Overview of Lyme Borreliosis (A Bioregulatory Medicine Approach)

by: James Odell, OMD, ND, L.Ac., BRMI Medical Director

The information in this monograph is intended to help users better understand current diagnostic and bioregulatory medicine treatment protocols related to tick-borne illnesses. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. The management of tick-borne illnesses in any given patient must be approached on an individual basis using the practitioner’s best judgment. Users should seek the advice of a physician before using any protocol listed in this monograph. The protocols raise many issues that are subject to change as new data emerge. The reader assumes the risk of any injuries. None of the suggested protocol regimens can guarantee health benefits. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions. ——————— Lyme disease, also called Borreliosis, might be the most insidious and least understood of infectious diseases of our day. Lyme disease is an infection that is caused by different genospecies of the Borrelia bacteria and primarily transmitted by the bite of an infected tick. According to Center for Disease Control (CDC) reports, Lyme disease caused by Borrelia is currently the most common vector-borne disease in the United States.1 There are several species, subspecies and strains of this bacteria. This great diversity of species and strains contributes to its ability to evade the immune system and antibiotic therapy, thus leading to a chronic infection (post-treatment Lyme disease syndrome or PTLDS). PTLDS is often associated with neurological symptoms that are both debilitating and increasingly difficult to treat with conventional antibiotics.2 The Borrelia spirochete has developed numerous adaptive features that makes it unique among pathogenic bacteria and thus can lead to PTLDS.3

Borrelia’s Adaptive Features

Borrelia’s adaptive features ensure its survival and confer resistance to antibiotics. Borrelia, like the bacteria that causes syphilis, is a spirochete. Spirochetes are a group of bacteria that have a unique mode of motility by means of axial filaments called endoflagella. When these filaments rotate, the spirochetes move in cork-screw fashion. This type of movement is thought to be an adaptation to viscous environments, such as aquatic sediments, biofilms, mucosal tissues, collagen tissue and the intestinal tracts of animals. This feature allows the spirochetes to hide their flagella from the host immune defenses. Borrelia’s membrane has a composition like the cells of mammals in that it contains phosphatidylcholine (PC), a type of phospholipid. Phospholipids are a class of lipids or fats that are a major component of all cell membranes. Because our nervous system is rich in PC, the spirochete tends to associate itself with our nervous system as a source of PC for its membrane. Hence, it feeds on us. It has also been suggested that having a cell membrane high in PC, and therefore “looking” like one of our own cells, may aid Borrelia in its effort to avoid our immune system.4

Borrelia has one of the most advanced and complex DNA structures of any bacteria known. This allows it to assess its surrounding chemistry and alter its cell membrane to ensure its survival. Thus, Borrelia is the ultimate escape artist. It can invade a variety of cells, including endothelium, fibroblasts, lymphocytes, macrophages, keratinocytes, synovium, and most recently neuronal and glial cells. By “hiding” inside these cells, the spirochete can evade the immune system and be protected to varying degrees against white cells and antibiotics, allowing the infection to persist.5 The spirochete can change its form to rounded forms, sometimes called spheroplasts, which either lack a cell wall or have a damaged cell wall.6 This too is a survival technique that can protect it from antibiotics. Data suggest these rounded cells are virulent and infectious, can survive under adverse environmental conditions, and may revert to the spiral form, once conditions are more favorable. Antibiotics are ineffective against these spheroplasts.7, 8, 9

Stages and Manifestations of Lyme Borreliosis

The disease is described as having three stages: early localized, early disseminated and late disseminated. However, the stages can overlap and not all patients go through all three. A bull’s-eye rash is usually considered one of the first signs of infection, but many people develop a different kind of rash or none at all. The last stage, because of domination of neurologic symptomatology, is called “neuroborreliosis”. The brain has a highly selective permeable barrier called the blood-brain barrier that normally protects the brain from foreign invaders. However, Borrelia‘s unique characteristics allow it to penetrate this protective barrier. Thus, neurological symptoms are present with chronic Lyme disease because Borrelia and its endotoxins (neurotoxins) infect the brain and central nervous system causing inflammation and various neurological symptoms such as pain, headaches, tremors, seizures, and brain fog.10

It has been said that the longer one is ill with Lyme the more endotoxin/neurotoxin is present in the body.  It probably is stored in fatty tissues, and once present, persists for a very long time.  This may be because of enterohepatic circulation, where the toxin is excreted via the bile into the intestinal tract, but then is reabsorbed from the intestinal tract back into the blood stream. Mainstream infectious disease doctors argue that there is no evidence that Lyme borreliosis remains in the body after a few weeks to a month of antibiotic treatment. The laundry list of symptoms in patients may be persistent, but these conventional doctors claim that it is not due to a chronic Lyme infection. On the other side, many doctors that specialize in Lyme disease blame Borrelia and coinfections for triggering chronic neurological and psychiatric symptoms.

A comprehensive therapeutic bioregulatory medicine approach considers the stage as well as the individual’s unique constitution and the biological terrain that is affected.

Spirochetes have an affinity for connective tissue. The following are 5 tissues that are commonly infected:

  • ligaments and joints (asymmetric affliction of large joints, especially hip and knee)

  • skin and subcutaneous tissues (collagen breakdown and premature aging)

  • meninges and astroglia (connective tissue of brain)

  • heart tissue

  • aqueous humor of the eye

Symptoms Borrelia spirochete releases bacterial lipoproteins (BLP) which cause numerous symptoms. The following is a checklist of common symptoms seen in various stages of Lyme disease:

Localized Early (Acute) Stage:

  • Solid red or bull’s-eye rash, usually at site of bite

  • Swelling of lymph glands near tick bite

  • Generalized achiness