Lyme Disease

Lyme from is named after the town in Connecticut USA, where the first outbreak was identified in 1975 after an unusually large number of young people contracted juvenile rheumatoid arthritis near the community of Lyme. A suspected arthropod vector was pinpointed as the cause, with attention focussed on the onset being late summer/early autumn.

 

In 1982, the etiologic agent of Lyme was discovered by Willy Burgdorfer who isolated SPIROCHETES belonging to the genus Borrelia. Burgdorfer was able to demonstrate that spirochetes reacted with IMMUNE SERUM from Lxodes ticks.

Lyme Spirochete resembles syphilis spirochete.

Lyme is now prevalent on six continents.

 

W.T. Harvey MD and Patricia Salvato MD in 2003 published research that demonstrated that the arthropod is not the exclusive vector of Lyme. In addition to ticks, Lyme can be carried/transmitted by FLEAS, MOSQUITOS, MITES.

 

Lyme can also be transmitted by human to human transfer (sexual and congenital)

Dairy and beef cattle can be infected with B Burgdorferi hence some raw food might be contaminated. It may be transmitted orally to laboratory animals. They concluded that Lyme may be a food infection.  

Blood transfusion may transmit it.  (Sacramento Medical Foundation Blood Centre 1989)

 

 

Dormancy and Activation – years can pass before symptoms appear in a patient infected with Borrelia Burgdorferi. Therefore Lyme can remain asymptomatic. (Swiss study 1998)

All asymptomatic carriers of Borrelia are at risk of developing Lyme at some point. Trigger factors may be stress, herpes simplex type 1 infection (cold sore). Suggestions of electro magnetic smog suppressing immune function is also being investigated. Dietrich Klinghardt recognises that this EM smog may also be a trigger/irritant to Borrelia itself.

 

 

Lyme is the fastest growing disease in the world. The Centre for Disease Control in Atlanta, Georgia affirms that ‘there is considerable under reporting of Lyme disease’, maintaining that the actual infection rate may be 1.8 million, not 180,000 currently reported (2003).

Considering vector, congenital, sexual, blood transfusion, Dr Harvey and Dr Salvato estimate that 15.5% of the global population, 1 billion people,  could be infected with Borrelia.

The Sierra Integrative Medicine clinic in Reno, Nevada states ‘Authorities estimate that up to 90% of the population could be carrying the Lyme spirochete and that Lyme is a factor in over 50% of chronic illnesses.

 

Toxins in Lyme Disease

 

MICROBIAL TOXINS and the damage they do to various organs and tissues on cellular and molecular level has been researched globally.

Research worldwide into bio-toxin induced illnesses are largely focused on Lyme Borreliosis.

Dr C Shoemaker MD and H Kenneth Hudnell PhD state ‘from a molecular toxicology point of view, Borrellia burgdorferi produces a large suite of bio-toxins that have tissue cells affinity, mainly NEUROTOXINS with high molecular tropism for lipid structures (i.e. central nervous system, peripheral nerves), muscles, joints (synovial membranes and joint cartilage), lungs and many others.

 

It is understood that Lyme Borreliosis can mimic a variety of diseases.

 

 

What is a SPIROCHETE?

 

SPIROCHETES are double membrane bacteria which are usually long and helically coiled. They propel themselves by twisting and spiralling, making movement rapid.

They can penetrate cell membranes, giving the potential to access all parts of the body.

B. Burgdorferi can change into three different forms to evade the immune system and anti biotics. The three known forms are the spiral form (spirochete) that has a cell wall, the Cell-Wall-Deficient form (CWD) and the cyst form.

Spirochete form – Causative bacteria of Lyme. Spiral shape allows penetration into tissue and bone. Capable of intracellular infection. Rapidly converts to CWD form when threatened with immune system or a/bs.

Cell-Wall-Deficient CWD form. Lack of cell wall makes targeting by immune cells and anti biotics more difficult.  Capable of intracellular infection. Clumps together in colonies – inner layers unreachable by anti biotics.

Cysts – Dormant form bacteria are not mobile and do not cause problems (asymptomatic presentation).  Can survive anti biotics, starvation, pH changes, temperature changes and most other adverse conditions. Converts back to spirochete form when conditions are favourable.

B.Bulgdorferi has a replication cycle of about seven days, one of the longest of any known bacteria.

 

Anti biotics are known to be most effective when a bacterium is replicating. Therefore the more cycles it goes through during an anti biotic treatment the better. Since the life cycle of a Streptococcus  throat infection is about eight hours, anti biotic treatment of ten days would cover thirty life cycles.

To treat Lyme for a comparable number of life cycles, treatment would need to be for at least thirty weeks. *see below.

~~~~~~~

 

*To  further complicate treatment, there are five sub-species of B. Burgdorferi and over one hundred strains of B.Burgdoferi in the USA., 300 strains world wide. This diversity is thought to contribute to the antigenic variability of the spirochete and its ability to evade the immune system and anti biotic therapy, leading to chronic infection under a plethora of disguises.

Persistence of B Burgdorferi gives access to sites that are inaccessible to immune cells and anti biotics, such as the brain and central nervous system. New evidence suggests that B. Burgdoferi may use the host’s fibrinolytic system to penetrate the blood/brain barrier.

Intracellular invasion has demonstrated that it can penetrate a host of cells such as endothelium, fibroblasts, lymphocytes, macrophages, keratinocytes and synovium. By hiding inside these cells B.B is able to evade the immune system and a/bs, allowing the infection to persist in a chronic state.

 

Antigenic variation B.B has the ability to vary its surface proteins in response to immune attack.

Immune system suppression. Complement inhibition, induction of anti-inflammatory cytokines such as IL-10 and the formation of immune complexes have all been documented in B. B. infections. The existence of immune complexes provides another explanation for sero-negative disease (i.e. false-negative antibody tests of blood and cerebrospinal fluid) as studies have shown that a number of sero-negative Lyme patients have antibodies bound up in these complexes.

For more information and a consultation please contact Cynthia Sillars DipIK KFRP ND MNLP and request a Registration form. Cynthia can be reached on mobile 07599520406 and land line 01325 730271.