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122 results for “Borrelia”
Figure 1 in Molecular detection of Borrelia anserina in Argas persicus (Acari: Argasidae) ticks collected from Lorestan province, west of Iran
Figure 1. The aggregated Argas persicus ticks at different stages around a thatched birdhouse in Lorestan province.
Figure 3 in Molecular detection of Borrelia anserina in Argas persicus (Acari: Argasidae) ticks collected from Lorestan province, west of Iran
Figure 3. The phylogenetic tree inferred from flaB amino acids sequence data of B. anserina (clade I) and other Borrelia taxa (clade II, KX171816 and JF693808) constructed using Neighbor-Joining (NJ) method with bootstrap test (1,000 replicates). The main clade in right side of tree separated with colored rectangular shape. Taxa are as species name following GenBank accession number, taxon of the present study indicated as bold. Nodes indicated with bootstrap value. Branch lengths are proportional to evolutionary changes, the units of the number of amino acid substitutions per site. The analysis involved 12 amino acid sequences. All positions containing gaps and missing data were eliminated. There were a total of 166 positions in the final dataset. The more diverged Pakistani strain of B. anserina (JF693808) located outside the main B. anserina (clade I). The members of clade II and B. hermsii are as outgroup.
Figure 2 in Molecular detection of Borrelia anserina in Argas persicus (Acari: Argasidae) ticks collected from Lorestan province, west of Iran
Figure 2. The stereomicroscopic view of dissected salivary glands (A); ovary and uterus (B) of female Argas tick in normal saline.
Figure 4 in Molecular detection of Borrelia anserina in Argas persicus (Acari: Argasidae) ticks collected from Lorestan province, west of Iran
Figure 4. The phylogenetic tree inferred from flaB nucleotide sequence data of B. anserina (clade I) and other Borrelia taxa (clade II and KX171816) constructed using Neighbor-Joining (NJ) method with bootstrap test (1000 replicates). The main clade in right side of tree separated with colored rectangular shape. Taxa are as species name following GenBank accession number, taxon of the present study indicated as bold. Nodes indicated with bootstrap value. Branch lengths are proportional to evolutionary changes, the units of the number of base substitutions per site the units of the number of amino acid substitutions per site. The analysis involved 12 nucleotide sequences. All positions containing gaps and missing data were eliminated. There were a total of 500 positions in the final dataset. The more diverged Pakistani strain of B. anserina (JF693808) located inside the main B. anserina (clade I). The members of clade II and B. hermsii are as outgroup.
Fig. 3 in Seroprevalence of Borrelia burgdorferi antibodies in white-tailed deer from Texas
Fig. 3. Assays used to demonstrate reactivity to Borrelia burgdorferi antigens in white-tailed deer serum samples. (A.) The molecular weight marker (Mk) showing estimated molecular weights of Borrelia antigens (Bb). (B.) From left to right, negative control samples (1—5) and samples highly sero-reactive (6—12). The three immunoassays used were ELISA, standardized western immunoblot (WB) and Marblot (MB) assays.
Fig. 2 in Seroprevalence of Borrelia burgdorferi antibodies in white-tailed deer from Texas
Fig. 2. Optical density values of the white-tailed deer (WTD) serum samples analyzed with indirect ELISA for Borrelia burgdorferi. (A.) ELISA data from 109 WTD serum samples used as negative controls, collected from 2003 to 2015. (B.) ELISA data from 1384 WTD serum samples collected from 2001 to 2013. The dashed line denotes the cut off value used in this study. The samples above this line were analyzed with standardized western immunoblot assay.
Fig. 4 in Seroprevalence of Borrelia burgdorferi antibodies in white-tailed deer from Texas
Fig. 4. Confirmed human Lyme Disease cases in Texas from 2000 to 2013 reported to the CDC (www.cdc.com).
Fig. 5 in Seroprevalence of Borrelia burgdorferi antibodies in white-tailed deer from Texas
Fig. 5. White-tailed deer (WTD) population density in Texas eco-regions from 2005 to 2013. This graph is a representation of WTD population density statewide in Texas; in two counties (Travis and Williamson) where sero-reactive samples, and negative control samples for Borrelia burgdorferi antibodies were found.
