Borrelia burgdorferi Persistence Post-antibiotic Treatment

Abstract

A basic precept of Borrelia burgdorferi biology is that persistent infection is the rule, not the exception, in immunocompetent hosts. Persistence occurs in many reservoir and incidental hosts of B. burgdorferi, and has been unequivocally proven experimentally in Peromyscus leucopus mice (Schwan et al. 1988), laboratory mice (Barthold et al. 1993a), rats (Moody et al. 1990), hamsters (Goodman et al. 1991), gerbils (Preac-Mursic et al. 1990), guinea pigs (Sonnesyn et al. 1993), dogs (Straubinger et al. 1997), and nonhuman primates (Roberts et al. 1995a). There is no reason to believe that humans are different, and indeed there are a number of documented reports confirming persistent infection in humans by both culture (Asbrink and Hovmark 1985; Kuiper et al. 1994; Maraspin et al. 2011; Miklossy et al. 2004; Snydman et al. 1986; Stanek et al. 1990; Strle et al. 1995) and polymerase chain reaction (PCR) (Bradley et al. 1994; Frazer et al. 1992; Moter et al. 1994; Nocton et al. 1994a; von Stedingk et al. 1995). Borrelia burgdorferi has evolved to persist in its varied hosts as a survival strategy for maintaining its natural 2-year life cycle through its hosts and vector tick stages. That life cycle requires survival of B. burgdorferi in reservoir hosts over winter, since there is no transovarial transmission from female ticks to larvae. Uninfected eggs are laid in the spring, and larvae emerge during the summer, when they feed upon persistently infected reservoir hosts to acquire infection and subsequently pass infection through the life stages (transstadial transmission) to nymphs and adults (Anderson and Magnarelli 1993). Without the essential role of persistently infected reservoir hosts, the life cycle of B. burgdorferi would fail. Mechanisms of B. burgdorferi immune evasion, dormancy, and activation in hosts and vectors are among the least studied, but most critically needed areas for research.