It has been over four decades since Connecticut health officials—investigating fifty-one child and adult residents of Lyme presenting with uncommon arthritic symptoms—formally concluded, in 1977, that they were witnessing the birth of a new illness.1 By 1987, the condition (named after the Connecticut location where it emerged) had progressed from a localized medical curiosity to a nationally reportable disease, meaning that American doctors had to report “any and all cases” to local and state health departments.1
Currently, the Centers for Disease Control and Prevention (CDC) receives reports of approximately thirty to forty thousand Lyme cases annually, a quadrupling since the 1990s.2 However, the CDC states that this figure likely represents a dramatic underestimate of Lyme’s true incidence, suggesting it could be as much as fifteen times higher.3 The vast majority of reported Lyme cases (95 percent) in the U.S. come from fourteen states in the Northeast and upper Midwest.4 Internationally, “information seems to support the occurrence of Lyme disease” in eighty-plus countries, although the Lyme Disease Association notes that officials in many of these locations are “reluctant to declare Lyme disease present.”5
NON-SPECIFIC SIGNS AND SYMPTOMS
From the outset, the condition labeled as Lyme disease has been perplexing and frustrating—both for those experiencing the weird panoply of difficult-to-pin-down symptoms and for those attempting diagnosis or treatment. Clinicians acknowledge that “Lyme” symptoms are little different from those seen in hundreds of other medical conditions.6
According to the CDC, early-stage “localized” Lyme “may”—but often does not—involve a rash, which “may” take on a bulls-eye conformation. (Lyme specialists nevertheless deem the bulls-eye rash as a “classic” feature of the illness.) At this stage, there “may” also be nonspecific flu-like symptoms such as fever, chills, headache, fatigue or achy joints and muscles.7 Later signs and symptoms (called the “disseminated” stage) “may” include rheumatologic, cardiac or neurologic manifestations such as arthritis, heart palpitations, nerve pain, facial palsy, brain or spinal cord inflammation or severe headaches.8 About one in eight Lyme patients (12 percent) “may” display neurologic or neuropsychiatric symptoms.9 Clinicians warn that the latter can emerge months to years down the road, resulting in “possibly irreversible mental illness.”10
The many conditions that overlap with Lyme symptomatology range from influenza and cellulitis to other hard-to-differentiate autoimmune ailments such as fibromyalgia, rheumatoid arthritis and multiple sclerosis.11 The lack of a clearcut disease profile is also evident in the International Lyme and Associated Diseases Society’s vague definition of chronic Lyme disease: “a multisystem illness with a wide range of symptoms and/or signs that are either continuously or intermittently present for a minimum of six months.” 12
THE CAUSALITY QUESTION
In the early 1980s, infectious disease specialists did not take long to rally around the explanation that Lyme was a tick-borne illness, pointing the finger at a particular spirochete harbored by a particular genus of tick. Spirochetes are any of a group of spiral- or corkscrew-shaped bacteria widely distributed in nature.13 The Lyme spirochete was named Borrelia burgdorferi (B. burgdorferi) in 1983 after William “Willy” Burgdorfer, the Swiss-born National Institutes of Health (NIH) medical entomologist credited with discovering it.14
As the NIH now tells it, Burgdorfer and colleagues at the National Institute of Allergy and Infectious Diseases (NIAID) Rocky Mountain Laboratories discovered in 1981 that the spirochete later named B. burgdorferi was the cause of “the mysterious Lyme disease.”14 (As an interesting historical footnote, Switzerland—Burgdorfer’s country of origin—was the first nation outside the U.S. to jump on the Lyme bandwagon, also reporting “Lyme arthritis” in 1981.15)
In 1982, Burgdorfer’s group published a three-page paper in Science (“Lyme disease—a tick-borne spirochetosis?”) that posed the spirochete hypothesis as a question rather than a certainty.16 In a narrative familiar to those who have followed the more recent story of SARS-CoV-2’s “isolation,”17 Burgdorfer and co-authors described their starting point as epidemiologic evidence that “suggested” infectious agent causality and “incriminated” a particular genus of tick. From that point forward, the efforts focused on “isolating” the presumed causative agent rather than demonstrating that the presumed causative agent actually leads to disease.