Fig. 1. Texas map showing 14 in Seroprevalence of Borrelia burgdorferi antibodies in white-tailed deer from Texas
Fig. 1. Texas map showing 14 counties in which white-tailed deer (WTD) were sampled for Borrelia burgdorferi antibodies from 2001 to 2015. Blue counties: samples negative by ELISA and standardized western immunoblot; Gray counties: negative control samples; Yellow counties: samples sero-reactive by standardized western immunoblot assay (Travis and Williamson counties). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
Fig. 2 in Prevalence of Borrelia burgdorferi sensu lato and Borrelia miyamotoi in ixodid ticks in the Far East of Russia
Fig. 2. Phylogenetic analysis of the nucleotide sequences of Borrelia 16S rRNA gene fragment of 733 bp long (A) and 5S‾23S ITS of 211–218 bp long (B) using Mega 6.06 software, UPGMA algorithm and 1,000 replications. Phylogenetic trees constructed by means of 5 alternative algorithms (Maximum likelihood, NeighborJoining, Minimum-Evolution, UPGMA and Maximum Parsimony) show similar topologies and reasonable bootstrap support. Nucleotide sequences of Borrelia isolates determined in our study are shown in bold. The number of identical sequences of Borrelia isolates determined in these ixodid ticks is shown in parentheses. Branches corresponding to the reference strains are underlined.
Fig. 1 in Borrelia miyamotoi infection in Apodemus spp. mice populating an urban habitat (Warsaw, Poland)
Fig. 1. Scheme of the study area (city of Warsaw, Poland) showing the arrangement of mice-trapping locations. Black points – locations where B. miyamotoi infected mice were present; White points – locations where none of the captured mice were B. miyamotoi infected; N1–N3 – locations within northern suburbs; C1–C5 - locations within city centre; S1–S2 – locations within southern suburbs; numbers in boxes – B. miyamotoi prevalence in mice inhabiting respective areas.
Sand lizards (Lacerta agilis) decrease nymphal infection prevalence for tick-borne pathogens Borrelia burgdorferi sensu lato and Anaplasma phagocytophilum in a coastal dune ecosystem
<p>1. Understanding which factors determine tick-borne disease hazard can contribute to effective disease control. In Europe, the hazard of the pathogens <em>Borrelia burgdorferi</em> s.l. and <em>Anaplasma phagocytophilum</em> is determined by local tick densities (mainly <em>Ixodes ricinus</em>) and the reservoir competence of the host species community. Sand lizards (<em>Lacerta agilis</em>) are common hosts for larvae and nymphs of <em>I. ricinus</em> and non-competent reservoirs for both pathogens. Consequently, high relative abundance of <em>L. agilis</em> is hypothesized to be associated with lower infection prevalence in nymphs. Here, we aimed to test whether this effectively occurs in natural settings.</p> <p>2. We sampled different habitat types within a heterogenous dune landscape at the Dutch coast and estimated 1) <em>L. agilis</em> densities, 2) host community competence, 3) the density and infection prevalence of questing<em> I. ricinus</em> ticks, and 4) the number and infection prevalence of ticks feeding on <em>L. agilis</em>.</p> <p>3. Captured <em>L. agilis</em> had high tick burdens and contributed substantially to feeding <em>I. ricinus</em> larvae in their natural habitat. <em>B. burgdorferi</em> s.l. and <em>A. phagocytophilum</em> were virtually absent from feeding larvae and nymphs.</p> <p>4. The nymphal infection prevalence of both pathogens in questing ticks was lower in habitat types where <em>L. agilis</em> was more abundant. Hence, <em>L. agilis</em> strongly reduced community competence.</p> <p>5. The density of questing nymphs was higher in habitat types with denser vegetation and also varied more between habitat types than infection prevalence. As a result, nymphal density had a stronger effect on the density of infected ticks than did nymphal infection prevalence.</p> <p>6. Synthesis and applications. Coastal dune habitats favourable for <em>L. agilis</em> have lower densities of questing nymphs, and a lower human infection hazard. These results might be applicable to similar ecosystems where <em>L. agilis</em> is present. From a public health perspective, this underlines the importance of preserving early successional habitat, as encroaching shrubs are associated with higher tick-borne disease hazard, and vegetation removal might be a solution to reduce hazard in coastal dunes. The high degree of spatial heterogeneity in the abundance of tick-borne pathogens also poses opportunities to manage recreational activities to limit human exposure to tick-borne diseases.</p>
Ecological interactions driving population dynamics of two tick-borne pathogens, Borrelia burgdorferi and Babesia microti
