts and credible scientists and not the propaganda of sick and suffering people who are being exploited due to their desperation, nor the charlatans who exploit them (whether knowingly or unknowingly).
If you have any questions for me or would like to better understand what the chronic Lyme community is truly like I would be happy to tell or show you anything you want to know. They have caused me and countless others too much harm for me to stay silent, the least I can do is speak up, especially when most who want to are too scared to or have a life to live and don't want to be under constant attack just for speaking up.
Thank you for your time, and I beg you to side with science rather than continuing to give a pseudoscientific cult and those who exploit them a platform to spread more misinformation and cause even more harm than they already have.
With the utmost sincerity,
Below is an excerpt from one of my journal entries from last January, a time when I was feeling especially frightened, anxious, hopeless - and above all, abandoned by the medical community. I hope it highlights the daily plight of someone like myself, someone who battles with chronic Lyme Disease and co-infections on a day to day basis.
January 15, 2017
“Today marks the 15th day of random, “wandering” leg muscle cramps and pains. I say wandering because one minute my right thigh will hurt or cramp or twitch, the next minute it will be my left calf, etc. There’s no pattern to it. We can add that to the already long list of symptoms presumably caused by Lyme disease (and likely another tickborne co-infection that is yet to be diagnosed) and I’m constantly about 30 seconds away from breaking down and crying lately. I’m tired on good days and exhausted on bad ones. Most days, there’s nerve pain down both arms into my fingers. Random other muscles in my body hurt, I have a varying left eye twitch, headaches, and brain fog. Oh, the brain fog – I will be in the middle of talking to someone and lose my train of thought or I can’t remember a word. I feel like I’m a terrible listener lately because people tell me things and then I don’t remember pieces of it. Or, I’ll tell someone something and then forget if I said it outloud or not.
My anxiety is through the roof; and due to all of these symptoms and the increased anxiety, I am constantly worrying that I have any number of fatal diseases or crises happening to me. I feel legitimately insane and am afraid if I speak of these fears outloud, other people will also think I’m crazy… and I wouldn’t blame them. I wake up in the middle of the night to readjust my heating pad to some other part of my body that hurts at the moment. I also wake up in the middle of the night with what can only be described as mini anxiety attacks over why my body is hurting so much.
All of this has only recently (the last 6 months or so) gotten so bad. I’d had knee pain and headaches and general fatigue for awhile and used to joke “it’s probably Lyme disease again” (I first was diagnosed with it in high school). I used the excuse that it would cost too much to go see my doctor and have labwork done because despite having health insurance, I have a very high deductible. 3 months ago, I finally made an appointment to go see my new PCP who agreed that my symptoms sounded like Lyme disease and ordered bloodwork – also a thorough workup to check my thyroid, liver function, adrenals, etc and test for autoimmune disorders like arthritis and gout. I got the call a few days later from a nurse telling me my initial ELISA test was positive and the Western blot would confirm it, but the doctor wanted me to start Doxycycline right away. A few days into the Doxycycline and I began to notice an increase in the severity of my symptoms (now I know it’s called a Herxheimer reaction). My doctor’s office then called to confirm that the Western blot test showed 7 out of 10 positive bands and told me to keep taking the Doxycycline despite my worsening symptoms. Okay, a week later and I was in hell… cue the start of me feeling like I was going crazy. I was told that this is common with Lyme and to keep taking my antibiotic. The usual 21 day dosage was increased to 30 days as I wasn’t getting better. At my follow-up a few days after my last dose, I told my doctor I was feeling about 75-80% better and she replied that this was normal and I may have some “post-Lyme symptoms” for a little while. She filled out my FMLA paperwork for work (in case I needed to miss work due to follow-ups or occasional bad days) and I was sent off.
Fast forward 1.5 months and my symptoms have all returned, plus new ones. A family member had told me about this Lyme Literate Medical Doctor her family was going to but as insurance won’t cover “chronic Lyme”, it was all out of pocket (re: cash). So I put it off. I figured my PCP would be able to treat me for this simple infection and then I’d be all cured and on my merry way again. Except... I was so very wrong. When I began to feel worse again, it finally hit me – I need to invest in my own health because if I don’t now, I could die from this. My body is telling me – and has been telling me for years – that something is wrong. No more thinking to myself that I must just be tired because I’m out of shape, or achey because maybe I’m just getting older (and I’m only 29). No more denying that I’ve slowly been getting worse, not better.
