1.
Hampshire College
NS­053: Natural History of Infectious Diseases
Professor Lynn Miller
Chronic Lyme Disease
and its Controversies
A Critical Review of the Literature and of Alternative Therapies
Justice Lynn Erikson
12/13/15

2. Erikson, 2015
Abstract
In this paper I will introduce Lyme borreliosis in its biological and clinical contexts, in concert with the
politics surrounding it. I will then discuss the basics of its complex history and biological characteristics. I will
critically review the current accepted treatment protocols for Lyme Disease, and go on to discuss Post­Treatment
Lyme Disease Syndrome and Chronic Lyme Disease. As a part of that discussion, I will introduce one proposed
revised model of borreliosis, and contrast it with the current CDC model. Finally, I will report alternative
therapies proposed by a couple of practitioners, and cursorily evaluate the scientific validity of their claims.
Introduction
Since I began my research on Lyme Disease just last semester, I have encountered dozens of people
whose lives have been affected by it. They often stop me mid­sentence, cutting me off with a sincere sense of
urgency, to tell me about the time that they, their mother, their best friend, or their neighbor had Lyme Disease. I
work as a college admissions tour guide, and I talk with families from all around the US every day. One girl,
during a walk around my garden plot that is quickly being taken over by Japanese Knotweed, tells me that she has
had chronic Lyme for years, and had to give up many of her favorite activities including hiking and sports,
because she was just too exhausted to do anything more than the bare minimum of physical activity. She also
expressed to me great concern that her grades had dropped because of her reduced energy to engage with her
schoolwork due to the fatigue that comes with Lyme; as well as a feeling of invisibility and hopelessness.
This is a young person’s epidemic as much as an older person’s epidemic; the CDC (2015a) reports that
in the last decade, the two groups with the highest prevalence of Lyme Disease diagnoses were five year olds and
fifty year olds. Researchers with the CDC estimate that around 329,000 cases of Lyme Disease occur in the
United States every year (Nelson et al. 2015), and while these are primarily in the Northeast part of the country,
almost every state in the union reports some diagnoses every year. It has become abundantly clear to me that more
research and understanding of this disease is a critical public health issue.
The Medical Science
Lyme Disease (more precisely known as Lyme Borreliosis) is typically caused by invasion by ​Borrelia
burgdorferi​ spirochetes, bacteria carried in the guts of deer ticks ​Ixodes scapularis.​ Or at least in the northeastern
US. It is notable that Steere, Coburn & Glickstein (2004) report that ticks ​Ixodes ricinus​ and ​Ixodes persulcatus
also carry american ​Borrelia burgdorferi​ in other areas of the US. Richter et al. (2006) indicate that there are also
a number of other Borrelia species ­ the most commonly associated with Lyme disease being ​B. garinii​ and ​B.
afzelii​ typically found in Europe and Asia. Many other ​Borrelia​ species are known worldwide, but may not be
pathogenic. These species cumulatively make up what is known as ​Borrelia burgdorferi sensu lato​, abbreviated
Bbsl​. While this paper focuses on Lyme disease in the US, we should remember that it is present in several
distinct forms across the globe. The Center for Disease Control (abbreviated CDC) (2015b) reports that ​B.
burgdorferi ​infection (borreliosis) almost always occurs through a tick bite, after which seventy to eighty percent
of people will exhibit a “bullseye rash” or erythema migrans (EM) about a week later. While our understanding of
the biology of borreliosis is still developing and pieces are constantly being called into question, most people
seem to agree on at least a few things: Steere, Coburn & Glickstein (2004) report that Lyme disease symptoms
include fatigue and malaise, joint and muscle pain, headaches and fever ­ all of which can be confused with flu
symptoms ­ except that they don’t end after a few days.
