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The Central Florida Research is dedicated to the research of Lyme Disease and other CSID (Chronic, systemic, infectious diseases).
Besides Borrelia burgdorferi (Bb), the Lyme bacteria recent research supports the fact that other pathogenic bacteria, and viruses contribute to the symptoms found in Lyme and CSID patients.
The bacteria Bb is transmitted by ticks and other vectors including mosquitoes, fleas and mites.
A recent study at the University of New Haven in Connecticut revealed that ticks tested carried not only Bb, but Babesia, Ehrlichia, Bartonella as well as other organism that have previously been found such as HHV6-A. Babesia, Ehrlichia and HHV6-A require different treatment protocols.
The life-cycle of Bb is related to the life cycle of the tick (usually Ixodes scapularis.) The tick has four stages in its two year life cycle: egg, larva, nymph and adult.
The spirochete is usually acquired during the tick's larval state. It is in this stage that the tick then becomes the host for the spirochete.
Willy Burgdorferi, Ph.D, who discovered the cause of Lyme disease in 1981, states that the complexity of the arthropod-borne spirochetes of Bb are well known.
Lyme diagnosis is complicated because Lyme disease mimics many other diseases. Like Syphilis, another disease caused by a spirochete, Lyme is called "The Great Imitator".
Two of the most common misdiagnosis are Chronic Fatigue and Fibromyalgia. The symptoms of other disease like RA, MS, Lupus and ALS often overlap Lyme disease symptoms. Most physicians look for the accepted tell tale sign of a Lyme infection which is the EM (bull's eye) rash seen at the bite's site.
However, only about 50% of those infected exhibit this rash. More often other symptoms appear after initial infection. These may include joint/muscle pain that migrates, stiffness of joints, flu like symptoms, headaches, neck pain and TMJ. Neurological, Neuropsychiatric, Cardiac/Pulmonary and Gastrointestinal problems appear to develop if the disease goes untreated and the infection is allowed to progress.
To better understand the complicated issues in diagnosing Lyme disease one should read the essay 'When to Suspect Lyme Disease' by John D. Bleiweiss, M.D. ( This can be found by typing in google.com the title).
The nature of the spirochete complicates the treatment of Lyme disease. Antibiotics are the chosen mainstream treatment, but success is difficult if the patient goes untreated and the disease becomes chronic. Prompt treatment within six weeks of antibiotics for a bite is recommended by ILADS ( International Lyme and Associated Disease Society) in order to prevent relapses and chronic illness. If not caught early longer treatment is usually needed.
Upon entering the body, the spirochete cloaks itself with a coating of the person's own DNA. The immune system which is normally in Cellular Immunity recognizes that there is a foreign invader and goes into Humeral Immunity, the state of attack.
The invader due to its ability to cloak itself and hide from the immune system evades detection. Hence, the referral to the spirochete as being a 'stealth pathogen'.
The white blood cells, the Neutrophils and Macrophages, whose job it is to engulf foreign pathogenic invasion allows the cloaked spirochetes to go in and out of these cells as they don't recognize it as the enemy. They see it as self (part of the person's own DNA).
Under these circumstances the immune system stays in 'Humeral Immunity' overdrive due to the fact that it can't locate the invader and destroy it. Normally when an enemy is destroyed the immune system returns to normal 'Cellular Immunity'. When an immune system is left in 'Humeral Immunity' overdrive, the results are negative.
Autoimmune issues occur and the immune system starts to attack many systems in the body. It is not unusual to see people with Borrelia or Mycoplasma infections to exhibit autoimmune issues such as diagnosed in Lupus, Parkinson's, ALS, Lupus, RA, and MS.
Chronic Fatigue Immune Dysfunction (CFIDS) and/or Fibromyalgia are other common misdiagnosis. Specific diagnosis is the result of a combination of factors present in the individual. These include the general health of the individual's immune system, their genetics, and the infectious agent. There are over 300 strains of Bb, and many species, therefore combinations of symptoms vary in each individual.
At the beginning of the last century, bacteriologist entered into an intense debate over 'pleomorphism', which is the ability of a bacteria to change from one form to another and as in the case of Bb back again into its original form.
The debate split microbiologist into two camps: the 'monomorphists' and the 'pleomorphists'. The 'monomorphists' believe that each bacterial cell by binary fission divides transversely to produce two new cells which evolve to replicate the original cell in size and shape.
The 'pleomorphists' believe that even common bacteria show complex life cycles, and have the ability to shed their cell wall. In the Spring of 2006, a research study was published on "A Life Cycle for Borrelia Spirochetes" by Dr. Alan MacDonald, Ph.D.