Tomorrow is my appointment with this specialist. I have a notebook with symptoms listed, questions to ask, and to take notes as I sit with him. He will test me for other co-infections as well as run another test for Lyme disease. Although maybe I was one of the “lucky” ones in the sense that both times I’ve been tested for Lyme, they have always come back positive – so I haven’t had to go through the whole thing of doctors telling you you don’t have it because the test would’ve been positive, misdiagnosing with other things, etc. Yet I am both anxious and also terrified for tomorrow’s appointment. I want to get better but I know I have a long road ahead and I’ve already had a taste of how hellish it can be when experiencing a Herxheimer reaction while on antibiotics. But I do know this, and this is what’s been keeping me going: I want my life back. I want to feel pain-free and normal again. I want to be able to tell someone, honestly, that I’m good when they ask how I am. I want to have a clear head to be able to think straight and remember things. I want this anxiety and depression to stop. I want to have a day where I don’t sit in the bathroom and cry and then wash my face to hide that I’ve been crying. I want to be able to get through a day without complaining to everyone and without feeling like I’m going insane. I just want my life back, and I’m not ready to give up.”
In the months after writing this entry, I went on to develop chest pains, shortness of breath, dizziness, panic attacks, worsening nerve and muscle pain, blurry vision and more. I was also later diagnosed with Babesia microti in addition to Lyme Disease. I’m still seeing my Lyme doctor (and paying out of pocket) and am currently improving on several antibiotics and supplements but it has been a very gradual, painful process.
I truly hope this account reaches someone who might be able to make a difference in the current state of how government agencies view Lyme Disease and tickborne co-infections. There needs to be more research done on testing and diagnoses methods and treatment for Lyme and co-infections. This is a growing problem; think of how many people the current accepted testing misses and how many are suffering without an accurate diagnosis. Please, on behalf of the many thousands of us who suffer and view each day as a renewed battle against these chronic illnesses, consider what I have written as testimony to the huge problem with current healthcare policies and beyond.
Aubrey Hines, Connecticut
Erica Keys Land
I believe that the mission of the newly formed committee should be a coordinated “Manhattan project” similar to the attack mounted against the HIV/AIDS epidemic in order to address the serious worldwide threat of Lyme disease. I base this believe upon the article published by Dr Raphael Stricker (below). If I am able to speak at the meeting, I will put these comments into my own words based upon my own experience and reflections.
Lyme disease is the most common tick-borne illness in the world today. Until recently, the Centers for Disease Control and Prevention (CDC) reported an average of only 30,000 cases of Lyme disease per year in the United States. Three preliminary CDC studies, however, have indicated that the true incidence of Lyme disease may be greater than 300,000 cases and as high as one million cases per year in the United States. A majority of these cases occur in women and children. Based on this new information, Lyme disease should be recognized as a virulent epidemic that is at least six times more common than HIV/AIDS. In response to these alarming statistics, we review the ongoing problems with diagnosis and treatment of Lyme disease. We propose the need for an HIV/AIDS-style “Manhattan project” to combat this serious epidemic that threatens the physical and mental health of millions of people around the world.
Almost from the moment of its discovery, Lyme disease has been a controversial illness , . The disease is caused by a spirochete, Borrelia burgdorferi, that is transmitted to humans by the bite of an Ixodes tick , . Following the discovery in 1982 that a spirochete was the agent of the disease, numerous reports described the protean clinical manifestations of the tick-borne illness, and laboratory testing for the disease was implemented in a haphazard fashion. This poorly directed approach to Lyme disease resulted in the perception in the early 1990s that the disease was being “overdiagnosed and overtreated” ,. This perception in turn led to a backlash, culminating in the development of stringent diagnostic and therapeutic criteria for Lyme disease , . As a result, the diagnosis and treatment of Lyme disease has been limited by a surveillance case definition formulated by the Centers for Disease Control and Prevention (CDC) and supported by the Infectious Diseases Society of America (IDSA) , . Use of this stringent case definition has restricted CDC reporting of the disease to about30,000 cases per year in the United States.
In response to this limited view of Lyme disease, a number of practitioners felt that the diagnostic criteria embraced by CDC/IDSA, such as the need for at least five antibodies against a laboratory strain of B. burgdorferi, geographical and seasonal restriction of the disease, and the presence of severe objective symptoms, were too restrictive and excluded many sick patients with tick-borne diseases. They also saw treatment failure with the short-term antibiotic regimens recommended by CDC/IDSA guidelines, and they recognized that Lyme disease may be complicated by infection with other tick-borne agents such as Babesia, Anaplasma, Ehrlichia, Rickettsia, and Bartonella. These practitioners formed the International Lyme and Associated Diseases Society (ILADS), an organization whose viewpoint is that Lyme disease is much more prevalent and complex than the CDC/IDSA criteria allow , . Based on the ILADS clinical perspective, it follows that the successful treatment of tick-borne diseases is more challenging than the limited recommendations of CDC/IDSA , . The contrasting CDC/IDSA and ILADS perspectives have given rise to the “Lyme Wars,” with sick patients stuck between the “overdiagnosed/overtreated” and “underdiagnosed/undertreated” camps ,. The controversial nature of Lyme disease, coupled with the relatively small number of cases reported by the CDC, has stunted progress in combatting this illness.
