A Sour Twist of Lyme, Overview

The Ticking Time Bomb of the Lyme Epidemic

by Geoff D'Arcy, Lic. Ac.

This past summer, after experiencing four days of a very high fever followed by intense chills, I was diagnosed with Lyme disease (LD). I live in the very small wooded Massachusetts town and in the months following my diagnosis and recovery, though I have been treating LD in my practice on and off for 10 years, I was astonished by the large number of friends and neighbors who shared with me that they, too, had been recently infected with Lyme. The stories I was hearing were so dramatic and recent that LD was clearly on a major up-swing, people spoke of having debilitating symptoms, months of recovery, intravenous antibiotics and more. I began to research and ask more questions. Where had this disease originated?  Why is it so mysterious, misdiagnosed, and misunderstood?  Why are the symptoms so varied?  I began to update myself and read lots of books and articles about this unusual tick-borne illness.  I discovered that the prevalence of Lyme in our area is increasing at astounding rates. It has become clear to me that there remains a lot of mystery about Lyme, and that there is a growing need to understand treatment options, and that we need to educate ourselves about prevention. In this article I will explain what I have learned and to try to make some sense about integrative treatment options and give some prevention guidelines.


Lyme disease (LD) is an infection caused by Borrelia burgdorferi, a type of bacterium called a spirochete that is carried inside the stomachs of ticks. These ticks are in turn, carried by deer, mice and chipmunks. (Ticks can be as small as the period at the end of this sentence, sometimes barely visible to the naked eye.) Transmission has also been confirmed to come from mites, and biting flies. When an infected tick bites, it can take up to 12 to 48 hours of feeding to transmit the spirochete bacteria. The degree of infection and how severe or chronic the symptoms become is directly related to the health of our immune system. If left un-treated or un-defeated by our immune system, and a beachhead is established, this amazing stealth bacterium can thrive and multiply. It travels through the bloodstream, and tries to establish itself in various body tissues. It has a special affinity for joints, collagen in skin, knees, (causing joint pain and swellings,) the aqueous humor of the eye, the meninges of the brain and heart tissue.


LD is called the “New Great Imitator” because, like syphilis, it attacks multiple organ systems and mimics many diseases. (Both diseases are caused by a spirochete.) If ignored, the early symptoms may disappear but more serious problems can develop months, even years later. LD has been linked to over 300 diseases including Parkinson’s, MS, ALS, Chronic Fatigue Syndrome and Fibromyalgia.


Many of us have heard of the “bull’s eye rash,” the known indicator that we’ve had a tick bite. The “bull’s-eye” usually appears 3 to 30 days after infection; however this is not fool proof; I have discovered that only 30-50% of those infected have had such a rash. (In my case there was no bulls-eye or sign of a bite). Some of us may also know that LD can produce arthritic-like symptoms; yet most are really surprised to learn that if left unchecked, it can become chronic. In these cases, symptoms may cover a broad spectrum, often appearing similar to other diseases, which can camouflage accurate diagnoses. Symptoms can range from meningitis, Bell’s palsy, heart problems, nervous system abnormalities, neurological complications, headaches, depression, disturbances in memory, and disruption of sleep.


LD was first recognized in the United States in 1975 by Dr. Allen Steere, following a “mysterious” outbreak of juvenile rheumatoid arthritis near the community of Lyme, Connecticut. The rural location of the Lyme outbreak and the onset of illness during summer and early fall, suggested that the transmission of the disease was by an insect, or tick. It was only in 1982 that researchers began to connect the dots. The trouble causing bacterium was discovered by Dr. Burgdorfer, who had the dubious honor of giving his name to this formidable spirochete, Borrelia burgdorferi (Bb). Since then, reports of LD have increased dramatically to the point where the disease has become a critical public health concern in some areas of the United States. Today, LD is the most prevalent tick-borne illness in the United States, spreading in a concentric circle from its epicenter, Lyme, CT, and infecting the suburban and rural Eastern seaboard at an alarming epidemic-like rate.


Presence of co-infections that go along on LD’s ride


Other tick-borne infections can further complicate an already complex picture.


Bb may be co-transmitted with Babesiosis, Ehrlichiosis, and Bartonella co-infections. One study found, that 1-in-5 were seropositive for Bb also Ehrlichiosis (DeMartino, Carlyon et al. 2001). 10%-to-60% for Babesiosis (Rubel, 2003c; Kraus, McKay et al, 2002).