The clinical description of Lyme disease is generally broken up into two stages. Early infection occurs in
the first month after a tick bite and is characterized by the erythema migrans rash. During this stage, the body is
responding to the invasion of ​Borrelia​ bacteria with its frontline response ­ the innate immune system. The innate
immune system includes macrophages (“big eaters”), white blood cells that are able to engulf and kill ​Borrelia
spirochetes (Montgomery & Malawista 1996). This crucial mechanism, as well as many other immune responses
to ​Borrelia,​ have been the focus of much study, and may lend later insights into the validity of various treatment
1

3. Erikson, 2015
methods. Early infection can in most cases be cured with a short round of antibiotics, in fact the Infectious
Diseases Society of America research group, Wormser et al. (2006) only recommends various oral or intravenous
short­term rounds of antibiotics for any stage of Lyme Disease or its most common co­infections (Table 1). At the
first clinical observation of EM, the physician is advised by the CDC to prescribe two weeks of basic antibiotics
such as doxycycline. In the CDC’s diagnosis guidelines, neurological symptoms such as meningitis and cerebral
nerve palsy still fall under “early Lyme disease”; and the standard treatment for these does not extend beyond
nearly the same two­week course of antibiotics. For carditis and lymphocytoma, the recommendation is again two
weeks of antibiotics. If the infection goes untreated or is unsuccessfully treated early on, late stage Lyme disease
develops.
Table 1: Official Lyme Disease Treatment Protocols.​ From ​Wormser et al., 2006
Late infection is when the more serious symptoms of Lyme develop: the broad neurological degradation,
arthritis, heart irregularities, facial palsy, and severe fatigue. Here we see a minor step up in the CDC treatment
protocols. For Lyme arthritis, a four­week course of antibiotics is recommended. And for patients with significant
and debilitating neurological symptoms, there is the option of 2­4 weeks of intravenous antibiotics, but if
symptoms do not subside, ​re­treatment is not recommended​. Limited symptomatic treatment beyond this is
suggested, especially anti inflammatory medications for arthritic symptoms, but no further treatment unless there
is “objective” evidence of reinfection (another tick bite). The CDC and National Institutes of Health call any
lingering symptoms beyond their limited treatment protocols “Post­Treatment Lyme Disease Syndrome”
(Abbreviated PTLDS) (CDC 2015c) and deny the existence of persistent infection or true Chronic Lyme Disease.
In fact, they specifically go out of their way to list treatments for PTLDS that are ​not​ recommended, citing a “lack
of biologic possibility, lack of efficacy, absence of supporting data, or the potential to harm the patient” including
long­term antibiotic therapy, and vitamins and nutritional managements. The same guidelines go on to thoroughly
discuss their evidence for why most PTLDS/chronic Lyme does not exist, dismissing it as depression, chronic
fatigue, etc. What I find most distressing about this is that the authors primarily cite their own research groups as
positive evidence, and everyone else as bad evidence. Conflicts of interest are everywhere in this field.
2

4. Erikson, 2015
History
Lyme Disease spent many years as a silent and mysterious epidemic. There remains a dizzying array of
hypotheses to how it may have originally appeared in the US, but I will represent the pieces that have assembled
themselves into a reasonable enough story for me. Alan Barbour (2015 p 1), one of the researchers that worked on
the identification of Lyme’s causative agent, introduces the history of Lyme with a case of an old woman with
Lyme­like symptoms that were supposed to be due to the bite of a European sheep tick (​Ixodes ricinus​) from
Germany sometime before 1909 (Figure 1). Some people have very dramatic or even conspiratorial ideas about
the origins of Lyme disease in the US. Michael Carroll (2005 p 3­27) and Tietjen (2005) write of German
researchers with histories of investigating use of ticks as biological weapons for the Nazi party being brought over
to do research on Plum Island; which is not too far from the areas in which Lyme was first identified. Carroll
describes substantial evidence that this research facility had issues with its containment of the ticks in its
laboratories. These hypotheses do seem to add up with each other, however, and may well have truth to them.
Regardless of where it came from, cases of Lyme Disease began to show up more and more in eastern
Connecticut during the early seventies; researchers were sent in after communities began putting the pieces
together and identifying what was quickly becoming a crippling epidemic among children in their communities.
In 1977, Steere et al. published a paper identifying this epidemic as “Lyme Arthritis” ­ naming the newfound
disease after the town of Old Lyme, where the disease was first reported to the State Health Department by a
concerned mother who had noticed an unusual prevalence of juvenile arthritis in the community. It wasn’t until
1982 that the causative agent, the spirochetal bacterium ​Borrelia burgdorferi​, was identified by Burgdorfer et al.
(1982), and sparked the ever­expanding research effort to understand the biology behind borreliosis.
