It is a popular misconception that Lyme disease was discovered in the late 1970's in Lyme, Connecticut. However, medical literature is actually rich with more than a century of writing about the condition, although most of it has been published only in Europe.

The first record of a condition associated with Lyme disease dates back to 1883 in Breslau, Germany, where a physician named Alfred Buchwald described a degenerative skin disorder now known as acrodermatitis chronica atrophicans (ACA).

In a 1909 meeting of the Swedish Society of Dermatology, where a physician named Arvid Afzelius presented research about an expanding, ringlike lesion he had observed. Afzelius published his work 12 years later and speculated that the rash came from the bite of an Ixodes tick.

Throughout the early twentieth century, associations were being made among many of the symptoms and signs that constitute Lyme disease. Some of these associations were: joint involvement in patients with late disease (1921), the link between the EM rash and neurologic problems (1922), psychiatric symptoms in patients with the EM rash (1930), patients with benign lymphocytomas observed to also have either EM or ACA (1934), and the description of heart involvement that appeared in patients with both the EM rash and arthritic symptoms (1934). By mid-century, physicians were experimenting with still-novel antibiotics and reporting successful results.

In 1970, for the first time, an incidence of EM known with certainty to have been acquired in the United States was reported by Rudolph Scrimenti, who diagnosed and treated a patient who had been bitten by a tick while hunting grouse in Wisconsin and acquired the disease.

In 1976, the first US case of clustering of this disease was reported by researchers at the Naval Submarine Medical in Southwestern Connecticut.

In 1977, physician Allen Steere et al described the first clustering of the disease misdiagnosed as juvenile rheumatoid arthritis. They named this condition 'Lyme arthritis'.

In the early 1980's, an entomologist at the United States Rocky Mountain Laboratories of the National Institutes of Health by the name of Willy Burgdorfer, MD, Ph.D., was investigating outbreaks of Rocky Mountain spotted fever. Research scientists Jorge Benach and Edward Bosler, Ph.D. collaborated in the dogged and dangerous work of gathering and testing ticks for disease-causing pathogens. During the course of the research, attention shifted from dog to black-legged ticks and in the fall of 1981, one of the batches of ticks yielded something dramatically new. Burgdorfer noticed an embryonic form of parasite in the body fluid of two of the ticks. Guided by his extensive knowledge of the early scientific writings of European researchers, he undertook a very close inspection of the tick--and found poorly stained, sluggish spirochetes. Within a year, the spirochetes had been named Borrelia burgdorferi (Bb), in his honor, and definitely identified as the causative agent of Lyme disease. Dr. Burgdorfer was the partner in the successful effort to culture the spirochete, along with Alan Barbour, MD.

Next came a period of consolidating and expanding of knowledge. After the discovery of Bb and the diseases associated with it, researchers began to learn more about how the infection lodges itself in the body. In 1985, Paul Duray, a Lyme disease researcher, declared that the Lyme disease bacterium disseminates itself through the body early in the course of infection. The prevailing wisdom at the time was that infection was slow to. Duray's findings are now the prevailing thought. Also in 1985, Burgdorfer was able to demonstrate that ticks infected with the Lyme spirochete could be found across the country.

In 1988, the LDF was founded and started the major push to bring Lyme disease in the spotlight. It was the effective partnerships among patients, government officials, and researchers that enabled volunteers around the world to bring Lyme disease the attention that has helped make it a household term.

The causative agent, Borrelia burgdorferi, is a type of spirochete. Spirochetes are long, thin, spiral-shaped bacteria. Other spirochetes include the causative agents of syphilis, relapsing fever, and gum disease.

The bacterium is thousands of times larger than a virus. However, it still requires a powerful microscope to see one. Roughly 1,500 Bb must be laid end to end to equal one inch. About 100,000 of Bb laid side to side would equal one inch.

When Bb was first discovered in 1982 it was thought that there was just one strain. Since then, about 100 U.S. and 300 worldwide strains of the bacterium have been discovered.

In the mid-1990's genospecies were formed to group the many variations into subcategories.

" Borrelia burgdorferi sensu lato" is name given to the overall category. In North America there is just one genospecies variant - Bb sensu stricto. In Europe there are three categories Bb sensu stricto, B. garinii, and B. afzelii. Asia has B. garinii and B. afzelii. Japan has B. japonica and B. miyamoto. These groups are evolving as new research discoveries occur.

A new pathogen causing Lyme or "Lyme-like" disease has been reported. While not culturable, it has been named B. lonestari sp.

The bacterium is able to move around the body through the bloodstream and between tissue. It can also invade tissue, replicate, and leave the cell - destroying the cell as it emerges. Sometimes, as the bacterium emerges, the cell wall collapses around the bacterium, forming a "cloaking device". This action may aid the bacteria's ability to hide from the immune system response.

Treatment varies and depends on how early a diagnosis is made and the organ system(s) involved. No definitive treatment regimens have been determined, and failures occur with all protocols.

Oral antibiotics may be sufficient for early stages of non-disseminated infection.

Long-standing or Disseminated Lyme Disease responds best to one or several courses of either oral or intravenous antibiotics.

Physicians and researchers agree that it is unethical not to treat people with demonstrated, persisting infection. Therefore, some people receive retreatment or longer treatment.

There is no test that can determine if a patient is infected with the LD bacterium and then demonstrate that the patient has become bacterium-free. Therefore, LD is clinical diagnosis, based on signs and symptoms, with the patients travel history to endemic areas and test results being additional pieces of information in the complete picture. No test can "rule-out" Lyme disease.

WHAT LABORATORY TESTS AID IN THE DIAGNOSIS?

