LNB is, in many cases, responsive to appropriate antimicrobial therapy and the clinical improvement sustained by the antibiotic treatment provide further evidence for the direct contribution of B. burgdorferi in disease pathogenesis. However, the chronic persistence, the frequent reoccurrence of LNB and the ability of B. burgdorferi to tolerate multiple cycles of antibiotic treatment is strongly suggestive for the formation of biofilm or biofilm-like protective structure (20–23). Indeed, different studies have shown that B. burgdorferi can switch from a motile to a stationary status, in which the cells are embedded within a biofilm matrix (22). B. burgdorferi biofilms have been observed both in vitro and in human infected skin tissues (22, 23). These structures express different mucopolysaccharides, particularly alginate, extracellular DNA and calcium, which are all typical markers of biofilm (22). The presence of biofilm may explain the low rate of Borrelia detection in the blood of infected patients as well as the ability of the spirochetes to evade the host immune system and resist the antibiotic therapy (21, 24–27).
This review investigates the differences in the epidemiology and clinical manifestations of LNB with particular emphasis on the pathogenetic role of B. burgdorferi biofilm in tissue adhesion, colonization and survival.