Desowitz (1981 p146­158), in his description of the zoonosis of babesiosis (a common Lyme coinfection,
and an obnoxious tick­borne infectious disease in its own right) describes how in the nineteenth century, there
were dramatic ecological changes to the Nantucket/Martha’s Vineyard/Shelter Island (Figure 1) etc. area due to
human settlement ­ ones that not­so­serendipitously created and ideal environment for ticks ­ and with an early
nineteenth century deer repopulation effort, it became a whole lot easier for tick­borne bacteria to make it from
mice, to deer, to grass, and to the clothes of humans. In addition to sharing a common vector, the presumed
zoonosis and identification of babesiosis and Lyme disease both occurred around the seventies and eighties in the
same areas; one can presume that the same or similar ecological factors impacted both. Because Lyme disease is
caused by ​B. burgdorferi ​, ​B. burgdorferi ​follows ​I. scapularis​ deer ticks, deer ticks follow white tailed deer
(Bosler et al. 1984; Duffy et al. 1994), and white tailed deer exist across the United States (Leopold, Sowls &
Spencer 1947), it wasn’t long before Lyme Disease became a national problem.
3

5. Erikson, 2015
Figure 1: Map showing Plum Island, Shelter Island, Lyme, Martha’s Vineyard, and Nantucket. ​Arrows
indicate possible initial routes of borreliosis spread. From Google Maps, December 12th, 2015.
Chronic Lyme Disease
I have been conducting an informal social survey in the lobby of the admissions office. Whenever I get
the chance, and before introducing what I study, I ask whether the families there are familiar with chronic Lyme
disease. I have yet to get anything but a resounding yes, generally accompanied by a personal story of connection
to chronic Lyme. As awareness of Lyme Disease spreads, the description of Lyme that the CDC and NIH have
been pushing since its discovery is becoming more and more obviously flawed. When I follow up my question
with the information that the CDC does not acknowledge the existence of a formal disorder known as “chronic
Lyme Disease” or even give much validity to its designated “Post Treatment Lyme Disease Syndrome”, I am met
with shock ­ how could it possibly not be an officially recognized disorder when everyone knows about it?
It is not just the public who is confused, either. Scientists and medical professionals alike have been
scratching their heads at what the CDC is doing in regards to Lyme for quite some time. Harvey and Salato
(2003), a pair of respected doctors in Houston, Texas wrote about their concerns about the CDC Lyme disease
model. I will discuss this paper as a representative work that seeks to present the truth about Borreliosis, but it is
by no means the only one. They reviewed a huge body of relevant literature (951 peer­reviewed papers and 13
books, in total) and discussed how the CDC model does not fit the range of scientific literature, or their clinical
observations. In concert, they develop a “Epidemic Borreliosis” model of the disease that is consistent with their
findings and experience (Table 2).
The CDC model often and sometimes entirely excludes: Patients who don’t exhibit a classical EM rash
living in a non­endemic area; patients with subclinical symptoms; patients who don’t test positive on the current
gold­standard IgG/IgM Western Blot tests; present false negatives in serological testing; or patients who may have
been infected by an expanding list of ​Bb sensu lato ​agents. In almost all of these cases, examples of interpersonal
or non­zoonotic infection such as sexual or gestational transfer; as well as other possible non­arthropod vectors
such as mosquitoes, fleas, and mites; are not accounted for by the model or given any mention or consideration in
CDC­approved publications. In addition to resulting in a lack of care for these patients, this also excludes these
patients from almost all borreliosis research. The CDC’s model has become a self­fulfilling paradigm, and
4

6. Erikson, 2015
wrongfully shuts out a huge portion of the borreliosis­affected population from their right to know what is
happening to their bodies, and to receive proper medical treatment for it. This is beyond negligent. It is immoral.
