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Lyme Disease and Humans

Lyme

Lyme disease is probably the most common vectored disease in the world. Its causative agent is a spirochete: Borrelia burgdorferi. Borrelia normally requires both a tick host of the Ixodes genus and a warm-blooded host to complete its infectious cycle, but insects may occasionally also be vectors, transmitting Borrelia from one host to another.

Spirochetes undergo multiple changes as the ticks are biting their warm-blooded host. But these pale in comparison with the changes that occur inside a human.

Inside the Human

If left alone once inside a warm-blooded host, spirochetes move through the blood stream, reproduce slowly, produce blebs, change shape, and move into the host's organs and tissues where they give off toxins that often reduce host mobility. Reduced host mobility increases the probability that new ticks will find and bite the infected host and transfer the spirochetes to more vertebrates.

Spirochetes Release “Cluster Bombs”

Each active bacterium releases into the body thousands of infectious packages, called blebs. Although the bacteria reproduce only about once every two weeks, these blebs are produced almost continuously, are hyper infective and appear to cause most of the symptoms of LD. Blebs are a sort of smoke screen against the immune system. As immune cells and antibodies are attacking the blebs, the bacteria (hidden inside other cells) can continue to release more blebs without injury. Since blebs are not true cells, they may be destroyed without eliminating the actual bacteria.

Borrelia Attacks our Immune System
Our immune response is slowed down and even rendered ineffective by bacteria that can rapidly change their surface characteristics. Borrelia's ability to swiftly generate new combinations of surface proteins while the tick is feeding makes it important to remove I. scapularis ticks early in the feeding bout. But it is even more important to be treated as soon after infection begins as possible. If Borrelia are given time to change their surface proteins and develop other defenses against our immune systems and antibiotics, Borrelia may become able to escape our most concerted efforts to eradicate them.

Spirochetes are Shape Shifters

As if the arsenal of attack by ticks and spirochetes does not perplex the host's immune system enough, the bacteria will change their characteristics when the host marshalls defenses against the spirochetes. They seem to have programs that instruct them to:
  • Produce new forms of both surface protein groups (vlsE and Osp).
  • Change shape and discard surface proteins.
  • Move from the blood stream into body fluids.
  • Enter cells and become invisible to antibodies and killer T-cells.
  • Destroy immune system cells.
  • Hide behind the blood-brain barrier where many antibiotics cannot penetrate.
There are no fewer than three shapes of Borrelia, two of which are highly infective:
  • the spirochetal form,
  • an L-form that discards its cell wall and integrated surface proteins, and
  • a cystic form that enters cells and becomes inactive.
The infective shapes of Borrelia disrupt cell function, destroy connections between them, and eventually kill the cells. Being inactive, the cystic form is resistant to antibiotics, does not present antigens to the immune system, and escapes destruction from most medications. The few medications that are active against the cystic forms are dangerous.

Neurological Damage

Most neurological damage in the body is caused by the L-form of Borrelia. This form easily enters cells, can break into small round cells (cocci), and in the nervous system, disrupts connections (synapses), destroys neurons and their supporting tissues, and produce holes (lesions) in the brain that cannot be repaired. These changes become manifest as:
  • altered sensory perception,
  • forgetfulness,
  • muscle weakness,
  • slow or rapid heartbeat,
  • low or high blood pressure,
  • personality changes,
  • dementia – sometimes extreme,
  • “Lyme rage,”
  • and many others.
A full blown disease with these characteristics needs a multi-pronged attack to be eliminated.

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Lyme Disease and Ticks

Lyme

Most people have been or know someone affected by Lyme Disease. The ticks that transmit this disease are found in all of the US, Canada, Mexico, European and most Asian countries. When they bite, they can inject the bacteria that cause Lyme disease and other diseases.

Early Symptoms of Lyme Disease

Lyme disease begins after a tick bite. This is sometimes followed by a bulls-eye rash, becoming exhausted in the middle of the day – totally incapable of continuing without collapsing in bed, flu-like symptoms that may or may not go away, or suddenly developing arthritis. Since any of these symptoms could be something else, diagnosing LD is difficult.

Diagnosis Difficulties

The bulls-eye rash is diagnostic for Lyme disease and treatment often begins with no further testing, but almost 50% of people affected have no or atypical rashes. When Lyme disease is suspected, doctors send blood samples for testing. This test looks for antibodies in response to the bacterium. If the test is positive, the standard treatment is two weeks of antibiotics. If it provides a false negative diagnosis (which it does about 40% of the time), the patient may be sent away and not properly treated for some time and require extensive treatments to cure the disease. Which antibiotics, the duration and mode of administration, and the bacterium's response to treatment vary widely.

