Lyme Disease

Lyme Disease

Dr. KennedyDefinition

Lyme disease, or borreliosis, is an infectious disease caused by a spirochete bacteria, primarily Borrelia burgdorferi in the U.S. and Borrelia afzelii or Borrelia garinii in

Europe. The vector for the infection is usually and classically an infected “black-legged” or “deer” tick, however other carriers, including other ticks in the Ixodes genus, have been

implicated in disease transmission. Borrelia is the predominant cause of Lyme disease in the U.S. The disease varies widely in its presentation which may include a rash and flu-like symptoms

in its initial stage, followed by musculoskeletal, arthritic, neurologic, psychiatric and cardiac symptoms. In most cases of Lyme disease symptoms can be eliminated with antibiotics if treatment is

begun early in the course of illness. Delayed or inadequate treatment may often lead to “late stage” or chronic Lyme disease that is disabling and difficult to treat. Thus, two different standards of

care for Lyme disease have emerged depending on the stage of infection.


The first record of a condition associated with Lyme disease dates to 1883 in Wroclaw, Poland ( which was at that time Breslau, Germany) where physician Alfred Buchwald described a

degenerative skin disorder now known as acrodermatitis chronica atrophicans. In 1909, Arvid Afzelius presented research about an expanding, ring-like lesion he had observed and published his

work 12 years later speculating that the rash came from the bite of an Ixodes tick, and that meningitic symptoms and signs in a number of case; this rash is now known as erythema

migrans which is the skin rash found in early stage Lyme disease. In the 1920s French physicians Garin and Bujadoux described a patient with meningoencephalitis, painful sensory

radiculitis, and erythema migrans following a tick bite, and they postulated the symptoms were due to a spirochetal infection. In the 1940s, German neurologist Alfred Bannwarth described

several cases of chronic lymphocytic meningitis and polyradiculoneuritis, some of which were accompanied by erythematous skin lesions. In 1948 spirochete-like structures were observed in

skin specimens by Swedish dermatologist Carl Lennhoff. In the 1950s, relations between tick bite, lymphocytoma, EM and Bannwarth’s syndrome are seen throughout Europe leading to the use

of penicillin for treatment. Interest in tick-borne infections in the U.S. began with the first report of tick-borne relapsing fever (Borrelia hermsii) in 1915, following the recognition of five

human patients in Colorado. In 1970 a physician in Wisconsin named Rudolph Scrimenti reports the first case of EM in the U.S. and treated it with penicillin based on European literature. The full

syndrome now known as Lyme disease was recognized when a cluster of cases originally thought to be juvenile rheumatoid arthritis was identified in three towns in southeastern Connecticut in

1975, including the towns Lyme and Old Lyme, which gave the disease its popular name. Before 1976, elements of B. burgdorferi sensu lato infection were called or known as tickborne

meningopolyneuritis, Garin-Bujadoux syndrome, Bannworth syndrome, Afzelius syndrome, Montauk Knee or sheep tick fever. Since 1976 the disease is most often referred to as Lyme

disease, Lyme borreliosis or simply borreliosis.

Signs and Symptoms

The acute phase of Lyme disease displays a characteristic reddish “bulls-eye” rash or “target lesion,” with accompanying fever, malaise, and muscle and joint pain. The characteristic “bull’s-eye” rash (known as

erythema chronicum migrans) may be seen in up to 80% of early stage Lyme disease patients, appearing from one day to one month after a tick bite. The rash represents a skin

infection with the Lyme bacteria, Borrelia burgdorferi. The time period from infection to the onset of symptoms is usually a few days up to 2 weeks, but can be months or years. Symptoms

most often occur from May through September because the nymphal stage of the tick is responsible for most cases. Asymptomatic infections can exist. Less common findings in acute Lyme

disease include cardiac manifestations – about 10% of patients have cardiac manifestations including heart block and palpitations. Neurologic symptoms (neuroborreliosis) occurs in

about 1/5 of cases. Simple altered mental status may be the only presenting symptom in early neuroborreliosis. Untreated or persistent cases may progress to a chronic form with

meningoencephalitis, cardiac inflammation (myocarditis), and arthritis. Chronic Lyme disease can have a multitude of symptoms affecting numerous physiological systems. Variations in

symptoms patterns may relate to innate immunity or variations in the Borrelia bacteria. Late symptoms of Lyme disease can appear months or years after initial infection and often progress in

cumulative fashion over time. Neuropsychiatric symptoms often develop much later in the disease progession, similar to tertiary neurosyphilis.