How fast is this danger to ourselves and our families growing?


Dan Kinderleher, M.D., an expert on Lyme disease, stated on the Today Show on June 10, 2002, that the number of cases may be 100 times higher than reported (With eighteen million in the United States alone).


Kenneth Singleton, M.D., in his book, The Lyme Disease Solution, reports, that:  “In 2005, there were potentially more than 460,000 new cases of Lyme disease.” However, in order to report a case to the Center for Disease Control and Prevention, [CDC] it takes 3 blood tests. Most people, (myself included), test positive to antibodies (giving proof that dead spirochetes have been cleaned-up,) and having no further symptoms, do not go on to get the second and third tests. Many researchers therefore believe that the real numbers the CDC reported should be much higher.


The double whammy that spikes the LD infection rates.


Two major factors contribute to the vast spread of LD. One, the deer population has increased extensively. Since 1900, the U.S. deer population has multiplied 70-80 times, from 500,000 to 35-40 million, providing the environment that contributes to a wild-fire spread of LD. Along with this, the percentage rate of infection of ticks has increasing alarmingly. The increasing hidden epidemic lurks in our back yards, woods and hiking trails. Add to this the school of medical thought that is denying the existence of chronic Lyme, and we have a potent mix for a dangerous epidemic. The time bomb is ticking...


In one of the few counties in the country where long-term studies have been done, an increase of infection of ticks 41.5% nymphal-tick stage was reported. The more that deer ticks are infected, the more people will become infected. The infection rate of ticks and people seems to be increasing dramatically, carried farther a field, every year by deer.


New Jersey infection rate of ticks doubles over four years.


In a random selection of ticks in 2004 in New Jersey, results showed that 33.6% tested positive for Borrelia burgdorferi (Bb), (Adelson, Rao et al., 2004). Recently in May of 2008, the Connecticut Easton Courier reported, “The average infection rate of ticks collected from multiple sites was reported at 60%; 78% at one location.” That’s an increase in the infection rate of ticks that has doubled over 4 years!! The time bomb is ticking louder...


A few towns are beginning to form alliances to better manage deer and understand ticks and their lyme infections. There are 14 towns in the alliance in Connecticut, the Courier also states, “Previously reported rates of infection in ticks have been in the range of 22% to 38% over the last four years. Increasing winter survival of deer and reduced hunting in the suburbs is contributing to the growing populations of ticks in our towns,” said Dr. Georgina Scholl, the Alliance’s research chairman. Clearly the infection rate within ticks is rapidly increasing and therefore increasing our exposure to LD. “It was as high as 78% at one site.”


Massachusetts, 109% increase over 2006

Acton, MA: 5% infection rate

Dover, MA: 10% infection rate

Nantucket, MA:  100% increase since 2006


In 2007, Massachusetts reported 2,988 blood test confirmed cases to the CDC; making the actual number well over 30,000 infected. Showing an increase of 109% over 2006. (lymediseaseassociation.org)


According to the Acton Health Department, in fiscal year 2008, there were 83 blood test-confirmed cases of LD in Acton, compared to just 19 the year before. So let’s take Acton’s population of 20,000 with a possible infection rate of ten times the reported number! That’s an infection rate increase up by 400% in the last year. Approximately 5% of Acton could be infected.


Quoted recently in the Dover Sherborn Press, Dr. Kruskall at Metro West Medical Center, and a Dover resident, said “Dover is ground zero for Lyme disease in Massachusetts, in my experience. I would venture to say that 10 percent of Dover residents have had Lyme disease, and that’s a horrendous number. Dr. Kruskall goes on to say, “…up to 500 deer may need to be killed or removed from Dover.”


According to the Boston Globe, “Nantucket is reporting a spike in cases of Lyme disease, with 262 people already diagnosed this summer of 2008, up nearly 39 percent from last year, with time (4 more months left) to climb.” This is a 100% increase in infection over 2006! (Multiply that number by 10, and you get the true probability.)


It appears we are reaching a tipping point of a pandemic. We need an urgent effort to reach out and educate people, especially in high risk towns and for those with high risk jobs.


In my opinion, it is not the deer alone that create the biggest risk factor, it is our pets. It is our beloved dogs and cats that are carrying the ticks into our homes. If we let our pets up on the furniture and beds, the risk factor increases again.