Harvey and Salato also detail extensive reasoning for their distrust of both Western Blot and serological
testing for the diagnosis of Lyme disease, outlining situations in which the tests produce false negatives. What is
probably the most unsettling place where the CDC and the actual body of literature don’t match up, is the notion
that Lyme borreliosis is not a persistent infection, and therefore any post­treatment symptoms must be due to
reinfection, past damage, or autoimmune responses. Harvey and Salato find that this is entirely premise­less or
based on indirect examples from unrelated diseases. However, there is an extensive body of evidence that very
strongly supports the formation of cystic and biofilm forms of ​Bb​ that can remain dormant for months to years
(Sapi et al. 2012). Based on this and studies of other spirochetal pathogens, we know that a dormant cystic
infection can persist indefinitely and continue to produce symptoms (or present as asymptomatic infection),
transmit infection, and still not invoke enough of an active immune response to test positive on immunological
assays. Additionally, ​Borrelia burgdorferi​ is known to possess numerous other mechanisms of evading and
possibly suppressing the immune response. (Berndtson, 2013. Bhattacharjee et al., 2013.) In light of these and
similar findings, Harvey and Salato propose a new model of borreliosis that places “Lyme Disease” as a small part
of a much larger global borreliosis pandemic (Table 2). This extensively challenges the current medical model of
borreliosis, and rightfully so. If we are to find a way to cure this awful pandemic, we must first recognize it for
what it is.
Table 2: Harvey and Salato (2003) proposed model of “Epidemic Borreliosis”
5

7. Erikson, 2015
Some of the most paradigm­shifting differences between the CDC model and the Harvey and Salato
Epidemic Borreliosis model are the epidemiological factors, placing the disease in a much larger worldwide
context. The idea that the primary vector is humans and that this is an ancient and worldwide epidemic, rather
than a new and localized zoonotic disease, in itself warrants a much larger and more serious investigation on the
part of medical science. Other major differences include the previously discussed inclusion of a broader
consideration of ​Borrelia​ agents and their vectors, characterization of persistent infection, more holistic diagnosis
criteria, a revised clinical timeline, and recognition of symptoms to fit this expansive consideration of the disease.
This model is a great step towards a better understanding of borreliosis, and it and similar work will hopefully
open the doors for patients to find recognition and understanding of their symptoms, as well as allow researchers
and practitioners to be supporting in developing effective and sustainable treatment protocols for all forms of
borreliosis.
Alternative Treatments of Epidemic Borreliosis
Although the mainstream medical community has not yet accepted a model of borreliosis that accounts
for persistent infection and a broader range of possible routes of infection and pathologies, alternative healthcare
practitioners and disillusioned doctors have been working very hard to develop effective treatment protocols for
patients denied effective care by the medical industry’s current Lyme Disease model. These practitioners are
required to look beyond antibiotics and consider the nuances of the realities of borreliosis ­ taking into
consideration its immune evasion tactics including cystic/biofilm forms, as well as holistically treating the wide
range of complex symptoms that come along with epidemic borreliosis infections that fall outside of the CDC
model. In this section I will talk about how a couple of practitioners have approached this in their practices.
Antioxidants and Thomas Levy
For years previous to starting this research, if you had asked me what I thought about antioxidants, I
would have gone on a long and passionate diatribe about the myths surrounding them. About how the public
conception of antioxidants resulted from a miscommunication between the scientific community and the public;
fueled by an extensive industry centered around marketing all kinds of common phytochemicals to misled people
looking for help fighting the hazards of 21st­century living at ridiculous prices (Melton, 2006.). I never would
have thought that I would be the person who just recently gave a 20­minute presentation to a group of pre­medical
students on the astounding potential health benefits of vitamin C. However, antioxidant therapy for borreliosis has
become the basis of my Division II (and probably III) research at Hampshire College.
Thomas Levy is well­known for his promotion of high­dose vitamin C for almost everything ­ or at least,
all diseases that are caused by oxidative stress, which he reports accounts for much of the diseases that we deal
with today. These include: cancer, atherosclerosis, autoimmune and infectious diseases, etc. Although he does not
discuss Lyme Disease specifically in his book, Levy cohesively describes the history and use of vitamin C to
prevent and treat disease in ​Primal Panacea​ (2011). He makes extensive and fantastic claims about the extent to
which this treatment can be useful, but seems to back it up with well­rationalized and broad scientific base. In
fact, he cites over 1,250 sources throughout the book, most of them peer­reviewed articles.
Figure 2: Ascorbic acid molecular structure and free radical reaction.
