Please see the following email addressed to the Co-chair of the Tick-Borne Disease Working Group
Recent passing of Dr. Nick Harris, the founder of IGeneX
https://www.lymedisease.org/nick-harris-igenex-has-died/
---------- Original Message ----------
From: CARL TUTTLE <runagain@comcast.net>
To: "linden.hu@tufts.edu" <linden.hu@tufts.edu>
Cc: All members of the TBDWG
Date: 04/28/2022 10:03 AM
Subject: Recent passing of Dr. Nick Harris, the founder of IGeneX
April 28, 2022
Graduate School of Biomedical Sciences
Tufts University
Suite 813
145 Harrison Avenue
Boston, MA 02111
Attn: Linden Hu, Professor of Immunology
Dear Prof Hu,
After the recent passing of Dr. Nick Harris, the founder of IGeneX, it was brought to my attention through the attached correspondence that you coauthored the controversial 2001 Klempner publication:
INTRALABORATORY RELIABILITY OF SEROLOGIC AND URINE TESTING FOR LYME DISEASE
https://pubmed.ncbi.nlm.nih.gov/11182109/
Dr. Nick Harris' complaint: (Personal Dropbox storage area)
https://www.dropbox.com/s/2eqe5p53x9852x5/Klempner%20LUAT2001%20%281%29.pdf?dl=0
Nick Harris claims that the lab specimens shipped to him were not stored properly and Klempner claims they were, so who's lying here?
The fact that Klempner refused Dr. Harris’ offer to retest at his own expense gives us a good indication.
Here is a comment from someone familiar with the situation:
I knew about it before going to Munich. This is what I remember. IGeneX had found very odd results on the LUATs, a mix of extreme highs and lows. They wanted to repeat the tests but NIH/Klempner said no, they should send what they had. They were under contract and they were obligated, they said. Nick was out of town, the lab capitulated and sent the squirrelly numbers. When he returned Nick was upset and called the lab Klempner was using. Someone there told him the specimens had been sitting in a regular refrigerator for an extended period--I don't know how long but definitely longer than the IGeneX protocol demanded for that test. Nick then called NIH--probably Phil Baker--and said he would retest at his own expense. Phil said no. Klempner was happy to take this to Munich where he could spread his lies that the LUAT was worthless. After all the LUAT was proving that ppl who tested negative on the bogus antibody tests could still have actual borrelial antigen in their urine. They couldn't allow that cat out of the bag.
__________________
Prof Hu,
Klempner as you know was the principal investigator for the antibiotic trials [1] that Dennis Dixon and other members of this TBDWG are fixated on despite mountains of evidence that Borrelia persist after extensive antibiotic treatment. It is interesting that you were a coauthor of these studies as well.
I reviewed those “antibiotic trials” and find it rather odd that “no evidence of B. burgdorferi was found in a total of more than 700 different blood and cerebrospinal fluid samples from the 129 patients in these studies.”
Statistically, that’s not possible so I wrote to Dr. Klempner and questioned those numbers (See attached correspondence). Klempner refused to answer my inquiry.
Correspondence to to Dr. Klempner (Personal Dropbox storage area)
https://www.dropbox.com/s/j0d6y4wxkak88gd/Mark%20Klempner%20700%20Samples.docx?dl=0
Those of us who have studied the mishandling of Lyme believe that the rush to create a vaccine led to it’s mishandling as a chronic relapsing seronegative disease did not fit the vaccine model and post-treatment Lyme disease syndrome is simply a fabricated medical condition disguising treatment failure.
It is obvious to me that this Working Group is being controlled by those who don’t want chronic Lyme recognized as it would threaten the vaccine business model [2] hence the focus on the Klempner antibiotic trials. Interesting to see that Klempner is involved in developing a yearly vaccine-like antibody injection. [3]
Prof Hu,
Have you read Monica Embers’ latest publication? Prof Embers as you know is a member of the TBDWG.