Ixodes scapularis (the black-legged tick or deer tick), a hard-bodied tick, is the primary vector of Lyme disease in eastern North America. In Europe, Ixodes ricinus (known

commonly as the sheep tick, castor bean tick, or European castor bean tick) is the primary vector. On the West Coast of the U.S. the primary vector is Ixodes pacificus (the “western

black-legged tick”). The majority of infections are caused by ticks in the nymph stage, as adult ticks do not become infected through feeding. Another possible vector is Amblyomma

americanum (the “Lone Star tick”) which is found throughout the southeastern U.S. as far west as Texas, and increasingly in northeastern states as well. Only about 20% of persons infected

with Lyme disease by the deer tick are aware of having had any tick bite, making early detection difficult in the absence of a rash. While Lyme spirochetes have been found in insects other than

ticks, reports of actual infectious transmission appear to be rare. Sexual transmission has been anecdotally reported and Lyme spirochetes have been found in semen and breast milk. However,

transmission of the spirochete by these routes, although seemingly likely, has not been proven. Congenital transmission of Lyme disease can occur from an infected mother to fetus through the

placenta during pregnancy. Prompt antibiotic treatment appears to prevent fetal damage.


Urbanization and other man-made factors can be implicated in the spread of the Lyme disease into the human population. Expansion of suburban neighborhoods has led to the gradual

deforestation of surrounding wooded areas and increasing contact between humans and ticks. Human expansion has also resulted in a gradual reduction of the predators that normally hunt deer

as well as mice, chipmunks and other small rodents – the primary reservoirs for Lyme disease. All of this increases the likelihood of transmission to Lyme residents has greatly increased. The

deer tick has a two-year life cycle, first progressing from larva to nymph, and then from nymph to adult. The tick feeds only once at each stage. In the fall, large acorn forests attract deer as well

as mice, chipmunks and other small rodents infected with B. burgdorferi. During the following spring, the ticks lay their eggs. The rodent population then “booms.” Tick eggs hatch into larvae,

which feed on the rodents; thus the larvae acquire infection from the rodents. Adult ticks may also transmit disease to humans. After feeding, female adult ticks lay their eggs on the ground, and

the cycle is complete. On the West Coast, Ixodes pacificus has a different life cycle. The risk of acquiring Lyme disease does not depend on the existence of a local deer population, as is

commonly assumed. New research suggests that eliminating deer from smaller areas may lead to an increase in tick density and the rise of “tick-borne disease hotspots.”


Lyme disease is the most common tick-borne disease in North America and Europe, and one of the fastest-growing infectious diseases in the United States. Of cases reported to the United

States Center for Disease Control, the ratio of Lyme disease infection is 7.9 cases for every 100,000 persons. In the ten states where Lyme disease is most common, the average was 31.6

cases for every 100,000 persons for the year 2005. Although Lyme disease has now been reported in 49 of 50 states in the U.S, about 99% of all reported cases are confined to just five

geographic areas (New England, Mid-Atlantic, East-North Central, South Atlantic, and West North-Central). The number of reported cases of the disease has been increasing, as are endemic

regions in North America.