What is a Bb life cycle?
According to Dr. MacDonald, study the "....life cycles are diverse arrays of life forms which emerge in an ordered sequence, which are 'connected' to one another across primary and secondary hosts, and constitute a cycle with 'circular ' relationship between hosts."
In "The Complexity of Arthropod-borne Spirochetes" by Dr. Burgdorferi, he states "...the most recent findings confirm the development of membrane-derived cysts, blebs, spherules, vesicles and potential transformation to motile, helical spirochetes.
These are not a part of a complex developmental cycle but rather as a "survival mechanism" of spirochetes to overcome and escape unfavorable conditions. Such conditions prevail during early phases of infection when spirochetes ingested into the midgut of ticks or lice become exposed to the vectors' digestive enzymes and tissue barriers. As a result, most detectable spirochetes produce numerous cysts often filled with granular material."
Understanding the microbiology behind the cyst or cell wall deficient form of Bb and its ability to hide from our immune system helps us understand the Lyme disease controversies and the complications for testing for the bacteria.
If the antibodies a person's body normally produces against an invading pathogen aren't always present then we must assume the accepted antibody test are flawed.
Testing for the spirochetes presents a problem because spirochetes are rarely found in the blood. However, the antigen Bb in its cysts, or cell wall deficient (CWD) form can be found in the blood.
There are only a couple of laboratories that do antigen testing for Bb. Antigen test check for the organism itself and aren't dependent upon a sick immune system to produce antibodies.
The Central Florida Research Laboratory in South Florida is a laboratory doing antigen testing.
The Central Florida Research Laboratory's antigen test is a one of a kind. It is an immune fluorescence test using a special kind of machine called Flow Cytometry. The Flow Cytometry is a specific instrument made to identify the various stages of Borrelia burgdorferi.
Cells acting with fluorescent antibodies are counted. The Flow Cytometry machine can read 50 thousand cells, WBC, RBC, and platelets in one minute, It prints out in a percentage ratio of how many cells are enumerated and fluoresing - .02 negative - .03 borderline -.04 above positive. The test is more definitive then the Bowen Q-RIBb test. However, it must be stated the diagnosis for Lyme disease is a clinical diagnosis.
Since Borrelia burgdorferi is a CWD and a stealth pathogen, an antigen test result is more accurate in detecting its presents in the blood than a test looking for antibodies . ( Our blood supply is protected by an antigen test to detect for HIV, thereby making the blood supply much safer for the detection of HIV).
The Flow Cytometry test from Central Florida Research is most beneficial in picking up Borrelia Burgdorferi the causative agent for Lyme Disease.
Mycoplasma organisms run the course from non-pathogenic to very pathogenic, Many patients suffering from Chronic Systemic Infectious Diseases are also found to have some of the pathogenic species of Mycoplasma present. Mycoplasma Fermentans (especially the Incognitos Strain) have been found in many CSID. Another pathogenic Mycoplasma that appears to be present in many CSID is Mycoplasma Pneumonia.
These organisms are very good at evading detection by the immune system and are also good at keeping the Immune system in Humural (overdrive). These organisms are Cell Wall Deficient from their inception. and can go into little DNA blebs making it difficult not only for the immune system to detect but also difficult for laboratory testing.
The above is part of a pamphlet that was inserted into the physicians and patients packets at the IACFS (International Alliance for Chronic Fatigue Syndrome and related disorders) conference held last month in Fort Lauderdale. It was hosted by PANDORA, the Miami Chronic Fatigue Syndrome support group.
Posts: 991 | From USA | Registered: Aug 2001
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bettyg
Unregistered
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sandi, you have an informative piece here.
there are so many posts about this NEW lab in florida; each one is different. could you copy your link here to all you see about them in medical and general?
there's just so much that should be in SAME spot so we all have a complete picture instead of 10-50% of picture.
just my thoughts; many of these are buried already!
if you agree, how about doing a search for this NEW LAB NAME in medical and general, and then posting your link to them all.
THANKS SO MUCH for your consideration!
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treepatrol
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-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
treepatrol
Honored Contributor (10K+ posts)
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quote:Originally posted by Al: This statment from the report concerns me !
"However, it must be stated the diagnosis for Lyme disease is a clinical diagnosis."
