Update On My Lyme Journey

It has been quite a while since I posted an update on my health and where I am in this Lyme journey. So I'll get straight to it.

I still have an active Lyme infection, even after three years of various kinds of treatment.

Long-term Lyme infection = chronic Lyme disease.

This was confirmed by a Ph.D. immune researcher (Dr. N) whom my doctor consulted with after I started breaking out with multiple large ring rashes on my back, chest, and abdomen during the past several months. Turns out, this is a sign of active Lyme. He said this happens when the body doesn't know what to do with the infection anymore, so it comes out through the skin (an organ itself).

He also told us some things we didn't know about how the Lyme infection has affected my immune system and how this happens when the Borrelia bacteria are in the body long term and isn't sufficiently treated or diagnosed correctly, to begin with, allowing greater dissemination. I think this is a common picture for many of us with chronic Lyme.

Dr. N says a long-term infection with the Lyme bacteria (Borrelias) confuses the immune system to such a degree; it causes it to "lose its intelligence." I'd never heard it put that way before, but I can see this is true.

Specifically, he told us the Lyme infection has caused my immune system to become stuck in a dominant Th2 (T-helper) cycle, an auto-immune cycle. He believes I've been stuck in this a very long time—years. This means my Th1 side is suppressed, and none of this is good because it creates a tremendous imbalance in how the immune system responds to pathogens, toxins, and allergens. One side of the immune system overacts, while the other underacts. If this goes on over time without correction, the immune system can literally burn itself out.

Interjection: I'm pretty sure God has been preserving me.

Interestingly, this explained some other issues I've had for years, like how I easily get and cannot get over certain infections, including some dormant infections that are chronically reactivated, particularly Epstein-Barr Virus (EBV), Cytomegalovirus (CMV), and Varicella-Zoster Virus (VZV). They can get layered in with the Lyme and other tick-borne co-infections. I've had respiratory infections I've never been able to recover from either fully, and now I know why—MTHFR mutations and this severe immune dysfunction, which is actually rooted in the Lyme infection itself.

T helper (Th) cells are immune cells. These cells are neutral until a pathogen (bacteria, virus, parasite, fungus), toxin, or allergen comes along, and they convert into either Th1 or Th2 cells, depending upon the threat.

Th1 cells fight viruses, cancer, yeast, and intracellular bacteria (bacteria inside cells that replicate like Lyme/Borrelias).

Th2 cells fight extracellular bacteria (bacteria that do not invade cells or replicate), parasites, toxins, and allergens.

Dr. Paul Cheney, M.D., explains immune dysfunction syndromes quite well. He says when a person is Th2 activated, they no longer have the defense mechanisms to keep dormant all the things caught in their past. They cannot suppress or control them anymore. Strep, EBV, CMV, etc., reactivate. Candida can also begin to appear. Go here to read more. If that link is broken, try here instead.

While I have had a few improvements, I am still unwell. But, as brutal as this all is, and as sick as I still am, I can't tell you how validating it feels to finally find a doctor who understands what long-term Lyme infections do to the immune and nervous systems—to my immune and nervous systems. 

Finally, somebody who has a deeper understanding of what's really been happening in my body! I'm so grateful to Dr. N. for the revelation he gave my doctor and me and for the time and expertise he graciously shared.

I am grateful to my doctor, too; I feel blessed to have her. She has walked with me through this for the past seven years that I've been seeing her. We've had many ups and downs, and over this last year, we both knew something else needed to be done. As she put it, while there have been some preserving benefits in my treatments, I'm still not getting well, which is a big problem. The fact that I was misdiagnosed for so long—16 years—has only complicated matters. For the record, she is the one who discovered I really have Lyme disease, which was a process in itself, but that's another story for another day. 

Clearly, a new protocol is in order, and I have started a new comprehensive treatment based on Dr. N's recommendations. It's totally herbal (with ongoing homeopathic and nutritional support), and while I've used some herbal therapies in the past, this is a protocol I've never done before. I have been on it for about a month now, and the most significant difference I can tell is that it's clearing up my Lyme rash. Nothing else helped before this.

Dr. N. laid out a very realistic picture of what he believes this treatment must entail. He said it must be comprehensive and not just focused on "killing" the Lyme bacteria, which is really difficult to do once Borrelia spirochetes invade the cells and replicate. It must also address inflammation, damage, and dysfunction in the entire nervous system and other affected organs and systems. And he said gaining back control of my immune system as soon as possible is highly crucial.

