A resulting persistent infection of the host can then result in the development of arthritis, carditis, or neuroborreliosis [4]. Arthritis is the primary manifestation of late and chronic Lyme disease by B. burgdorferi sensu stricto, the predominant genospecies in the United States. The genetic basis of bacterial virulence and disease has been investigated in a large number of Gram-negative and Gram-positive bacteria in the last three decades and major virulence factors of each microbe have been identified. These studies have shown that various strains of bacterial

pathogens often exhibit different levels of pathogenicity and Erastin cell line disease manifestations in the hosts. In most cases, the high pathogenicity is associated with specific variations in the set of virulence factors [5–11]. In many microbes, the respective virulence factor-encoding genes are clustered selleck inhibitor together in specific regions defined as pathogenicity islands [12]. Strains of B. burgdorferi

show a high variation in their ability to cause disseminated infection. Since genetic studies have been developed in this spirochete only in the past decade, classification based upon its virulence factor diversity has not yet been fully developed. Furthermore, the presence of a segmented genome has hampered studies with different spirochete strains. However, B. burgdorferi sensu stricto strains have been divided into different groups either on the basis of allelic variation in the Outer surface protein C (OspC), which is essential for causing infection in the mammalian hosts [13–16], or the polymerase chain reaction (PCR) and restriction fragment length polymorphism analysis of 16 S-23 Interleukin-3 receptor S rRNA spacer types (RST). Furthermore, ospC or RST groups were used as markers to determine pathogenicity of different B. burgdorferi strains with only some groups considered invasive [17–24]. Studies involving the two most widely investigated strains, B31 and N40, have contributed significantly to the understanding of Lyme disease pathogenesis and assessment of the virulence

factors of B. burgdorferi[25–27]. B31 and N40 strains were isolated from Ixodes scapularis ticks from Shelter Island and Westchester county of New York, respectively, and both are highly infectious in the mouse model [2, 28]. Indeed, N40 C188-9 clinical trial strain was selected for its high pathogenicity from a large number of isolates recovered from ticks by Durland Fish. By a thorough genetic analysis of various clones of N40 used in various laboratories, we have recently shown that the original culture was a mixed culture and different researchers isolated two different clones independently and retained the original name, N40, for both [29]. The clones designated as cN40 and the sequenced N40B are the derivatives of the same strain and N40 clone D10/E9 (N40D10/E9) and N40C appear to be derivatives of the second strain that is different from cN40/N40B.