In the 1982 paper,16 Burgdorfer and colleagues described their sequence of investigatory steps as follows:
- Initially, “attempts to isolate the causative agent either from ticks or from patients were unsuccessful.”
- The researchers then collected ticks from a “known endemic” Lyme region, dissected them and found spirochetes in certain gut tissues (although the spirochetes “moved sluggishly and rotated slowly” after being “moderately well” stained with dark-microscopy dyes).
- The researchers used electron microscopy to further investigate the organisms’ “structural features.”
- The scientists then “isolated” the spirochete “by inoculating 0.1 ml of a suspension prepared from midgut tissues of four infected ticks into 8.5 ml of modified Kelly’s medium” (a culture medium containing, among other ingredients, “bovine albumin solution, gelatin solution and serum”).18
- When the researchers then allowed three hundred ticks to feed on eight rabbits to the point of engorgement, the rabbits developed tiny lesions (though only one rabbit showed lesions at the site of tick attachment). However, fourteen days of daily blood smears “were negative for spirochetes.” Moreover, “limited attempts to isolate spirochetes from suspensions of biopsied skin lesions in Kelly’s medium were negative.” The authors stated, “Even though. . . at least two ticks harboring spirochetes had fed on each rabbit, we are not certain whether the described skin reaction. . . is causally related to the spirochetes or is due to other factors associated with the ticks’ feeding process.”
After some mucking about with antibody testing in the rabbits and in nine Lyme patients, what was the authors’ tentative conclusion? “Our observations suggest that the. . . organism isolated from [the ticks in question] may be involved in the etiology of Lyme disease” [emphasis added].16
In 1983, Burgdorfer and NIAID colleagues published another short paper in The New England Journal of Medicine describing the “isolation” of spirochetes from the blood of two Lyme patients.19 “Isolation” procedures again included inoculation with modified Kelly’s medium, as well as “serial dilutions” and testing for reactivity “with tick-derived spirochetes from stock cultures.”
In 2019, two of the three surviving authors of the Science article felt compelled to publish a detailed follow-up to their self-confessed “circumstantial” 1982 paper.20 Making up for the brevity of the 1982 and 1983 reports, the follow-up article rambled through labored descriptions of the authors’ training and qualifications, affectionate accounts of friendly mentorship from “Willy,” nods to other “astute” researchers and discussion of lab techniques to “grow” spirochetes. The paper also added a few colorful details about the attempts to “isolate” spirochetes from ticks—noting, for example, that the ticks had been “dipped in ethanol and then briefly flamed to sterilize their exterior before dissection.”20
The 2019 paper contained another interesting admission: The “eventual pure culture” obtained by the scientists turned out to be contaminated with another bacterium. As one of the authors reported: “I spent several days trying to clear what we presumed to be a contaminant with different antibiotics. I eventually found that nalidixic acid and 5-fluorouracil. . . could suppress if not eliminate the other organism while allowing growth of the spirochete. While we could not make a serious claim with a contaminated culture, it was the first recovery of the spirochete outside the tick and the only one with which to work at the time.” The researchers then admitted that they continued to use cell suspensions that contained the contaminant. They stated: “Again, these were not results that could be included in a paper, but they gave us confidence that we were onto something.”20
The laboratory efforts by Burgdorfer and colleagues in the 1980s likely would appear crude by twenty-first-century standards. In 2008, for example, scientists bragged of efforts to genetically modify B. burdorferi—justifying these efforts as a strategy to assess “putative virulence factors” in the lab.21 Using these “powerful genetic techniques,” they remain interested in genetically manipulating spirochetes, lab animals such as mice “and even the tick” to study host-vector “interactions.”21
