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 2): Motility of the Lyme Bacteria

This is Part 2 of the series The Complexities of Lyme Disease by Thomas Grier, M.S. Click here to read Part 1. I'll post Part 3 next week.  ~ Michelle

Motility of the Lyme Bacteria: 

How does the Lyme bacteria travel from the bloodstream to other tissues? While we have known for a long time that the Lyme spirochetes can show up in the brain, eyes, joints, skin, spleen, liver, GI tract, bladder, and other organs, we didn't understand the mechanism by which it could travel through capillaries and cell membranes. Then, Dr. Mark Klempner, M.D., presented at the 1996 LDF International Lyme Conference an interesting paper that gave us part of the answer.

Many researchers have observed that the Lyme spirochete attaches to the tip of the human cells first. It then wiggles and squirms until it enters the cell. What Dr. Klempner showed was that when the spirochete attached to the human host cell, it caused that cell to release digestive enzymes that would dissolve the cell and allow the spirochete to go where ever it pleases. This is very economical for the bacteria to use our own cell's enzymes against us because it does not need to carry the genes and enzymes around when it travels.

Dr. Klempner also showed that the spirochete could enter cells such as the human fibroblast cell (the skin cell that makes scar tissue) and hide. Here the pathogen was protected from the immune system and could thrive without assault. More importantly, when these Bb-fibroblast cultures were incubated with Rocephin (ceftriaxone), two-thirds of the cultures still gave rise to live spirochetes after two weeks and in later experiments for more than 30 days.

If we can't kill it in a test tube at these high concentrations of Rocephin in four weeks, how can we hope to kill it in the human body?

This means: The infection can enter the best tissue that is optimal for its survival. Once it gains an intracellular position, it may evade the immune system and antibiotic therapy by remaining sequestered away from these hostile environs.

Another interesting observation about this bacteria is how it interacts with our body's immune system.

Dr. David Dorward of the NIH Rocky Mountain Laboratories showed that when healthy normal human B-cells were placed in a culture with live Borrelia burgdorferi, it was only a matter of moments before the spirochetes started to attach and penetrate the antibody-producing white blood cells. Once inside the cell, the bacteria should be killed by a process wherein B-cell lysosomal enzymes dissolve the bacteria. But this does not happen. Instead, the bacteria actually thrive and eventually destroy the lymphocyte.

What is much more disconcerting is that by using a time-lapse video camera, the spirochete can be seen to enter the B-cell and exit a short distance later. But when it exits, it appears to be wearing the membrane of the B-cell. The live motile bacteria then swims about unharmed in the sea of B-cells because by wearing the cloak of its enemy, it goes undetected. This stealth-type camouflage will prevent antibodies from attaching to it; it prevents the complement enzymes in the blood from finding and destroying it, and it eludes the scavenger white blood cells such as macrophages and killer T-cells that normally hunt and destroy foreign pathogens.

This means: We have a highly evolved bacteria that is highly mobile, can dissolve any tissue it desires so it can find immune-privileged sites, and can camouflage itself from our own immune system by wearing the membrane of the very cells that are supposed to track it down and kill it. This bacteria seems to have evolved a sophisticated defense mechanism to avoid our immune system.

Lyme bacteria (Borrelia burgdorferi spirochete) in human blood

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