All of this has suddenly changed. Three preliminary reports from the CDC have drastically altered our view of Lyme disease –. The first report, by Hinckley et al., examined laboratory test results for Lyme disease in 2008. The authors concluded that the true annual rate of diagnosed Lyme disease was on the order of 312,000 cases, more than ten times the official number reported by the CDC . The second report, by Hook et al., examined self-reported cases of Lyme disease in the years 2009, 2011, and 2012. The study found that in 2012, Lyme disease was diagnosed in 0.3% of respondents during the previous year; extrapolating from a population of >300 million, as many as one million people would have been diagnosed with Lyme disease in that timeframe. Furthermore, 42% of Lyme disease patients remained ill after 6 months, 12% were ill for more than 3 years, and 36% were treated with antibiotics for more than 8 weeks. Based on these results, the authors concluded that “a very large number of individuals in the US have been diagnosed with Lyme disease” .
The third study, by Nelson et al., analyzed private insurance claims related to Lyme disease between 2001 and 2010. The study found that a large number of Lyme disease cases not formally reported are nevertheless diagnosed and treated by healthcare providers. Among inpatients, children aged 5–9 years had the highest rate of Lyme disease diagnosis, while women were diagnosed with Lyme disease more often than men in the outpatient setting. The reason for this gender discrepancy is unclear . In summary, these CDC studies indicate that Lyme disease is far more prevalent than official reporting statistics indicate, with at least 300,000 new Lyme disease cases and as many as one million cases (a majority of them women and children) diagnosed each year in the United States. In comparison to HIV/AIDS, which is diagnosed at a rate of 55,000 new cases per year, Lyme disease appears to be at least six times more common in the United States.
How did Lyme disease reach these epidemic proportions? Three major factors play a role. First, the clinical diagnostic criteria for Lyme disease are too stringent, with only objective signs of the disease, such as an erythema migrans rash, arthritis, meningitis, or carditis, considered relevant . Many patients with late Lyme disease (up to 90%) will only display subjective symptoms of the disease such as fatigue, musculoskeletal pain, and neurocognitive problems, and these patients will often fail.
PLOS Pathogens: Lyme Disease: Call for a “Manhattan Project” to Combat the Epidemic (http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1003796) to be diagnosed and treated for the disease , . Second, commercial laboratory testing for Lyme disease yields poor results, with a sensitivity of only 46% in patients who have been infected for more than 4–6 weeks. Thus, these tests miss more than half of Lyme disease cases , . In contrast, testing for HIV/AIDS has a sensitivity of >99.5% and misses less than one in 200 HIV/AIDS cases , . Third, treatment for Lyme disease is very restrictive, with CDC/IDSA clinging to the use of monotherapy with questionably effective short courses of antibiotics. This outdated approach contrasts with other serious infectious diseases such as tuberculosis and HIV/AIDS, where long-term combination antimicrobial therapy is the norm , .
Controversy also persists over the existence of chronic Lyme disease due to persistent infection with B. burgdorferi in patients who are untreated or undertreated for the spirochetal illness , , . While some researchers continue to insist that there is no “credible scientific evidence” for chronic Lyme disease, a growing body of clinical and research evidence supports persistent symptomatic infection with the Lyme spirochete –. Recognition of the 10-fold greater magnitude of the Lyme disease epidemic and persistence of symptoms for more than 3 years supports the concept of chronic Lyme disease , . It remains to be determined how the chronic form of the disease is related to the ability of B. burgdorferi to penetrate tissue sites, evade the immune response and survive antibiotic therapy.
What needs to be done to combat the growing Lyme disease epidemic? As suggested by others , we need to establish a “Manhattan project” along the lines of the approach to the HIV/AIDS epidemic. First, an inclusive panel of clinicians, researchers, patients, and government officials should be established to determine the new approach to Lyme disease using the type of panel balancing recommended by government guidelines for controversial diseases . This panel should revoke the archaic and ineffective IDSA Lyme guidelines and establish new clinical parameters for Lyme disease diagnosis , . Second, a uniform standard for Lyme disease testing should be established, with emphasis on a “gold standard” culture and/or PCR test for the spirochete –. This effort would mirror the government-supervised approach to HIV/AIDS that was used to ensure high test sensitivity for that disease, as described above , . Third, further trials of antibiotic therapy should be conducted once the “gold standard” testing is in place, with emphasis on combination antimicrobial therapy and encouragement of pharmaceutical industry participation , , . Although development of a safe and effective Lyme vaccine would be desirable, the failure of a previous Lyme vaccine and the inability over 30 years to develop an effective HIV/AIDS vaccine should serve as a cautionary note that vaccine-based prevention of Lyme disease may not be feasible in the near future –.
In summary, preliminary studies from the CDC indicate that the Lyme disease epidemic has reached an unprecedented level with at least 300,000 people and as many as one million people, a majority of them women and children, diagnosed with Lyme disease each year in the United States. The staggering magnitude of the epidemic should prompt the CDC to show leadership in developing new guidelines for the diagnosis and treatment of Lyme disease. A coordinated “Manhattan project” similar to the attack mounted against the HIV/AIDS epidemic is urgently needed to address the serious worldwide threat of Lyme disease.
