https://www.ncbi.nlm.nih.gov/m/pubmed/30257905/
Limitations and Confusing Aspects of Diagnostic Testing for Neurologic Lyme Disease in the United States.
Theel ES, et al. J Clin Microbiol. 2018.
Abstract
In the United States, laboratories frequently offer multiple different assays for testing of cerebrospinal fluid (CSF) samples to provide laboratory support for the diagnosis of central nervous system Lyme disease (CNSLD). Often included among these diagnostic tests are the same enzyme immunoassays and immunoblots that are routinely used to detect the presence of antibodies to Borrelia burgdorferi in serum. However, performing these assays on CSF alone may yield positive results simply from passive diffusion of serum antibodies into the CSF. In addition, such tests are only United States Food and Drug Administration-cleared and well-validated for testing serum, not CSF. When performed using CSF, positive results from these assays do not establish the presence of intrathecal antibody production to B. burgdorferi and therefore should not be offered. The preferred test to detect intrathecal production of antibodies to B. burgdorferi is the antibody index assay, which corrects for passive diffusion of serum antibodies into CSF and requires testing of paired serum and CSF collected at approximately the same time. However, this assay also has limitations and should only be used to establish a diagnosis of CNSLD in conjunction with patient exposure history, clinical presentation and other laboratory findings.
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**Comment**
ALL testing for tick-borne infections is abysmal. Diagnosis should still be clinical, which is why medical practitioners MUST become educated on this beast.
Also, the past is riddled with thousands who have not made the “antibody” cut and have been essentially left to die. Trust me when I say there are far more false negatives than positives!
For instance, read about the story of Vicki Logan: https://madisonarealymesupportgroup.com/2017/03/09/remember-vicki-logan/
Please read the entire article as zinger after zinger is exposed as to the corruption involved, but Liegner requested an autopsy on Vicki and the pathologist not only refused, he refused to even let an outside pathologist use the facilities to perform it.
The reason? Wait for it…..
……danger of infection to himself and his staff.
I thought Lyme disease was benign and similar to the common cold – easily cured with 21 days of doxy?
By now you know that Liegner wasn’t about to let the ball drop and found a way to get Vicki to the Chief of Neuropathology at Columbia Presbyterian where her autopsy results are now available to all. Without this critical step, propelled by Liegner, the pathologist at Hudson Valley Hospital would have successfully prevented medical knowledge of chronic and neurologic Lyme disease as well as the cause of her hypotension, a missed diagnosis of myocardial infarction.
Then there’s this little gem proving seronegativity with active infection occurs:
Seronegative Chronic Relapsing Neuroborreliosis.
https://www.ncbi.nlm.nih.gov/pubmed/7796837
Lawrence C.a · Lipton R.B.b · Lowy F.D.c · Coyle P.K.d
aDepartment of Medicine, bDepartment of Neurology, and cDivision of Infectious Diseases, Albert Einstein College of Medicine, and dDepartment of Neurology, State University of New York at Stony Brook, New York, NY., USA
Eur Neurol 1995; 35:113–117 (DOI:10.1159/000117104)
Abstract
We report an unusual patient with evidence of Borrelia burgdorferi infection who experienced repeated neurologic relapses despite aggressive antibiotic therapy. Each course of therapy was associated with a Jarisch-Herxheimer-like reaction. Although the patient never had detectable free antibodies to B. burgdorferi in serum or spinal fluid, the CSF was positive on multiple occasions for complexed anti-B. burgdorferi antibodies, B. burgdorferi nucleic acids and free antigen.
[Title modified on 11 April 2018 by Sharon Davies, The BMJ]
Last year’s influenza vaccine also contained the same H3N2 strain as this year’s vaccine (A/Hong Kong/4801/2014 (H3N2)-like virus). Many people would have developed long term IgE mediated sensitization to the H3N2 viral proteins due to last year’s vaccine [1–4]. Those who received the Flublok vaccine can be expected to have an even stronger IgE response due to its 3X viral protein content [5,4]. This year’s vaccine H3N2 proteins would have been neutralized by these IgE antibodies. Thus resulting in the observed low vaccine efficacy. [6]
When a person making anti-H3N2 IgE is infected with H3N2, one can expect the course of the flu to be significantly worse. So the “cytokine storm” being observed in severe cases is likely to be an infection concurrent with an allergic reaction. Death is caused by anaphylactic shock but due to the presence of an infection, it is wrongly classified as septic shock.