INDIRECT TESTS (Antibody Tests)

Antibodies are the immune system's response to "fight off" infection. Tests strive to be both sensitive (detecting any LD antibodies) and specific (detecting just LD antibodies).

Test Interpretation

• False Negative tests occur due to defects in test sensitivity; too low an antibody level to detect (e.g. they are bound to the bacteria, with too few free-floating; the patient taking antibiotics or other drugs; naturally low antibody production); the bacterium has changed, limiting recognition by the immune system; or bacterial strain variations.
• False positive tests occur due to test failure or cross-reacting antibodies (e.g. syphilis, periodontal disease, ANA or RF).

Types of Tests

• Titer (ELISA, EIA, IFA) - These tests measure the level of Bb antibodies in fluid. Laboratories use different detection criteria, cut-off points, types of measurements, and reagents.
• Western blot - This test produces bands indicating the immune system's reactivity to Bb. Laboratories differ in their interpretation and reporting of these bands.
• C6 Lyme Peptide ELISA - identifies antibodies to a consistent surface protein that is present on every known strain of the Lyme disease bacteria, Borrelia burgdorferi (Bb). The C6LPE is more sensitive for diagnosing all stages of Lyme disease, including those patients with late stage Lyme disease.

DIRECT DETECTION TESTS

• Antigen detection - These tests detect a unique Bb protein in fluid (e.g. urine) of patients. This may be useful for detecting LD in patients taking antibiotics or during symptom flare-up.
• Polymerase chain reaction (PCR) - This test multiplies the number of Bb DNA to a detectable measurable level.
• Culturing - Growing the bacterium in culture is difficult and can take months.

LD symptoms can imitate other diseases and can be misdiagnosed.

EARLY LOCALIZED DISEASE

Signs and symptoms of Early Local Lyme Disease often starts with flu-like feelings of headache, stiff neck, fever, muscle aches, and fatigue. About 60% of light-skinned patients notice a unique enlarging rash, referred to as erythema migrans (EM), days to weeks after the bite. On dark-skinned people, this rash resembles a bruise.

The rash may appear within a day of the bite or as late as a month later. This rash may start as a small, reddish bump about one-half inch in diameter. It may be slightly raised or flat. It soon expands outward, often leaving a clearing (normal flesh color) in the center. It can enlarge to the size of a thumb-print or cover a persons back.

To be considered local disease the rash must be at the tick bite site with no other major organ system involvement. A rash occurring at other than the bite site in an indication of Disseminated Lyme Disease.

Don't confuse a local reaction to a tick bite, with signs of infection. A small inflamed skin bump or discoloration that develops within hours of a bite and over the next day or two is not likely to be due to infection - but rather a local reaction to the disruption of the skin.

DISSEMINATED LYME DISEASE

Some people do not notice these early indicators of infection. Early manifestations usually disappear, and disseminated (other organ system involvement) infection may occur. General symptoms alone do not indicate Lyme disease.

GENERAL
Profound fatigue, severe headache, fever(s), severe muscle aches/pain.

BRAIN
Nerve conduction defects (weakness/paralysis of limbs, loss of reflexes, tingling sensations of the extremities - peripheral neuropathy), severe headaches, stiff neck, meningitis, cranial nerve involvement (e.g. change in smell/taste; difficulty chewing, swallowing, or speaking; hoarseness or vocal cord problems; facial paralysis - Bell's palsy; dizziness/fainting; drooping shoulders; inability to turn head; light or sound sensitivity; change in hearing; deviation of eyeball [wandering or lazy eye], drooping eyelid), stroke, abnormal brain waves or seizures, sleep disorders, cognitive changes (memory problems, difficulty in word finding, confusion, decreased concentration, problems with numbers) and, behavioral changes (depression, personality changes).

Other psychiatric manifestations that have been reported in the scientific literature include: panic attacks; disorientation; hallucinations; extreme agitation; impulsive violence, manic, or obsessive behavior; paranoia; schiziphrenic-like states, dementia, and eating disorders. Several patients have committed suicide.

EYES
Vision changes, including blindness, retinal damage, optic atrophy, red eye, conjunctivitis, "spots" before eyes, inflammation of various parts of the eye, pain, double vision.

SKIN
Rash not at the bite site (EM) - This skin discoloration varies in size and shape; usually has rings of varying shades, but can be uniformly discolored; may be hot to the touch or itch; ranges in color from reddish to purple to bruised-looking; and can be necrotic (crusty/oozy). The rash may develop a bull's-eye rash or target look. The shape my be circular, oval, triangular, or a long-thin ragged line.

Other disseminated skin problems include:

• lymphocytoma, which is a benign nodule or tumor, and
• acrodermatitis chronica atrophicans (ACA) which is discoloration/degeneration usually of the hands or feet.

HEART and BLOOD VESSELS
Irregular beats, heart block, myocarditis, chest pain, vasculitis.

JOINTS
Pain - intermittent or chronic, usually not symmetrical; sometimes swelling; TMJ-like pain in jaw.

LIVER
Mild liver function abnormalities.

LUNGS
Difficulty breathing, pneumonia.

MUSCLE
Pain, inflammation, cramps, loss of tone.

STOMACH and INTESTINES
Nausea, vomiting, diarrhea, loss of appetite, anorexia.

SPLEEN
Tenderness, enlargement.

PREGNANCY
Miscarriage, premature birth, stillbirth, and neonatal deaths (rare). Congenital LD has been described in medical literature.

It is possible for the bacterium to pass from mother to fetus across the placenta, resulting in congenitally acquired LD. A link between LD and adverse outcomes in pregnancy is under investigation. However, most studie