- Treatment of Lyme disease: a medicolegal assessment. Expert Rev Anti Infect Ther 2: 533–557. doi: 10.1586/14787184.108.40.2063 Google Scholar
- Lyme disease: The next decade. Infect Drug Resist 4: 1–9. doi: 10.2147/idr.s15653 Google Scholar
- Lyme disease diagnosis and treatment: Lessons from the AIDS epidemic. Minerva Med 101: 419–425. Google Scholar
- Harvey WT, Salvato P (2003) ‘Lyme disease’: ancient engine of an unrecognized borreliosis pandemic? Med Hypotheses 60: 742–759. doi: 10.1016/s0306-9877(03)00060-4
- Johnson L, Stricker RB (2004) View Article PubMed/NCBI
- Stricker RB, Johnson L (2011) View Article PubMed/NCBI
- Stricker RB, Johnson L (2010) View Article PubMed/NCBI
- Steere AC, Taylor E, McHugh GL, Logigian EL (1993) The overdiagnosis of Lyme disease. JAMA 269: 1812–1816. doi: 10.1001/jama.269.14.1812. View Article PubMed/NCBI Google Scholar.
- Dressler F, Whalen JA, Reinhardt BN, Steere AC (1993) Western blotting in the serodiagnosis of Lyme disease. J Infect Dis 167: 392–400. doi: 10.1093/infdis /167.2.392. View Article PubMed/NCBI Google Scholar.
- Wormser GP, Dattwyler RJ, Shapiro ED, et al. (2006) The clinical assessment, treatment, and prevention of Lyme disease, Human Granulocytic Anaplasmosis, and Babesiosis: Clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis 41: 1089–1134. doi: 10.1086/508667. View Article PubMed/NCBI Google Scholar.
- Feder HM Jr, Johnson BJ, O'Connell S, Shapiro ED, Steere AC, Wormser GP (2007) Ad Hoc International Lyme Disease Group (2007) A critical appraisal of ‘chronic Lyme disease’. N Engl J Med 357: 1422–30. doi: 10.1056/nejmra072023. View Article PubMed/NCBI Google Scholar.
- Johnson L, Aylward A, Stricker RB (2011) Healthcare access and burden of care for patients with Lyme disease: a large United States survey. Health Policy 102: 64–71. doi: 10.1016/j.healthpol.2011.05.007. View Article PubMed/NCBI Google Scholar.
- Stricker RB, Johnson L (2011) The pain of chronic Lyme disease: moving the discourse backward? FASEB J 25: 4085–7. doi: 10.1096/fj.11-1203ltr. View Article PubMed/NCBI Google Scholar.
- Burrascano JJ (1993) The overdiagnosis of Lyme disease. JAMA 270: 2682. doi: 10.1001/jama.1993.03510220038016. View Article PubMed/NCBI Google Scholar.
- Cameron D, Gaito A, Harris N, et al. (2004) Evidence-based guidelines for the management of Lyme disease. Expert Rev Anti-Infect Ther 2(1 Suppl): S1–13. doi: 10.1586/14789072.2.1.s1, View Article PubMed/NCBI Google Scholar.
- Stricker RB, Lautin A (2003) The Lyme Wars: time to listen. Expert Opin Investig Drugs 12: 1609–1614. doi: 10.1517/135437220.127.116.119. View Article PubMed/NCBI Google Scholar.
- Kullberg BJ, Berende A, van der Meer JW (2011) The challenge of Lyme disease: tired of the Lyme wars. Neth J Med 69: 98–100.
- Hinckley A, Connally N, Meek J, Johnson BJ, Kemperman M, et al.. (2013) TickNET: A survey of testing practices for Lyme disease by large commercial laboratories –United States, 2008. Presented at the 13th International Conference on Lyme Borreliosis and other Tick-Borne Diseases, Boston, MA, August 19, 2013. Available: http://www.poughkeepsiejournal.com/assets/pdf/BK211782914.pdf.
- Hook S, Nelson C, Mead P (2013) Self-reported Lyme disease diagnosis, treatment, and recovery: Results from 2009, 2011, & 2012 HealthStyles nationwide surveys. Presented at the 13th International Conference on Lyme Borreliosis and other Tick-Borne Diseases, Boston, MA, August 19, 2013. Available: http://www.poughkeepsiejournal.com/assets/pdf/BK211780914.pdf.
- Nelson C, Saha S, Shankar M, Kugeler K, Hinckley A, et al.. (2013) Epidemiology and clinical characteristics of Lyme disease diagnosed by health care providers: Results from a large national database study. Presented at the 13th International Conference on Lyme Borreliosis and other Tick-Borne Diseases, Boston, MA, August 19, 2013. Available: http://www.poughkeepsiejournal.com/assets/pdf/BK211781914.pdf.