Three Stages of LD identified


1. Early Infection. Some get a bull’s-eye rash. However, not all rashes that occur at the site of a tick bite are due to Lyme disease. An allergic reaction to tick saliva can be the trigger.


2. Spreading Stage. Occurs days-to-weeks following infection. At this stage the spirochetes spread through the blood to other far-flung body tissues. Often those infected complain of: fatigue, chills and fever, headache, muscle and joint pain, swollen lymph nodes, secondary annular skin lesions.


3. Persistent Infection. Some symptoms and signs of Lyme disease may not appear until weeks, months, or years after a tick bite. This typically involves intermittent episodes of joint pain, meningitis, Bell’s palsy, cardiac involvement, migratory pain to joints, tendons, muscle and bone. Arthritis-like symptoms, especially in the knees is common, also erosion of cartilage and/or bone. Nervous system abnormalities can include numbness, pain, and depression, disturbances in memory, mood, or sleep patterns, and sensations of numbness and tingling in the hands or feet. Neuro-psychiatric symptoms are common, due to brain swelling.


Joseph Burrascano, MD, known for his work on Lyme, defines chronic Lyme disease: “To be said to have chronic LB (Lyme Borrelia), these three criteria must be present:


1. Illness present for at least one year (this is approximately when immune breakdown attains clinically significant levels)


2. Have persistent major neurological involvement (such as encephalitis/encephalopathy, meningitis, etc.) or active arthritic manifestations (active synovitis)


3. Still have active infection with B. burgdorferi (Bb), regardless of prior antibiotic therapy (if any).”


Blood Tests are not 100% accurate because Bb is known to dwell deep within the body’s tissues, making it really difficulty for proper detection. If that’s not bad enough it shape-shifts… Bb is known as "polymorphic", meaning that it "morphs" into different forms in the body. Three forms are known to date including: spirochete, spheroplast and cyst forms, probably the result of an evolutionary adaptation to stressful environments where the organism can change into "dormant" forms to avoid harsh conditions. They gravitate to areas in the body that exhibit a high density of fatty acids such as the brain, and feed there. Spirochetes also utilize sugar as an energy source which is why a diet low in sugar intake is recommended during treatment to prevent further proliferation.


Bb also has an uncanny ability to "evade" the immune system by hanging-out deep within tissues and in areas such as joint capsules that are insulated from immune system effects. This may be one of the reasons that LD can be a "latent" infection that requires some sort of "trigger" to initiate symptom onset. Other factors such as the strength of the host’s immune system, the spirochetal load inserted at the time of the tick bite, and the presence of co infections may contribute to a "dormant" appearance of the disease. Nonetheless, silent proliferation of the bacteria over time can render a host chronically ill with fatigue, malaise and a plethora of other disabling symptoms.


The CD-57 Test


Dr. Burrascano also states: “Our ability to measure CD-57 counts, represents a breakthrough in LB, (Lyme Borrelia) diagnosis and treatment. Chronic LB infections are known to suppress the immune system and can decrease the quantity of the CD-57 subset of the natural killer cells. In HIV infection, abnormally low T-cell counts are routinely used as a marker of the activity level of the infection; in LB, we can use the degree of decrease of the CD-57 count as an indicator how active the Lyme infection is and whether, after treatment ends, a relapse is likely to occur. It can even be used as a simple, inexpensive screening test, because at this point we believe that only Borrelia (Bb) will depress the CD-57. Thus, a sick patient with a high CD-57 is probably ill with something other than Lyme, such as a co-infection.”



More evidence has accumulated indicating the severe detrimental effects of the concurrent use of immunosuppressant drugs, including steroids in the patient with active B. burgdorferi infection. Many LD friendly M.D.s believe strongly that steroids or any other immunosuppressant should never be given to any patient who may even remotely be suffering from LD, because serious, permanent damage may result, especially if given for anything greater than a short course.

LD’s Minefields


I want to offer some background information about the two major controversies bubbling around LD. One is related to the two warring conventional treatment camps. And the second is related to the location of what is known as the epicenter of the disease: Lyme, Connecticut.


