A Brief Overview of
Lyme Bacteria Behavior
Lyme Disease is a complex systemic disease that is caused by highly motile bacterium in the spirochete family. The bacteria Borrelia burgdorferi was first isolated from the skin of a Lyme patient with the distinctive bull’s-eye rash in the early 1980s. Since that time, culturing the elusive bacterium has been difficult, frustratingly unpredictable, and miserably inconsistent.
Borrelia burgdorferi can very quickly move from the site of a tick bite directly into the circulatory system where it can circulate throughout the entire body. Most bacterial infections that enter the blood stream are trapped within the blood vessels and consequently are easier to kill with antibiotics than bacteria that are dispersed throughout many tissues and organs.
Borrelia burgdorferi is a unique bacterium that has a distinct and insidious method for passing through the capillary walls of human blood vessels and making its way into whatever tissue that waits on the other side of the capillary wall.
If the spirochete finds a tissue it likes and a place where it can thrive, the bacteria will survive and multiply. If conditions are unfavorable the bacteria may die, but more disturbing than the bacteria’s ability to migrate and penetrate blood vessels is recent evidence from the NIH Rocky Mountain Labs that this particular species of spirochete like many of its cousins may have a protective cyst-like form.
When stressed the Lyme bacteria under certain conditions will shed a portion of its cell wall and extrude a membrane wrapped vesicle that is a spherical shaped blob.
These blebs appear to be minimally metabolically active which means they can essentially lay dormant and resist antibiotics. They stimulate the immune system and contain the bacteria’s DNA. In some species of spirochetes blebs have been observed to harbor classical-form spirochetes inside them.
The cyst-like L-form or bleb may become metabolically active at a more favorable time and then go on to produce fully functional classical-form spirochetes that can once again roam the human body in a motile form.
The Lyme bacteria begin their passage through blood vessels by attaching themselves to the endothelial cells lining the inside of the blood vessel. Then it 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 starts a cascade of cellular degradation that ultimately leads to leaky gaps between the cells that make up the blood vessel walls.
Once the bacteria are out of the blood stream they are able to travel deep inside many organs and tissues of the human body. 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 Lyme tests are so fallible and why there may never be a 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 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!)
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.
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.
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.
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.
The Borrelia genus of bacteria represent over 40 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.
Lyme Bacteria Behavior
Lyme Disease is a complex systemic disease that is caused by highly motile bacterium in the spirochete family. The bacteria Borrelia burgdorferi was first isolated from the skin of a Lyme patient with the distinctive bull’s-eye rash in the early 1980s. Since that time, culturing the elusive bacterium has been difficult, frustratingly unpredictable, and miserably inconsistent.
Borrelia burgdorferi can very quickly move from the site of a tick bite directly into the circulatory system where it can circulate throughout the entire body. Most bacterial infections that enter the blood stream are trapped within the blood vessels and consequently are easier to kill with antibiotics than bacteria that are dispersed throughout many tissues and organs.
Borrelia burgdorferi is a unique bacterium that has a distinct and insidious method for passing through the capillary walls of human blood vessels and making its way into whatever tissue that waits on the other side of the capillary wall.
If the spirochete finds a tissue it likes and a place where it can thrive, the bacteria will survive and multiply. If conditions are unfavorable the bacteria may die, but more disturbing than the bacteria’s ability to migrate and penetrate blood vessels is recent evidence from the NIH Rocky Mountain Labs that this particular species of spirochete like many of its cousins may have a protective cyst-like form.
When stressed the Lyme bacteria under certain conditions will shed a portion of its cell wall and extrude a membrane wrapped vesicle that is a spherical shaped blob.
These blebs appear to be minimally metabolically active which means they can essentially lay dormant and resist antibiotics. They stimulate the immune system and contain the bacteria’s DNA. In some species of spirochetes blebs have been observed to harbor classical-form spirochetes inside them.
The cyst-like L-form or bleb may become metabolically active at a more favorable time and then go on to produce fully functional classical-form spirochetes that can once again roam the human body in a motile form.
The Lyme bacteria begin their passage through blood vessels by attaching themselves to the endothelial cells lining the inside of the blood vessel. Then it 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 starts a cascade of cellular degradation that ultimately leads to leaky gaps between the cells that make up the blood vessel walls.
Once the bacteria are out of the blood stream they are able to travel deep inside many organs and tissues of the human body. 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 Lyme tests are so fallible and why there may never be a 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 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!)
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.
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.
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.
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.
The Borrelia genus of bacteria represent over 40 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.