Protocol Challenges

Lyme disease presents some difficult challenges, so a protocol approach has to keep them in mind.  They include:

Challenge #1: Biofilms – A Cloaking Disguise

Biofilms are a cloaking device bacteria use to survive in adverse conditions. Lyme bacteria can form a slimy matrix over themselves that shields them from antibodies and white blood cells from the immune system. Biofilms are also notorious for their ability to withstand extraordinarily high concentrations of antibiotics that are otherwise lethal in smaller doses to their planktonic counterparts.

Biofilms are well described with other bacteria such as dental bacteria, Pseudomonas and E. coli. Biofilms have even been seen in brain tissue.  This may be why neuroborreliosis, or “neuro Lyme,” is so hard to cure and why it causes dementia.

Biofilm is comprised, in part, of heavy metals.  Heavy metals are perhaps the most troublesome toxins because they have been found to feed and make up the biofilm that surrounds the spirochete Borrelia burgdorferi.  Combining systemic enzymes like our Fibrin Dissolving Formula with heavy metal chelators like our Heavy Metal Detox Formula is one strategy for “punching holes” in the biofilm. Once this is done, then antimicrobials, like those in our Monolaurin Formula, can better attack bacteria, yeast, and other bugs.

Challenge #2: Lyme spirochetes can change shape. 

This makes it hard for the immune system to detect them – and hard for anything to destroy them. The strength of one’s immune system often dictates the severity of symptoms.  The longer symptoms go untreated, the less removable they can become.

When Lyme spirochetes encounter antibiotics, they can go into cyst form immediately.  Most researchers feel the cyst form is impervious to antibiotics, although some physicians have had success with metronidazole (Flagyl) and tinidazole and the non-drug, grapefruit seed extract found in our Biofilm formula.¹

Cysts are small sacs containing immature spirochetes.  Eventually, the sacs might lodge in tissue or travel the blood stream where white blood cells sense their foreign presence but have little ammunition to kill them.

Challenge #3: Penetrating Cells

The tip of the B. burgdorferi spirochete can spin and twirl until it stimulates the cell’s own enzymes to digest a part of the membrane, allowing entry.  Once inside, the spirochete can lie dormant, protected from both the immune system and the action of antibiotics.  This ability to burrow into or between cells and hide, gains them protection from the immune system.

Challenge #4: Outer Membranes and Division

Both B. burgdorferi and Treponema pallidum, the causative agent for syphilis, have highly unusual outer membranes.  The molecular architecture of these membranes is responsible for their ability to cause persistent infection.  The cell division time of B. burgdorferi is very long compared to other bacteria.

Strep and staph cells, for example, divide in less than 20 minutes.  B. burgdorferi takes 12-24 hours to divide.  The problems is that most antibiotics are effective at the moment when bacteria are dividing because antibiotics inhibit the creation of a new cell wall.  This is a key reason Lyme is so hard to knock out.  Fortunately, our Monolaurin formula operates on a different method of absorption.  Division time is not a large factor.

Challenge #5: Antibiotics

Most doctors agree that, if you have just been infected, a course of penicillin-type antibiotics for at least 6 weeks is the best treatment. The idea here is to knock it out before it can mutate and burrow into tissues.  After initial infection, B. burgdorferi travels rapidly via the bloodstream,² and can be found within the central nervous system as soon as twelve hours after entering the bloodstream.

Early infections require full dose antibiotic therapy with an agent able to penetrate all tissues in concentrations known to be bactericidal to the organism.  However, it is increasingly months or years after the initial infection that people suspect or confirm they have Lyme.

In other articles, we showed that B. burgdorferi exists in three distinct forms:

1. Spirochete
2. Cyst
3. Cell-wall-deficient (CWD) form

Since it can change from one form to another means that, when you throw an antibiotic at a spirochete, it can simply morph into its cyst or CWD form.  Then it can hide in a biofilm, to escape destruction. When the Lyme bug no longer senses the stress of antibiotics, it can morph again into the spirochete form and continue burrowing into new tissues.

Some people infected with chronic, subclinical infections do not handle Vitamin D the way nature intended.  Their bodies convert too much of it to a type of secosteroid that triggers a production of macrophages (like soldiers with inflammatory ammunition to overwhelm the bacteria).  But the soldiers cannot see the bacteria because the bugs are hiding behind a wall of biofilm.  So, the person is left with lots of inflammation – like an army dressed for battle who can’t find the enemy. Since soldiers will do battle, they attack whatever moves; in this case, it happens to be our own cells. (See our Chronic Inflammation Recommendation.)

The Difficulty of Lyme Protocols

B. burgdorferi also has a three-layer cell wall, helping to determine the spiral shape of the spirochete.  This distinctive cell wall resembles those of Gram-negative bacteria (which our Monolaurin formula kills).