<p><em>Borrelia</em> <em>burgdorferi</em> (<em>Bb</em>) and <em>Babesia</em> <em>microti</em> (<em>Bm</em>) are vector-borne zoonotic pathogens commonly found co-circulating in <em>Ixodes</em> <em>scapularis</em> and <em>Peromyscus</em> <em>leucopus</em> populations. The restricted distribution and lower prevalence of <em>Bm</em> has been historically attributed to lower host-to-tick transmission efficiency and limited host ranges. We hypothesized that prevalence patterns are driven by coinfection dynamics and vertical transmission. We use a multi-year, multiple-location, longitudinal dataset with mathematical modelling to elucidate coinfection dynamics between <em>Bb</em> and <em>Bm</em> in natural populations of <em>P. leucopus</em>, the most competent reservoir host for both pathogens in the eastern USA. Our analysis indicates that, in the absence of vertical transmission, <em>Bb</em> is viable at lower tick numbers than <em>Bm</em>. However, with vertical transmission, Bm is viable at lower tick numbers than <em>Bb</em>. Vertical transmission has a particularly strong effect on <em>Bm</em> prevalence early in the active season while coinfection has an increasing role during the nymphal peak. Our analyses indicate that coinfection processes, such as facilitation of <em>Bm</em> infection by <em>Bb</em>, have relatively little influence on the persistence of either parasite. We suggest future work examines the sensitivity of <em>Bm</em> vertical transmission and other key processes to local environmental conditions to inform surveillance and control of tick-borne pathogens.</p>
Ecological interactions driving population dynamics of two tick-borne pathogens, Borrelia burgdorferi and Babesia microti
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Sand lizards (Lacerta agilis) decrease nymphal infection prevalence for tick-borne pathogens Borrelia burgdorferi sensu lato and Anaplasma phagocytophilum in a coastal dune ecosystem
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Data from: Comparison of spleen transcriptomes of two wild rodent species reveals differences in the immune response against Borrelia afzelii
<p>Different host species often differ considerably in susceptibility to a given pathogen, but the causes of such differences are rarely known. The natural hosts of the tick-transmitted bacterium <i>Borrelia afzelii</i>, which is one of causative agents of Lyme borreliosis in humans, include a variety of small mammals like voles and mice. Previous studies have shown that <i>B. afzelii-</i>infected bank voles (<i>Myodes glareolus</i>) have about ten times higher bacterial load than infected yellow-necked mice (<i>Apodemus flavicollis</i>), indicating that these two species differ in resistance. In this study, we compared the immune response to <i>B. afzelii </i>infection in these host species by using RNA-sequencing to quantify gene expression in spleen. Gene set enrichment analysis (GSEA) showed that several immune pathways were down-regulated in infected animals in both bank voles and yellow-necked mice. Moreover, IFNα response was up-regulated in <i>B. afzelii</i>-infected yellow-necked mice, while IL6 signaling and the complement pathway were down-regulated in infected bank voles; differences in regulation of these three pathways between bank voles and yellow-necked mice could thus contribute to the difference in resistance to <i>B. afzelii</i> between the species. This study provides knowledge of gene expression induced by a zoonotic pathogen in its natural host, and possible species-specific regulation of immune responses associated with resistance.</p>
Combining GWAS and FST-based approaches to identify targets of Borrelia-mediated selection in natural rodent hosts
Recent advances in high-throughput sequencing technologies provide opportunities to gain novel insights into the genetic basis of phenotypic trait variation. Yet to date, progress in our understanding of genotype-phenotype associations in non-model organisms in general and natural vertebrate populations in particular has been hampered by small sample sizes typically available for wildlife populations and a resulting lack of statistical power, as well as a limited ability to control for false positive signals. Here we propose to combine a genome-wide association (GWAS) and FST-based approach with population-level replication to partly overcome these limitations. We present a case study in which we used this approach in combination with Genotyping-by-Sequencing (GBS) SNP data to identify genomic regions associated with Borrelia afzelii resistance or susceptibility in the natural rodent host of this Lyme disease-causing spirochete, the bank vole (Myodes glareolus). Using this combined approach we identified four consensus SNPs located in exonic regions of the genes Slc26a4, Tns3, Wscd1 and Espnl, which were significantly associated with the voles' Borrelia infectious status within and across populations. Functional links between host responses to bacterial infections and most of these genes have previously been demonstrated in other rodent systems, making them promising new candidates for the study of evolutionary host responses to Borrelia emergence. Our approach is applicable to other systems and may facilitate the identification of genetic variants underlying disease resistance or susceptibility, as well as other ecologically relevant traits, in wildlife populations.
