The Complexities of Lyme Disease (Part 4): Lyme Receptors

This is Part 4 in the series The Complexities of Lyme Disease by Thomas Grier, M.S. Click here to read Part 1. Here to read Part 2. And here to read Part 3.

Lyme Receptors 

It now appears that there are specific receptors in the Lyme spirochete to attach to endothelial
cells, N-Acetyl-glucasomine, B-cells, glial cells, nerves, and neurons.

The way our immune system is supposed to work is that it recognizes foreign invaders as being different from self, and it attacks the infection. Unfortunately, the immune system sometimes attacks our own cells. This is called autoimmune disease. If a foreign invader has a chemical structure similar to our own tissue antigens, our bodies sometimes make antibodies against our own tissues. In people with Lyme disease, scientists have discovered auto-antibodies against our own tissues, including:

• Nerve Cells (Axons)
• Cardiolipin 
• Myelin (also seen in MS)
• Myelin Basic Protein (also seen in MS)
• Neurons (brain cells)

When the immune system finds a foreign invader, it tags that invader in a number of ways. A cell called the macrophage can engulf the bacteria and then communicate to other immune cells the exact description of the bacteria. Another cell might mark the cell with an antibody, which attracts killer T-cells. Some types of T-cells communicate to other cells what to attack and regulates the immune assault. But sometimes, the body can produce a type of antibody that doesn't attack or help. A blocking antibody will attach and coat the intruder, but it won't fix *compliment, and it shields the bacteria from further immune recognition. In Lyme, we have seen quantities of IgG4 blocking antibody such as is seen in some parasitic infections (Tom Schwann RML 92 LDF Conference).

[* Note: Compliment is a term used for a series of 18 + digestive proteins that are only activated by signals from our immune system, such as complement-fixing antibodies that attach to foreign antigens.]

In order for the immune system to make an attacking antibody, the immune system must first find an antigen that it can attack. Unfortunately, as seen by freeze-fracture electron microscope, photographs of the Lyme bacteria show that most of the antigens are on the inside of the inner membrane and not on the outside. This makes the bacteria less visible to the immune system and more difficult to attack.

The most intriguing fact about Borrelia spirochetes is their well-documented ability to change the shape of their surface antigens when they are attacked by the human immune system. When this occurs, it takes several weeks for the immune system to produce new antibodies. During this time, the infection continues to divide and hide. It appears that Borrelia are able to change their surface antigens many times and can do it quickly.

Borrelia burgdorferi (Bb) correlates with the enhancement of Toll-like 

receptor 2 (TLR2) expression by microglia 

American Society for Microbiology

In one study by Dr. Andrew Pachner, M.D., he infected mice with a single strain of Borrelia burgdorferi. After several weeks he was able to isolate two slightly different forms of the bacteria. The bacteria from the bloodstream was attacked and killed by the mouse's immune sera, but the bacteria isolated from the mouse's brain was unaffected by the immune sera. The bacteria isolated from the mouse's brain had a new set of surface antigens.

It appears that contact with the CNS caused the bacteria to change its appearance. Since the brain is isolated from the immune system and is an immune-privileged site, the bacteria became its own separate strain.

This means: Infections of the bloodstream may be different from the infections that are sequestered in the brain. While we continue to have active immunity in the bloodstream, the brain has no immune defenses except for circulating antibodies. So if those circulating antibodies are ineffective to attack the bacteria in the brain, then the brain is left without any defenses, and the infection goes unabated.

Another peculiar observation of this bacteria is seen inside the bacteria. When the genetic control mechanisms of this bacteria are inhibited with antibiotics known as DNA Gyrase Inhibitors (ciprofloxin), the bacteria start to produce bacteriophage.

A phage is a virus that specifically attacks bacteria. In this case, there are two distinct forms. This means the Lyme bacteria at one time was attacked by viruses; it was able to suppress them, but the DNA to make the phage is still incorporated within the DNA of the bacteria. Perhaps activation of this phage could one day be beneficial to treating chronic Lyme patients?

The Complexities of Lyme Disease ( A Microbiology Tutorial) by Thomas Grier, M.S.

