Figure 1.

Possible mechanisms for persistent symptoms after antibiotic treatment for LD. 1) Autoimmunity in which self-antigens are targeted by B- and/or T-cells due to molecular mimicry or other immune dysregulated mechanisms. 2) Post-infectious immune mediated sequalae from the spirochete or its cellular components such as peptidoglycan could cause damage to tissues/organs during the initial infection. Evidence for these first two mechanisms doesn’t involve the recovery of whole, intact spirochetes after treatment. 3) Persistent infection in which a small number of spirochetes survive after antibiotic treatment as viable, viable non-cultivable (VBNC), or non-viable cells. Evidence for B. burgdorferi antibiotic persistence can be found in in vitro culture studies and several in vivo animal models such as mice, dogs, and non-human primates (NHPs). It should be notes that these mechanisms may not exist independently of one another and involve other unknown mechanisms.