Borrelia Virulence Factors
Unlike many pathogenic bacteria, B. burgdorferi lacks many traditional virulence factors. While possessing two membranes like Gram-negative bacteria, B. burgdorferi lacks endotoxin (lipopolysaccharide) (Fraser et al. 1997; Casjens et al. 2000). In addition, B. burgdorferi makes no known exotoxins (Fraser et al. 1997; Casjens et al. 2000). Many pathogens express specialized secretion systems that allow for injection of effectors directly into host cells; B. burgdorferi lacks Type III or IV secretion systems (Fraser et al. 1997; Casjens et al. 2000). While B. burgdorferi has been detected inside mammalian cells, there is little evidence that B. burgdorferi is a true intracellular pathogen with the ability to create a niche within a host cell vacuole to evade host immune responses (Comstock and Thomas 1989; Ma et al. 1991; Klempner et al. 1993; Girschick et al. 1996; Fraser et al. 1997; Casjens et al. 2000; Livengood and Gilmore 2006; Wu et al. 2011). Many bacterial pathogens have sophisticated strategies to sequester iron, an essential and limiting nutrient. B. burgdorferi, however, has no need for iron (Posey and Gherardini 2000). B. burgdorferi does have an impressive array of adhesins to facilitate binding to host tissues (Antonara et al. 2011; Brissette and Gaultney 2014). B. burgdorferi also has the ability to evade host complement through the binding of host complement regulators (Kraiczy and Stevenson 2013). Complement evasion is especially important, as hematogenous spread is a critical component of the bacterium's ability to disseminate to a wide variety of tissues. Despite spreading throughout a host, the bacterium's strategy is one of evasion rather than confrontation. The vector host, the Ixodes tick, and the mammalian reservoir hosts, such as white-footed mice, do not seem to suffer any ill effects from B. burgdorferi infection (Hersh et al. 2014; Herrmann and
Gern 2015). Humans are accidental and dead-end hosts, and the bulk of disease pathology is a result of our immune responses to the bacterium rather than an effect of the bacterium itself.