1. Conflicting Medical Treatment Camps Confuse Patients


One conventional medical camp the Infectious Disease Society of America (IDSA) says for treatment of Lyme, take 10 to 21 days of antibiotics and you are cured! The other says LD can be chronic for many years. The existence of chronic and persistent LD is hotly debated in medical communities. The 2006 guidelines of the IDSA denies a need for long-term treatment, effectively leaving chronic LD sufferers high and dry, recommending no more than 21-28 days of antibiotic treatment, (after that, its all in your head). Many health professionals and researchers in this camp, claim that chronic LD is over-diagnosed and not only that, it will censure MDs practicing outside of their guidelines.


In the other camp, are the Lyme-literate health practitioners, the International Lyme and Associated Diseases Society (ILADS) takes a much more progressive approach to treatment and diagnosis, claiming under-diagnosis is rife among non-Lyme-literate-medical-professionals and that long-term antibiotic treatment may be necessary. Many chronic LD sufferers have found themselves cut-off by their insurance companies and their MDs because of IDSA guidelines.


However, things are shifting. An investigation by the Attorney General of Connecticut forced the ISDA to re-consider. Attorney General Richard Blumenthal’s antitrust investigation has uncovered serious flaws in the Infectious Diseases Society of America’s (IDSA) process for writing it’s 2006 LD guidelines and the IDSA has agreed to reassess them with the assistance of an outside arbiter.


2. LD’s Lyme, Connecticut Origin Controversy


Enter the conspiracy theorists. Some things to consider: the LD bacteria, Bb is an ancient bacteria, estimated to have lived in ticks for a 100 million years (Buhner). There is some evidence of Bb in the Tchefuncte Indians of Louisiana between 500 BCE and 300 CE and, Bb may have spread to Europe around 1492. So, these bacteria have co-existed with humans causing disease for quite a while. Why, then, did it spring up suddenly in 1976 in a cluster of juvenile arthritis cases? Why is Lyme, Connecticut the epicenter? Since 1976, Bb has spread out, like a wild fire in a concentric circle from Lyme, Connecticut.




Less than 2 miles off the East end of Long Island and a few miles from Lyme in Connecticut lies Plum Island, an 840-acre island not listed on any map (try mapquesting it). A top secret government Type 3 Bio-Hazard lab is authorized to use lethal force for any incursion on the island. Workers have been ferried over to this Island, from yes, you’ve guessed it, Lyme, Connecticut for decades. The first cases of LD in 1976 were reported in people living yards from the ferry dock.


According to Michael Carroll in his book, Lab 257, reveals the frightening true story of an unknown island situated in the shadow of New York City, nestled within the playground of America’s elite, the Hamptons. Unveiled as a Cold War biological warfare laboratory, Plum Island struggled for half a century in the name of animal science for the U.S. Department of Agriculture, and is now in the hands of the new Department of Homeland Security. Yet its achievements have been marred by outrageous biological and environmental mishaps. A shoddily built and poorly managed germ lab that threatens our environs with biological and ecological pollution, Plum Island remains -- at this very moment, as Lab 257 shows -- a ticking time bomb.


Is it a coincidence that there was work being conducted on Plum Island with dangerous animal diseases, that there were apparently sloppy safety measures of its weaponizing bacteria protocols in the 1950’s and 60’s*, that there is some evidence of its work with ticks, that the workers are ferried to the island from Lyme, that there was an outbreak of LD in Lyme, Connecticut? (*Note that the Lab had to aggressively suppress a full scale foot-and-mouth virus outbreak on the Island that leaked from its research.) Is it a far-fetched idea that this weaponizing research into, or enhancing, a tick’s ability to infect, has leaked out into the tinder-box like environment of the mainland, and sparked the wild-fire spread throughout the Eastern seaboard? It may sound incredible, but I’ve heard that some reputable researchers quietly, consider this a highly possible and credible contributing factor to the outbreak of LD in this area, if not the downright instigator.


There are two sides to every story, however. The prevailing scientific view suggests that Bb infections were a fact of life in early American history that went largely unnoticed amid the harsh reality of frontier life. They argue that mass deforestation of the Northeast due to the clearing of land for agriculture and settlement in the 19th and early 20th century resulted in a collapse of white-tailed deer populations, the primary carriers of the deer tick, and hence the tick became too scarce to infect people with Bb. Many theorize that Long Island served as a refuge for relict populations of deer in the area. Then, as land-use patterns changed in the latter half of the 20th century, woodlands and forests recovered in the Northeast, along with deer and deer ticks. (Ranga, Trivedi, et al. 1997; Stricker, 2006). Infected ticks have been found on migratory birds that travel between states, countries and continents (Gardner, 2001).