Diversity and host specificity of Borrelia burgdorferi's outer surface protein C (ospC) alleles in synanthropic mammals, with a notable ospC allele U absence from mixed infections
<p>Interactions among pathogen genotypes that vary in host specificity may affect overall transmission dynamics in multi-host systems. <em>Borrelia burgdorferi</em>, a bacterium that causes Lyme disease, is typically transmitted among wildlife by <em>Ixodes</em> ticks. Despite the existence of many alleles of <em>B. burgdorferi</em>'s <em>sensu stricto</em> outer surface protein C (<em>ospC</em>) gene, most human infections are caused by a small number of <em>ospC</em> alleles ["human infectious alleles" (HIAs)], suggesting variation in host specificity associated with <em>ospC</em>. To characterize the wildlife host association of <em>B. burgdorferi</em>'s <em>ospC</em> alleles, we used metagenomics to sequence <em>ospC</em> alleles from 68 infected individuals belonging to eight mammalian species trapped at three sites in suburban New Brunswick, New Jersey (USA). We found that multiple allele ("mixed") infections were common. HIAs were most common in mice (<em>Peromyscus</em> spp.) and only one HIA was detected at a site where mice were rarely captured. <em>OspC </em>allele U was exclusively found in chipmunks (<em>Tamias striatus</em>), and although a significant number of different alleles were observed in chipmunks, including HIAs, allele U never co-occurred with other alleles in mixed infections. Our results suggest that allele U may be excluding other alleles, thereby reducing the capacity of chipmunks to act as reservoirs for HIAs.</p>
Antibodies to Borrelia burgdorferi and Bartonella species in serum and synovial fluid from people with rheumatic diseases
<p>Vector-borne infections may underlie some rheumatic diseases, particularly in people with joint effusions. The aim of this study was to compare serum and synovial fluid antibodies to<em> B. burgdorferi </em>and <em>Bartonella </em>spp. in patients with rheumatic diseases.</p> <p>This observational, cross-sectional study examined paired synovial fluid and serum specimens collected from 110 patients with joint effusion between October 2017 and January 2022. Testing for antibodies to <em>B. burgdorferi </em>(using CDC criteria) and <em>Bartonella </em>spp. via two Indirect Fluorescent Antibody [IFA] assays, was performed as part of routine patient care.</p> <p>There were 30 participants (27%) with positive two-tier <em>B. burgdorferi</em> serology, and 26 participants (24%) with IFA seroreactivity (≥1:256) to <em>B. henselae </em>and/or <em>B. quintana. </em>Both <em>B. burgdorferi</em> IgM and IgG were detected more frequently in synovial fluid than serum: 27% of patients were either IgM or IgG positive in synovial fluid, compared to 15.5% in serum (p = 0.048). Conversely, <em>B. henselae </em>and <em>B. quintana </em>antibodies were detected more frequently in serum than synovial fluid; overall only 2% of patients had positive IFA titers in synovial fluid, compared to 24% who had positive IFA titers in serum (p <0.001). There were no significant associations between <em>B. burgdorferi</em> or <em>Bartonella</em> spp. seroreactivity with any of the clinical rheumatological diagnoses.</p> <p>This study provides preliminary support for the importance of synovial fluid antibody testing for documenting exposure to <em>B. burgdorferi</em>, but not for documenting exposure to <em>Bartonella </em>spp.</p>
MHC class II genotype-by-pathogen genotype interaction for infection prevalence in a natural rodent-Borrelia system
<p><span>MHC genes are extraordinarily polymorphic in most taxa. Host-pathogen coevolution driven by negative frequency-dependent selection (NFDS) is one of the main hypotheses for the maintenance of such immunogenetic variation. Here we test a critical but rarely tested assumption of this hypothesis—that MHC alleles affect resistance/susceptibility to a pathogen in a strain-specific way, i.e. that there is a host genotype-by-pathogen genotype interaction. </span><span>In a field study of bank voles naturally infected with the tick-transmitted bacterium </span><em><span>Borrelia afzelii</span></em><span>, we tested for MHC class II (</span><em><span>DQB</span></em><span>) genotype-by-</span><span><em>B. afzelii</em> </span><span>strain interactions for infection prevalence between ten </span><em><span>DQB</span></em><span><em> </em>alleles and seven strains. One allele (<em>DQB</em>*37) showed an interaction</span><span>, </span><span>such that voles carrying <em>DQB</em>*37 had higher prevalence of two strains and lower prevalence of one strain than individuals without the allele. These findings were corroborated by analyses of strain composition of infections, which revealed an effect of <em>DQB</em>*37 in the form of lower </span><span>b</span><span> diversity among infections in voles carrying the allele. Taken together, these results provide rare support at the molecular genetic level for a key assumption of models of antagonistic coevolution through NFDS. </span></p>
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