SPECIAL REPORT from STAT, October 12, 2016:
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Burgdorfer’s final clue–is “Swiss agent” the key to Lyme disease?
STAT, a health and science publication affiliated with the Boston Globe, has published an explosive article about a long-ignored factor that may hold a clue to the mystery of Lyme disease.
The ‘Swiss Agent’: Long-forgotten research unearths new mystery about Lyme disease
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By Charles Piller @cpiller
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The tick hunter was hopeful he had found the cause of the disabling illness, recently named Lyme disease, that was spreading anxiety through leafy communities east of New York City. At a government lab in Montana, Willy Burgdorfer typed a letter to a colleague, reporting that blood from Lyme patients showed “very strong reactions” on a test for an obscure, tick-borne bacterium. He called it the “Swiss Agent.”
But further studies raised doubts about whether he had the right culprit, and 18 months later, in 1981, Burgdorfer instead pinned Lyme on another microbe. The Swiss Agent test results were forgotten.
Now STAT has obtained those documents, including some discovered in boxes of Burgdorfer’s personal papers found in his garage after his death in 2014. The papers — including letters to collaborators, lab records, and blood test results — indicate that the Swiss Agent was infecting people in Connecticut and Long Island in the late 1970s. READ MORE.
While undergoing hepatitis C long term interferon/ribavirin therapy from 1997-2006, I was bitten by a tick during the 1999-2000 time frame while employed as a land surveying technician . Ultimately, my physicians believed that my unusual increasing visual disturbances, muscle aches and cognitive
decline were caused by my HCV infection & therapy, and I became disabled by 2002. I tested positive for Lyme in December 2006 after a late October febrile illness necessitated a hospital emergency room visit. While at the ER, the attending physician performed a spinal tap which revealed elevated CSF protein.
Between October-December 2006, an environmental inspection determined our home was inundated with high levels of multiple mold species and my wife and I were compelled to move after Aspergillus fumigatu was detected in my blood and our house cat tested “Strong Positive” for bartonella.
Although I ended long term interferon/ribavirin HCV therapy in December 2006, no treatment or follow up was initiated for my Aspergillus exposure or my “positive” Lyme test but our cat was treated for bartonella and survived. In 2007, I developed increasing visual disturbances, double vision (diplopia) photopias & floaters, ultimately necessitating laser retina surgery. During 2006-2010, my neurological, visual (uveitis & iritis), low platelet count (thrombocytopenia) and re-occurring febrile/rash issues continued, increasing then decreasing, only to increase again in a cycle, while my physicians believed these symptoms to be related to my HCV infection. By the end of 2008, my liver specialist diagnosed primary sclerosing cholangitis (PSC) and
prescribed long term ursodiol therapy to keep my bile ducts open and decrease my ever increasing GGT levels. By January 2009, my liver specialist revised his diagnosis to “PSC-Vanishing Bile Duct Syndrome” and referred me to the National Institutes of Health (NIH) Undiagnosed Disease program, which never acknowledged my liver specialist’s referral.
In January 2010, I returned to the ER with severe gas, severe myalgia, right upper quadrant and right
eye/optic nerve pain but the ER’s CT scan detected nothing unusual. Later in January 2010 a HIDA scan and “Motility Study” were ordered by my liver specialist, the results being inconclusive. The doctor conducting the motility study mentioned that they observed “something unusual” at the juncture of the jejunum & illeum, but they didn’t know what it was and took no biopsy. My liver specialist suggested subsequent cardiac and neurological followup. My cardiac workup detected Left Ventricular Hypertrophy (LVH) w/Diastolic Dysfunction Grade 1 and the neurological workup confirmed a sensory motor demyelinating neuropathy.
When I mentioned to the neurologist that I had been bitten by a tick in the 1999-2000 time frame, he sent me to an infectious disease specialist, who begrudgingly tested me for Rocky Mountain Spotted Fever (RMSF). My June 2, 2010 RMSF test result was IgG=>256, but IgM was “negative”. When this Santa Barbara ID
specialist refused to test me for other vector borne illnesses and refused follow appointments, I sought care at UCLA’s Infectious Disease Clinic in Santa Monica, CA. Subsequent testing at UCLA-Santa Monica revealed that my RMSF IgG was 512, but all other vector borne illness testing were either negative or very low AB titers. After my third (6-29-2010) RMSF test by my wife’s primary care physician revealed my IgG test had risen to 1024, the UCLA ID specialist ultimately initiated 8 weeks of doxycycline therapy and said he would send my “paired sera sample” to the California Department of Health, Viral & Rickettsial Disease Laboratory-Richmond, CA (CDPH-VRDL-Richmond) and the CDC.
The paired sera sample testing (June 2nd and June 29th 2010) for RMSF at CDPH-VRDL-Richmond detected IgM titers, verbally reported as 1:40 (06-02) and 1:10 (06-29), both IgM levels being below the “reportable level” of commercial RMSF testing. This same “paired sera sample” was sent to the CDC Rickettsial Zoonoses Branch and detected antibody titers to rickettsia Rickettsi and rickettsia Akari. During and initially after my RMSF doxycycline therapy, my symptoms improved, but ultimately my symptoms returned and my antibody titers have persisted to this day, rising and falling above the detection limit (1:64) up to and beyond 1:512.
My subsequent consultations with infectious disease specialists at UC San Diego (2011) opined that the CDC test results were false positives related to his HCV infection, but the UCSD doctors made no mention whatsoever in their report of the IgG & IgM titers detected at CDPH-VRDL-Richmond. Since 2011, all of my efforts to determine if I am still infected with Rocky Mountain Spotted Fever have been thwarted by doctors specifically omitting that I had been treated for RMSFand fail to make any mention of the CDPH-VRDL-Richmond testing results, which showed elevating IgG and decreasing IgM antibody titers were detected in June 2010.
Now that I have successfully attained (05-2015) and maintained my sero-negative hepatitis C (HCV) status, my rheumatological/neurological sequela continue without a definitive diagnosis, with my rheumatologist at Stanford Palo Alto offering another referral to the NIH Undiagnosed Disease Program. I can only conclude that America’s medical establishment is woefully ignorant regarding rickettsial bacteria symptomology, research and treatment because my contacts at the CDC state that researchers in France are decades ahead of American researchers and French researchers have a large rickettsial disease clinic in Marseilles, France.
Walter Taylor-Lompoc, CA