Spirochetes are considered unique22 because of their endocellular whip-like flagella—a feature that allows them to “twist and move.”23 According to biologists, spirochetes are “characteristically found in a liquid environment (e.g., mud and water, blood and lymph),”22 with free-living species populating aquatic habitats and symbiont species playing a “mutualistic role”24 in hosts ranging from ruminants25 to termites.26 For example, a “physiologically and morphologically diverse population of spirochetes” inhabits the rumen of cows, significantly contributing “to the degradation of plant materials ingested by the ruminants.”25 In termites—the world’s most prolific digesters of cellulose—spirochetes are essential in helping break down the cellulose; in fact, without spirochetes in the termite gut, the insects cannot survive.27 In hosts such as mollusks, spirochetes serve no apparent purpose but nevertheless “coexist peacefully.”27
Early on, researchers theorized that the Borrelia spirochetes function as beneficial symbionts in ticks but become “parasites” in mammals.28 In humans, the belief is that various spirochetes cause not just Lyme disease but also conditions such as syphilis29 and periodontal disease.30 Notably, the spirochete explanation for syphilis emerged concurrently with the one-microbe-one-disease theory popularized by figures like Robert Koch and Louis Pasteur in the late 1800s and the rise of dark-field microscopy.31 Competing with other historical explanations for syphilis—including theories that it was a spin-off of leprosy (resulting from sex between prostitutes and lepers) or punishment for immoral behavior or the result of a “grand astrological conjunction”—scientists in 1905-1906 converged on (and then never again deviated from) the view that microscope-detectable spirochetes were the definitive syphilis-causing agent.32 In the modern era, this has led to misdiagnosis of syphilis as Lyme (and probably vice-versa) because of spirochete antibody “cross-reactivity.”33
Where the Lyme spirochete is concerned, descriptions are heavily reliant on creepy, science-fiction-like language that encourages a parasitic and even predatory perspective. One writer says, for example, that Lyme spirochetes resemble “biological smart cars—burrowing into tissues, nerves and joints with the aid of a tiny molecular motor with gear-like switches for forward and reverse navigation.”34 Using similar transportation imagery, a doctor specializing in Lyme treatment warns that the bacteria “feed on connective tissue of every kind and use the blood stream as their super-highway in order to get around.”6 Writing for the Global Lyme Alliance, a Lyme victim describes the spirochetes as both “savvy” and “difficult to catch,” evocatively depicting them as “glowing gummy worms buzzing around [the] body” and “coiling around [the] arms and legs,” with “headlamps guiding their way through [the] joints, cells, and organs, including [the] brain.”23
From the sound of it, the “savvy” spirochete appears to belong to the same cast of “fairy tale” characters as the “wily” virus.17 In fact, there are reasons to wonder whether the fairy tale’s punch line might be “the emperor has no clothes.” Take, for example, the manner in which a Lyme disease diagnosis is worked up. By and large, Lyme is not laboratory-diagnosed; instead, clinicians mostly rely on subjective assessment of the “clinical picture,”35 which, as already noted, can resemble hundreds of other conditions. Operating on the assumption that B. burgdorferi “infection” is not up for debate as the cause of Lyme disease, laboratories have developed B. burgdorferi antibody tests, but they are notoriously problematic. Rated as “no better than a coin toss” by many,36 the tests are a major source of frustration for patients whose treatment and insurance coverage hinge on a hard-and-fast diagnosis.37
Patients are not the only parties struggling to deal with Lyme’s diagnostic challenges. The following phrasing suggests the flimsiness of the diagnostic edifice [emphases added]:
[A] major problem is the inability of documenting the existence and location of the bacteria. After the initial transfer of the bacteria from the. . . tick into the person, the spirochetes spread locally, but after an initial bacteremic phase, the organisms can no longer be reliably found in body fluids. The bacteria are probably present in subcutaneous sites and intracellular loci. Currently, the use of circulating antibodies directed against specific antigens of the Lyme borrelia are the standard means to diagnose the disease, but specific antibodies are not an adequate means to assess the presence or absence of the organism. What is needed is a more Lyme-specific antigen as a more definitive adjunct to the clinical diagnosis.35
