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Lyme
Disease: What We Know and What We Don’t Know
An Editorial by Tom Grier
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In
1975 the term “Lyme Arthritis” first entered the vocabulary
of the physicians in America. Since that time Lyme disease and Lyme-like
diseases have become recognized worldwide. But in the 28 years since “Lyme
Arthritis” was first described: What do we actually know? And what
do we yet need to learn about this illness?
Why is it that in the three decades since Lyme disease was first described that it still perplexes us and vexes us with controversy and puzzlement?
In a nutshell it comes down to the inescapable fact that victims of Lyme disease all too often have lingering symptoms that remain or return even after aggressive and multiple antibiotic treatments. They remember wellness, but with each passing year the fog that fills their brain, the palpitations that shake their hearts, and the fatigue that plagues their bodies becomes the ever present reminder that they were stricken with a poorly understood and often underestimated pathogen.
Here are some things we know: The pathogen that causes Lyme disease is Borrelia burgdorferi and it is a highly motile spirochete that belongs to a genus of bacteria that are notorious for giving rise to variant strains. Borrelia are bacteria that are associated with dozens of tick and louse-borne Relapsing Fevers that are found throughout the world. These related illnesses range in symptoms from cases of mild fevers to rapidly fatal encephalitis’. The hallmark attribute that most Borrelia bacteria have in common is their ability to adapt, change and infect host animals that in turn infect many species of ticks and lice.
We know for example that if you rank all the known Borrelia pathogens in a phylogenetic tree based on related genetics, you will find many disease causing pathogens that cause similar symptoms will often end up close together in related groups on the phylogenetic family-tree.
In other words Borrelia burgdorferi, Borrelia afzellii and Borrelia garinii that cause Lyme disease in America and Europe are all genetically similar to each other and have similar tick vectors. It is believed that they are closely related and variations occurred as separate tick populations over thousands of years migrated with animal populations and the bacteria became isolated populations. At one time all Borrelia had a common ancestor.
Exactly how long ago we don’t know, but the evidence of common ancestry is in their related and similar genes. This year when the genomic sequence of Borrelia burgdorferi was determined, it came as quite a shock that most of the genes in this large bacterium had no known counterparts or similarities to other known bacterial genes. This means the function of the majority of the genes in the Borrelia species has yet to be determined.
What we don’t know: The Lyme bacteria Borrelia burgdorferi likes to preferentially express certain genes and suppress others. This allows the bacteria to adapt to new environments. But what does it take for Borrelia burgdorferi to express one of the suppressed genes of an ancient pathogen cousin? Borrelia burgdorferi like all Borrelias have genes that are latent but intact. If a gene is expressed or triggered by the environment as it is suggested by research done of Relapsing Fever strains, then could a latent but deadly gene be triggered in one individual with unique genetic markers and not expressed in another patient? Could pathogen-host interactions based on patient genetic markers explain why some Lyme patients have persisting symptoms?
What we know: Dr. Andrew Pachner infected mice with Borrelia burgdorferi and later extracted the bacteria from the blood and from the brains of the infected mice. What he found was basically that the Bacteria in the brain changed: they now expressed a new set of genes. The result was bacteria so different from what he started with, that the antibodies from the peripheral blood could no longer detect the bacteria isolated from the brain.
This is bad news as the CNS is isolated from the rest of the body. If the Lyme spirochete can adapt to the human brain and circumvent the immune system, it is less likely to be inhibited by our natural immune defenses. Further studies by Pachner in primates using PCR suggested persistent infection post-antibiotic treatment. This is more bad news as this suggests that the CNS of primates is an isolated and protective incubator for Borrelia bacteria.
What other gene expressions of these bacteria do we need to understand better?
What we need to find out: Occasionally patients infected with Relapsing Fever will report a Bull’s-Eye rash identical to Lyme disease, and experience symptoms similar to Lyme without a recurring febrile states (Recurring fevers). If Relapsing Fevers can behave like Lyme disease, does this mean Lyme could suddenly cause an aggressive encephalitis in a patient similar to East African Relapsing Fever? Since we don’t know or understand the reasons for patient variation in symptoms, it is something we need to investigate and learn. We know for instance from early work done by Dr. Patricia Coyle M.D. PhD that the Lyme bacteria can get into the CNS of a lyme patient very early, but only a small fraction of these patients develop serious mennigo-encephalopathies.
Understanding the recently sequenced genomic sequence of Borrelia burgdorferi and gene expression is essential to understanding both chronic and acute Lyme disease. In patients with HLA-DR4 tissue type, are there markers in the joints responsible for chronic Lyme arthritis ? We need to study the role of genetics, and receptor sites in both humans and within the Lyme spirochete. How the bacteria interacts with one person may be radically different than how it acts in another patient.