- Cairns V, Godwin J (2005) Post-Lyme borreliosis syndrome: a meta-analysis of reported symptoms. Int J Epidemiol 34: 1340–1345. doi: 10.1093/ije/dyi129 View Article PubMed/NCBI Google Scholar
- Phillips SE, Burrascano JJ, Horowitz R, Savely VR, Stricker RB (2006) Lyme disease testing. Lancet Infect Dis 6: 122. doi: 10.1016/s1473-3099(06)70387-5 View Article PubMed/NCBI Google Scholar
- Stricker RB (2007) Counterpoint: long-term antibiotic therapy improves persistent symptoms associated with Lyme disease. Clin Infect Dis 45: 149–57. doi: 10.1086/518853
- Berndtson K (2013) Review of evidence for immune evasion and persistent infection in Lyme disease. Int J Gen Med 6: 291–306. doi: 10.2147/ijgm.s44114 View Article PubMed/NCBI Google Scholar
- Stricker RB, Johnson L (2013) Persistent infection in chronic Lyme disease: does form matter? Res J Infect Dis 1: 2. doi: 10.7243/2052-5958-1-2 View Article PubMed/NCBI Google Scholar
- Miklossy J (2012) Chronic or late Lyme neuroborreliosis: analysis of evidence compared to chronic or late neurosyphilis. Open Neurol J 6: 146–157. doi: 10.2174/1874205x01206010146. View Article PubMed/NCBI Google Scholar.
- Ljøstad U, Mygland Å (2013) Chronic Lyme; diagnostic and therapeutic challenges. Acta Neurol Scand Suppl 196: 38–47. doi: 10.1111/ane.12048 View Article PubMed/NCBI Google Scholar
- Liegner K (2012) Valley views: Major initiative needed to fight tick-borne infections. Poughkeepsie Journal, August 21, 2012. Available: http://www.poughkeepsiejournal.com/article/20120822/OPINION04/308220005/Valley-Views-Major-initiative-needed-fight-tick-borne-infections.
- Viswanathan M, Carey TS, Belinson SE, et al.. (2013) Identifying and managing nonfinancial conflicts of interest for systematic reviews. Methods Research Report. AHRQ Publication No. 13-EHC085-EF. Rockville, MD: Agency for Healthcare Research and Quality; May 2013. Available: www.effectivehealthcare.ahrq.gov/reports/final.cfm.
- Johnson L, Stricker RB (2010) The Infectious Diseases Society of America Lyme guidelines: a cautionary tale about development of clinical practice guidelines. Philos Ethics Humanit Med 5: 9. doi: 10.1186/1747-5341-5-9. View Article PubMed/NCBI Google Scholar
- Johnson L, Stricker RB (2010) Final report of the Lyme Disease Review Panel of the Infectious Diseases Society of America: A Pyrrhic victory? Clin Infect Dis 51: 1108–1109. doi: 10.1086/656690. View Article PubMed/NCBI Google Scholar
- Sapi E, Kaur N, Anyanwu S, Luecke DF, Datar A, et al. (2011) Evaluation of in-vitro antibiotic susceptibility of different morphological forms of Borrelia burgdorferi. Infect Drug Resist 4: 97–113. doi: 10.2147/idr.s19201. View Article PubMed/NCBI Google Scholar
- Sapi E, Pabbati N, Datar A, Davies EM, Rattelle A, et al. (2013) Improved culture conditions or the growth and detection of Borrelia from human serum. Int J Med Sci 10: 362–376. doi: 10.7150/ijms.5698. View Article PubMed/NCBI Google Scholar
- Nolte O (2012) Nucleic acid amplification based diagnostic of Lyme (neuro-)borreliosis - Lost in the jungle of methods, targets, and assays? Open Neurol J 6: 129–139. doi: 10.2174/1874205x01206010129. View Article PubMed/NCBI Google Scholar
- Stricker RB, Delong AK, Green CL, Savely VR, Chamallas SN, et al. (2011) Benefit of intravenous antibiotic therapy in patients referred for treatment of neurologic Lyme disease. Int J Gen Med 4: 639–646. doi: 10.2147/ijgm.s23829. View Article PubMed/NCBI Google Scholar
- Donta ST (2012) Issues in the diagnosis and treatment of Lyme disease. Open Neurol J 6: 140–145. doi: 10.2174/1874205x01206010140 View Article PubMed/NCBI Google Scholar
- Stricker RB (2008) Lymerix® risks revisited. Microbe 3: 1–2. View Article PubMed/NCBI Google Scholar.
- Marks DH (2011) Neurological complications of vaccination with outer surface protein A (OspA). Int J Risk Saf Med 23: 89–96.
- Cohen J (2013) AIDS research. More woes for struggling HIV vaccine field. Science 340: 667. doi: 10.1126/science.340.6133.667. View Article PubMed/NCBI Google Scholar
Erica Keys Land, Esq.
