Genotypic Diversity of<i>Borrelia burgdorferi</i>Strains Detected in<i>Ixodes scapularis</i>Larvae Collected from North American Songbirds

Brinkerhoff, R. Jory; Bent, Stephen J.; Folsom-O'Keefe, Corrine M.; Tsao, Kimberly; Hoen, Anne G.; Barbour, Alan G.; Diuk‐Wasser, Maria A.

doi:10.1128/aem.01585-10

Cited by 25 publications

(28 citation statements)

References 19 publications

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“…Northward migrating birds, either by carrying immature infected ticks, or by serving as a reservoir themselves for B. burgdorferi (Brinkerhoff et al 2010), are the most likely means of spirochete introduction (Dennis et al 1998). At other sites, B. burgdorferi incidence in newly colonized I. scapularis populations mirrored infection rates in ticks removed from birds.…”

Section: Discussionmentioning

confidence: 96%

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Genotypic Diversity of an Emergent Population ofBorrelia burgdorferiat a Coastal Maine Island Recently Colonized byIxodes scapularis

MacQueen

Lubelczyk²,

Elias³

et al. 2012

Vector-Borne and Zoonotic Diseases

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The recent range expansion of Ixodes scapularis has been accompanied by the emergence of Borrelia burgdorferi. The development of genetic diversity in B. burgdorferi at these sites of emergence and its relationship to range expansion is poorly understood. We followed colonization of I. scapularis on a coastal Maine island over a 17-year period. B. burgdorferi's emergence was documented, as was expansion of ospC strain diversity. Ticks collected from rodents and vegetation were examined for the presence of B. burgdorferi. Sequencing and reverse line blot were used to detect B. burgdorferi ospC major groups (oMG). No I. scapularis were found until year four of the study, after which time they increased in abundance. No B. burgdorferi was detected by darkfield microscopy in I. scapularis until 10 years into the study, when 4% of adult ticks were infected. Seven years later, 43% of adult ticks were infected. In 2003, one oMG accounted for 91% of B. burgdorferi strains. This "founder" strain persisted in 2005, but by 2007 was a minority of the 7 oMGs present. Given the island's isolation, gene flow by avian introduction of multiple strains is suggested in the development of B. burgdorferi oMG diversity.

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Section: Discussionmentioning

confidence: 96%

“…This may be accomplished when the spirochete is dispersed to a new area by infected reservoir hosts, such as birds (Brinkerhoff et al 2010), or by larval deer ticks that are attached to infected small mammals or birds (Rand et al 1998;Ginsberg et al 2005;Brinkerhoff al. 2011).…”

Section: Introductionmentioning

confidence: 99%

Genotypic Diversity of an Emergent Population ofBorrelia burgdorferiat a Coastal Maine Island Recently Colonized byIxodes scapularis

MacQueen

Lubelczyk²,

Elias³

et al. 2012

Vector-Borne and Zoonotic Diseases

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“…To our knowledge, this is the first documented example of a B. burgdorferi gene product whose absence directly affects the ability of the spirochete to complete its infectious cycle in a competitive environment. With an increasing body of data addressing the occurrence of multiple genotypes of B. burgdorferi cohabiting Ixodes ticks (6,11,17,24,28) and the prevalence at which a specific genotype is associated with human infection (12,26,46), continued investigation of how proteins such as BBA03 contribute to the spirochete's fitness in the natural infectious cycle will provide greater insight into the ecological and functional biology of this zoonotic pathogen.…”

Section: Discussionmentioning

confidence: 99%

Competitive Advantage of Borrelia burgdorferi with Outer Surface Protein BBA03 during Tick-Mediated Infection of the Mammalian Host