Adding to the confusion, the author of the above passage observes that “there is often no separation between early and late or persistent/ chronic Lyme disease,” stating that one patient might progress directly to “persisting symptoms” while another might “have early disease, but then no further symptoms for a number of weeks or months.” 35
ONE THING LEADS TO ANOTHER
Inevitably, the conviction that Lyme disease is the result of infection with a bacterial parasite run amok has led to the parallel conviction that antibiotics are the solution. It seems to matter little that many patients experience “unspecific persisting symptoms such as fatigue, myalgia, arthralgia or cognitive dysfunction. . . months to years after adequate treatment.”38
In a study published in May 2021, Tulane researchers examined the brain of a sixty-nine year-old female donor who had experienced the “classic” symptoms of Lyme fifteen years previously, followed by a steady decline into dementia and death.39 To their astonishment, the researchers reported finding “intact spirochetes” in the brain, notwithstanding “aggressive antibiotic therapy. . . at different times throughout her illness.” 40 Ignoring evidence linking widely used antibiotics to “serious disruption[s] in brain function. . . and other brain problems,” 41 or the increased risks of dementia from other drugs commonly taken by U.S. adults,42 the Tulane researchers are sticking with the spirochetes, with plans to investigate B. burgdorferi’s role in severe neurological disease.
The CDC admits that long-term antibiotic treatment is associated with “serious, sometimes deadly complications.”43 To continue making the case that “appropriate” antibiotic therapy is necessary to achieve favorable Lyme outcomes, the CDC and others have coined a new diagnostic category to cover the stubborn subgroup for whom aggressive antibiotic therapy provides no relief: “post-treatment Lyme disease syndrome,” or PTLDS.43 As per the CDC definition, PTLDS sufferers experience pain, fatigue and difficulty thinking that lasts for over six months post-treatment. The best that CDC can offer by way of explanation for PTLDS is to say that it either is a post-infection “autoimmune response,” or the result of “a persistent but difficult-to-detect infection” or that PTLDS symptoms “are due to other causes unrelated to the patient’s Borrelia burgdorferi infection.”43 Other researchers agree that it is difficult to differentiate between “active infection or post-infectious auto-immunity.”44
The wily spirochetes that manage to survive bombardment with antibiotics also get their own name: “Borrelia persisters,” defined as bacteria that “survive the killing action of antibiotics by changing its [sic] physiological state.”45 As a 2019 study describes them, these “elusive” persisters are multi-drug-tolerant and can “remain viable despite aggressive antibiotic challenge,” sometimes by hiding out in biofilms. To combat these challenges, the authors recommend the development of drugs “with a high activity against multiple persister forms.” They also note, however, that natural compounds such as stevia, oregano oil and cinnamon bark or clove bud oils have been effective in killing “all forms of Borrelia.”45
ALTERNATIVES TO ANTIBIOTICS
Although mainstream medicine has no meaningful treatments to offer for Lyme other than antibiotics, Lyme sufferers and alternative healers have explored a number of options, ranging from nutritional interventions to herbal protocols.
On the nutrition front, the fat-soluble vitamins A and D are (unsurprisingly to those eating a Wise Traditions diet) of central importance. Studies indicate that vitamin A deficiency not only fosters susceptibility to Lyme but may exacerbate Lyme arthritis; evidence suggests that boosting vitamins A and D (preferably from food sources such as cod liver oil) can minimize or prevent Lyme symptoms.46,47
A 2016 study reported low serum carnitine concentrations in Lyme patients.48 Carnitine plays a key role in fat metabolism. The best source of carnitine is red meat, beef in particular. The authors of the 2016 paper recommend carnitine supplementation “to prevent late complications of the disease.”