Borreliella burgdorferi Antimicrobial-Tolerant Persistence in Lyme Disease and Posttreatment Lyme Disease Syndromes
Cabello, F. C., Embers, M. E., Newman, S. A., & Godfrey, H. P.
mBio, e0344021, advance online publication April 25, 2022.
https://doi.org/10.1128/mbio.03440-21
Excerpts:
burgdorferi is endowed with several genetic and metabolic mechanisms that in other bacteria are responsible for generation of antimicrobial tolerance. Apart from in vitroand animal experiments, their relevance to the presence of antimicrobial-tolerant B. burgdorferi in humans remains to be experimentally established. There is, however, strong experimental evidence from in vitrostudies (14–16), animal models (17–20, 32, 155–159), and patients (21, 185–187) that B. burgdorferi can become tolerant to antimicrobials and remain in host tissues for extended periods of time in dynamic equilibrium with the host immune response (70, 155–159). This is underlined by the presence of B. burgdorferi DNA and RNA in xenodiagnostic ticks fed on animals and patients with potential antimicrobial-tolerant B. burgdorferi organisms, since tick midgut contents and salivary glands are likely to contain tissue nucleases able to clear naked DNA and RNA not associated with viable organisms (172, 175, 201). While the continuing presence of borrelial DNA in humans, animals, and ticks has been compared to that of bacterial DNA found in valves of patients with treated bacterial endocarditis years after treatment (202–204), this comparison is at best inexact, since valvular tissues are potentially immunologically privileged sites where access to antimicrobials and host endonucleases is limited and where DNA (even if generated by unculturable organisms) could be protected from degradation.
One promising approach is to generate mutants of B. burgdorferi genes potentially involved in antimicrobial tolerance (e.g., rel, dksA, and rpoS) in isogenic strains of B. burgdorferi. The ability of these strains to generate antimicrobial-tolerant persisters in vitro and in animals can be compared with that of wild-type strains and their epistatic interactions, regulatory hierarchies, and potential epigenetic markers assessed (39, 205, 206). Potential epigenetic modifications, such as DNA methylation of isogenic antimicrobial-tolerant borrelias, could similarly be assessed by nanopore-based DNA sequencing (39), while genome-wide mutagenesis and genome editing could permit identification of new genes and functions involved in antimicrobial tolerance-mediated persistence in vitro and in vivo in animals (206, 207). The recent rescue of potential antimicrobial-tolerant B. burgdorferi persisters by culture of heart tissues from chronically infected macaques can be expected to facilitate metagenomic and metatranscriptomic analysis and identification of the genetic elements underlying their inability to be readily cultured as well as those involved in persistence in mammals (156, 208, 209). It can also be expected to enable identification of therapeutic modalities capable of blocking functions needed for antimicrobial-mediated spirochetal persistence, tolerance, and revival and thus forestall development of PTLDS in some patients (9, 15, 16, 58, 66, 70).
___________________________________
From someone who’s entire family progressed to late-stage debilitating Lyme and recovered through long term antibiotic treatment, it is crystal clear to me that the following statement is absolutely true:
In the fullness of time, the mainstream handling of Chronic Lyme disease will be viewed as one of the most shameful episodes in the history of medicine because elements of academic medicine, elements of government and virtually the entire insurance industry have colluded to deny a disease. -Dr. Kenneth Liegner
Respectfully submitted,
Carl Tuttle
Hudson, NH
Cc: All members of the Prevention and Treatment Subcommittee
References
1. TWO CONTROLLED TRIALS OF ANTIBIOTIC TREATMENT IN PATIENTS WITH PERSISTENT SYMPTOMS AND A HISTORY OF LYME DISEASE
https://pubmed.ncbi.nlm.nih.gov/11450676/
2. Valneva Receives FDA Fast Track Designation for its Lyme Disease Vaccine Candidate VLA15
https://www.pfizer.com/sites/default/files/partnering/recent_partnership/2017_07_24_VLA_Lyme_FDA_Fast_track_PR_EN.pdf
3. A Lyme disease vaccine doesn’t exist, but a yearly antibody shot shows promise at preventing infection
https://theconversation.com/a-lyme-disease-vaccine-doesnt-exist-but-a-yearly-antibody-shot-shows-promise-at-preventing-infection-138230