Borrelia burgdorferi and its Effects
Borrelia burgdorferi, is a spirochete transmitted by the black-legged tick, Ixodes scapularis (previously called I. dammini). Once infected, spirochetes travel through the blood stream and affect many organs, often burrowing into the cells, and wreaking havoc wherever they settle: They trigger arthritis; cause heart arrhythmias, (rarely) heart attack, weaken cardiac muscle; alter sensory input, motor control, disrupt thought processes, may cause paralysis of facial muscles (Bell's palsy) and other muscle groups; trigger muscle pain (myalgia), weakness, and sometimes tetany; produce rashes – often with a bullseye appearance; and can cross the placenta, causing fetal abnormalities.

The Ticks

The tick's role in transmitting Lyme Disease was noted shortly after the identification and naming of Lyme Disease in 1977. Ticks usually hatch without internal parasites, obtaining them over a period of several days as they feed from previously infected hosts.

About 50% of black-legged ticks carry B. burgdorferi. Almost 20% carry the agent for Babesiosis or Ehrlichiosis, and half of this second group carries two of the three agents. As treatments are different, doctors often test for all three agents when a patient presents an infection after a tick bite.
Tick development includes four stages: egg, larva, nymph, and adult. As sit and wait predators, they feed only once during each stage after the egg. They climb vegetation and hold on until something knocks them off or they are carried away by an animal.

Tick Development: Three Stages

Larvae, the size of the dot in the letter “i,” usually hatch in the spring, wait low in the vegetation, and feed on small mammals or birds. Larvae molt about three months after feeding, and the nymphs climb about a foot off the ground to feed on medium or large mammals and birds that walk by. At the end of the summer, the nymph molts to the adult stage.

Most feeding adult ticks are females. Males attempt to mate shortly after molting, may not feed again, and die soon after mating. A female must feed so her eggs can develop, and can live up to a year without feeding. She only becomes sexually receptive after engorging while feeding for at least a day. After mating, she swells to ten times her already swollen size, all the time transferring bacteria to the host. See the article “Lyme Disease: Warding Off The Disease” to find out how to reduce your chances of obtaining Lyme disease.

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Incorrect Diagnosis of Lyme Disease

Lyme Disease

Misdiagnosis of Lyme disease is rampant. In the 40% to 45% of cases where there is no rash after infection, the early symptoms of Lyme disease are difficult to classify. Diagnostic tests are only 50% to 60% reliable. The disease mimics many other conditions, and some doctors will not diagnose it based on symptoms if test results are negative.

The Basis for Misdiagnosis

Without seeing a tick or rash, the symptoms are varied, vague, and mimic many maladies: flu, chronic fatigue syndrome, multiple sclerosis (MS), lupus, rheumatoid arthritis, neurological disorders, cardiac arrhythmias, muscle weakness, and others.

During the progression of Lyme disease, the symptoms change as bacteria move out of the blood, transform, and mutate. The immune response is depressed, and the organism becomes extremely difficult to detect. In addition, the bacteria produce blebs (packages of active Borrelia enzymes) that attach to antibodies and divert T-cells (attack cells) from the bacteria themselves.

The Necessary Tests for Diagnosis

Positive results on both the ELISA test and Western Blot test are required by the Center for Disease Control (CDC) in order to report a case of Lyme disease. Because there are large numbers of antigens on bleb surfaces, antibodies bind to the blebs and become invisible to the ELISA test for Lyme disease, and ELISA test results are falsely negative forty to sixty percent of the time.

The Western Blot test is far more accurate because it looks for proteins shed from the bacteria and the blebs. The Infectious Diseases Society of America (IDSA) requires that five of the sixteen possible protein bands be present for a positive diagnosis. Yet IDSA instructs physicians to ignore the presence of the bands for OspA and OspB, found in all strains of Borrelia, because these bands might show up in patients if they were previously vaccinated against Lyme disease.

Opposing Ideas Regarding Diagnosis

IDSA guidelines restrict physicians from ordering the Western Blot test before the ELISA test or if the ELISA test results are negative. Thus, the better of the two diagnostic tests is not available if the weaker of the two tests does not first indicate the presence of Lyme disease antibodies. Unfortunately, most physicians honor IDSA guidelines.

The International Lyme and Associated Diseases Society (ILADS) has determined that requiring this combination of test results means that about 90% of all cases of Lyme disease are not reportable. Unfortunately for many patients, physicians who follow the IDSA guidelines also misdiagnose approximately 90% of their patients, whereas physicians who understand the ILADS view provide the necessary treatment.

There are two new tests for Lyme disease: a C6 test where an artificially produced complex of surface proteins binds to antibodies already attached to the surfaces of blebs, allowing them to be identified; the other looks for OspA. These tests are supposed to have few false negatives and almost zero false positives. Unfortunately for patients, IDSA (but not ILAD) refuses to acknowledge the validity of these tests.

