Lyme Basics

What is Lyme?

Borrelia (causes Lyme, picture on the left) is a long spiraled shape cell that is called a spirochete. Spirochetes look like a spiraled worm under a microscope which are classified as a bacteria. Historically, Borrelia had been hard to classify because it has both bacterial qualities and non-bacterial qualities including more complex eukaryote qualities [1](ticks and humans are in this category) that bacteria's aren't known to have, and for years it was thought of as a Protozoa; a unicellular eukaryotic organism. [2] It also contains the largest number of DNA replicons which makes Borrelia the most complex bacteria (if it is to be labelled a bacteria that is) in the world. There is no close relative to Borrelia that we know of, but the closest organisms are the syphilis spirochetes which have about a 40% similarity in genome structure.[3] Instead of needing iron to survive like most other parasites, Borrelia has learned how to survive without iron, and can feed on magnesium which is a vital element to the human immune system, as well as for muscles which includes the heart. There are three main known species of Borrelia that cause Lyme disease throughout the world which are Borrelia (B. for short) burgdorferi (more common in the United States), B. afzelii, and B. garinii, but recent discoveres have also added B. miyamotoi, B. lonestari, B. valaisiana, B. andersonii, B. japonica, B. lusitanie, B. turdae, B. tanukii, B. spielmani, and B. bissetti. It is highly likely that we are going to continue to discover new species of Borrelia.


What can Lyme do?

Borrelia is a master of disguise because it can hide from the immune system in numerous ways.  It changes shape like a shape shifter and has 3 different preferred shapes. The reason why it changes shape is because it confuses the immune system, and each shape protects itself from specific antibiotics. It can turn into a cyst in seconds and can form biofilms which are slime coverings, or shields, that they form around themselves which protects them from the immune system and from antibiotics. Some strands of Borrelia can stay in their biofilm form hibernating and well protected for 2.5 years. It can change its outer surface protein coating (Osp) which is like changing its identity making it have chameleon like properties. The immune system works by identifying the protein coating of an invading antigen, then it creates antibodies specifically for attacking those proteins. Once Borrelia realizes that antibodies are being made to combat its current protein coating, it begins to change its protein coating.

Once invaded into a host, Borrelia shuts down specific parts of the immune system that are lethal to itself including Natural Killer cells. (NK cells).[5] NK cells are the most dangerous for Lyme because they can independently find foreign intruders and cause instant death on contact. When Lyme realizes its being tracked, it hides inside a hosts cells which makes itself invisible to the host's immune system. Because of how fast Borrelia can change its shape, change its protein coating to mimic the hosts coatings, and hide in the hosts cells, the immune system of a host may not even know that it had been infected by Borrelia for months on end. This means that the body will not produce antibodies against Lyme, and Lyme patients will have a high chance of testing negative for Lyme on their Lyme tests.

When Borrelia invades, the body activates a Th-1 immune response which secretes pro-inflammatory cytokines to combat any invading antigen, and to combat this, Borrelia uses the hosts immune system and induces Th2 (IL-2), an anti-inflammation cytokine responses which shuts down the Th-1 response allowing Lyme to penetrate deeper into the host. [6] This means that Borrelia can control the hosts immune system for its own benefit. They can reproduce through replication by cloning and through genetic exchange with another spirochete. [7] When Borrelia get ready to invade a host, they first determine the species of the host by looking at it's pH level, and then it transforms into a spirochete designed to survive that specific type of host. They then clone themselves to rapidly increase their numbers that are naturally immune to the new host, and eventually when it's best for their survival, they begin to replicate through genetic exchange.


Borrelia Burgdorferi in it's biofilm form
This picture won the 2012 Microbial Photo contest
for the American Type Culture Collection

Ancient history of Lyme

Lyme disease is an ancient parasite that has been infecting humans worldwide for thousands of years. A 5,000 year old mummy named Otzi is the oldest case found with Lyme disease who was found in northern Italy.[8] The disease is also commonly found among many civilizations such as the Louisiana Tchefuncte Indians that existed between the years 500 BCE and 300 CE.[9] Although Borrelia has been identified in tribes throughout the ancient world, Borrelia may have become more aggressive since the 1970s.

Our first modern written European medical records identified Lyme in 1883 under the name Erythema Chronicum Migrans (ECM) by Dr. Alfred Buchwald. Karl Herxheimer and Kuno Hartmann later renamed the disease as Acrodermatitis Chronica Atrophicans (ACA) in 1902.

By 1955, a German team established that ECM was susceptible to penicillin and doctors began to treat ECM with antibiotics. [10] The first American physician that came in contact with Lyme disease was in October 1968 by a Milwaukee dermatologist, Rudolph Scrimenti who successfully treated the patient with antibiotics 2 years before the controversy started. [11]

Lyme didn't become an issue until there were several rat population booms that occurred across our country because we reduced the population of the predators of rats and mice who are known carriers of Lyme disease, and we also expanded their environment by planting more trees expanding their habitats, and this wasn't just happening in the United States, it was happening throughout the world.


[1] Buhner, Stephen: Healing Lyme, Silver City: Raven Press, 2005. Print p.15

[2] http://www.horizonpress.com/jmmb/v2/v2n4/09.pdf

[3] p.16 buhner

[4]Singleton, Kenneth (2010-08-19). The Lyme Disease Solution (p. 5). Kindle Edition.

[5] Buhner, Stephen Healing Lyme, Silver City: Raven Press, 2005. Print p.55

[6] Singleton, Kenneth (2010-08-19). The Lyme Disease Solution (p. 144). . Kindle Edition.

[7] Weintraub, Pamela (2010-04-01). Cure Unknown: Inside the Lyme Epidemic (p. 349). Macmillan. Kindle Edition.

[8]http://abcnews.go.com/Technology/oetzi-iceman-mummy-alps-lyme-disease-lactose-intolerance/story?id=15816788#.UJUvfMWCnJI

[9] http://www.ncbi.nlm.nih.gov/pubmed/8048468

[10] Weintraub, Pamela (2010-04-01). Cure Unknown: Inside the Lyme Epidemic (p. 82). Macmillan. Kindle Edition.

[11] Weintraub, Pamela (2010-04-01). Cure Unknown: Inside the Lyme Epidemic (p. 83). Macmillan. Kindle Edition.