Orthomolecular physician Thomas E. Levy, MD, JD has described the successful use of intravenous vitamin C therapy for both acute and chronic Lyme disease.49 In one case, a woman fell extremely ill seven to ten days after a tick bite, received several rounds of IV vitamin C and became “completely well, never having a clinical relapse or any chronic Lyme symptoms.” In the case of a woman with a twelve-year history of chronic Lyme, one month of IV vitamin C therapy resolved the condition. Levy notes that the dramatic turnaround did not begin to manifest until day twenty-three, when a “switch was flipped” and the patient “looked like a new person.”
Many other healing modalities have proven useful for at least some Lyme patients. These include hyperbaric oxygen therapy, light therapy, Rife machines, essential oils, traditional Chinese medicine and homeopathy.50 Herbal approaches have also attracted many grateful testimonials. Master herbalist Stephen Harrod Buhner’s website (buhnerhealinglyme.com) and book, Healing Lyme, outline a protocol involving astragalus as well as a paste made up of andrographis tincture and green clay.51
SHAPING PUBLIC PERCEPTIONS
Half a century into the Lyme story, it seems clear that many questions—whether about causality or treatment—remain unanswered. Even researchers wedded to conventional narratives state that “it remains paramount to. . . better understand the disease pathway and its pathophysiologic mechanisms” and to acknowledge the controversies that surround antibiotic treatment.44
Cutting-edge thinkers like Drs. Stephanie Seneff and Natasha Campbell-McBride have noted the strong correlation between the introduction of glyphosate into the food supply and the rise of Lyme disease. Given what we know about glyphosate in other contexts, the possibility that Lyme is at least in part the result of herbicide poisoning makes a lot of sense. And as The Forbidden Doctor website (forbiddendoctor. com) suggests, this may be the reason the spirochetes show up: “This is a situation where the presence of a bacterium is considered the cause of the disease, rather than being associated with it. This is like blaming the rats in the alley for the presence of a collection of garbage spilled all around. . . . [G]et rid of the glyphosate and the bacterium goes away.” It also stands to reason that further poisoning with strong antibiotics is bound to make things worse.
Another possible explanation is toxins in tick saliva. Like all blood-sucking insects, ticks produce vasodilators in their saliva to ensure that the blood stays liquid during their meal. These compounds can cause side effects like rapid heartbeat, heart palpitations, headaches and joint pain in those unable to clear these toxins.
Sadly, individuals with Lyme disease, like those with chronic fatigue syndrome and other conditions with slippery symptom profiles,52 have often had difficulty getting medical practitioners to take their disease seriously. At this juncture, there should be no doubt that the condition known as Lyme—whatever it is—can cause considerable suffering. One writer notes that many of the chronically ill “are unable to work or go to school,” adding: “Some go bankrupt. Families break up. There’s a high rate of suicide among Lyme disease patients, reflected in a common saying among the afflicted: ‘Lyme doesn’t kill you; it only makes you wish you were dead.’”2
When examining the Lyme narrative—or, for that matter, SARS-CoV-2—we must bear in mind the leading role played by NIAID and related government agencies in shaping public perceptions of disease and epidemics. These agencies, with their vaccine patents and related agendas, can scarcely be considered disinterested or neutral parties. For example, federal agencies are currently allowing testing of experimental Lyme vaccines (including one developed by Pfizer),53 despite a disastrous experience with a three-dose recombinant Lyme vaccine in the late 1990s. The vaccine generated numerous reports of musculoskeletal “side effects” (including arthritis!) that resulted in a class-action lawsuit.54 The prosecuting attorneys, according to one account, asserted that the manufacturer, GlaxoSmithKline (GSK), “suppressed reports of adverse events from the licensing trial and provided inadequate warnings to genetically susceptible individuals.”54 Though GSK ultimately withdrew the vaccine from the market, those who experienced serious adverse events received no compensation.