The fact that blood donors are not screened as to whether Borellia is in their blood is simply incomprehensible. With CDC announcing in 2016 that there are 300,000 NEW lyme disease infections yearly it is counterintuitive NOT TO perform such screening. My daughter was diagnosed with chronic lyme Borellia by both blood tests and clinical evaluation over 9 years ago and 2 years after she was bitten by a tick at her grandmother’s home in Avondale, Jacksonville Florida. I personally witnessed the classic bulls eye rash on her thigh which she thought was ring worm. Two years and 9 doctors later (all of who dismissed her serious physical condition which exhibited the now known and acknowledged results of lyme infection) she was diagnosed in New York by a physician who had moved his practice from Lyme Conn. to NY in order to better serve the multitudes of individuals who had been tick bitten and were suffering life threatening illnesses directly from such infections.
So it is ok to NOT screen the blood supply?????? Are you nuts??? The blood and pain and suffering of those who have or who hereafter become infected because of this insane policy will be on you unless you reverse this disasterous and wrong headed policy. I am a retired litigation attorney. I can assure you that eventually many very capable and wise attorneys will be suing everyone in sight who created this policy and/or who failed to reverse it despite overwhelming evidence that Borellia is in the blood supply. You will most likely be included in those lawsuits.
Not convinced? Please refer to the recently filed lawsuit by 28 plaintiffs against multiple insurers and individuals including the IDSA in Federal Court in Texas. Individual defendants include Dr.Gary Wormser et al.
Seeing is believing!!!!!!!!!
I am an American citizen who is currently living in Australia where post-Lyme Disease or persistent symptoms post-antibiotic treatment are not accepted. I was diagnosed with Lyme Disease by an Infectious Disease Specialist in 1995, who is a member of the IDSA and ILADS. He has served on the Kansas City Mayor's AIDS Council and is a well informed specialist who has treated and written peer review articles on a number of topics in infectious disease ranging from HIV-AIDS patients with Histoplasmosis in Kansas City to H1N1 Influenza induced Myocarditis. When I was referred to Dr. Brewer, I had been sick for at least 9-10 years with a multi-system illness which he diagnosed as late stage disseminated Lyme Disease, which had by that time affected my central nervous system, my heart, lungs and muscular-skeletal system. Despite long term oral antibiotics, I was left with the effects of Lyme Disease which for me has been a remitting/relapsing progressive course so that today, I have lost most of my hearing in my right ear, I have new hearing loss in my left ear, I have an immune system that looks like someone with advanced AIDS, with a CD4/CD8 ratio of only 0.46, kappa and lambda light chains of only 0.10 and 0.13 respectively, an absolute increase in CD8 +CD3 T cells (as shown by flow cytometry of leukocyte surface antigens). I also have non-specific sub-cortical brain lesions, painful radiculopathy with frank degenerative changes in my cervical and thoracic spine, the onset of multi-focal painful Myoclonus in my brain, neck, heart, and abdomen which presents with involuntary sudden shock-like jerking motions. The Myoclonus was brought on following a severe adverse reaction to the antibiotic Flagyl for a dental abscess and severe deterioration in my medical symptoms. I have become so ill, that I can no longer work and have applied for disability through the bilateral agreement between the US and Australia, but this has been problematic because my ongoing symptomatic Lyme Disease has not been recognized. I am trying to repatriate so I can resume my treatment under Dr. Brewer but I have deteriorated so much since I originally applied last year that I would have difficulty flying a commercial flight just to mainland USA (San Francisco) which is a 13-hour non-stop flight because I am unable to sit up for very long without having the onset of these painful Myoclonic events, where I am unable to control the vocalization of the painful jerk, and which at its worst is a loud wailing shrill sound, which would not be permitted on a commercial flight unless I had a medical attendant who could assist me with medical management. I give you this background so you are able to hear my story and understand the reasons for my request for the following three requests as you undertake your work on the national Tick-borne Working Group.
- As a replacement to Dr. Gary Wormser, I ask that you consider in addition to the people on your alternate list, Dr. Neil Spector, an Oncologist from Duke University Medical Center who literally lost his heart due to undiagnosed Lyme Disease which caused heart failure. Despite three months of IV antibiotics, Dr. Spector's heart continued to deteriorate over a period of 10 years following antibiotics until he required a heart transplant. The worst part of his story as a medical insider, is that his illness was minimized by even his own colleagues. He is now very interested in translational medicine for Lyme Disease using methods he has used in treating cancer patients specifically with targeted immunotherapy. He has developed a model to show how the Borrelia bacteria is similar to cancer and is working on his first grant aimed at targeted immunotherapy for Lyme Disease, as each patient is unique. Even if you are not able to include him on the panel, I would ask that you invite him to share his research so that it will inform your work on finding a cure for Lyme Disease.
