By Erica Verrillo*
Lyme disease is a complex of bacterial, viral and parasitic infections that are transmitted to humans principally through the bite of an infected tick, although research shows that the infections may also be transmitted via mosquito, flea, mite, sand fly and other insect bites. In addition, they can be transmitted in-utero from mother to child, as well as through bodily fluids such as saliva, vaginal secretions and semen, and via blood transfusions. Co-morbidity with other conditions, such as mold illness, environmental toxicity, hypothyroidism and adrenal fatigue, is common.
Lyme disease is often misdiagnosed as chronic fatigue syndrome (CFS), myalgic encephalomyelitis (ME), fibromyalgia, Parkinson’s, multiple sclerosis (MS), lupus, arthritis and other illnesses as it mimics many dozens of other conditions and diseases, although these conditions are not always caused by Lyme.
Lyme disease is the most prevalent vector-borne illness in the United States and Canada, and it has surpassed HIV as the fastest growing infectious disease in both countries, as well as possibly in some European countries, Mexico and Australia. In 2013, the CDC estimated that there are upwards of 300,000 new cases of Lyme disease every year, although many thousands of cases are undiagnosed or misdiagnosed.
Lyme disease presents as a multisystem inflammatory disease that may first affect the skin as a rash. Symptoms may resemble those of the flu, including fever, chills, fatigue, body aches, and headache. Early Lyme disease is typically improperly treated, as most doctors have been taught that it can be cured with two weeks of antibiotic therapy, or people don’t typically manifest the characteristic bulls-eye rash for which Lyme disease is known. However, if it isn’t caught early, it quickly spreads to the joints, nervous system and other organ systems, by which time physicians may be baffled by the wide array of symptoms. Even if a proper diagnosis and treatment are given at this stage, many patients will continue to exhibit symptoms for many months or years, until the disease is brought into remission, or the ongoing inflammatory response is mitigated and damage to the organs/systems has been healed.
Typically, Lyme disease presents in three stages:
- Stage 1 occurs within 30 days of a tick bite and causes nonspecific symptoms, including fatigue, myalgias, arthralgias, headache, fever, chills, and neck stiffness.
- Stage 2, called the “early disseminated” stage, can set in soon after stage 1, but symptoms also manifest weeks to months after the bite. Musculoskeletal and neurologic symptoms are common.
- Stage 3, like early disseminated disease, can set in relatively soon after the initial infection, but can also be delayed months to years, depending upon the immune response of the host, virulence of the Lyme organisms, and other factors. At this stage, every system in the body is affected, including the neuroendocrine, musculoskeletal, digestive, cardiac and central nervous systems. Many people incubate the infections for years and manifest symptoms only after a stressful event.
Exposure to Lyme disease is sometimes indicated by a skin rash, called erythema migrans, which begins with a red bull’s eye of roughly five to six inches surrounding the tick bite. The appearance of the rash can be delayed for up to one to two weeks after disease transmission and can persist for three to five weeks. However, as many as 50-70% of all Lyme disease patients either do not get a rash or remember seeing one.
The highest infection rates are in the Northeastern United States, but Lyme disease is epidemic in every US region, including the Midwest, South, and West. It has spread rapidly throughout the US via the migration of infected animals and insects. Ticks known to carry Lyme disease have been identified in all 50 states and on every continent worldwide.
The History of Lyme Disease
Lyme disease is named after the towns of Lyme and Old Lyme, Connecticut, two adjacent communities located at the base of the Connecticut River where it meets the Atlantic. In 1975, Polly Murray, a woman from Lyme, Connecticut, contacted the Connecticut Department of Health Services to report a strange illness that was afflicting her as well as her husband and children, and many other inhabitants of the town. Polly had experienced a baffling array of symptoms that had stumped doctors since the 1960s, but when her husband and children began to experience similar symptoms – joint pain, headaches, sore throats, rash – she realized that they were all suffering from the same disease.
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Coincidentally, Judith Mensch, who lived just a few miles away in Old Lyme, Connecticut, called the Department of Health Services at about the same time. Her daughter, Anne, had been diagnosed with juvenile rheumatoid arthritis. Judith, who was married to a pathologist at Memorial Hospital in New London, questioned the diagnosis after noticing the same symptoms in her neighbors and her neighbors’ children.