Another unusual structural feature is a single flagellum, attached to each end of the spirochete.  This runs the length of the organism and is surrounded by it. This feature is significant in relation to immune protection (most bacterial flagella are highly antigenic).  Still another difference in B. burgdorferi structural architecture is a clear gel-like “biofilm” coating surrounding the bacteria, giving it protection from the immune system (and important to our enzyme step).¹

The DNA of B. burgdorferi is also arranged in a different manner than in other bacteria, lying along the inside of the inner membrane.  The bacteria replicate specific genes, inserts them into its own cell wall.  It then pinches off that part of the cell membrane, releasing it into the surrounding medium.  This fragment of the spirochete membrane with incorporated DNA is known as a “bleb” – perhaps protecting the organism from the immune system.²

The cell division time of B. burgdorferi is very long compared to other bacteria.  A typical cell wall reproduction time for Streptococcus or Staphylococcus is less than 20 minutes, while the total reproduction time of B. burgdorferi is from 12-24 hours.  (Most antibiotics are effective only when the bacteria are dividing with the formation of new cell wall). Given this, an antibiotic would have to be present 24 hours a day for 1.5 years to be present during the cell wall reproduction period.³

Lyme Brain Toxins

Because many of the symptoms of Lyme disease involve the nervous system, it seemed natural that the spirochete produced a toxin that disrupted normal nerve function. A match was made with a selected B. burgdorferi gene and the organism causing many other well-known infectious diseases. The structures of this family of toxins all contain zinc.  They all cut the chemical bond between two specific amino acids in a particular protein found in nerve cells.⁴

This inhibits the release of neurotransmitter chemical signals that nerve cells use communicate with another.  One such neurotransmitter is a simple organic substance known as acetylcholine. (Nutrients to increase acetylcholine ^5,6 are provided in our Multi-Nutrient formula supplement.)

As we talk about in other articles, many brain disease autopsies (on Alheizmer’s and Autism) have been done and are finding that 70-90% of them had Lyme disease!  With our Lyme protocol, we may be bringing new hope to these people.

Hibernating

There are two mechanisms by which B. burgdorferi can survive within the host and remain unknown for long periods of time.

1.  The invasion of tissues by the spirochete.  The tip of the organism has the ability to bind to cells, spin and twirl until it stimulates the cell’s own enzymes to digest a part of the membrane, allowing it to enter. Once inside, the spirochete results in either the death of the cell or takes up residency within.  It may lie dormant for years, protected from both the immune system and the action of antibiotics.
2.  Cysts: If B. burgdorferi senses it is being attacked or starved, it generates a type of biofilm called“cysts”.  These are small cocoons attached to the body by slender threads.  Cysts contain immature spirochetes in a metabolically inactive form.  The immune system and antibiotics can attempt to destroy the invading foreign bodies (cysts) but are not successful.⁶

B. burgdorferi can quickly change surface antigens to protect itself.  Antibodies made against one strain may be effective in killing that strain.  However, the new strain, having different surface antigens, will take up residence in a different tissue where it escapes detection and survives.  It is apparent that B. burgdorferi has evolved disguises and biological techniques to guarantee its survival and thwart any attempts to circumvent it.⁶

4 Major Diseases Linked to Lyme Disease

(There are many other diseases linked to Lyme disease, but some of these have few answers.)

Alzheimer’s:   Spirochetes found in the brain of many Alzheimer disease (AD) patients were positively identified as B. burgdorferi.  Borrelia antigens and genes were also co-localized with beta-amyloid deposits in these AD cases.⁷

Multiple Sclerosis:   The spirochete B. burgdorferi has been found in the brain of many multiple sclerosis (MS) patients along with amyloid deposits. MS has been linked to Lyme disease both seasonally and by location.

Systemic Scleroderma:   The spirochete B. burgdorferi has been found in the blood in systemic scleroderma. Treatment with antibiotics effective against B. burgdorferi returned the skin to normal.⁸

Lyme-Induced Arthritis:   Some Lyme-induced arthritis patients are affected by the disease to different degrees.  A laboratory study demonstrated that different strains of B. burgdorferi were capable of activating arthritis to various degrees.  The proteolytic enzymes in our Biofilm formula are capable of eliminating most of the proteins in the extracellular matrix.⁹

References

1. http://www.lymenet.de/literatur/Microbiology.htm
2. Zajkowska JM, Hermanowska-Szpakowicz T. Subpopulations of the peripheral lymphocytes in the early clinical forms of Lyme disease.Med Sci Monit. 2000;6:278-84.
3. Grier, T. The Complexities of Lyme Disease, from: Lyme Disease Survival Manual, 1997.
4. Schmidt JJ, Stafford RG. Fluorigenic substrates for the protease activities of botulinum neurotoxins, serotypes A, B, and F.Appl Environmental Microbiol. 2003;69:297-303.
5. Vaz FM, Wanders R. Carnitine biosynthesis in mammals.Biochem J. 2002;361:417-29.
6. http://www.orbit6.com/cognition/neurotr1.htm
7. Miklossy J, Khalili K, Gern L et al. Borrelia burgdorferi persists in the brain in chronic lyme neuroborreliosis and may be associated with Alzheimer disease.J Alzheimers Dis. 2004;6:639-49.
8. Wackernagel A, Bergmann AR, Aberer E. Acute exacerbation of systemic scleroderma in Borrelia burgdorferi infection.J Eur Acad Dermatol Venereol.
9. Singh SK, Morbach H, Nanki T et al. Differential expression of matrix metalloproteinases and cyclooxygenases in synovial cells exposed to borrelia burgdorferi.Inflamm Res. 2004;53:689-96.