The Lyme bacteria begin their passage through blood vessels by attaching themselves to the endothelial cells lining the inside of the blood vessel. (see Tara Moriarty PhD video Spirochetes Unwound)
Then the spirochetes continually twitches and pushes itself as deep as it can go. The simple act of attaching to the endothelial cells lining the blood vessels initiates the endothelial cells to release digestive enzymes including tissue plasminogen, proteases, and basement membrane laminase.
This digestive enzyme cascade starts a localized attack of cellular degradation that ultimately leads to leaky gaps between the endothelial cells that make up the blood vessel walls. (See Blood-Brain-Barrier photo)
Once the bacteria are out of the blood stream they are able to travel deep inside many organs and tissues of the human body.(see transplacental fetal autopsies and brain-Alzheimer's photos.)
In animal models, the Lyme spirochete within mere hours of a tick bite, causes a dramatic breakdown of the blood-brain-barrier. This breakdown of the BBB has been observed in rats, mice, hamsters, dogs, cats, and monkeys.
Why is it important to understand this mechanism of blood vessel penetration when we are discussing Lyme disease diagnostic tests?
The fact that the Lyme bacteria can escape the blood stream very early in the infection is fundamental to understanding why the antibody Lyme tests are so fallible and why there may never be a antibody based serology Lyme test that is truly trustworthy.
Just because you kill all the cockroaches that you see in your basement doesn’t mean there aren’t some in hidden in the walls, rugs and cupboards!
(The blood vessels in the brain usually prevent bacteria and toxins from entering the brain. A loss of this barrier not only allows the Lyme bacteria to enter the brain but also other undesirable substances such as inflammatory cells, toxins and other bacteria enter the brain. Creating a perforated BBB opens the patient up to further complications!) (See Sci American graphic)
It is the bacteria’s ability to exit the blood stream, hide, and survive that makes Lyme disease so difficult to detect with any one test. It is the unique microbiology of this bacterium that gives it the ability to hide and survive undetected within the human body.
It takes time fr the human immune system to respond to an infection. An example is pneumonia. Before antibiotics the patient got sick, then they got a fever, then the sweats, then either the fever broke or the patient died.
What caused the fever was an initial response to the bacteria and the immediate release of cytokines from the WBCs, but this action is not connected to antibodies.
The antibodies will take 2-4 weeks to develop and this is what breaks the fevers. The antibodies tag the bacteria and the phagocytes (special white blood cells) engulf the tagged pneumococci bacteria and the patient lives.
First a large antibody forms in about two weeks called IgM, then in four weeks IgG antibodies develop. It is the IgG that usually saves the day, and memory B-Cells will remember the infection so next time the same patient may not even get sick or may have a shortened convalescence because now the patient can make antibodies in mere days. This is how the pneumonia vaccine protects a patient.
But here is the bad news with Borrelia burgdorferi: the bacteria can move out of the bloodstream so fast that the immune system may not have time to make an IgG response. The infection goes deep, where the antibodies and WBCs cant reach the infection. To facilitate this the Lyme bacteria blocks compliment in at least two ways.
Compliment first spots the infection and a series dozens of blood enzymes poke holes in the bacteria to weaken it, and tags the bacteria so the WBCs will spot it sooner and eliminate the invaders. But Bb evades the compliment cascade and leaves the Blood stream. Antibodies may not develop at levels to be measured because the immune system has a thresh-hold response, and a small infection load may not trigger a strong immune response.
The uniqueness of this bacterium is why using other bacterial diseases as a model for Lyme disease is not only inaccurate but it leads to misunderstandings within the medical community on how to properly diagnose and treat Lyme disease.
In the early days before we knew Lyme was caused by a spirochete, early Lyme treatment papers compared Lyme disease to a sore throat by saying that since Lyme patients respond to tetracycline (1978) then Lyme disease must be caused by a bacterium. Since most bacterial infections like strep throat are successfully treated in 10-14 days then it makes sense to use tetracycline for 10-14 days.
Sadly the medical community has not budged from this position in 35 years.
For years the Lyme pathogen has been treated as though it were like other bacteria that are obligated to stay within the bloodstream, but Borrelia burgdorferi does not play by the same rules as other bacterial infections!
When physicians try to simplify their understanding of this disease by treating it like other bacterial infections, they disregard the uniqueness of these bacteria to hide, thrive and survive.
If a doctor uses a “one-size-fits-all” approach to diagnosis and treatment, the result will be one population of patients that never get diagnosed, and another population of patients that will relapse from incomplete treatment.
It is not a failure of medical science that allows relapses to occur. It is a lack of understanding medical science that allows patients with Lyme disease to suffer needlessly.
The Lyme spirochete has evolved
to hide, thrive and survive!
Infections caused by the family of bacteria known as Borrelia are unique in their microbiology and cannot be dismissed with a rubber stamped one-treatment-fits-all approach. Lyme disease is not a sore throat, it is not Syphilis, and it is not Tuberculosis. It is Borreliosis: A very misunderstood collection of diseases cause by the Borrelia group of bacteria.
One of the hallmarks of the Borrelia genus is that the bacteria is constantly changing and evolves before our very eyes. Their unique genetics allows the bacteria to change every time it divides.
In 1995 we had one bacterium species that caused Lyme disease, now we have more than 14 species of Borrelia in the "Lyme family" and a dozen Borrelia species in the "Tick-Borne Relapsing Fever" group.
The Borrelia genus of bacteria represent over 30 disease causing bacteria that are all related to each other and all share the common gift of being highly variable and adaptive.
Lyme disease is not a single disease, it is part of a growing family of pathogens that basically cause variations of Relapsing Fever. These similar Lyme-like bacteria should really be considered collectively as one disease. Lyme disease is part of the bigger picture that we can refer to as Borreliosis.