The Complexities Of Lyme Disease (Part 1): The Structure of the Lyme Bacteria

I recently came across this fantastic excerpt written by Lyme researcher and lecturer, Thomas Grier, M.S., who was misdiagnosed with M.S. for years when he had chronic relapsing Lyme disease. Sounds familiar to many of us, I know. He is now the Executive Director of Pathology Studies at MIBDEC (Minnesota Insect-Borne Disease Education Counsel), a non-profit organization. He has a background in microbiology and immunology and continues to do research in both the Lyme and M.S. communities. 

The article is so long that I'm breaking it into parts and using excepts that might not be as well known or understood. I found it extremely interesting. While I already knew some of the basic information; it truly helped me better understand the complexities of Borrelia (Bb) and its effect on and within the human body. I felt the need to share it.

Perhaps some of you are familiar with Grier and/or his work. I had previously read his personal story a couple years ago but never knew he had written the manual (Lyme Disease Survival Manual) this excerpt is taken from. 

I'll post Part 2 in a week or so but I've included a link to the full article at the end of this post for those who want to read it in it's entirety now.    ~ Michelle

Excerpts from The Complexities of Lyme Disease 

by Thomas Grier, M.S.

Why is Lyme disease such a mystery? Why does it mimic so many other diseases? Why is it so difficult to detect? The reasons come from the microbiology of the bacteria that causes Lyme. This paper will look at the biology of this bacteria and the consequences of the organism's unique microbiology on human victims.

Lyme disease is caused by a spiral-shaped bacterium known as a spirochete. Diseases that are caused by spirochetes are notorious for being relapsing in nature, difficult to detect, and great imitators of other diseases. Syphilis, Tick-Borne Relapsing Fever, and Leptospirosis are other examples of spirochetal diseases. Lyme disease is caused by a bacteria called Borrelia burgdorferi, named after the man who isolated it from a Deer Tick in 1981, Dr. Willy Burgdorfer. The following is a tutorial to help explain away the mysteries of this bacteria, and why it causes so much controversy between patients and the medical community.

The Structure of the Lyme Bacteria:

The structure of the Lyme spirochete is unlike any other bacteria that has ever been studied before. It is one of the largest of the spirochetes (0.25 microns x 50 microns). It is as long as a fine human hair is thick. Borrelia burgdorferi is a highly motile bacteria. It can swim extremely efficiently through both blood and tissue because of internal propulsion. It's propelled by an internal arrangement of flagella, bundled together, that runs the length of the bacteria from tip to tip.

Like other Borrelia bacteria, Borrelia burgdorferi (Bb) has a three-layer cell wall which helps determine the spiral shape of the bacteria. What makes this bacteria different from other species is that it also has a clear gel-like coat of glycoproteins that surround the bacteria. This extra layer is sometimes called the Slime Layer or S-layer.

This means: This extra layer of glycoproteins (exaggerated in thickness here) may act like a stealthy coat of armor that protects and hides the bacteria from the immune system. The human immune system uses proteins that are on the surface of the bacteria as markers and sends attacking antibodies and killer T-cells to those markers called outer surface protein antigens (OSP antigens). This nearly invisible layer is rarely seen in washed cultures but can be seen regularly in tissue biopsies.

The Lyme bacteria is also different from other bacteria in its arrangement of DNA.

Most bacteria have distinct chromosomes that are found floating around inside the cytoplasm. When the bacteria starts to divide, it forms a new cell wall in the middle and begins to split in two. The chromosomes also divide, and the new copies of the chromosomes enter the new cell. The arrangement of DNA within Borrelia burgdorferi, however, is radically different from other bacteria. It is arranged along the inside of the inner membrane of the cell. It looks something like a net embedded just underneath the skin of the bacteria.

This means: We really don't understand the mechanisms of how Bb regulates its genetic material during its division. The bacterial DNA is uniformly embedded inside the inner membrane of the Bb bacteria, like nylon stocking.

Another unique feature to Borrelia burgdorferi are Blebs. This bacteria replicates specific genes and inserts them into its own cell wall, and then pinches off that part of its cell membrane and sends the Bleb into the host. Why it does this, we don't know? But we do know that these blebs can irritate our immune system.

Dr. Claude Garon of Rocky Mountain Laboratories has shown that there is a precise mechanism that regulates the ratio of the different types of blebs that are shed. In other bacteria, the appearance of blebs often means the bacteria can share genetic information between themselves. We don't know if this is possible with Borrelia species.

