Staphylococcus Lyme spirochetes
* Note: Antibiotics kill bacteria by binding to RNA rich organelles inside the bacteria called ribosomes*, and interrupting the formation of cell wall proteins, or proteins involved in cell metabolism. (See LD Survival Manual) Some newer antibiotics kill by disrupting DNA/RNA synthesis. (Cipros and other quinilones interrupt DNA gyrase and enzyme that unwinds DNA for replication)

If a bacteria is in a non-metabolic state (dormant) no antibiotic is effective. To be lethal the antibiotic must be absorbed and processed through the bacteria’s metabolic machinery and cause a disruption of metabolism.

Unlike antiseptics, antibiotics don’t kill on contact. If there are any dormant bacteria hidden in sequestered sites, then regardless of the length of treatment, antibiotics can fail until the bacteria become metabolically active. (The Forgotten Plague see reference to Tuberculosis)

A ribosome translates messenger RNA into proteins. In other words, cellular genes are expressed as proteins that are created at the site of the ribosomes.

Ribosomes are protein creating factory assembly lines. Like other spirochetes, such as those that cause Syphilis, the Lyme spirochete can remain in the human body for years in a non-metabolic state. We know this because patients with ACA rash for years are often culture positive when the skin is biopsied and cultured. Non metabolic bacteria is essentially suspended animation. The bacteria does not metabolize in this state, antibiotics are not absorbed or effective. When the conditions are right, those bacteria that survive, can seed back into the blood stream and initiate a relapse. It is a beautiful and patient survival mechanism. (59-62,70)

This means: Just because a person is symptom free for long lengths of time doesn’t mean they aren’t infected. It may simply be a matter of time before the re-emergence of sequestered non-metabolic bacteria. Whereas viral infections often impart a lifelong immunity, and may suppress subsequent relapses or reinfections. Lyme like other bacterial infections, does not impart an active immunity for long a period of time. People are often reinfected with Lyme. A relapse of symptoms could actually be thought of as a reinfection or a reseeding of infection from immune privileged sites.(96)

POLYMORPHISM: The ability of a bacteria to change its structural identity. During cell division this bacteria has the ability to change its cell wall structure, and surface antigens thus making it more difficult for the human immune system to recognize. Like its cousins, the RELAPSING FEVER SPIROCHETES , the Lyme spirochete has a sequence of surface antigens it can choose to express or not express. There are more than two dozen species of Relapsing Fever Borrelia bacteria which have been clearly identified. We are now beginning to see a similar diversity within the Lyme spirochete family as well. Polymorphism makes recognition and identification more difficult, it is like a criminal putting on a new disguise after every time he has committed a new crime. While there are four generally accepted genospecies of Lyme disease Borrelia burgdorferi, afzellii, garinii, and lonstarrii, there are hundreds of identified strains of the first three species. Borrelia spirochetes are polymorphic because they have built in genetic mechanisms to vary their antigens.

This Means: Just as the immune system recognizes the bacteria and tries to kill it. The bacteria changes its clothes and fools the immune system and survives a little longer. Soon the bacteria finds safer areas of the body to hide in and the immune system stops looking for it. But another aspect of polymorphism is that once the cell changes it may become even more lethal to some cells. For example when Borrelia burgdorferi was introduced into the mouse via the blood stream, the bacteria traveled to the brain. But the bacteria recovered from the brain was more adapted to the brain and could no longer be killed from antibodies in the bloodstream. Polymorphism is a clever way to survive and may offer reasons to multiple symptoms.

CELL WALL DEFICIENT SPIROCHETES:
The nice clearly definable spiral shape of the Lyme spirochete is formed by the presence of the bacteria’s cell wall. Without this cell wall to determine its shape, the bacteria only has a thin pliable membrane to hold its structure together. When the bacteria turns off its genes that govern cell wall synthesis, the bacteria can change from a spiral shape, to a sphere. These spherical forms are known as L-forms or Cell Wall Deficient (CWD) forms. They represent a new hazard in the diagnosis and treatment of common diseases.

Many doctors and microbiologists have a hard time understanding that spirochetes can actually be fuzzy blobby looking spheres, but they are a reality. As a defense mechanism to mammalian immune systems, the Lyme spirochete has learned to turn off its group of genes that result in cell wall formation. This also eliminates all associated cell wall antigens.

How does a microbiologist recognize Borrelia burgdorferi once it is no longer a spirochetea? In order to prove that these spheres floating around in human blood are actually spirochetes is difficult because they do not culture well. Instead a microbiologist will make a wet mount of the infected blood on a slide, and then add acrodine orange stain to stain the nucleic acids. Then a second stain that is specific for Borrelia burgdorferi is added. It is prepared by first making a monoclonal antibody specific to a Borrelia membrane antigen. Then that monoclonal antibody is tagged with a fluorescent dye. When this dye is added to the wet mount slide it stains only the Borrelia species of bacteria. Suddenly what was once totally invisible in blood by normal staining techniques, becomes visible. Spirochetes can in fact become cell wall deficient spheres.

Another technique to identify spheroplasts as being Borrelia bacteria is to take antibodies unique against Borrelia and tag them with inert gold spheres. Then culture the L-forms with the antibody-tagged-gold . When these cultures are viewed under electron-microscopes, the gold can clearly be seen attached to the membrane indicating that the antibody has attached to a protein specific to Borrelia. Therefore the spheroplasts must have once been spirochetes.

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