Dr James Schaller
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In 1992 and 1993, IDSA author Dr. Mark Klempner published two studies in the Journal of Infectious Diseases documenting how Lyme "spirochetes can survive antibiotic treatment through intracellular sequestion within fibroblasts" making them "among the small number of bacteria that can cause chronic infection by localizing within host cells where they remain sequestered from some antimicrobial agents" (1993; 167:1074-1081).

Or as he stated in the same journal" The Lyme disease spirochete . . . can be recovered long after initial infection, even from antibiotic-treated patients, indicating that it resists eradication by host defense mechanisms and antibiotics . . . several eukaryotic cell types provide the Lyme disease spirochete with a protective environment contributing to its long-term survival" (1992; 166(2):440-4).

Likewise, Dr. Raymond Dattwyler proclaimed in Reviews of Infectious Diseases 1989, 11(6)S6; S1494-8, "Lyme borreliosis is a chronic infectious disease caused by the spirochete Borrelia burgdorferi. They [Lyme spirochetes] have been demonstrated in tissues obtained from individuals with high levels of antiborrelial antibodies, a finding that indicates the presence of immunity alone does not guarantee eradication of this organism."

In a New England Journal of Medicine study, Drs. Dattwyler and John Halperin (also of the IDSA) "studied 17 patients who had presented with acute Lyme disease and received prompt treatment with oral antibiotics, but in whom chronic Lyme disease subsequently developed."

These "chronic Lyme" patients tested negative on currently-available blood tests: "Although these patients had clinically active disease, none had diagnostic levels of antibodies to B. burgdorferi on either a standard enzyme-linked immunosorbent assay or immunoflourescence assay. We conclude that the presence of chronic Lyme disease cannot be excluded by the absence of antibodies against B. burgdorferi and that a specific T-cell blastogenic response to B. burgdorferi is evidence of infection in seronegative patients with clinical indications of chronic Lyme disease."

Dattwyler RJ; Volkman DJ; Luft BJ; Halperin JJ; Thomas J; Golightly MG. Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi.

New England Journal of Medicine 1988, 319(22):1441-6 A year earlier these same two researchers reported on "the clinical courses of 5 patients with Lyme disease who developed significant late complications, despite receiving tetracycline early in the course of their illness.

All 5 patients had been treated for erythema chronicum migrans with a course of tetracycline that met or exceeded current recommendations" (Failure of tetracycline therapy in early Lyme disease. Arthritis & Rheumatism 1987, 30:448-450.)

In 1993, Dr. Halperin co-authored an article entitled "Recurrent erythema migrans despite extended antibiotic treatment with minocycline in a patient with persisting Borrelia burgdorferi infection" in the Journal of the American Academy of Dermatology, 28(2 Pt 2):312-4. The title says it all: Even "persisting Borrelia burgdorferi infections" can occur, with manifestations as odd as a recurrent bull's-eye rash (erythema migrans).

Or as Dr. Halperin wrote in Neurology in 1992 ((42):43-50), "In many instances continued infection appears to be essential for symptoms to persist, no matter how small the number of organisms, as antimicrobial therapy is generally followed by clinical improvement."

Or as Gerold Stanek (also of IDSA) put it in the British Journal of Dermatology in 2001, "The relapses she repeatedly suffered despite initially successful antibiotic treatment could be related to the observation that Borrelia [the Lyme disease bacteria] may possibly be able to remain dormant in certain tissue compartments, thus escaping bactericidal antibiotic activity" (144(2):387-392).

Or as Allan Steere, guru of IDSA on Lyme, told the American Journal of Medicine in 1995 (88:4A-44S-51S), "Similarly [as in tertiary syphilis or tuberculoid leprosy], the antigenic stimulus in Lyme arthritis would appear to be a small number of live spirochetes, demonstrated here by monoclonal antibodies, which may persist in the synovial lesion for years (p.494)".

Or as Dr. Steere, wrote in the New England Journal of Medicine (1990 Nov 22; 323(21):1438-44), "The likely reason for relapse is failure to eradicate the spirochete . . . This last article is one of many studies that show continuing symptoms are most likely due to persistence of the spirochete [type of Lyme bacteria]." Indeed, many articles have been published before AND since 1990 demonstrating the possible persistence of Lyme infection in antibiotic-treated patients.

These studies have been written by members of the IDSA Lyme "team" and many other reputable scientists. And they are among the 98% of available literature on Lyme not cited in the IDSA's newest treatment guidelines!


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