- I ask that the CDC remove all of the misleading information about post-treatment Lyme Disease which very much minimizes how sick people can become. Dr. Neil Spector is one example. I am another. Marisol Thomas, wife of rock singer Rob Thomas is another who has severe neurological Lyme Disease despite antibiotic treatment. It is very harmful to the public for the CDC to minimize Lyme Disease as its public website does. Even the CDC's most recent webinar in 2014 on Lyme Disease persistence showed that in all of the animal models the bacteria has the capacity to persist in animals post-antibiotic treatment even up to 12 months (which is far as the research has examined), as the animals have continued disease and presence of the organism at autopsy. If the panel is not aware of this webinar, it should be made available to all members, including the transcript, slide and video which is available on YouTube: https://www.youtube.com/watch?v=Xzuwv3OkMBA It is important to remove this misleading information not only for American health practitioners but for foreign health practitioners and foreign health departments such as Australia which get their information directly from the CDC website which is not up to speed with clinical treatment experience in humans infected with Lyme Disease or the animal research. This mis-information by the CDC has directly impacted on my life severely as one of 10 million Americans living abroad, not to mention the 330 million Americans living state-side or the millions/billions of people around the world who look to the CDC for information. Please I ask as a patient whose life has been forever altered by Lyme Disease for more than 30 years that you help facilitate this.
- I ask that the Tick-borne group compile a list of all relevant animal and human research in a special compendium that would be available to the public and would be easily cross-referenced with the CDC, NIH, the NIH e-Reporter of Lyme Disease research etc, so that information about Lyme Disease is more transparent and available to the public, such as is periodically available through various advocacy forums. It was only last year that I even knew that forums and advocacy organizations like Lyme Disease.org existed and I am now a participant in their patient-driven research. As an example of such a compendium, I provide the undernoted of just a few examples of how devastating Lyme Disease can be which in reading the CDC website, does not appear to be the case. This is why it is so important that the CDC correct their information on Lyme Disease and post-treatment Lyme Disease which minimizes the seriousness of what happens to patients after the antibiotics are withdrawn and the disease progresses. Even Allen Steere 1990 article on "Chronic Manifestations of Neurological Lyme Disease" stated that one third of patients relapsed and had disease progression either due to failure to eradicate spirochetes or irreversible sequela.
Example of Articles for a Compendium of Lyme Disease Research
Lyme Disease Morbidity & Persistence
Inflammation a Source of Pathology in Lyme Disease
- Histopathology of clinical phases of human Lyme disease www.ncbi.nlm.nih.gov/pubmed/2685926
- Serum inflammatory mediators as markers of human Lyme disease activity www.ncbi.nlm.nih.gov/pubmed/24740099
- Borrelia burgdorferi RST1 (OspC type A) genotype is associated with greater inflammation and more severe Lyme disease www.ncbi.nlm.nih.gov/pubmed/21641395
Lyme Cardiac Disease
- CDC Information on Lyme Carditis & Sudden Cardiac Death in CDC Morbidity & Death Report 2013 http://www.cdc.gov/mmwr/pdf/wk/mm6249.pdf
- Junctional ectopic tachycardia (in Lyme Disease) secondary to myocarditis associated with sudden cardiac arrest☆ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5420052/
- Range of atrioventricular conduction disturbances in Lyme borreliosis http://www.ncbi.nlm.nih.gov/pubmed/2183859
- Detection of Borrelia bissettii in Cardiac Valve Tissue of a Patient with Endocarditis and Aortic Valve Stenosis in the Czech Republic http://www.ncbi.nlm.nih.gov/pubmed/18650352
- Lyme Endocarditis http://www.ncbi.nlm.nih.gov/pubmed/23043635
Neurological Lyme Disease
- Neuro-Lyme Disease: MRI Imaging Findings http://pubs.rsna.org/doi/10.1148/radiol.2531081103?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed&
- Inflammation and central nervous system Lyme disease https://www.ncbi.nlm.nih.gov/pubmed/19944760
- Acute ischemic pontine stroke revealing lyme neuroborreliosis in a young adult http://www.ncbi.nlm.nih.gov/pubmed/19115674
- Cerebrovascular Events in Lyme Neuroborreliosis http://www.ncbi.nlm.nih.gov/pubmed/26002071
- Neuroborreliosis-associated cerebral vasculitis: long-term outcome and health-related quality of life http://www.ncbi.nlm.nih.gov/pubmed/23329377
- Lyme neuroborreliosis: manifestations of a rapidly emerging zoonosis http://www.ncbi.nlm.nih.gov/pubmed/19346313
- Interaction of the Lyme Disease Spirochete Borrelia burgdorferiwith Brain Parenchyma Elicits Inflammatory Mediators from Glial Cells as Well as Glial and Neuronal Apoptosishttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570132/