6

8. Erikson, 2015
Levy’s claims may be dramatic, but the molecular and clinical biology does seem to pan out. Vitamin C,
also known as ascorbic acid, is uniquely good at “scavenging” free radicals. Denisov and ​Afanas' ev (2005)
describe that ​as an acid, ascorbic acid readily loses protons, and is able to stabilize the resulting negative charge
across its ketone and alcohol groups (Figure 2), making the reaction favorable. Because of this it is readily able to
donate protons to “free radicals” ­ compounds with an unpaired electron in their outer shell ­ and balance that
radical electron like it does negative charge. Scandalios (2007) reports that ascorbic acid is also able to regenerate
itself via other biochemical processes within the cell so that it can go on to scavenge more free radicals. These
properties make ascorbic acid a very efficient and useful antioxidant. Valko et al. (2006) describes the role that
antioxidants and free radicals play in normal human health and disease states. They state that free radicals are
produced by a variety of normal cellular processes, and they play vital roles in some parts of signaling and even
immune responses. However, too many of them in the wrong places can cause serious damage. Pratt and Cornely
(2013) report the biochemical basis for the fact that free radicals cause chain reactions that can lead to DNA and
other cellular damage. This is known to cause a huge range of health problems including cancer, cardiovascular
disease, hypertension, neurodegenerative diseases, rheumatoid arthritis, and even ageing.
The destructive mechanisms of borreliosis are not well­known, but Pancewicz et al. (2001) and others
state that free radicals and antioxidants definitely play a crucial role in how the bacteria causes disease. Primarily,
Borrelia seems to be activated by free radicals and produces free radicals. Garcia­Monco and Benach (1997) find
that this causes a massive immune response, which creates tissue­damaging inflammation, and accounts for many
borreliosis symptoms such as erythema migrans and arthritis. However, the immune response’s primary way of
attempting to kill the bacteria is through the use of localized free radicals, and therefore small doses of vitamin C
have been both shown to suppress this immune response on a molecular level, as seen by Goldschmidt (1991) and
stimulate it on a cellular level, as seen by Li and Lovell (1985), and Leibovitz and Siegel (1977). Researchers
such as Miller (1969) have also investigated potential direct bactericidal mechanisms of ascorbic acid. So the idea
is that if we can utterly overwhelm the system with ascorbic acid, it is able to quench these free radical chain
reactions from the ​Borrelia​, but it won’t be counter productive by intercepting the useful bactericidal immune
response, because ascorbic acid is also potentially capable of killing the ​Borrelia​ on it own. A brand new study
from Goc et al. (2015) finds that ascorbic acid is an effective bactericidal agent against ​B.burgdorferi​ and
B.garinii ​spirochetes as compared to doxycycline and other plant­derived compounds, but found no susceptibility
against latent forms of ​Borrelia​. My research is in the same vein: testing the bactericidal effects of ascorbic acid
on ​Borrelia burgdorferi​ spirochetes and biofilms. There is still a lot to be researched on these mechanisms, but at
the end of it all we might finally find a treatment that works for all forms of borreliosis.
Herbalism and Stephen Harrod Buhner
Herbalism as it exists in the United States today primarily helps those who the biomedical institutions and
industry have failed. It picks up slack where mainstream medicine is unable to fulfill a need in people’s medical
experiences, and therefore often needs to develop its own protocols without the assistance of much medical
science. Because usually the science, for one reason or another, just isn’t there.
Stephen Harrod Buhner is a prominent author in Natural Medicine, having many popular titles under his
belt such as ​The Secret Language of Plants​, which many herbalists will refer to regularly for an understanding of
plant medicine that most of the scientific community just doesn’t address. Plants are more than just their
“primary” or “active” chemical constituents. They are living systems, every bit as varied and mysterious as any
other organism. So why does the biomedical community act as if it can “prove” or “disprove” a plant medicine by
extracting its active constituent and performing double­blind randomized placebo­controlled clinical trials? They
aren’t disproving herbal medicine if they aren’t actually using it. That being said, laboratory research can give us
crucial information in trying to understand ​why​ these medicines might be working.