There have been reports of a granular form of Borrelia, which can grow to full size, fully autonomous spirochetes and can reproduce. These granules are so small that they can be filtered and separated from live adult spirochetes by means of a micropore filter. The granular/spore form of Borrelia burgdorferi is still being debated. (Stealth Pathogens Lida Mattman Ph.D. 66, Phillips/Mattman 98, Preac-Mursic)

The division time of Borrelia burgdorferi is very long. Most other pathogens, such as Streptococcus or Staphylococcus, only take 20 minutes to double. The doubling time of Borrelia burgdorferi is usually estimated to be 12-24 hours. Since most antibiotics are cell wall agent inhibitors, they can only kill bacteria when the bacteria begins to divide and form new cell walls.

This means: Since most antibiotics can only kill bacteria when they are dividing, a slow doubling time means less lethal exposure to antibiotics. Most bacteria are killed in 10-14 days of antibiotics. To get the same amount of lethal exposure during new cell wall formation of a Lyme spirochete, the antibiotic would have to be present 24 hours a day for 1 year and six months!

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).

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 bloodstream and initiate a relapse. It is a beautiful and patient survival mechanism.

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 the 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 a long period of time. People are often reinfected with Lyme. A relapse of symptoms could actually be thought of as reinfection or a reseeding of infection from immune-privileged sites.

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 that have been clearly identified. We are now beginning to see a similar diversity within the Lyme spirochete family as well. Polymorphism, which is the ability of the bacteria to change its structural identity, 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, Borrelia afzellii, Borrelia garinii, and Borrelia 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 bloodstream, 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 for multiple symptoms.

The Complexities of Lyme Disease (A Microbiology Tutorial) By Thomas Grier, M.S.

Borrelia burgdorferi (Bb) bacteria (spirochetes) magnified using dark-field microscopy.

Oral Spirochetosis, Lyme, and Other Chronic Diseases

I believe the book, The Stealth Killer: Is Oral Spirochetosis the Missing Link in the Dental and Heart Disease Labyrinth? is very relevant and important not only for those of us with Lyme but for everyone. It's definitely informative and seriously worth the read, in my opinion. Dr. William Nordquist, DMD, connects a big dot between spirochetes and many chronic diseases, including periodontal, cardiovascular, and neurological diseases.

Many of my major health problems began after having oral surgery in 1994. I did have optic neuritis before 1992, but the etiology could never be fully explained. The reason for the surgery was to remove an abscessed portion of bone from my maxilla (which, interestingly, was on the same side as the neuritis). Actually, there was more bone abscessed than the surgeon could initially tell from my x-rays. Of course, he later discovered this fact during the actual surgery. Afterward, I felt very ill. In fact, my recovery did not go well at all.

I tried returning to work two weeks later but took a medical leave of absence for over two months because I was just too exhausted, sick, and debilitated. I couldn't physically function.

After several rounds of labs, it appeared I had developed mono (Epstein-Barr) following the surgery, which was true. This was thought to be the sole reason for my feeling so badly and that I would recover in time. Little did I know; it was only the beginning.

I've never felt the same since.

And I've had so many questions.

Nineteen years later, I still have many questions. Yet I began digging even deeper after discovering chronic Lyme was at the root of my illness a few years ago (of course, we all know the complicating problem with undiagnosed or misdiagnosed Lyme disease is that it becomes chronic or persistent Lyme with multiple co-infections. And that's not even taking into account the weakening or damaging of cells, organs, and systems that occurs through the many taxing months and years of untreated chronic infections and inflammation).

Were oral spirochetes responsible for the abscess in my jaw?

Was Borrelia burgdorferi (Bb), the Lyme bacteria, already present in my system before the surgery? Or other vector-borne bacteria or viruses, for that matter?

Did the invasiveness of that initial surgery (I had two other subsequent surgeries a few years later due to complications, but that's for another time) suppress my immune function, which in turn allowed the release of spirochetes more systemically?

I have my own thoughts about all of this. I've found some solid answers along the way, but I also have my arrived-at-answers too. You know, piecing together certain parts of this health puzzle yourself and arriving at the most apparent answer. Sound familiar?