How Borrelia Fools the Immune System
Borrelia presents many complexes of surface antigens. Presentation of a large number of complexes delays or renders our immune responses ineffective. Additionally, the bacteria soon leave the blood stream, moving into tissue fluids and cells, reducing the intensity of the antibody response. After entering a warm-blooded host, Bb continues to remove and produce newly altered surface proteins, presenting new antigen complexes to the immune system. These complexes give the bacteria respite from attack. They grow and keep the disease active. As the immune system cannot produce antibodies against molecules that it has not been exposed to, it remains a step or two behind the bacteria.

The Results of Incorrect Diagnosis

Many people suffer or have their lives destroyed because Lyme disease is not properly diagnosed. It happens every day: a patient tells his doctor he is experiencing extreme fatigue, aches and pains in his joints and major muscles, lack of concentration, depression, and digestive upset.

She asks, “Did you see a tick?” “No.”

“Did you get a rash?” “No.”

“Then you do not have Lyme Disease.”

When he asks to be tested for Lyme disease, some doctors refuse, others will reluctantly order a test. If the test comes back negative, the doctor states the patient does not have Lyme disease, and the patient's symptoms may be treated. Because of misdiagnosis or late diagnosis, these patients suffer years of misery and hospitalizations. When the tests come back positive, and the patient is given minimal treatment with antibiotics, he is told he is cured, but now has developed autoimmune problems or post Lyme syndrome, and there is nothing further that can be done.

The most damaging feature of Lyme disease care is not misdiagnosis, however: It is the absence of treatment or insufficient treatment.

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Lyme Disease Ticks and Spirochetes

Since Lyme disease is the most common vectored disease in the US, possibly in the world, researchers are studying the organisms intensely. In the US, its causative agent is aspirochete: Borrelia burgdorferi. Borrelia requires both a tick host of the Ixodes genus and a warm-blooded host to complete its infectious cycle, reproducing inside both hosts. These bacteria are transmitted primarily by I. scapularis in the Eastern US, I. pacifica in the Western US.

After hatching, ticks pass through three life stages, each lasting about a year: larva, nymph, and adult. Ticks usually feed only once during each life stage. The transfer of Lyme Disease begins when a tick becomes infected by feeding on a vertebrate host with Bb. Inside the tick, the spirochetes are dormant. When the tick feeds on a new host, spirochetes reproduce, are passed to the warm-blooded host, and this host becomes infected. Spirochetes that remain in the tick become dormant again and wait for another feeding bout.

Ticks do not just transfer bacteria from one host to another. The ticks, the spirochetes, and the hosts are all altered by the transfers. The changes that Bb undergoes within the tick and the warm-blooded hosts are complicated, but knowing what they are will help understand why finding a vaccine against or cure for Lyme Disease is problematical.

Inside the Tick

Upon being drawn into a tick, the bacteria discard most of their surface proteins, produce new ones, attach to proteins on the surface of the tick's intestinal cells, and become quiescent. While quiescent inside the tick gut, the spirochetes manufacture only one or two variants of surface protein vlsE and possibly one variant of protein Osp. The change in nutrients and acidity when the tick eats again stimulates renewed bacterial reproduction.

A spirochete protein, BptA (Borrelia protein A) is needed for this reproduction to take place. The protein either allows the spirochete to utilize the fresh blood for nourishment or it prevents the hemoglobin newly released from the host cells from killing the bacteria. Bacteria in which BptA is inactive cannot reproduce and ticks that house the mutated BptA- strain of Bb eventually lose these spirochete symbionts.

When the Tick Bites

Spirochetes
Tick saliva contains anesthetics that inhibit host awareness of the bite. Other chemicals in tick saliva stimulate an increase in blood supply to the area, inhibit the blood from clotting, and inhibit the host's immune system.

The introduction of fresh blood cells into the tick causes the bacteria to leave the tick's gut wall, stimulates spirochete growth and reproduction, and triggers rapid changes in spirochete surface proteins that the vertebrate host's immune system uses to fight off this disease agent. The bacteria also move to the tick's salivary glands and when the tick begins to spit the blood fluids back into the host, Bb is injected into its new host along with these fluids.

Over the course of the three or four days that the tick feeds, individual spirochetes produce up to five variants of vlsE proteins and one or two Osp variants. There are four possible combinations of the two Osp variants (A and B): no Osp, OspA, OspB, and OspA and B together. Mix those four combinations with several variants of vlsE proteins, and there may be well over a hundred different protein combinations on the surface of the spirochetesentering the new host. This means that the host's immune system is receiving a double whammy: being assaulted by the equivalent of 100 or more different types of bacteria at the same time that it is being attacked by tick salivary proteins that suppress its immune system.