In ​Healing Lyme​, Buhner (2005) discusses his experiences with and perspectives on what he calls “The
Lyme Wars” ­ many of the controversies I have discussed, and more. He then details his protocol for treating
patients that have not received adequate care from mainstream physicians. His core protocol contains:
Andrographis paniculata​, Japanese Knotweed (resveratrol, ​Polygonum cuspidatum​), Cat’s Claw (​Uncaria
7

9. Erikson, 2015
tomentosa​), and the optional Astragalus and Smilax (sarsaparilla). These herbs are discussed individually in detail
for their uses, history, role in Lyme disease, chemistry, etc. They are, supposedly, ​both antispirochetal and
bolstering to the immune system​. I believe that this particular concert of effects is what may make them a better
treatment option than antibiotics in many cases. Despite being a much more under­studied topic than Vitamin C
therapies, ​Healing Lyme​ still contains many references to primary literature. Buhner has published a book titled
Herbal Antibiotics​ (2012), which covers some of the herbs used in his protocols in greater depth. I will evaluate
some of this research as a representative example.
Example: Andrographis
The first and core herb in the protocol is andrographis, ​Andrographis paniculatum​. Buhner (2005)
describes the primary mechanisms of andrographis as immunostimulant, antibacterial, antiinflammatory, and
analgesic (pain­relieving), among other things. He justifies its use in the protocol with descriptions of its
antispirochetal, nervous calming and protecting, and liver protecting and enhancing. He emphasizes its ability to
readily cross the blood­brain barrier. It is also notable that it is supposedly clinically effective for a variety of
neglected tropical diseases. A cursory survey of the bibliography indicates that there may be good evidence for
the actions of andrographis and its “active” compound andrographolide against the neglected tropical diseases as
found by Dutta and Sakul (1985), some bacteria, as an antiinflammatory agent as seen by Balu and
Alagesaboopathi (1993), as an active agent against free radical damage in the liver as found by Koul and Kapil
(1994), and as an immunostimulant as shown by Puri et al. (1993). It seems that most of the logic of its use in
treating borreliosis must be inferred from these actions. Which is not unreasonable, as ​Borrelia​ does behave much
like a parasite in many ways, such as its immune evasion techniques. And of course, immune stimulation against
other bacteria, parasites, and viruses can somewhat reasonably be assumed to be helpful against ​Borrelia​ as well.
Overall, this research and logic holds up reasonably well, but there is still a sore lack of dedicated research on
alternative and especially herbal treatments for borreliosis.
Conclusion
Borreliosis exists within a massive mess of confusing and often conflicting information from many
sources, and it’s incredibly difficult to know who to trust, both as a scientist and as a patient. However, careful
digging into the available information can begin to uncover a fairly cohesive story that fits together without
contradictions. But this effort is greatly hindered by the CDC’s aggressive insistence on its Lyme disease model,
which is increasingly being questioned by the biomedical communities and the public at large. Various groups
have begun to propose models of the epidemiology and biology of borreliosis that fit the available scientific data
and reflect the clinical reality that this disease is a lot more prevalent, severe, complex, and difficult to treat than
the CDC would have us believe. It is therefore not unreasonable to consider borreliosis in its varied forms a true
pandemic. Because of the lack of available treatments for any patient falling outside of the very narrow CDC
definition of clinical Lyme disease, healthcare practitioners of all sorts are risking their credibility and even ability
to practice medicine by developing their own treatment protocols to fit these emerging independent models of
epidemic borreliosis. This pandemic urgently needs high­quality research to develop a clear understanding of its
biology and to develop effective treatment protocols for all manifestations of borreliosis and its co­infections. It is
my hope that as awareness of these realities spread, an increasing independent effort on the part of all sorts of
biologists, medical scientists, clinicians, etc. to create a body of research that simply cannot be overlooked. I am
very much looking forward to joining this effort as I proceed with my research on ascorbic acid and ​Borrelia
biofilms, and move on to Naturopathic medical school in the future.
8

10. Erikson, 2015
Bibliography:
Balu, S. and Alagesaboopathi, C.. 1993. “Anti­inflammatory activities of some species of Andrographis
Wall.(Acanthaceae).” ​Ancient science of life​, ​13​(1­2): 180.
Barbour, Alan G. 2015. ​Lyme Disease: Why It’s Spreading, How It Makes You Sick, and What to Do
about It​. Johns Hopkins University Press, Baltimore.
Berndtson K. 2013 “Review of evidence for immune evasion and persistent infection in lyme disease.”
International journal of general medicine​. ​6​: 291­306.
Bhattacharjee, A., Oeemig, J.S., Kolodziejczyk, R., Meri, T., Kajander, T., Lehtinen, M.J., Iwaï, H., Jokiranta,
T.S. and Goldman, A.. 2013. “Structural basis for complement evasion by Lyme disease pathogen
Borrelia burgdorferi.” ​Journal of Biological Chemistry​, ​288​(26): 18685­18695.
