Borrelia burgdorferi Genetic Markers and Disseminated Disease in Patients with Early Lyme Disease

Abstract

Three genetic markers of Borrelia burgdorferi have been associated with disseminated disease: the OspC type, the 16S-23S rRNA intergenic spacer type (RST), and vlsE. Here, we modified previous methods so as to identify the three markers by PCR and restriction fragment length polymorphism in parallel, analyzed B. burgdorferi isolates from erythema migrans (EM) skin lesions in 91 patients, and correlated the results with evidence of dissemination. OspC type A was found approximately twice as frequently in patients with disseminated disease, whereas type K was identified approximately twice as often in those without evidence of dissemination, but these trends were not statistically significant. The remaining seven types identified were found nearly equally in patients with or without evidence of dissemination. RST 1 strains were significantly associated with dissemination (P ‫؍‬ 0.03), whereas RST 2 and RST 3 strains tended to have an inverse association with this outcome. The vlsE gene was identified in all 91 cases, using primer sets specific for an N-terminal sequence of B. burgdorferi strain B31 (vlsE B31 ) or strain 297 (vlsE 297 ), but neither marker was associated with dissemination. Specific combinations of the three genetic markers usually occurred together. OspC type A was always found with RST 1 and vlsE B31 , type K was always identified with RST 2 and more often with vlsE 297 , and types E and I were almost always found with RST 3 and equally often with vlsE B31 and vlsE 297 . We conclude that B. burgdorferi strains vary in their capacity to disseminate, but almost all strains isolated from EM lesions sometimes caused disseminated disease.

Geographic Variation in the Relationship between Human Lyme Disease Incidence and Density of Infected Host-Seeking Ixodes scapularis Nymphs in the Eastern United States

“…26,32 Differences in virulence 37 and transmission efficiency 25,38 may lead to differences in infection risk and/or reporting rates by humans infected with different strains. Thus, areas with low incidence but high rDIN could be explained by an overrepresentation Table 4. of strains with a low virulence in or transmission to humans.…”

Pervasive Recombination and Sympatric Genome Diversification Driven by Frequency-Dependent Selection in Borrelia burgdorferi, the Lyme Disease Bacterium

“…Third, the severe human virulence of B. burgdorferi s.s. is itself evidence for it being a generalist parasite of mammalian hosts, since despite the fact that humans are not its natural reservoir hosts, B. burgdorferi s.s. is capable of invading and infecting the human tissues. Although B. burgdorferi s.s. strains appear to vary in human virulence (Dykhuizen et al 2008;Wormser et al 2008), it has been argued that associations between human pathogenecity and genomic groups are weak and all groups have the potential to cause invasive infections in humans (Alghaferi et al 2005;Jones et al 2006).…”

Genetic Diversity of Borrelia burgdorferi and Detection of B. bissettii-Like DNA in Serum of North-Coastal California Residents

“…Of the 20 B. burgdorferi samples from study subjects whose DNA could be typed, 19 (95%) were of ospC genotype A. This proportion is significantly higher than in some northeastern United States communities, in which ospC A was detected in 23.5% of blood cultures (P Ͻ 0.001) (41) and 36.2% of skin isolates (P ϭ 0.012) (15). The B. burgdorferi clonal complex defined by ospC genotype A is ecologically highly invasive and established in a broad range of host species in Europe and North America (27).…”

“…The B. burgdorferi clonal complex defined by ospC genotype A is ecologically highly invasive and established in a broad range of host species in Europe and North America (27). In the northeastern United States, where the frequency of ospC A alleles is high in I. scapularis populations (40,41), this genotype is often one of the most, if not the most, commonly found in organisms that cause disseminated B. burgdorferi infections (8,9,15,34,41). Its predominance in this small Californian population is a further testament to its virulence and to its ability to disseminate from the initial site of infection, particularly considering that the prevalence of ospC A alleles in host-seeking I. pacificus nymphs collected within CHR and throughout Mendocino County is only 10% (unpublished data) and 10.9%, respectively (13).…”