We already knew some of these things and have been working to accomplish them. However, Dr. N's insight into how the Lyme infection has affected my immune system changed how we look at the overall picture and proceed with a different treatment. It's like he's given us a huge, missing piece to this crazy, complicated puzzle; an essential element.

Our primary treatment keys:

1.) Treat the long-term Lyme infection as outright as possible using Berberine as a primary herbal antibiotic. Then switch to another herbal combo after 2 months. Back this up with homeopathic remedies.

2.) Reduce overall inflammation in the body, especially in my immune and nervous systems, including my brain. Dr. N says absolutely no one can fully heal or be well with high levels of inflammation in the body. We must also help repair and support the entire nervous system. This is a longer process.

3.) Correct immune dysfunction by helping restore intelligence back to the immune system. This will help with chronic viral infections as well as the Lyme infection.

According to Dr. N, we must do numbers one, two, and three simultaneously to be successful. And so we are. 

4.) Once my immune and nervous systems are stronger, we will start working to correct other dysfunctions in the body like adrenals, thyroid, liver, etc.

Also, maintaining the ability to detoxify is always near the top of the list. If one cannot detox, then one cannot heal. This is something we've been working on for a while and continue doing.

I'd be lying if I didn't say I felt somewhat disheartened by this, and that this has been going on for so long just adds to it; nineteen years total, to be exact. However, I knew deep down that the Lyme infection is still an issue for me because I know my body. If nothing else, this certainly speaks to the complexity and chronicity of Lyme disease. And it speaks of how stealth the Borrelia bacteria are, like it literally hijacks the immune system.

I know this has been rather long, and honestly, I wrestled with writing it because it takes a lot of energy to put it all together. Still, I needed to write an update, if only to document it all for myself. I will try to post periodic updates as I work through this new protocol.

Please pray for my endurance as it would be much appreciated.

I can't even begin to tell you the different treatments I've tried over the years (I know those of you who are also struggling with Lyme totally understand) and how I've worked my butt off to be well. So I really hope and pray this will be a key or at least a big step forward. Some days, it's just plain hard, but I'm still holding to my faith.

The Lord's brought me this far, and I know He will see me through.

With love,

Michelle

The Biology of Lyme Disease: An Expert's Perspective

I wanted to share this informative interview (May 2013) with Dr. Alan MacDonald, MD, clinical pathologist and researcher. He explains the microbiology of Lyme (Borrelia spirochetes) disease and the connection he has found in his many years of research to degenerative neurological conditions, including Alzheimer's disease.

He starts by explaining some of his medical background and training and how he became interested in studying and researching spirochetal diseases, first with Syphilis (Treponema pallidum), and then more specifically, Lyme disease (Borreliosis).

Of note is an interesting case study regarding a German physician who had Alzheimer's disease. Dr. MacDonald and his team found high antibody levels of three different strains of Lyme spirochetes in his spinal fluid as well as Lyme spirochetes in his brain.

He also stated he could grow Lyme spirochetes from four Alzheimer's brains in his work with culturing brain tissues through the George Glenner Alzheimer's Brain Bank at the University of California at San Diego.

He discusses biofilms, DNA changes, and mutations of the Borrelia bacteria. During the last ten minutes, he eloquently explains why Lyme testing methods are flawed here in the USA. As many of us with Lyme already know, standard labs only test for one strain of Borrelia when testing for Lyme infection. At the same time, there are about 100 different genotypes of Borrelia burgdorferi (Bb) alone and many other species of Borrelia bacteria as well, i.e., B. afzelli, B. andersonii, B. microti, B. miyamotoi, etc.

Dr. MacDonald is a true pioneer in Lyme research, and his vast knowledge of Lyme disease biology is over-the-top excellent. He's done most of his work at Harvard and in his own basement. He's best known and beloved in the Lyme community for his role in the Lyme documentary, Under Our Skin.

At the filming of this interview, he stated that he now collaborates with Dr. Eva Sapi, Ph.D., in her ongoing Lyme research at the University of New Haven while also continuing his research in Alzheimer's and Lyme Neuroborreliosis. Two great scientific minds for sure!

I think that Dr. MacDonald has laid a solid foundation of research for the role Lyme spirochetes can play in many neurological diseases, including MS and ALS. Instead of calling Lyme "The Great Imitator," perhaps it should be called The True Root of Many Disease Processes more fittingly.

This video is just under thirty minutes. It's clearly worth watching if you have Lyme or someone you love does. I found it very interesting and enlightening. Also, it will prompt you to go directly to YouTube to watch.