What we don’t know: One of the most frequent complaints from Lyme patients is the loss of cognitive abilities. Their minds are fuzzy, foggy and they complain of short term memory loss and poor word retrieval. Their fear is: How permanent is this memory impairment? And will it progress? We don’t know why so few bacteria can cause such a profound affect on conscious thought, but unlike Syphilis, a related and similar spirochetal infection, the Lyme bacteria is found in the human body in extremely low numbers?
Why are there so few bacteria in a Lyme infection? Are their other forms (spheroplast or cell-wall deficient forms) of the bacteria in greater numbers that we just aren’t recognizing? How can so few bacteria cause such horrible symptoms like cardiomyopathy, encephalitis, hepato-spleenamegaly, heart arrhythmias, rheumatoid-like arthritis, optical neuritis, Bell’s Palsy, muscle spasms, fibromyalgia, and multiple sclerosis-like presentations. Can it be that a small number of bacteria initiate cascade responses of inflammation and autoimmunity in the human body? If autoimmunity is playing a role, how does it affect the various tissues?.
Why is it that in the three decades since Lyme disease was first described that it still perplexes us and vexes us with controversy and puzzlement?
In a nutshell it comes down to the inescapable fact that victims of Lyme disease all too often have lingering symptoms that remain or return even after aggressive and multiple antibiotic treatments. They remember wellness, but with each passing year the fog that fills their brain, the palpitations that shake their hearts, and the fatigue that plagues their bodies becomes the ever present reminder that they were stricken with a poorly understood and often underestimated pathogen.
Here are some things we know: The pathogen that causes Lyme disease is Borrelia burgdorferi and it is a highly motile spirochete that belongs to a genus of bacteria that are notorious for giving rise to variant strains. Borrelia are bacteria that are associated with dozens of tick and louse-borne Relapsing Fevers that are found throughout the world. These related illnesses range in symptoms from cases of mild fevers to rapidly fatal encephalitis’. The hallmark attribute that most Borrelia bacteria have in common is their ability to adapt, change and infect host animals that in turn infect many species of ticks and lice.
We know for example that if you rank all the known Borrelia pathogens in a phylogenetic tree based on related genetics, you will find many disease causing pathogens that cause similar symptoms will often end up close together in related groups on the phylogenetic family-tree.
In other words Borrelia burgdorferi, Borrelia afzellii and Borrelia garinii that cause Lyme disease in America and Europe are all genetically similar to each other and have similar tick vectors. It is believed that they are closely related and variations occurred as separate tick populations over thousands of years migrated with animal populations and the bacteria became isolated populations. At one time all Borrelia had a common ancestor.
Exactly how long ago we don’t know, but the evidence of common ancestry is in their related and similar genes. This year when the genomic sequence of Borrelia burgdorferi was determined, it came as quite a shock that most of the genes in this large bacterium had no known counterparts or similarities to other known bacterial genes. This means the function of the majority of the genes in the Borrelia species has yet to be determined.
What we don’t know: The Lyme bacteria Borrelia burgdorferi likes to preferentially express certain genes and suppress others. This allows the bacteria to adapt to new environments. But what does it take for Borrelia burgdorferi to express one of the suppressed genes of an ancient pathogen cousin? Borrelia burgdorferi like all Borrelias have genes that are latent but intact. If a gene is expressed or triggered by the environment as it is suggested by research done of Relapsing Fever strains, then could a latent but deadly gene be triggered in one individual with unique genetic markers and not expressed in another patient? Could pathogen-host interactions based on patient genetic markers explain why some Lyme patients have persisting symptoms?
What we know: Dr. Andrew Pachner infected mice with Borrelia burgdorferi and later extracted the bacteria from the blood and from the brains of the infected mice. What he found was basically that the Bacteria in the brain changed: they now expressed a new set of genes. The result was bacteria so different from what he started with, that the antibodies from the peripheral blood could no longer detect the bacteria isolated from the brain.
This is bad news as the CNS is isolated from the rest of the body. If the Lyme spirochete can adapt to the human brain and circumvent the immune system, it is less likely to be inhibited by our natural immune defenses. Further studies by Pachner in primates using PCR suggested persistent infection post-antibiotic treatment. This is more bad news as this suggests that the CNS of primates is an isolated and protective incubator for Borrelia bacteria.
What other gene expressions of these bacteria do we need to understand better?
What we need to find out: Occasionally patients infected with Relapsing Fever will report a Bull’s-Eye rash identical to Lyme disease, and experience symptoms similar to Lyme without a recurring febrile states (Recurring fevers). If Relapsing Fevers can behave like Lyme disease, does this mean Lyme could suddenly cause an aggressive encephalitis in a patient similar to East African Relapsing Fever? Since we don’t know or understand the reasons for patient variation in symptoms, it is something we need to investigate and learn. We know for instance from early work done by Dr. Patricia Coyle M.D. PhD that the Lyme bacteria can get into the CNS of a lyme patient very early, but only a small fraction of these patients develop serious mennigo-encephalopathies.