THE BIOWEAPON HYPOTHESIS
Although the first formal case reports of what has come to be known as Lyme disease emerged in the late 1970s, independent researchers have traced Lyme’s Long Island origins further back to 1968, when Lyme emerged alongside two other novel conditions (Rocky Mountain spotted fever and babesiosis).2 Describing subsequent investigations into the “triple threat” outbreaks as “fragmented,” science and technology writer Kris Newby—herself a one-time Lyme and babesiosis sufferer—points out that officials never asked “why these strange diseases had appeared seemingly out of nowhere in the same place and at the same time.”2
According to Newby—author of the 2020 book Bitten: The Secret History of Lyme Disease and Biological Weapons—the 1960s were a fertile period for tests of live biological and chemical warfare agents conducted by scientists from the Central Intelligence Agency (CIA), the U.S. Army and the Department of Defense.55 In Lab 257: The Disturbing Story of the Government’s Secret Germ Laboratory, investigator Michael Christopher Carroll broke the story of the government’s Plum Island research in 2004.56 (A 2019 CounterPunch story notes that Newby avoids discussion of Plum Island and Carroll’s findings.)57 The experimental testing of warfare agents took place in many locations, both domestically and internationally. After learning about these “grossly immoral” experiments from Newby’s book, New Jersey Congressman Chris Smith, whose adult daughter has chronic Lyme, called for a comprehensive government investigation.58
“Willy” Burgdorfer was a key player in the U.S. biological weapons program, says Newby, artificially infecting fleas, ticks and mosquitoes with “deadly pathogens” and working with other tick experts at Fort Detrick to “mass-produce infected ticks so that they could be dropped from airplanes.”59 According to Newby’s research, the U.S. military experimented with both “fast-acting fatal and slow-acting incapacitating disease agents.” Ticks, moreover, “were the perfect stealth weapon, virtually untraceable and able to sicken a large population without damaging societal infrastructure.” Later efforts also focused on tick-borne microbes “that could be mass-produced and deployed in aerosol form without the ticks.”59 Among the military activities outlined in Bitten, Army scientists reportedly dropped “infected ticks” on Cuban sugar cane workers and released “hundreds of thousands of radioactive, aggressive, Lone Star ticks on the Atlantic coastal bird flyway.”59
Perhaps the biggest bombshell in Bitten is that Burgdorfer (now deceased) publicly copped to being a bioweapons expert in a 2013 videotaped interview, explicitly stating that the cause of the original Lyme-area outbreak was a bioweapon. Burgdorfer did not name the eponymous Lyme spirochete as the bioweapon, however, instead fingering a rickettsia—the “tiny virus-like bacterium” that scientists blame for Rocky Mountain spotted fever—which Burgdorfer nicknamed “The Swiss Agent.”59
Though these and other tales of bioweapons-crazed mad scientists are ominous and deserve scrutiny, journalist and veteran medical cartel deconstructor Jon Rappoport offers an important and possibly reassuring counter-perspective. Rappoport’s logical analysis—also highly relevant to current debates about SARS-CoV-2—calls attention to the fundamental fact that many of the pathogens supposedly being weaponized are figments of genomic sequencing rather than properly isolated pathogens. “Automatically jumping from attempt to success,” Rappoport says, is “unwarranted.” Stated another way, just because scientists claim to be capable of weaponizing viruses—or spirochetes—does not mean that they have been successful in doing so. Rappoport also notes that the “intentional deployment of a highly dangerous chemical” generally produces far more “predictable” effects, both in terms of intensity and duration, than biological agents.60 His conclusion: “Self-styled experts” and others who “assume that an ATTEMPT to weaponize a virus equals success” may have been “watching too many sci-fi movies.” 61
MORGELLONS AND LYME: ENVIRONMENTAL FACTORS?