Due to the difficulty in culturing Borrelia bacteria in the laboratory, diagnosis of Lyme disease is typically based on the clinical exam findings and a history of exposure to endemic Lyme areas.[1]

The classical rash, which does not occur in all cases, is considered sufficient to establish a diagnosis of Lyme disease even when serologies are negative. Serological testing can be useful, but

is not diagnostic due to frequent false positives and false negatives. Lyme is a deep tissue infection and by the time encephalopathy is established, few if any cerbro-spinal fluid antibodies can be

detetected. Also, the PCR (Polymerase Chain Reaction) is unreliable. Seronegative (“false negative”) disease can occur for the same reason that this phenomenon occurs in neurosyphilis with

incomplete antibiotic treatment which blocks the serum antibody response, but dose not eliminate the infection. Advanced imaging studies like SPECT or PET can provide objective evidence of

global brain dysfunction. Neuropsychological testing can be utilized, but a normal result does not rule out the illness, which can be very subtle and manifest as a disabling mood disorder

accompanied by debilitating fatigue, with few objective signs and all of this can, of course, have other causes. Thus diagnosis of late-stage Lyme disease is often difficult due to the multi-faceted

appearance which can mimic symptoms of other diseases. For this reason Lyme has often been called the new “great imitator” (syphilis was the old “great imitator”). Lyme disease may be

misdiagnosed as multiple sclerosis, rheumatoid arthritis, fibromyalgia, chronic fatigue syndrome, or other autoimmune and neurodegenerative diseases.

The serological laboratory tests most widely available and employed are the Western blot and ELISA. A two-tiered protocol is recommended by the CDC. The more sensitive

ELISA is performed first and if it is positive or equivocal, the more specific Western blot is run. However, the reliability of testing in diagnosis remains controversial. Studies show the Western blot

IgM has a specificity of 94–96% for patients with clinical symptoms of early Lyme disease. But, erroneous test results have been widely reported in both early and late stages of the disease.

These errors can be caused by several factors, including antibody cross-reactions from other infections including Epstein-Barr virus and cytomegalovirus, as well as herpes simplex virus.

Polymerase chain reaction (PCR) tests for Lyme disease have also been developed to detect the genetic material (DNA) of the Lyme disease spirochete. PCR tests are rarely susceptible to

false-positive results but can often show false-negative results, and the overall reliability of PCR in this role remains unclear. With the exception of PCR, there is no currently practical means for

detection of the presence of the organism, as serologic studies only test for host antibodies against Borrelia. High titers of either immunoglobulin G (IgG) or immunoglobulin M (IgM) antibodies to

Borrelia antigens indicate disease, but lower titers can be misleading. The IgM antibodies may remain after the initial infection, and IgG antibodies may remain for years. Western blot, ELISA and

PCR can be performed by either blood test via venipuncture or cerebral spinal fluid (CSF) via lumbar puncture. Though lumbar puncture is more definitive of diagnosis, antigen capture in the

CSF is much more elusive – reportedly CSF yields positive results in only 10-30% of patients cultured. The diagnosis of neurologic infection by Borrelia should not be excluded solely on the basis

of normal routine CSF or negative CSF antibody analyses.

At least 37 Borrelia species have been described, only 12 of which are Lyme related. The Borrelia species known to cause Lyme disease are collectively known as Borrelia burgdorferi sensu lato, “sunsu lato” meaning “in the broad sense” and have been found to have greater diversity than originally suspected. Until recently it was thought that only three sub-species of Borellia burgdorferi caused Lyme disease, however, newly discovered sub-species have also been found to cause disease in humans. Clinician skilled in dark field microscopy can see spirochetes when they are present, but the pathogenic sub-species cannot be distinguished from the non-pathogenic and failure to see any spirochetes does not mean they are absent.

At the bottom line, as frustrating as it is for doctor and patient, testing for Lyme disease is almost useless in the judgment of most doctors. Even though the CDC urges testing and does not say

specifically that Lyme is a clinical diagnosis, that is what it all boils down to. It alls comes back to clinical exam findings and a history of exposure to endemic Lyme areas.