Understanding the recently sequenced genomic sequence of Borrelia burgdorferi and gene expression is essential to understanding both chronic and acute Lyme disease. In patients with HLA-DR4 tissue type, are there markers in the joints responsible for chronic Lyme arthritis ? We need to study the role of genetics, and receptor sites in both humans and within the Lyme spirochete. How the bacteria interacts with one person may be radically different than how it acts in another patient.
What we don’t know: One of the most frequent complaints from Lyme patients is the loss of cognitive abilities. Their minds are fuzzy, foggy and they complain of short term memory loss and poor word retrieval. Their fear is: How permanent is this memory impairment? And will it progress? We don’t know why so few bacteria can cause such a profound affect on conscious thought, but unlike Syphilis, a related and similar spirochetal infection, the Lyme bacteria is found in the human body in extremely low numbers?
Why are there so few bacteria in a Lyme infection? Are their other forms (spheroplast or cell-wall deficient forms) of the bacteria in greater numbers that we just aren’t recognizing? How can so few bacteria cause such horrible symptoms like cardiomyopathy, encephalitis, hepato-spleenamegaly, heart arrhythmias, rheumatoid-like arthritis, optical neuritis, Bell’s Palsy, muscle spasms, fibromyalgia, and multiple sclerosis-like presentations. Can it be that a small number of bacteria initiate cascade responses of inflammation and autoimmunity in the human body? If autoimmunity is playing a role, how does it affect the various tissues?.
Ticks carry more than just
Lyme disease! Including:
0 -Ehrlichia;
o -Bartonella;
0 -Babesia;
o -Q- Fever;
0 -Tularemia;
o -Tick-borne Encephalitis;
0 -Mycoplasma;
o -Relapsing Fever;
0 -Rocky Mountain Spotted Fever and others.
Never WAIT and SEE about a tick bite, please! Quickly and properly treated infections are less likely to progress to later stage or chronic disease.
Sometimes tick bites are
mistaken for spider bites!
Some diseases may be spread by animal bites or scratches and from mosquitoes, fleas or lice.
There is still so much to learn about Lyme disease and related infections.
Sometimes Lyme disease and related infectious diseases are undiagnosed for years, even decades!
Watch closely for symptoms after tick bites. Some never see a tick or a bulls-eye rash.
Don't ignore tick-borne disease symptoms!
If you feel sick, ask a doctor!
SYMPTOMS may include:
0 -Tick bites;
o -Fever; Flu symptoms;
0 -All kinds of Rashes;
o -Muscle; Joint; Neck Pain;
0 -Body Aches; Weakness
o -Light /Sound Sensitivity;
0 -Bells Palsy; Nerve pain;
o -Insomnia; Poor memory
0 -Headaches; Numbness;
o -Mood disorders; Confusion;
0 -Extreme Fatigue; Exhaustion
Never let tick-borne diseases progress!
Lyme and associated diseases are often MISTAKEN FOR OTHER ILLNESSES, Including:
0 -Chronic Fatigue;
o -Fibromyalgia;
0 -Hypochondria;
o -Multiple Sclerosis;
0 -Lupus;
o -Rheumatoid Arthritis;
0 -Lou Gehrig's disease (ALS);
o -Alzheimer's and
0 -Parkinson's disease
******************
Don't be fooled about ticks and their diseases.
******************
Directly affecting humankind, worldwide:
W H A T H A P P E N E D
when the U.S. Senate addressed the Centers for Disease Control regarding Lyme disease?
Consult a good doctor!
Visit ILADS, LDF, LymeNet or LDA to find a specialist in your location.
Protect your children and your family.
Learn about ticks and their many diseases.
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Tick-borne diseases are spreading rapidly in many countries across the world -not only in Scandinavia, UK, Hungary, Scotland, USA, France, Germany, China, and Australia.
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- TICKS KNOW NO BOUNDARIES -
Tick-borne diseases are spreading rapidly in many countries across the world -not only in Scandinavia, UK, Hungary, Scotland, USA, France, Germany, China, and Australia.
- ONE BIG PROBLEM WITH TESTS -
There is NO 100% accurate Lyme disease test currently available to detect infection or cure. more...
- WHERE TICKS LIVE -
Ticks can be found in and around leaf litter; grass; logs; animal fur; bird feeders; and deer, mice, squirrel, and other small animal habitats.
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Never let tick-borne
infections progress !
Tick-borne diseases can
affect any body part,
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Lyme disease and Syphilis are both caused by a type of bacteria called a spirochete.
Tick-borne diseases can KILL!
Ticks travel on mice!
ALWAYS Get Ticks Tested!
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