- American neuroborreliosis presenting as cranial polyneuritis and radiculoneuritis http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4204232/
- Neurogenic Bladder in Lyme Disease http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3547183/
- Primary Central Nervous System Lymphoma, "Relatively strong evidence for this mechanism exists for Borrelia burgdorferi-associated cutaneous marginal zone lymphoma..." http://www.medscape.com/viewarticle/550516_3
Other Lyme Disease Morbidity
- Clinical manifestations of Lyme disease http://www.ncbi.nlm.nih.gov/pubmed/3554839
- Clinical pathologic correlations of Lyme disease www.ncbi.nlm.nih.gov/pubmed/2814170
- Ixodes tick-borne borreliosis with erythema nodosum https://www.ncbi.nlm.nih.gov/pubmed/16445235
- Chronic Lymphomonocytic Meningoencephalitis, Oligoarthritis and Erythema Nodosum: Report of Baggio-Yoshinari Syndrome of Long and Relapsing Evolution. https://www.ncbi.nlm.nih.gov/pubmed/24878862
- Chronic Lyme Disease and Co-infections: Differential Diagnosis http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3565243/
- Lyme borreliosis in the severe combined immunodeficiency (scid) mouse manifests predominantly in the joints, heart, and liver http://www.ncbi.nlm.nih.gov/pubmed/2221014
- Borrelia burgdorferi infection may be the cause of sarcoidosis http://www.ncbi.nlm.nih.gov/pubmed/1333393
- Gastrointestinal and hepatic manifestations of tickborne diseases in the United States https://www.ncbi.nlm.nih.gov/pubmed/11941547
- Urinary dysfunction in Lyme disease https://www.ncbi.nlm.nih.gov/pubmed/8417211
- Borrelia infection and risk of non-Hodgkin lymphoma http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2972577/
- Lyme borreliosis and multiple sclerosis are associated with primary effusion lymphoma www.ncbi.nlm.nih.gov/pubmed/17197115
- Primary cutaneous B-cell lymphoma and Borrelia burgdorferi infection in patients from the Highlands of Scotland www.ncbi.nlm.nih.gov/pubmed/10976703
- Acute lyme infection presenting with amyopathic dermatomyositis and rapidly fatal interstitial pulmonary fibrosis www.ncbi.nlm.nih.gov/pmc/articles/PMC2898701/
- The expanding clinical spectrum of ocular lyme borreliosis http://www.ncbi.nlm.nih.gov/pubmed/10711899
- Lyme borreliosis mimicking central nervous system malignancy: the diagnostic pitfall of cerebrospinal fluid cytology https://www.ncbi.nlm.nih.gov/pubmed/11185583
- Current Trends Update: Lyme Disease and Cases Occurring during Pregnancy -- United States http://www.cdc.gov/mmwr/preview/mmwrhtml/00000569.htm
- (Otzi) New insights into the Tyrolean Iceman's origin and phenotype as inferred by whole-genome sequencing http://www.ncbi.nlm.nih.gov/pubmed/22426219
- The musculoskeletal abnormalities of the Similaun Iceman (Otzi): clues to chronic pain and possible treatments http://www.ncbi.nlm.nih.gov/pubmed/23096483
- Lyme disease associated with sudden sensorineural hearing loss: case report and literature review. https://www.ncbi.nlm.nih.gov/pubmed/23303170
- Long-Term Assessment of Fibromyalgia in Patients with Culture-Confirmed Lyme Disease https://www.ncbi.nlm.nih.gov/pubmed/25470117
- Long-term assessment of fatigue in patients with culture-confirmed Lyme disease. https://www.ncbi.nlm.nih.gov/pubmed/25447620
- Severity of chronic Lyme disease compared to other chronic conditions: a quality of life survey http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3976119/
Lyme Disease Persistence
- CDC Webinar on Lyme Persistence https://www.youtube.com/watch?v=Xzuwv3OkMBA
- CDC Webinar on Lyme Persistence Seminar Slides http://www.cdc.gov/lyme/pdfs/PersistenceWebinarSlides.pdf
- Evaluation of in-vitro antibiotic susceptibility of different morphological forms of Borrelia burgdorferi http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3132871/
- Eva Sapi, PhD, Biofilms and antibiotic resistance of Borrelia burgdorferi, NorVect 2014 https://www.youtube.com/watch?v=StKyCfuRdns
- Review of evidence for immune evasion and persistent infection in Lyme disease http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3636972/
- Culture of the Entire Mouse To Determine whether CultivableBorrelia burgdorferi Persists in Infected Mice Treated with a Five-Day Course of Ceftriaxone http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4249442/
- Persistence of Borrelia burgdorferi in experimentally infected dogs after antibiotic treatment http://www.ncbi.nlm.nih.gov/pmc/articles/PMC229521/
- Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3256191/
- Persistent infection in chronic Lyme disease: does form matter? http://www.hoajonline.com/journals/pdf/2052-5958-1-2.pdf
- Persistence of Borrelia burgdorferi sensu lato in patients with Lyme borreliosis http://www.ncbi.nlm.nih.gov/pubmed/11233667
- Long term and repeated electron microscopy and PCR detection of Borrelia burgdorferi sensu lato after an antibiotic treatment http://www.ncbi.nlm.nih.gov/pubmed/15068199