Bosler, E.M., Ormiston, B.G., Coleman, J.L., Hanrahan, J.P. & Benach, J.L. 1984, "Prevalence of the
Lyme Disease Spirochete in Populations of White­Tailed Deer and White­Footed Mice", ​Yale
Journal of Biology and Medicine, 57:​ 651­659.
Boylan, J.A., Lawrence, K.A., Downey, J.S. and Gherardini, F.C., 2008. “Borrelia burgdorferi membranes are the
primary targets of reactive oxygen species.” ​Molecular microbiology​, ​68​(3):786­799.
Buhner, S.H. 2005. ​Healing Lyme.​ Raven Press.
Buhner, S.H.. 2012. ​Herbal antibiotics: natural alternatives for treating drug­resistant bacteria​. Storey
Publishing.
Burgdorfer, W., Barbour, A.G., Hayes, S.F., Benach, J.L., Grunwaldt, E. & Davis, J.P. 1982. "Lyme
Disease­­A Tick­Borne Spirochetosis?" ​Science. 216(4552)​: 1317­1319.
Carroll, Michael C. 2005. ​Lab 257: The Disturbing Story of the Government’s Secret Germ Laboratory
HarperCollins, New York.
CDC, 2015a “Confirmed Lyme disease cases by age and sex ­­ United States, 2001­2010”
http://www.cdc.gov/lyme/stats/chartstables/incidencebyagesex.html
CDC, 2015b “Signs and Symptoms of Untreated Lyme Disease”
http://www.cdc.gov/lyme/signs_symptoms/index.html
CDC, 2015c “Post­Treament Lyme Disease Syndrome” http://www.cdc.gov/lyme/postlds/index.html
Denisov, E.T. and Afanas' ev, I.B., 2005. ​Oxidation and antioxidants in organic chemistry and biology​. CRC
press.
Desowitz, Robert S. 1981. ​New Guinea Tapeworms and Jewish Grandmothers ​W.W. Norton &
Company, New York.
Duffy, D.C., Campbell, S.R., Clark, D., DiMotta, C. & Gurney, S. 1994. "Ixodes scapularis (Acari:
Ixodidae) Deer Tick Mesoscale Populations in Natural Areas: Effects of Deer, Area, and
Location", ​Journal of Medical Entomology. vol. 31(1):​ 152­158.
Dutta, A. and Sukul, N.C.. 1982. “Filaricidal properties of a wild herb, Andrographis paniculata.” ​Journal of
helminthology​, ​56​(02): 81­84.
Garcia­Monco, J.C. and Benach, J.L.. 1997. “Mechanisms of injury in Lyme neuroborreliosis.” ​Seminars in
neurology.​ ​17​(1): 57­62.
Goc, A., Niedzwiecki, A. and Rath, M.. 2015. “In vitro evaluation of antibacterial activity of phytochemicals and
micronutrients against Borrelia burgdorferi and Borrelia garinii.” ​Journal of applied microbiology​,
119​(6): 1561­1572.
Goldschmidt, M.C.. 1991. “Reduced bactericidal activity in neutrophils from scorbutic animals and the effect of
ascorbic acid on these target bacteria in vivo and in vitro”. ​The American journal of clinical nutrition​,
54​(6): 1214S­1220S.
Harvey, W. T.; Salato, J. 2003. “‘Lyme Disease’: and ancient engine of an unrecognized borreliosis pandemic?”
Medical Hypotheses. 60:​ 742­759.
Koul, I.B. and Kapil, A.. 1994. “Effect of diterpenes from Andrographis paniculata on antioxidant defense system
9

11. Erikson, 2015
and lipid peroxidation.” ​Indian Journal of Pharmacology​, ​26​(4): 296.
Leibovitz, B. and Siegel, B.V. 1977. “Ascorbic acid, neutrophil function, and the immune response.”
International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin­und
Ernahrungsforschung. Journal international de vitaminologie et de nutrition​. ​48​(2): 159­164.
Leopold, A., Sowls, L.K. & Spencer, D.L. 1947, "A Survey of Over­Populated Deer Ranges in the United
States", ​The Journal of Wildlife Management, 11(2):​ 162­177.