In the case of food allergy for example, the allergen exposure can be large enough to cause an immediate hypersensitivity reaction and anaphylactic shock within minutes/hours. In the case of influenza allergy, it may take a day or two for the virus to replicate and produce enough viral exposure for anaphylaxis. So the anaphylaxis unfolds over a couple of days.
This result makes a lot of sense. When you have influenza virus allergy and are infected, you have more mast cell degranulation, more histamine, more mucus, more sneezing, more viral shedding.
Increased hospitalization rates have been observed in asthma patients that have received the influenza vaccine. Again, this is as predicted because asthma patients are likely to produce stronger IgE responses to the viral proteins upon vaccination. [8] On subsequent virus exposure, they can be expected to develop severe IgE mediated asthma.
Consider dengue infection. The initial mosquito bite that injects dengue virus into a person, causes the induction of IgE against dengue proteins. [9] Upon a subsequent bite that introduces the dengue virus again, the person develops hives due to a dengue specific-IgE mediated allergic reaction. As the infection (and thus allergic reaction) progresses and more histamine is released, vascular permeability increases. The result is hypotension and dengue shock syndrome. [10] Basically, a type 1 hypersensitivity reaction caused upon dengue virus exposure following IgE mediated sensitization to dengue viral proteins.
The route of exposure for natural influenza infection is the respiratory tract, not subcutaneous (SC) or intramuscular (IM) injection. Influenza vaccines artificially changed the route of initial viral protein exposure to SC or IM injection thus making it similar to the route of exposure for dengue.
The result is an IgE response to influenza proteins, similar to the response for dengue. It should therefore not come as a surprise that we are modifying the course of influenza infection such that it is acquiring characteristics of a dengue infection (hives and shock).
As a result, allergy medications such as antihistamines and anaphylaxis treatments may have to be considered to avoid or treat this man-made influenza shock syndrome.
References
1. Smith-Norowitz T a, Wong D, Kusonruksa M, Norowitz KB, Joks R, Durkin HG, et al. Long term persistence of IgE anti-influenza virus antibodies in pediatric and adult serum post vaccination with influenza virus vaccine. Int J Med Sci. 2011;8(3):239–44.
2. Davidsson A, Eriksson JC, Rudblad S, Brokstad KA. Influenza specific serum IgE is present in non-allergic subjects. Scand J Immunol. 2005 Dec;62(6):560–1.
3. Nakayama T, Kumagai T, Nishimura N, Ozaki T, Okafuji T, Suzuki E, et al. Seasonal split influenza vaccine induced IgE sensitization against influenza vaccine. Vaccine. 2015;
4. Arumugham V. Short sighted influenza control policy based on poorly designed vaccines will sicken more people [Internet]. Available from: https://www.zenodo.org/record/1038445
5. Corporation PS. Flublok Quadrivalent 2017-2018 [Internet]. 2018. Available from: https://www.fda.gov/downloads/BiologicsBloodVaccines/Vaccines/ApprovedPr…
6. McLean HQ, Thompson MG, Sundaram ME, Meece JK, McClure DL, Friedrich TC, et al. Impact of repeated vaccination on vaccine effectiveness against influenza A(H3N2) and B during 8 seasons. Clin Infect Dis. 2014;59(10):1375–85.
7. Yan J, Grantham M, Pantelic J, de Mesquita PJ, Albert B, Liu F, et al. Infectious virus in exhaled breath of symptomatic seasonal influenza cases from a college community. Adamson W, Beato-Arribas B, Bischoff W, Booth W, Cauchemez S, Ehrman S, et al., editors. Proc Natl Acad Sci. National Academy of Sciences; 2018;
8. Joshi AY, Iyer VN, Hartz MF, Patel AM, Li JT. Effectiveness of trivalent inactivated influenza vaccine in influenza-related hospitalization in children: a case-control study. Allergy asthma Proc. United States; 2012;33(2):e23–7.
9. Koraka P, Murgue B, Deparis X, Setiati TE, Suharti C, Van Gorp ECM, et al. Elevated levels of total and dengue virus-specific immunoglobulin E in patients with varying disease severity. J Med Virol. 2003;70(1):91–8.
10. Tuchinda M, Dhorranintra B, Tuchinda P. Histamine content in 24-hour urine in patients with dengue haemorrhagic fever. Southeast Asian J Trop Med Public Health. Thailand; 1977 Mar;8(1):80–3.
Competing interests: No competing interests
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