Shapiro ED.F1000Prime Rep. 2015.1 comment
In this one-sided opinion piece about Lyme disease, Eugene Shapiro once again finds "no evidence that viable B. burgdorferi persist in humans after conventional treatment with antimicrobials". Shapiro is a well known member of the shrinking "Lyme Denialist" cabal that views Lyme disease as a trivial illness that is "hard to catch and easy to cure", apparently ignoring the latest CDC figures showing more than 300,000 new cases per year in the USA. The fact that Lyme disease has become a major epidemic that is six times more common than HIV/AIDS in this country fails to impress Shapiro, who adheres to the dogma that persistent infection with B. burgdorferi, the Lyme spirochete, does not exist following short-course antibiotic therapy despite extensive evidence to the contrary (Stricker & Johnson, Infect Drug Resist 4: 1-9, 2011; Cameron et al, Expert Rev. Anti Infect. Ther. 12:1103-1135, 2014).
Significant controversy over Lyme disease exists for three main reasons: (1) lack of accurate and/or universally accepted testing for the disease, (2) disagreement about symptoms associated with persistent infection in chronic Lyme disease, and (3) misinterpretation and misrepresentation of underpowered Lyme antibiotic treatment trials. While many studies describe the constellation of musculoskeletal, neurocognitive and/or cardiac symptoms associated with chronic Lyme disease, Shapiro views these as "medically unexplained symptoms" not necessarily related to persistent B. burgdorferi infection. Without a universally accepted "gold standard" test, the controversy over persistent infection and optimal therapy continues to smoulder while thousands of patients continue to suffer due to the dogma espoused by Shapiro (Johnson et al. PeerJ 2:e322, 2014).
A major problem faced by Shapiro is that he is trying to prove a negative. Thus if there is any evidence that persistent infection with B. burgdorferi does exist following short-course antibiotic therapy, his opinion is obviously wrong. To address this problem, Shapiro narrows his evidence to two recent Lyme disease articles, ignoring numerous studies in animals and humans that support persistent infection or leave the issue unsettled (Cairns & Godwin, Int J Epidemiol 34: 1340-1345, 2005; Berndtson, Int J Gen Med 6: 291-306, 2013; Stricker & Johnson, PLoS Pathog 10: e1003796, 2014). Shapiro dismisses this contrary evidence as "speculative", but his narrow selection of two "convincing" studies is insufficient to support his biased conclusion.
The first study examined a group of 17 patients with recurrent erythema migrans (EM) rashes who were promptly treated for their initial episode of Lyme disease and then developed one or more EM rashes at a later date. Culture of the rashes revealed different strains of B. burgdorferi in the subsequent episodes, and Shapiro points to this as evidence for new infection rather than relapse in these patients. However as pointed out in a letter addressing the article, this is a poor model for chronic Lyme disease due to persistent infection because all patients were promptly treated for their initial illness, lived in endemic areas and most likely were reinfected with a different strain of the spirochete from a subsequent tickbite. This is a very different situation from a patient who may have been infected and never treated for months to years and develops the constellation of musculoskeletal, neurocognitive and/or cardiac symptoms that are characteristic of persistent infection with the Lyme spirochete (Donta, N Engl J Med 368:1063-1064, 2013). Thus the model for persistent infection in this study is flawed.
The second study was a xenodiagnosis safety study of 36 patients (26 Lyme patients in different stages of disease and 10 controls) who allowed ticks to feed on them, and the ticks were then examined for B. burgdorferi transmission. Shapiro states that "no viable B. burgdorferi were cultured from ticks fed on any of these patients". This conclusion is flawed for two reasons: First, 30-50% of ticks were lost during the study, rendering the transmission results uninterpretable. Second, one patient with post-treatment Lyme disease syndrome (PTLDS) was found to have a positive culture from one tick, as stated in the Results: "One nymph was found to be positive by PCR of the nymph lysate culture, but direct PCR of the nymph lysate and microscopic evaluation of the culture were negative....The original positive OspA PCR of the tick culture was confirmed by PCRs for other B. burgdorferi genes.... The DNA extracted from this culture sample was then tested by IA/PCR/ESI-MS, which was positive for 7 of the 8 assay primer pairs" (emphasis added). Thus this patient had culture-confirmed evidence of persistent infection with the Lyme spirochete in PTLDS. Shapiro generously states that this finding is "provocative" when in fact it provides definitive evidence that he is wrong.
In summary, this one-sided opinion piece will only add to the confusion and misinformation surrounding Lyme disease. With better testing and novel treatments, a solution to this tickborne disease will someday be found. Shapiro's muddled article fails to contribute to this solution.
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