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In 2019, investigators reported that post-Lyme disease arthritis might be triggered by a peptidoglycan molecule in the cell envelope of Borrelia burgdorferi — a molecule that is released but not degraded when the bacterium dies (NEJM JW Gen Med Aug 15 2019 and Proc Natl Acad Sci U S A 2019; 116:13498). Systemic administration of this residual molecule into mice led to development of acute arthritis. The investigators speculated that this molecule also might trigger other post-Lyme complications — including meningitis and the fatigue and cognitive problems associated with posttreatment Lyme disease syndrome (PTLDS).
In a new study, many of the same investigators looked at human joint fluid and cells from patients with post-Lyme arthritis, as …