Debugging the bug

Lyme disease is caused by Borrelia burgdorferi and other related species of Borrelia.  “Lyme disease” was coined by Steere in 1977.  Microbiologist Willie Burgdorfer discovered the germ in 1981 -- A thin, elongated spiral shaped bacteria, or spirochete residing in the gut of ticks. 

These bacteria are persistent and frequently cause chronic disease.   The belief that the bacteria persist has been refuted by the IDSA for decades.  The IDSA is wrong.  The narrative oft repeated describing the structure and function of the spirochete by those in my camp, is outdated and incorrect.  

This post is an effort to correct the record. 

The following statements are wrong and I explain why. 

#1 Lyme bacteria have 3 forms:  spirochete, L-form and cyst form. 

Lyme does not exist in an L-form.  An L form is a cell wall deficient bacterium derived from a bacterium that ordinarily has a cell wall.   Lyme lacks a cell wall to begin with so this is an impossibility. Lyme bacteria possess a double outer membrane and no cell wall.  Bacterial cysts do no occur. This is a feature of protozoa. Lyme bacteria are pleomorphic with “phenotypic” variation.  These chameleons of the bacterial world frequently present as a round bodied forms which are treatment resistant.  In summary: No L-forms, No true cysts. Yes, spirochetes have shape shifting ability – pleomorphic variation, commonly observed as round body forms, blebs and many others.  

#2 Lyme bacteria persist in large measure because they hide in cells (are intracellular).

Lyme bacteria primarily exist outside host cells (extracellular).  Intracellular forms exist but are relatively uncommon. The bacteria adhere to a protein matrix between cells.  Primary mechanisms of persistence are biofilm formation and pleomorphic variability.  The spirochetes are anaerobic (do not require oxygen) and therefore are able to live in tissues with a poor blood/oxygen supply, e.g. joint cartilage. These bacteria easily cross the blood brain barrier which is a safe-haven because immune responses are limited. The bacteria may survive in other “immune privileged” areas. Intracellular localization is a relatively minor means of immune evasion. 

#3 Treatment must include: cell wall drugs (beta-lactams), intracellular drugs and “cyst busters.”  

Assuming we are talking about the bacterial cells (not host) With Lyme spirochetes all antibiotics inhibit or kill Lyme work via an intracellular mechanism.   The molecules that form the bacterial cell wall are called peptidoglycans.  Borrelia spirochetes possess strands of peptidoglycans internally, acting as an internal skeleton.  When beta-lactams kill Lyme, the action is inside the cells. The other classes of antibiotics generally work inside the cells, disrupting DNA/RNA, metabolic pathways or protein synthesis.  If we are instead referring to drugs which penetrate host cells, antibiotics from many classes may penetrate host cells, including beta-lactams. 

4#  Flagyl is a cyst buster.  

If one is referred to round forms of Lyme, Flagyl is no more effective (in a test tube) than doxycycline.  Empiric evidence and clinical practice inform us that Flagyl is very effective and may be synergistic with other drugs. 

In summary:  No L forms.  No cyst forms.  No cyst busters.  Ceftin, amoxicillin, others function as intracellular antibiotics when used against Lyme. 

Lyme spirochetes have a developed ability to persist in the face of adversity.  This phenomenon is not unknown in the world of bacteriology. For example, tuberculosis.  TB is treated with a 4-drug combination for 2 months and a 2-drug combination for another 2 months.  This complicated formula is the results of decades of research.  

Lyme (chronic) has not had this sort of attention from the medical community which maintains the persistent delusion the disease does not exist.