Spirochetes have more time to alter their surface proteins toward the end of the tick's feeding bout making it important to have the tick removed as early as possible when a human or pet is bitten as their immune systems have fewer types of bacteria to identify and destroy. But this alone would not be sufficient to prevent Lyme disease. It is of utmost importance to obtain treatment early.

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Incorrect Treatment For Lyme Disease

lyme disease
Delays in proper treatment, inhibition of our immune systems by tick and bacterial defenses, and development of resistance of Borrelia to common antibiotics allow the bacteria to escape eradication. Caught early enough, most cases are cured with a short series of oral antibiotics. There is even talk about a single dose of long-release doxycycline being sufficient if given early enough. Yet many people are being misdiagnosed, given insufficient treatments (Burrascano 2005), and not cured even after prolonged antibiotic administration.

The Physician Factor

Physicians who follow the guidelines of the Infectious Diseases Society of America (IDSA) feel that the regime of antibiotics proscribed by IDSA is sufficient to eliminate Lyme disease. Thus, these doctors prescribe 14 days of doxycycline when they assume the patient has had the disease for less than a month, and 28 days when they feel there is neurological involvement.

When the patient symptoms are not relieved by this antibiotic regime, the doctor, following IDSA's guidelines, states the disease is cured, but now the patient is demonstrating “post Lyme disease syndrome”, and there is nothing further that can or will be done. The International Lyme and Associated Diseases Society (ILADS) produced different guidelines. ILADS physicians understand that the disease has entered a “chronic Lyme disease” state, and more intense measures must be taken to eradicate the disease.

How Borrelia Escape the Immune System During Chronic Lyme Disease
Borrelia penetrate into the cells of various tissues where they become isolated from both antibodies and killer T-cells (phagocytes) that would eat them. The blood brain barrier prevents many antibiotics from entering the tissues of the brain and spinal cord. When Borrelia penetrate that barrier, they are isolated from most antibiotics and wreak mayhem inside our nervous system, causing major alterations in nerve function – breaking the synaptic network and even destroying nerve cells.

The bacteria also burrow into and kill T-lymphocytes, the very cells designed to trap and kill them. As they destroy lymphocytes, Borrelia can hide inside a stolen portion of the lymphocyte's membrane and move through the bloodstream and tissue fluids looking to the immune system like a lymphocyte. The bacteria leave the lymphocyte membrane for only a short time before they enter a new cell.

How Borrelia Escape Antibiotics

  • Once inside the host, the bacteria reproduce about once every two weeks. (E. coli can reproduce once every twenty minutes.) Since most antibiotics prevent the bacteria from reproducing, ILADS feels a two week antibiotic treatment is ineffective as the bacteria may not reproduce during the period of treatment.
  • Each spirochete releases hundreds of membrane covered blebs, from their outer surface, and it appears these blebs are in part responsible for causing the symptoms of LD. Some antibiotics destroy these blebs, although the bacteria escape the antibiotic. In this case, the antibiotic reduces the severity of the illness because, although the blebs are rapidly destroyed by the antibiotic, bacteria continue to make blebs, so a few blebs remain active during treatment. The patient feels “better” but is not cured. Once the antibiotic is stopped, the blebs increase to pre-antibiotic levels and the disease comes back in full force – often producing new and more serious symptoms.
  • Borrelia has the ability to change from a spirochete into two other cell forms and enter body cells (Alan B. MacDonald, MD, power point presentation entitled: “Borrelia and Alzheimer's Disease”, presented to the ILADS national meeting Oct 30, 2007).
  • The first is an inactive cystic form that is able to produce new spirochetes at a later time. MacDonald feels this form is responsible for resurging Lyme disease after periods of remission.
  • The second is an L-form or spheroid without a cell wall. This form is often found inside T-cells and neurons and appears to be responsible for damaging these tissues. Each of the three forms of Borrelia requires different antibiotics or medications to destroy (Burrascano 2005). If these different medications are not provided at the proper times, the disease may return. IDSA does not agree the cyclic and L-forms develop in humans – even though Dr. McDonald has been demonstrating this for years. Thus, IDSA does not provide for treating any form but the spirochetal one.
  • Bacteria can acquire genes for antibiotic resistance from resistant strains of other species. If a few Borrelia become resistant to an antibiotic, the sensitive forms are destroyed by it - effecting a temporary “cure.” When the resistant ones reproduce and form a resistant population, LD returns but now must be treated with a different antibiotic.

Patients May Need Several Medications

The key to treatment of LD is to have the treatment started as soon as you suspect you have the disease - before the bacterium transform, mutate, or obtains antibiotic resistance. Once the bacteria are altered, a single antibiotic can not treat all of its forms, but there are many antibiotics available. If a particular antibiotic fails, another one might be effective.

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