There appears to be some inconsistencies with what is being published regarding laboratory diagnostics for Lyme disease. Is this “flip-flopping” a result of pressure from the Centers for Disease Control to maintain the status quo or is it a case off do whatever is best for one’s accedemic career? First email to Professor Stephen E. Schutzer, M.D.: --------- Original Message ---------- From: Carl Tuttle To: tickbornedisease@hhs.gov, schutzer@njms.rutgers.edu Cc: CID.EditorialOffice@oup.com, All members of the Working Group Date: December 17, 2017 at 10:22 AM Subject: Advances in Serodiagnostic Testing for Lyme Disease Are at Hand Dec 17, 2017 Rutgers New Jersey Medical School 185 South Orange Avenue Newark, New Jersey 07103 Attn: Stephen E. Schutzer, M.D., Professor Dear Dr. Schutzer, I would like to call attention to the following study you published in the Lancet in February 1990 highlighting seronegative Lyme disease (No antibody production against infection): Lancet. 1990 Feb 10;335(8685):312-5. Sequestration of antibody to Borrelia burgdorferi in immune complexes in seronegative Lyme disease. Schutzer SE1, Coyle PK, Belman AL, Golightly MG, Drulle J. Abstract To find out whether apparent seronegativity in patients strongly suspected of having Lyme disease can be due to sequestration of antibodies in immune complexes, such complexes were isolated and tested for antibody to Borrelia burgdorferi. In a blinded analysis the antibody was detected in all 10 seronegative Lyme disease patients with erythema chronicum migrans (ECM), in none of 19 patients with other diseases, and in 4 of 12 seronegative patients who probably had Lyme disease but had no ECM. These findings were confirmed by western blot, which also showed that immune complex dissociation liberated mainly antibody reactive to the 41 kD antigen and sometimes antibody to an approximate 30 kD antigen. Complexed B burgdorferi antibody was also found in 21 of 22 (95%) of seropositive patients with active disease, 3 additional seronegative but cell mediated immune reactive patients, and 3 other seronegative patients who eventually became seropositive. Apparent B burgdorferi seronegativity in serum immune complexes may thus be due to sequestration of antibody in immune complexes. PMID:1967770 ________________________ In addition to your study above, please take a moment to review the following case study from Stony Brook Lyme clinic. I understand the patient received thirteen spinal taps, multiple courses of IV and oral meds, and relapsed after each one, proven by CSF antigens and/or PCR. The only way this patient (said to be a physician) remained in remission was to keep her on open ended clarithromycin- was on it for 22 months by the time of publication: 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. ____________________ In addition to these examples of seronegative Lyme disease, were you aware that Duke University Oncologist Dr. Neil Spector required a heart transplant after his Lyme disease went untreated for four years as his serologic tests for Lyme were repeatedly negative and did not become seropositive until the damage to his heart was irreversible? Source: https://www.dukehealth.org/blog/doctor-hopes-his-medical-journey-inspires-others Dr. Schutzer, I understand that you were involved in the recent Cold Spring Harbor Laboratory Banbury conference and coauthored the following article: Advances in Serodiagnostic Testing for Lyme Disease Are at Hand https://academic.oup.com/cid/advance-article-abstract/doi/10.1093/cid/cix943/4706288?redirectedFrom=fulltext In addition, you were interviewed by Contagion on Dec 7, 2017 and made the following statement regarding the case definition of the Western blot which was established in 1994 at the closed door Dearborn Conference: “This confusion is because when the Western blot criteria were formulated, “it was not known that some key proteins of the Lyme agent were only produced during an actual infection and these proteins were left out of the criteria,” Dr. Schutzer noted.” Source: http://www.contagionlive.com/news/advances-are-being-made-in-diagnostic-testing-for-early-lyme-disease I read through your interview with Contagion a number of times and I could not find any references to seronegative Lyme disease. (No antibody production against infection) As you know, a Tick-Borne Disease Working Group has been established as part of the 21st Century Cures Act to review federal efforts related to all tick-borne diseases. Source: https://www.hhs.gov/ash/advisory-committees/tickbornedisease/index.html I have taken the liberty to carbon copy all members of the TBD Working Group on this communication so perhaps you would be kind enough to hit reply to all and explain to the group how these “Advances in Serodiagnostic Testing for Lyme Disease” will not allow any patient who does not produce antibodies to slip through the cracks as experienced by Dr. Neil Spector. Your prompt attention to this inquiry is appreciated. Sincerely, Carl Tuttle Independent Researcher Lyme Endemic Hudson, NH Cc: -Robert T. Schooley, M.D. Editor-in-Chief, Clinical Infectious Diseases -All members of the Working Group -Barbara D. Alexander, M.D. Professor of Medicine Director of Transplant Infectious Disease Duke University Second email to Dr. Schutzer: --------- Original Message ---------- From: Carl Tuttle To: schutzer@njms.rutgers.edu, tickbornedisease@hhs.gov Cc: All members of the Working Group Date: December 18, 2017 at 10:20 AM Subject: Re: Advances in Serodiagnostic Testing for Lyme Disease Are at Hand Dr. Schutzer, It was brought to my attention that you coauthored the following article in 2013: Achieving molecular diagnostics for Lyme disease Mark W Eshoo,Steven E Schutzer,Christopher D Crowder,Heather E Carolan &David J Ecker https://www.ncbi.nlm.nih.gov/pubmed/24151851 Pages 875-883 | Published online: 09 Jan 2014 Excerpt: "Early Lyme disease is often difficult to diagnose. Left untreated, symptoms can last for many years leading to chronic health problems. Serological tests for the presence of antibodies that react to Borrelia burgdorferi antigens are generally used to support a clinical diagnosis. Due to the biologically delayed antibody response, serology is negative in many patients in the initial 3 weeks after infection and a single test cannot be used to demonstrate active disease, although certain specialized tests provide strong correlation. Because of these limitations there exists a need for better diagnostics for Lyme disease that can detect Borrelia genomic material at the onset of symptoms." _____________________ Could you please explain the flip-flopping between molecular diagnostics and now serology? What is going on here exactly? Carl Tuttle Hudson, NH