Levy, T. E. 2011. ​Primal Panacea.​ MedFox Publishing. Henderson, NV.
Li, Y. and Lovell, R.T.. 1985. “Elevated levels of dietary ascorbic acid increase immune responses in channel
catfish.” ​The Journal of nutrition​, ​115​(1): 123­131.
Melton, Lisa. 2006 “The antioxidant myth: a medical fairy tale” NewScientist.com
Miller, T.E.. 1969. “Killing and lysis of gram­negative bacteria through the synergistic effect of hydrogen
peroxide, ascorbic acid, and lysozyme.” ​Journal of Bacteriology​, ​98​(3): 949­955.
Montgomery, RR & Malawista, SS. 1996, "Entry of Borrelia burgdorferi into macrophages is end­on and
leads to degradation in lysosomes", ​Infection and Immunity. 64(7): ​2867­2872.
Nelson, Christina A., Shubhayu Saha, Kiersten J. Kugeler, Mark J. Delorey, Manjunath B. Shankar,
Alison F. Hinckley & Paul S. Mead. 2015. “Incidence of Clinician­Diagnosed Lyme Disease,
United States, 2005–2010”. ​Emerg Infect Dis.​ ​21:​ 1625­1631
Pancewicz, S.A., Skrzydlewska, E., Hermanowska­Szpakowicz, T., Zajkowska, J. and Kondrusik, M., 2001.
“Role of reactive oxygen species (ROS) in patients with erythema migrans, an early manifestation of
Lyme borreliosis.” ​Medical Science Monitor​, 7(6): 1230­1235.
Pratt, C.W., Cornely, K. 2014. “Free Radicals and Aging”. ​Essential Biochemistry.​ Third Edition. Wiley
Publishing. 407.
Puri, A., Saxena, R., Saxena, R.P., Saxena, K.C., Srivastava, V. and Tandon, J.S.. 1993. “Immunostimulant agents
from Andrographis paniculata.” ​Journal of Natural products​, ​56​(7): 995­999.
Richter, D., Postic, D., Sertour, N., Livey, I., Matuschka, F.R. and Baranton, G.. 2006. “Delineation of Borrelia
burgdorferi sensu lato species by multilocus sequence analysis and confirmation of the delineation of
Borrelia spielmanii” ​International journal of systematic and evolutionary microbiology​. ​56​(4): 873­881.
Sapi, E.; Bastian, S.L.; Mpoy, C.M.; Scott, S.; Rattelle, A.; Pabbati, N.; Poruri, A.; Burugu, D.; Theophilus,
P.A.S.; Pham, T.V.; Datar, A.; Dhaliwal, N.K.; MacDonald, A.; Rossi, M.J.; Sinha, S.K.; Luecke, D.F..
2012. "Characterization of biofilm formation by Borrelia burgdorferi in vitro", ​PloS one 7(10):​ e48277.
Scandalios, J.G., 1997. ​Oxidative stress and the molecular biology of antioxidant defenses​. Cold Spring Harbor
Laboratory Press.
Steere, A. C., Malawista, S. E., Snydman, D. R., Shope, R. E., Andiman, W. A., Ross, M. R. and Steele,
F. M. 1977. “An epidemic of oligoarticular arthritis in children and adults in three connecticut
communities”. ​Arthritis & Rheumatism. 20(1): ​7­17
Steere, A.C., Coburn, J. & Glickstein, L. 2004, "The emergence of Lyme disease", ​The Journal of
Clinical Investigation. 113(8): ​1093­1101.
Tietjen, Marjorie. 2005. “Lyme Disease ­ A biological weapon?”
http://www.rense.com/general63/lyme.htm
Valko, M., Liebfritz, D., Moncol, J., Cronin, M.T.D., Mazur, M., Telser, J.. 2007. “Free radicals and antioxidants
in normal physiological functions and human disease.” ​IJBCB. 39​: 44­84.
Wormser, G.P., Dattwyler, R.J., Shapiro, E.D., Halperin, J.J., Steere, A.C., Klempner, M.S., Krause, P.J.,
Bakken, J.S., Strle, F., Stanek, G., Bockenstedt, L., Fish, D., Dumler, S.J. & Nadelman, R.B.
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. ​43(9):​1089­134.
10