A physician at the Connecticut Department of Health Services, Dr. David Snydman, was concerned by the odd combination of symptoms, particularly the rashes, headaches and swollen joints, and promptly called Dr. Allen Steere at Yale University. The two physicians had worked together at the CDC’s Epidemic Intelligence Service, a program set up in the 1950s to track epidemics worldwide. As a consequence, they were both trained to look for the indications of an epidemic. Like Dr. Snydman, Dr. Steere realized that something novel, and possibly infectious, was happening in Lyme. He met with Polly Murray and soon afterward began testing the 39 children and 12 adults that Polly had identified in her neighborhood as having similar symptoms to her own.
Two years later, Dr. Steere published the paper that was to put Lyme disease on the map: “Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three Connecticut communities.” While the paper suggested an arthropod vector, it wasn’t until 1982 that an entomologist, Dr. Willy Burgdorfer, discovered the bacterium that caused Lyme disease. Dr. Burgdorfer had been analyzing deer ticks suspected of carrying Rocky Mountain Spotted Fever (RMSF) when he saw something unexpected under the microscope. In the mid-gut of the tick, he noticed spirochetes, spiral-shaped disease-causing bacteria. Deer ticks had not been known to carry spirochetes, but further testing confirmed the bacteria caused Lyme disease. This discovery gained Burgdorfer worldwide recognition, and the honor of having the bacterium named after him.
Manifestations of what we now call Lyme disease were first reported in the medical literature in Europe in 1883 when Alfred Buchwald, a physician in Breslau, Germany (now Wroclaw, Poland), reported a degenerative skin condition called “acrodermatitis chronic atrophicans” in his patients. It was later found that this condition was a symptom of the European strain of Lyme disease. In 1909, Swedish dermatologist Arvid Afzelius was the first to identify the classic ring-shaped rash associated with Lyme disease. He named it “erythema migrans.” Publishing his research 12 years later, he theorized that the rash was the result of a tick-borne infection, specifically members of the genus Ixodes. Neurological symptoms associated with an Ixodes tick bite, including paralysis, palsy, headache, and double vision, were reported in 1922 by two French physicians, Charles Garin and A. Bujadoux, and again in the early 1940s by the German neurologist Alfred Bannwarth. The neurological symptoms associated with Lyme are known as Garin-Bujadoux-Bannwarth, or Bannwarth’s, Syndrome.
Although the disease did not gain full recognition in the United States until the Lyme outbreak in the 1970s, the first report of relapsing fever due to a tick bite (Borrelia hermsii) was as long ago as 1915 when five patients fell ill in Colorado. In 1970 a physician in Wisconsin, Rudolph Scrimenti, reported the first case of erythema migrans in the U.S. Based on European reports regarding tick-related infection, he treated it with penicillin, which had become commercially available in 1942.
Since Willy Burgdorfer’s discovery of the bacterium that causes Lyme disease, over 36 species of borrelia have been identified, over 20 of which are capable of causing disease, and several dozens of strains of Babesia, Bartonella and other Lyme co-infections have also been identified.
* Erica Verrillo is ProHealth’s expert editor for the ME/CFS HealthWatch and Natural Wellness newsletters. She is the author of Chronic Fatigue Syndrome: A Treatment Guide, 2nd Edition, available as an electronic book on Amazon,Barnes & Noble, Kobo and Payhip (PDF file). Her website,CFSTreatmentGuide.com, provides practical resources for patients with ME/CFS. She also writes a blog, Onward Through the Fog, with up-to-date news and information about the illness, as well as the full text of CFS: A Treatment Guide, 1st Edition (available in translation).
Afzelius , Arvid. Erythema chronicum migrans. Acta dermato-venereologica, Stockholm, 1921, 2: 120-125.
Brody, Jane E . Lyme Disease Broadens Its Range. New York Times, June 28, 1983
Burgdorfer W, Barbour AG, Hayes SF, Benach JL, Grunwaldt E, Davis JP. Lyme disease-a tick-borne spirochetosis? Science. 1982 Jun 18;216(4552):1317-9.
Garin, Ch. and A. Bujadoux. Paralysie par les Tiques. Journal de médecine de Lyon, 1922, 71: 765-767.
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Murray, Polly. The Widening Circle: A Lyme Disease Pioneer Tells Her Story
Steere AC, Malawista SE, Snydman DR, Shope RE, Andiman WA, Ross MR, Steele FM. Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three Connecticut communities. Arthritis Rheum. 1977 Jan-Feb;20(1):7-17
Last Updated: 4/21/15
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