Morgellons disease is an “unexplained” skin condition characterized by “small fibers or other particles emerging from skin sores.”62 As the Morgellons Research Foundation states, a hallmark aspect of the condition is the experience of “disturbing crawling, stinging, and biting sensations.”63 Interestingly, individuals with Lyme sometimes describe “a spinning sensation under [the] skin” as well as the feeling of “twisting spirochetes coiling around [the] arms and legs” and “a buzzing like electricity.”23 Many individuals with Morgellons experience symptoms similar to Lyme such as fatigue, mental confusion and joint pain.63 According to a 2013 report in GreenMedInfo, some physicians believe that Morgellons may in fact represent “an unusual morphing of Lyme disease.”64
Studies in cattle have led to the suggestion that there are parallels between Morgellons and a condition called bovine digital dermatitis that is suspected to have “spirochetal involvement.”65 Spirochetal infection has likewise emerged as a possibility in connection with Morgellons disease in humans, due to the finding that spirochetes are found in Morgellons skin lesions.64 Of course, causality cannot be inferred from the mere presence of spirochetes, which could be serving an unknown or unacknowledged purpose that might even be beneficial.
In the cases of both Lyme and Morgellons, there is little dispute that environmental factors play a significant role. Synthetic contaminants—whether from genetically modified organisms (GMOs) in food and agriculture64 or glyphosate or nanoparticles in geoengineering aerosols66—are troubling contenders that deserve further attention.
- Connecticut State Department of Health. A brief history of Lyme disease in Connecticut. https://portal.ct.gov/DPH/Epidemiology-and-Emerging-Infections/A-Brief-History-of-Lyme-Disease-in-Connecticut (page last updated 7/1/2019).
- Newby K. On the link between Lyme disease and bioweapons. Literary Hub, May 15, 2019. https://lithub.com/on-the-link-between-lyme-disease-and-bioweapons/.
- Centers for Disease Control and Prevention. Lyme disease: data and surveillance. https://www.cdc.gov/lyme/datasurveillance/index.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Flyme%2Fstats%2Findex.html.
- Centers for Disease Control and Prevention. Lyme disease: where found. https://www.cdc.gov/ticks/tickbornediseases/lyme.html.
- Lyme Disease Association, Inc. Lyme in 80+ countries worldwide. Aug. 27, 2013. https://lymediseaseassociation.org/about-lyme/cases-stats-maps-a-graphs/lyme-in-more-than-80-countries-worldwide/.
- Talty J. Diagnosis and treatment of Lyme disease. http://drjaninetalty.com/Diagnosis%20and%20treatment%20of%20lyme%20disease.
- Centers for Disease Control and Prevention. Signs and symptoms of untreated Lyme disease. https://www.cdc.gov/lyme/signs_symptoms/index.html.
- Centers for Disease Control and Prevention. Lyme disease: signs and symptoms. https://www.cdc.gov/ticks/tickbornediseases/lyme.html.
- Koedel U, Fingerle V, Pfister HW. Lyme neuroborreliosis–epidemiology, diagnosis and management. Nat Rev Neurol. 2015;11(8):446-456.
- Paparone PW. Neuropsychiatric manifestations of Lyme disease. J Am Osteopath Assoc. 1998;98(7):373-378.
- Greenhalgh T. 3 conditions that may be mistaken for Lyme disease. Rheumatology Advisor, May 28, 2019.
- Shor S, Green C, Szantyr B, et al. Chronic Lyme disease: an evidence-based definition by the ILADS Working Group. Antibiotics (Basel). 2019;8(4):269.
- Spirochetes: definition, characteristics, Gram stain and culture. Microscope Master. https://www.microscopemaster.com/spirochetes.html.
- National Institutes of Health Intramural Research Program. Discovery of the disease agent causing Lyme disease. https://irp.nih.gov/accomplishments/discovery-of-the-disease-agent-causing-lyme-disease.