And then there are those questions that still remain. And perhaps they always will. I'm not sure I'll ever find complete answers for them. Sound familiar too?

According to Dr. Dietrich KlingharM.D.M.D., Ph.D., one of the many presentations of Borrelia, as well as Babesia and Bartonella (two other tick-borne bacteria), can be "non-healing infections of the jaw bone, devitalized teeth, and dental pain."

The more I've researched, the more I've discovered that Borrelia (Lyme) spirochetes, among many things, like bone. A lot. Particularly bones of the jaw and hip. They seem to have an affinity for it. I've heard through the grapevine, if you will, some stories of others with Lyme disease who also had bone infections (osteomyelitis) of the jaw and/or hip. I directly heard a woman tell the story of her mother, who had spirochetes eat through the head of her femur to such a degree; she had to have a hip replacement. And then, the spirochetes began eating through the plastic part of the implant. Crazy!

This is what led me to find Dr. Nordquist's book, The Stealth Killer. Of course, it is written from a dental viewpoint, but that's precisely the point. He discusses, among many things, how all spirochetes, including oral spirochetes and Borrelia, the causative agent of Lyme, share similar, if not identical, survival strategies. Very interesting, don't you think?

When I first started reading it, my mouth dropped open. No pun intended. It spoke to me on so many levels because of the previous dental and jaw bone infections I'd had, as well as a heart arrhythmia I developed several years later. The arrhythmia continually grew worse over the course of two years, and we had no idea what was causing it.

In the meantime, Lyme came into the picture. Long story, but the arrhythmia totally subsided once I started on a Lyme treatment (specifically beginning with Borrelia Remedy Series Therapies from Desbio). It took about three months for my rhythm to completely correct itself, but it did indeed. That's when my doctor and I both knew the Borrelia bacteria had gotten into my heart tissue and was the source of this mysterious arrhythmia.

Dr. Nordquist has also co-written another relevant book that I've yet to read but plan to, The Silent Saboteurs: Unmasking Our Own Oral Spirochetes as the Key to Saving Trillions in Health Care Costs.

On a side note, Dr. David Jernigan, DC, wrote an interesting article entitled, Are You Harboring Bacteria in Your Teeth? that bears witness to this discussion. Beyond daily brushing and flossing, he recommends using a Waterpik Waterflosser Ultra with purified water and a cap full of Thieves Mouthwash, the highly anti-bacterial/anti-viral/anti-fungal essential oil blend, to eliminate any bacteria in the mouth, including Borrelia. This I have tried and like.

Dr. Douglas Martin, DDS, recommends brushing with baking soda and using a Waterpik with Dakin's solution (1 part Clorox to 20 parts water) to eradicate spirochetes, an oral care regimen advocated by Dr. Jurgen Slots, Ph.D., head of the Periodontics program at the University of Southern California. Click here to read more. While I often use baking soda to brush, I've never tried Dakin's solution. Anybody?

I share all this because I absolutely believe that spirochetes have played a role in my health problems from the beginning. And this isn't only a Lyme disease issue. I know many who've had similar experiences. I wonder how many people with Alzheimer's or arteriosclerosis or congestive heart failure, MS, or gingivitis actually have a problem with spirochetes of some kind?

Believe me, I clearly know and understand there are usually many factors that play a role in developing chronic illness. But I also believe there are key triggers involved in the process, including spirochetes. Knowing they can evade detection by the immune system and still cause major havoc in the body unbeknownst to the average person, including many doctors, is what makes me want to share this even more. I'd say stealth is a spot-on description.

I sincerely hope and pray the dental and medical fields will awaken more to this truth. And perhaps in doing so, more lives can be spared the tremendous suffering, debilitation, and loss that comes with pathogenic spirochetal infections like Borrelia, including oral spirochetes.

I'm certainly not advocating living in fear. That is no way to live. I won't. One has to choose to live in hope because there is always hope for something better despite all the difficulty, suffering, and uncertainty. And there are those wonderful doctors, researchers, scientists, and advocates who are diligently working for this very thing - something better. You and I are working for something better too; a better life for ourselves, for our loved ones, and for the next generation.

I have to keep hoping and believing. Let's hope and believe together.

Michelle

P.S. If any of you have had similar experiences that you want to share, I'd love to hear about them.