The currently recommended prevention involves avoiding areas in which ticks are found; this can reduce the probability of contracting Lyme disease. Other good prevention practices include

wearing clothing that covers the entire body when in a wooded area; using mosquito/tick repellent; after exposure to wooded areas, checking all parts of the body (including hair) and clothing for

ticks. If going to the woods, wear long-sleeve shirts and pants that are tucked into socks or boots. Also wear light-colored clothing so that you can see the tick on you before it attaches itself. An

effective method of preventing Lyme disease is a reduction in numbers of the primary host on which the deer tick depends. Lyme and all other deer-tick borne diseases can be prevented on a

regional level by reducing the deer population that the ticks depend on for reproductive success. By reducing the deer population to healthy levels of 8 to 10 per square mile (from the current

levels of 60 or more deer per square mile in the areas of the country with the highest Lyme disease rates) the tick numbers can be brought down to very low levels, too few to spread Lyme and

other tick-borne diseases.


Complete removal of the tick head is important; if the head is not completely removed, local infection with various bacteria may result. Persons from whom attached ticks have been removed

should be monitored closely for signs and symptoms of tick-borne diseases for up to 30 days and personally I recommend immediate prophylactic treatment in such a case. Antibiotics are the

primary treatment for early stage Lyme disease. Penicillin was first demonstrated by researchers to be useful against Borrellia in the 1950s; today the antibiotics of choice are doxycycline,

amoxicillin and ceftriaxone. Macrolide antibiotics are also used such as azithromycin (Zithromax), clarithromycin (Biaxin), dirithromycin (Dynabac), erythromycin and roxithromycin (which is not

available in the U.S.). A three day course of doxycycline therapy may be considered for deer tick bites. Patients should report any Erythema migrans (red rashes around the body) over the

subsequent two to six weeks. If there should be suspicion of disease, then a course of Doxycycline should be immediately given for ten days without awaiting serology tests (which only yield

positive results after an interval of one to two months). In later stages, the bacteria disseminate throughout the body and may cross the blood-brain barrier, making the infection more difficult to

treat. Late diagnosed Lyme is treated with oral or IV antibiotics, frequently ceftriaxone, 2 grams per day, for a minimum of four weeks. Minocycline is also indicated for neuroborreliosis for its

ability to cross the blood-brain barrier.

With little research conducted specifically on treatment for late/chronic Lyme disease, particularly Lyme encephalopathy, treatment remains controversial. Currently there are two sets of

peer-reviewed published guidelines in the United States; the International Lyme and Associated Diseases Society advocates extended courses of antibiotics for chronic Lyme patients in light of

evidence of persistent infection, while the Infectious Diseases Society of America does not recognize chronic infection and recommends no treatment for persistent symptoms. Double-blind,

placebo-controlled trials of long-term antibiotics for chronic Lyme have produced mixed results. The latest double blind, randomized, placebo-controlled multicenter clincal study, done in Finland, results indicated that oral adjunct antibiotics were not justified in the treatment of patients with disseminated Lyme borreliosis who initially received intravenous antibiotics for 3 weeks. The researchers noted the clinical outcome of said patients should not be evaluated at the completion of intravenous antibiotic treatment but rather 6-12 months afterwards. In patients with chronic post-treatment symptoms, persistent positive levels of antibodies did not seem to provide any useful information for further care of the patient. In mainstream medicine, antibiotic treatment is the central pillar in the management of Lyme disease. However, in the late stages of borreliosis, symptoms may persist despite extensive and repeated antibiotic treatment. Lyme arthritis which is antibiotic resistant may be treated with hydroxychloroquine or methotrexate. Corticosteroids should never be given to Lyme patients.

Most clinicians agree on the treatment of early Lyme disease infections. There is, however, considerable disagreement regarding prevalence of the disease, diagnostic criteria, treatment of

late-stage Lyme disease, and the likelihood of a chronic, antibiotic-resistant infections. Some authorities contend that Lyme disease is relatively rare, easily diagnosed with available blood tests,

and most often easily treated with two to four weeks of antibiotics while others propose that the disease is under-diagnosed, available blood tests are unreliable, and that extended antibiotic

treatment is often necessary. The majority of public health agencies such as the U.S. Centers for Disease Control maintain the former position. While this narrower position is sometimes

described as the “mainstream” view of Lyme disease, published studies involving non-randomized surveys of physicians in endemic areas found physicians evenly split in their views, with the

majority recognizing seronegative Lyme disease, and roughly half prescribing extended courses of antibiotics for chronic Lyme disease.