- Gerster JC, Guggi S, Perroud H, Bovet R. Lyme arthritis appearing outside the United States: a case report from Switzerland. BMJ. 1981;283:951-952.
- Burgdorfer W, Barbour AG, Hayes SF, et al. Lyme disease—a tick-borne spirochetosis? Science. 1982;216(4552):1317-1319.
- Cowan T, Morell SF. The contagion fairy tale. Wise Traditions. Winter 2020;21(4):14-25.
- Stoenner HG. Biology of Borrelia hermsii in Kelly medium. Appl Microbiol. 1974;28(4):540-543.
- Benach JL, Bosler EM, Hanrahan JP, et al. Spirochetes isolated from the blood of two patients with Lyme Disease. N Engl J Med. 1983;308:740-742.
20. Barbour AG, Benach JL. Discovery of the Lyme disease agent. mBio. 2019;10(5):e02166-19.
- Tilly K, Rosa PA, Stewart PE. Biology of infection with Borrelia burgdorferi. Infect Dis Clin North Am. 2008;22(2):217-234.
- “Spirochete.” Encyclopaedia Britannica. https://www.britannica.com/science/spirochete.
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- Crystal J. Unraveling spirochetes. Global Lyme Alliance, Oct. 15, 2019. https://www.globallymealliance.org/blog/unraveling-spirochetes.
- Murphy GE, Matson EG, Leadbetter JR, et al. Novel ultrastructures of Treponema primitia and their implications for motility. Mol Microbiol. 2008;67(6):1184-1195.
- Paster BJ, Canale-Parola E. Physiological diversity of rumen spirochetes. Appl Environ Microbiol. 1982;43(3):686-693.
- Collins P. Team building: symbiosis between termites and microbes. Research Nature Laboratory, 2016. https://researchnature.wordpress.com/2016/02/22/ team-building-symbiosis-between-termites-and-microbes/.
- Symbiotic spirochetes in animal models. Lyme Disease, Science, & Society, Oct. 28, 2012. https://campother.blogspot.com/2012/10/symbiotic-spirochetes-in-animal-models.html.
- Hoogstraal H. Ticks and spirochetes. Acta Trop. 1979;36(2):133-136.
- Halperin JJ. A tale of two spirochetes: lyme disease and syphilis. Neurol Clin. 2010;28(1):277-291.
- Pérez-Chaparro PJ, Gonçalves C, Figueiredo LC, et al. Newly identified pathogens associated with periodontitis: a systematic review. J Dent Res. 2014;93(9):846-858.
- The germ theory of disease. https://bio.libretexts.org/Courses/Mansfield_University_of_Pennsylvania/BSC_3271%3A_Microbiology_for_Health_Sciences_Sp21_(Kagle)/01%3A_Introduction/1.01%3A_An_Invisible_World/1.1.04%3A_The_Beginnings_of_Modern_Microbiology/1.1.4.01%3A_Pasteur_and_Spontaneous_Generation/220.127.116.11.01%3A_The_Germ_Theory_of_Disease.
- Tampa M, Sarbu I, Matei C, et al. Brief history of syphilis. J Med Life. 2014;7(1):4-10.
- Naesens R, Vermeiren S, Van Shaeren J, Jeurissen A. False positive Lyme serology due to syphilis: report of 6 cases and review of the literature. Acta Clin Belg. 2011;66(1):58-59.
- Atherton J. Yale scientists take the driving seat in pursuit of Lyme disease answers. 2021. https://westcampus.yale.edu/news/yale-scientists-take-driving-seat-pursuit-lyme-disease-answers.
- Donta ST. Issues in the diagnosis and treatment of Lyme disease. Open Neurol J. 2012;6:140-145.
- Kling R, Galanis E, Morshed M, Patrick DM. Diagnostic testing for Lyme disease: beware of false positives. BCMJ. 2015;57(9):396, 399.
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This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation, Summer 2021🖨️ Print post