I must very strongly emphasize that all diagnoses of tick-borne infections remains a clinical one. Clinical clues will be presented later in this monograph, but testing information is briefly summarized below. In Lyme Borreliosis, western blot is the preferred serologic test. Antigen detection tests (antigen capture and PCR), although insensitive, are very specific and are especially helpful in evaluating the seronegative patient and those still ill or relapsing after therapy. Often, these antigen detection tests are the only positive markers of Bb infection, as seronegativity has been reported to occur in as many as 30% to 50% of cases. Nevertheless, active LB can be present even if all of these tests are non-reactive! Clinical diagnosis is therefore required. In Babesiosis, no single test is reliable enough to be used alone. Only in early infections (less than two weeks duration) can the standard blood smear be helpful. In later stages, one can use serology, PCR, and fluorescent in-situ hybridization (``FISH'') assay. Unfortunately, over a dozen other protozoans can be found in ticks, most likely representing species other than B. microti, yet commercial tests for only B. microti and WA-1 are available at this time! In other words, the patient may have an infection that cannot be tested for. Here, as in Borrelia, clinical assessment is the primary diagnostic tool. In Ehrlichiosis and Anaplasmosis, by definition you must test for both the monocytic and granulocytic forms. This may be accomplished by blood smear, PCR and serology. Many presently uncharacterized Ehrlichia-like organisms can be found in ticks and may not be picked up by currently available assays, so in this illness too, these tests are only an adjunct in making the diagnosis. Rarely, Rocky Mountain Spotted Fever can coexist, and even be chronic. Fortunately, treatment regimens are similar for all agents in this group. In Bartonella, use both serology and PCR. PCR can be performed not only on blood and CSF, but as in LB, can be performed on biopsy specimens. Unfortunately, in my experience, these tests, even when both types are done, will presently miss over half the cases diagnosed clinically. Frequent exposures to Mycoplasmas are common, resulting in a high prevalence of seropositivity, so the best way to confirm active infection is by PCR. Chronic viral infections may be active in the chronic patient, due to their weakened immune response. PCR testing, and not serologies, should be used for diagnosis. Commonly seen viruses include HHV-6, CMV, and EBV.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
treepatrol
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-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
CaliforniaLyme
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YUP tree, I agree&!!*)!*)!
Important!!! I always harp ion getting treated for all the coinfections regardless of serology because of this!!!!!!!!!!!!!!!!!!!
Babesiosis is often sero-!!! Krause says that!
Anaplasmosis as well- 1/3 of people who DIED from it in one abstract were seronegative repeatedly!!!
Yikes.
-------------------- There is no wealth but life. -John Ruskin
All truth goes through 3 stages: first it is ridiculed: then it is violently opposed: finally it is accepted as self evident. - Schopenhauer Posts: 5639 | From Aptos CA USA | Registered: Apr 2005
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I thought the treatment for Ehrlichia was with Doxy. Which is one of the treatments for Lyme. It says in the article that the treatment for Ehrlichia differs than the treatment for Lyme.
Posts: 310 | From TN | Registered: Jan 2007
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treepatrol
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upsy
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
Marnie
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I have a problem with "cloaks".
DNA is composed of chains of amino acids held together by weak hydrogen bonds.
Those bonds can be easily broken in times of oxidative stress. This is DNA damage.
Then the amino acids are available for Bb to utilize.
Specifically, tyrosine and phenylalanine. We use tryptophan and histidine to counter.
When Bb is on its way out of the tick, it picks up a protein from the tick's saliva called Salp15.
Salp15, an ixodes scapularis salivary protein, inhibits CD4(+) T cell activation .
This is OspC protein expression. This is what determines infection. This protein must be expressed for Bb to infect.
"Salp15 inhibits the subsequent TCR ligation-induced T cell signaling at the earliest steps
including tyrosine phosphorylation of the Src kinase Lck,
downstream effector proteins, and lipid raft reorganization."
It is believed if we can develop a vaccine to counter Salp15, we have a better chance to prevent infection.
Is Salp = sodium aluminum phosphate?
Do we have an immediate Al-Mg displacement problem?
So Bb uses OspC to gain a foothold.
Once infected, the question becomes...does OspA and OspB become the predominent proteins expressed?
And which PDE enzymes do we need to inhibit?
Those related to anti-inflammatory actions only?
OR
Those related to anti-histamine actions?
OR
BOTH.
I suspect CWD forms are "infants". These are easily destroyed via ultrasound or osmotic pressure changes (I suspect barometric pressure changes can effect them as well.) The steps to destroy any gram negative pathogen begin with damaging the cell walls OR prevent its formation in the first place. Bb's cell wall IS made up of lipoproteins. Inactivate HMG CoA reductase. Halt VLDL - choline rich - release.
Posts: 9430 | From Sunshine State | Registered: Mar 2001
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