Love and blessings,
Michelle

P.S. If you're interested in reading more about the microbiology of Lyme, Borrelia bacteria, or how it affects the immune system and other cells, consider reading The Complexities of Lyme Disease by Thomas Grier, MS which is also excellent. Click here to read Part 1 or find the whole series listed in my blog archive under March and April 2013.

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 3): When Lyme Bacteria Infects the Brain

This is Part 3 of the series, The Complexities of Lyme Disease by Thomas Grier, M.S. Click here to read Part 1 and here to read Part 2. Part 4 is soon to come.  ~ Michelle

When Lyme Bacteria Infects The Brain:

As we have previously discussed, the pathogen that causes Lyme disease is a highly motile spirochete within the Borrelia family of bacteria. This is the same group of bacteria that cause Relapsing Fevers in Africa and around the world. Like other Relapsing Fever bacteria, Borrelia burgdorferi (Lyme bacteria) has both an affinity for the brain and a mechanism to penetrate into it.

While Lyme may be a bit more subtle upon penetrating the brain, its silent but insidious invasion may be the reason that brain involvement can and is often overlooked by physicians for months or even years in neurological Lyme patients.

In the case of Lyme disease, every animal model to date shows that the Lyme spirochete can go from the site of the bite of an infected tick to the brain in just a few days. While we know this bacteria can break down individual cell membranes and capillaries, its entrance into the brain is too pronounced for such a localized effect.

When the Lyme bacteria enters the human body, we react by producing several immune regulatory substances known as cytokines and lymphokines. Several of these act in concert to break down the blood-brain barrier (e.g., IL-6, Tumor Necrosis Factor-alpha, IL-1, Transforming Growth Factor-beta, etc.). In addition to affecting the blood-brain barrier, these cytokines can make us feel ill and give us fevers.

Since the brain has no immune system, it prevents infection by limiting what can enter the brain. The capillary bed that surrounds the brain is so tight that not even white blood cells are allowed to enter. Many drugs can’t enter either, making treatment of the brain especially hard.

For the first ten days of a Lyme infection, the blood-brain barrier (BBB) is virtually nonexistent. This not only allows the Lyme bacteria to get in but also immune cells that can cause inflammation of the brain.

* Note: The breakdown of BBB was shown to occur by tagging WBCs, albumin, and other substances known not to cross the BBB with radioactive iodine. The CSF (cerebrospinal fluid) of mice was tested, and then they were infected with Bb (Borrelia burgdorferi). The CSF was then retested every day after for several weeks. The result? No crossover of iodine was present in the control group, but 100% crossover was in the infected group for 10 days. The infection had the same result on the BBB as if you were injecting the radioactive iodine directly into the brain.

Once the Lyme bacteria enter the brain, they continue to divide and become entrenched within the brain's tissues and cells. Borrelia burgdorferi is directly neurotoxic upon contact with neurons and also has a negative effect on glial cells trying to repair brain injury. This, in turn, further increases the permeability of the blood-brain barrier, allowing, even more, blood-borne agents to enter the brain. The immune system responds to the new flood of internal bacterial antigens and produces more inflammatory cytokines. The result can cause brain edema or encephalitis, intracranial pressure, and focal areas of demyelination.

Also, when the human brain becomes inflamed due to infection with the Lyme bacteria, cells called macrophages respond by releasing a neuro-toxin called quinolinic acid. This toxin is also elevated in Parkinson’s Disease, MS, and ALS. What quinolinic acid does is to stimulate neurons to repeatedly depolarize. If this goes on unabated, it eventually causes the neurons to demyelinate and die. Basically, people with elevated quinolinic acid have short-term memory problems.

This means: If we think of our brain cells like telephone lines, we can visualize the problem. If all of the lines coming in are busy, we can’t learn anything. If all of the lines going out are busy, we can’t recall any memories. Our thinking process becomes impaired.

A second impairment to clear thinking that Lymies can experience is the restriction of proper circulation within the blood vessels inside the brain. Using an instrument called the Single Photon Emission Computerized Tomography scanner (SPECT scans), we are able to visualize the blood flow throughout the human brain in 3-D detail. What was seen in the brains of chronic neurological Lyme patients was an abnormal “Swiss-Cheese” pattern of blood flow. The cortical or thinking region of the brain was being deprived of good circulation, while the occipital (eyesight) regions had an increased flow. This could help explain why most Lyme patients complain of poor concentration and overly sensitive eyes.

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