Alternative Therapies

A number of other alternative therapies have been suggested, though clinical trials have not been conducted. For example, the use of hyperbaric oxygen therapy (which is used conventionally to

treat a number of other conditions), as an adjunct to antibiotics for Lyme has been discussed. Though there are no published data from clinical trials to support its use, preliminary results using a

mouse model suggest its effectiveness against B. burgdorferi both in vitro and in vivo. Anecdotal clinical research has shown potential for the antifungal azole medications such as Diflucan in the

treatment of Lyme. Alternative medicine approaches include bee venom because it contains the peptide melittin, which has been shown to exert inhibitory effects on Lyme bacteria in vitro; no

clinical trials of this treatment have been carried out, however.

Samento is a form of cat’s claw from the Peruvian jungle that is superior to typical forms. The beneficial effects of most cat’s claw preparations are blunted by the presence of TOA (tetracyclic oxindole alkaloids), which inhibit the real active agents, called POA (pentacyclic oxindole alkaloids). The latter, more favorable compounds are known to modulate and up-regulate the immune system. Many commercially available cat’s claw preparations contain up to 80 percent TOA. As little as one percent TOA can reduce POA effectiveness up to 80 percent. In addition, the specific species of TOA-free cat’s claw contains considerable quantities of quinovic acid glycosides. These compounds are what the latest generation of quinolone antibiotics (such as Cipro) are based on. The natural compounds provide safe and significant direct antimicrobial effects on Lyme disease.

Treatment with TOA-free cat’s claw isn’t an instant cure-all. It can take a long treatment process because of the variety of forms of Bb, the long length of time it can exist in the body in the CWD form, and because it can hide out inside cells. It is when they emerge that they are susceptible to white cell attack and elimination. The mature spirochete form is sensitive to attack by antibiotics or the immune system, as well as the improved cat’s claw. The organism can lie dormant for months or years after infection. In fact, a 1998 Swiss study showed that only 12.5 percent of Bb positive patients have symptoms. Conventional medicine has grown up thinking bacterial infections can be cured in 10-60 days. They believe that if antibiotics don’t cure you, what remains can’t be Lyme. That is wrong. This mistaken idea rests on the lack of knowledge about the characteristics of the cell wall deficient form of bacteria.

Three companies currently market the improved cat’s claw. Allergy Research Group/Nutricology, which also distributes artemisinin, can be reached at 800-545-9960 or Ask for Prima Una de Gato. Nutramedix’s product is called Samento Plus, and is available by calling 561-745-2917 or on the web site: Farmacopia also carries the product ( or 800-896-1484). I don’t recommend any other commercially available cat’s claw at this time because of the likelihood of TOA content.

A comprehensive strategy to detoxify, replenish nutrition, and strengthen mental/spiritual well being is absolutely essential. Do not rely on TOA-free cat’s claw alone for this monster bacteria! Removal of mercury fillings and treatment for heavy metals may be required for best results as well as treatment of underlying conditions, notably chronic (usually undetected) gut wall infection..


For early cases, prompt treatment is usually curative, however, the severity and treatment of Lyme disease may be complicated due to late diagnosis, failure of antibiotic treatment, simultaneous

infection with other tick-borne diseases including ehrlichiosis, babesiosis, and bartonella, and immune suppression in the patient. A meta-analysis published in 2005 found that some patients with

Lyme disease have fatigue, joint and/or muscle pain, and neurocognitive symptoms persisting for years despite antibiotic treatment. Patients with late Stage Lyme disease have been shown to

experience a level of physical disability equivalent to that seen in congestive heart failure. Though rare, Lyme disease can be fatal.

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