et al. 2012

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Linear plasmid lp54 is one of the most highly conserved and differentially expressed elements of the segmented genome of the Lyme disease spirochete Borrelia burgdorferi. We previously reported that deletion of a 4.1-kb region of lp54 (bba01 to bba07 [bba01-bba07]) led to a slight attenuation of tick-transmitted infection in mice following challenge with a large number of infected ticks. In the current study, we reduced the number of ticks in the challenge to more closely mimic the natural dose and found a profound defect in tick-transmitted infection of the bba01-bba07 mutant relative to wild-type B. burgdorferi. We next focused on deletion of bba03 as the most likely cause of this mutant phenotype, as previous studies have shown that expression of bba03 is increased by culture conditions that simulate tick feeding. Consistent with this hypothesis, we demonstrated increased expression of bba03 by spirochetes in fed relative to unfed ticks. We also observed that a bba03 deletion mutant, although fully competent by itself, did not efficiently infect mice when transmitted by ticks that were simultaneously coinfected with wild-type B. burgdorferi. These results suggest that BBA03 provides a competitive advantage to spirochetes carrying this protein during tick transmission to a mammalian host in the natural infectious cycle.T he genome of Borrelia burgdorferi, the causative agent of Lyme disease, consists of a linear chromosome and numerous linear and circular plasmids (9,15). Several of these extrachromosomal plasmids have been shown to carry genes that are critical for B. burgdorferi viability during the infectious cycle, as it must adapt to two very different environments, i.e., the Ixodes tick vector and a mammalian host (18,25,38,39,57). One of the most highly conserved plasmids, which also has one of the largest proportions of differentially regulated genes in the B. burgdorferi genome, is the linear plasmid lp54 (7,10,21,30,32,39,40,44,51,52,56). Although several genes on lp54 have been identified as contributing to (5,14,41,48) or essential for (3,39,58) spirochete fitness in vivo, the majority of the proteins encoded on this plasmid are of unknown function and lack homologs in other organisms (9,15). We previously used the Cre-lox system to delete the genes encompassing a 4.1-kb region of lp54, from bba01 to bba07 (bba01-bba07 region) (A3⌬A1-7 mutant) (4). In addition to a delay in colony formation and distinct colony morphology, a slight defect was observed in the ability of the A3⌬A1-7 mutant to establish mammalian infection by tick bite in a challenge with 20 infected nymphs per mouse. In this study, to create a more biologically relevant model, we reduced the tick challenge to 3 ticks per mouse and found that the A3⌬A1-7 mutant was significantly attenuated in the ability to infect mice by tick bite in this challenge, whereas wild-type (WT) B. burgdorferi could routinely establish mammalian infection at a dose as low as 1 tick per mouse.Since all attempts to complement the full A3⌬A1-7 mutant were unsuc...

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“…In the northeastern United States, B. burgdorferi is transmitted among wildlife hosts, predominantly small mammals and ground-dwelling birds, by the immature stages (nymphs and larvae) of Ixodes scapularis ticks (Anderson 1988, LoGiudice et al 2003, Brisson and Dykhuizen 2004, Brisson et al 2008, Ogden et al 2008, Brinkerhoff et al 2010, Ogden et al 2011. The human risk of contracting Lyme disease is strongly correlated with the prevalence of B. burgdorferiinfected nymphs , Mather et al 1996, Stafford et al 1998, Diuk-Wasser et al 2012.…”

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confidence: 99%

Reductions in Human Lyme Disease Risk Due to the Effects of Oral Vaccination on Tick-to-Mouse and Mouse-to-Tick Transmission

Voordouw

Tupper

Önder

et al. 2013

Vector-Borne and Zoonotic Diseases

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Vaccinating wildlife is becoming an increasingly popular method to reduce human disease risks from pathogens such as Borrelia burgdorferi, the causative agent of Lyme disease. To successfully limit human disease risk, vaccines targeting the wildlife reservoirs of B. burgdorferi must be easily distributable and must effectively reduce pathogen transmission from infected animals, given that many animals in nature will be infected prior to vaccination. We assessed the efficacy of an easily distributable oral bait vaccine based on the immunogenic outer surface protein A (OspA) to protect uninfected mice from infection and to reduce transmission from previously infected white-footed mice, an important reservoir host of B. burgdorferi. Oral vaccination of white-footed mice effectively reduces transmission of B. burgdorferi at both critical stages of the Lyme disease transmission cycle. First, oral vaccination of uninfected white-footed mice elicits an immune response that protects mice from B. burgdorferi infection. Second, oral vaccination of previously infected mice significantly reduces the transmission of B. burgdorferi to feeding ticks despite a statistically nonsignificant immune response. We used the estimates of pathogen transmission to and from vaccinated and unvaccinated mice to model the efficacy of an oral vaccination campaign targeting wild white-footed mice. Projection models suggest that the effects of the vaccine on both critical stages of the transmission cycle of B. burgdorferi act synergistically in a positive feedback loop to reduce the nymphal infection prevalence, and thus human Lyme disease risk, well below what would be expected from either effect alone. This study suggests that oral immunization of wildlife with an OspA-based vaccine can be a promising long-term strategy to reduce human Lyme disease risk.

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Genotypic Diversity ofBorrelia burgdorferiStrains Detected inIxodes scapularisLarvae Collected from North American Songbirds

Cited by 25 publications

References 19 publications

Genotypic Diversity of an Emergent Population ofBorrelia burgdorferiat a Coastal Maine Island Recently Colonized byIxodes scapularis

Genotypic Diversity of an Emergent Population ofBorrelia burgdorferiat a Coastal Maine Island Recently Colonized byIxodes scapularis

Competitive Advantage of Borrelia burgdorferi with Outer Surface Protein BBA03 during Tick-Mediated Infection of the Mammalian Host

Reductions in Human Lyme Disease Risk Due to the Effects of Oral Vaccination on Tick-to-Mouse and Mouse-to-Tick Transmission

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