Question: Anti-Flagellar Antibody as VALID for diagnosis?

QUESTION: I just listened to Robert Giguere from IGeneX and he said that 41kD is for any bacteria with a tail. Is the Yale patent more specific?
ANSWERS: Yes, it is 100% SPECIFIC (and spirochetal flagellin is internal and is not a tail), or does not detect the flagellins from any other species and detects all stages and types of Lyme including neurologic Lyme, which we all know was excluded from the Dearborn case definition. This is Yale’s US patent 5, 618,533 and states:
“This is a continuation of application Ser. No. 837,193, filed Feb. 11, 1992, entitled FLAGELLIN-BASED COMPOSITIONS AND METHODS FOR THE DIAGNOSIS AND TREATMENT OF LYME DISEASE, now abandoned.Claims
“We claim:
“1. A flagellin polypeptide capable of detecting B. burgdorferi-specific antibodies in a majority of seropositive samples and comprising an immunodominant region of a B. burgdorferi flagellin antigen or derivatives thereof, which polypeptide is recognized by antibodies elicited by infection with B. burgdorferi, ****but is substantially less reactive than the full-length flagellin protein when reacted with antibodies elicited by infection with other bacteria or treponemes.***
“Lyme disease generally occurs in three stages. Stage one involves localized skin lesions (ECM) from which the spirochete is cultured more readily than at any other time during infection [B. W. Berger et al., “Isolation And Characterization Of The Lyme Disease Spirochete From The Skin Of Patients With Erythema Chronicum Migrans”, J. Am. Acad. Dermatol., 3, pp. 444-49 (1985)].
“Flu-like or meningitis-like symptoms are common at this time.
Stage two occurs within days or weeks, and involves spread of the spirochete through the patient’s blood or lymph to many different sites in the body including the brain and joints.
“Varied symptoms of this disseminated infection occur in the skin, nervous system, and musculoskeletal system, although they are typically intermittent. Stage three, or late infection, is defined as persistent infection, and can be severely disabling. Chronic arthritis, and syndromes of the central and peripheral nervous system appear during this stage, as a result of the ongoing infection and perhaps a resulting auto-immune disease [R. Martin et al., “Borrelia burgdorferi–Specific And Autoreactive T-Cell Lines From Cerebrospinal Fluid In Lyme Radiculomyelitis”, Ann Neurol., 24, pp 509-16 (1988)]
.
“The neurologic manifestations of Lyme disease are protean and include weakness, peripheral nerve palsy, radiculitis, meningitis and encephalitis. The pathogenesis of neuroborreliosis, however, is unclear. Examination of the cerebrospinal fluid (CSF) of patients with neuroborreliosis shows a mononuclear pleocytosis and production of B. burgdorferi specific antibody, suggesting that inflammation is involved in disease. In some cases, spirochetes have been cultured from the CSF of patients with neurologic symptoms, implicating the organism directly with disease. Experiments using mice suggest that spirochete virulence may play a role in the development of neurologic infection.
“Infection with B. burgdorferi induces a strong humoral immune response. Early in human infection, antibodies are generated primarily against the 41-kDa flagellar protein. In later stages, antibodies to the outer surface proteins OspA and OspB, among others, appear [J. E. Craft et al., “Antigens Of Borrelia burgdorferi Recognized During Lyme Disease”, J. Clin. Invest., 78, pp. 934-39 (1986)]. “
This test is SPECIFIC to Lyme borrelia, does not detect other flagellins, is the earliest antibody to show up, and most people will make at least this antibody, whereas the Osps and the Vmps, being lipoproteins, no, lipoproteins cause immunosuppression in most people. People prone to a reactive arthritis, yes, they will have a hypersensitivity response to fungal antigens like LYMErix (OspA) or the Vmps of the other Borrelia (these are the ones who test Dearborn positive and have no other illness signs except a bad knee).
Yale did not use this valid method to assess their other patent, LYMErix, because they knew LYMErix did not prevent spirochetes. OspA may have tolerized against arthritis, and certainly in animals, but no Lyme vaccine was ever proven to prevent spirochetes in any animal; read more about that aspect of the Lyme science fraud here in the 9th charge sheet:
When I talked to the Number 2 guy under Fauci (NIAID.gov), Joe Breen, he agreed with me that there should be Yale-Fla-Patent-Like recombinant, specific flagellins test that includes from all the at least dominant species of Borreliae – used at the same time – for all potential Borreliosis patients. This was 2012.
According to the FDA, your test should detect 100% of the known positive cases/samples (this is verbatim by the FDA when I called them about it – a one John Bishop III of the FDA). That means we have to go with detecting anti-flagellar antibodies because it is the only one KNOWN to occur in most patients. And Yale was not the only group to propose such a fla-specific-antibody test. There were at least 2 other groups who proposed and developed similar methods at that time, in the late 1980s and early 1990s.
The Bowen Lab used a fluorescent monoclonal anti-Borrelia fla antibody (H9724) proposed by Barbour as a standard for ALL BORRELIA detection. The CDC wanted to shut them down but they could not. Why. It was Barbour’s idea to use this standard, band 41, general antibody to find Borreliosis.
The problem with that is you’ll find more anti-flagellar antibodies than free flagellin antigen floating around in the blood.
Infect Immun. 1986 May;52(2):549-54.
A Borrelia-specific monoclonal antibody binds to a flagellar epitope.
Abstract
In immunofluorescence assays monoclonal antibody H9724 recognized eight species of the spirochetal genus Borrelia but not representatives of the genera Treponema, Leptospira, and Spirochaeta. We examined the reactivity of H9724 against subcellular components of Borrelia hermsii, an agent of relapsing fever, and B. burgdorferi, the cause of Lyme disease. H9724 bound to isolated periplasmic flagella of the two borreliae. In Western blots the antibody reacted with the predominant protein in flagellar preparations from B. hermsii and B. burgdorferi; the apparent molecular weights of these flagellins were 39,000 and 41,000, respectively.
You can order that thru commercial labs, H9724.
There are new tests out there that claim to detect flagellin in the blood and not flagellar antibodies, like Ceres. They will miss most patients; it’s a waste of time and money not to mention lives. Not every new technology is an improvement. Here is another blog post about these new technologies:
The next problem is that detecting spirochetes does not really help with your diagnosis of post-tick-bite sepsis. This is more like an AIDS like disease and apparently needs to be treated as if it is a lymphoma – with leukemia drugs and perhaps anti-virals:
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