scholarly journals Variable Tick Protein in Two Genomic Groups of the Relapsing Fever Spirochete Borrelia hermsii in Western North America

2005 ◽  
Vol 73 (10) ◽  
pp. 6647-6658 ◽  
Author(s):  
Stephen F. Porcella ◽  
Sandra J. Raffel ◽  
Donald E. Anderson ◽  
Stacey D. Gilk ◽  
James L. Bono ◽  
...  
Keyword(s):  
North America ◽  
Outer Surface ◽  
Surface Protein ◽  
Relapsing Fever ◽  
Gene Encoding ◽  
Borrelia Hermsii ◽  
Tick Vector ◽  
Tick Transmission ◽  
Sequence Relatedness ◽  
Variable Major Proteins

ABSTRACT Borrelia hermsii is the primary cause of tick-borne relapsing fever in North America. When its tick vector, Ornithodoros hermsi, acquires these spirochetes from the blood of an infected mammal, the bacteria switch their outer surface from one of many bloodstream variable major proteins (Vmps) to a unique protein, Vtp (Vsp33). Vtp may be critical for successful tick transmission of B. hermsii; however, the gene encoding this protein has been described previously in only one isolate. Here we identified and sequenced the vtp gene in 31 isolates of B. hermsii collected over 40 years from localities throughout much of its known geographic distribution. Seven major Vtp types were found. Little or no sequence variation existed within types, but between them significant variation was observed, similar to the pattern of diversity described for the outer surface protein C (OspC) gene in Lyme disease spirochetes. The pattern of sequence relatedness among the Vtp types was incongruent in two branches compared to two genomic groups identified among the isolates by multilocus sequence typing of the 16S rRNA, flaB, gyrB, and glpQ genes. Therefore, both horizontal transfer and recombination within and between the two genomic groups were responsible for some of the variation observed in the vtp gene. O. hermsi ticks were capable of transmitting spirochetes in the newly identified genomic group. Therefore, given the longevity of the tick vector and persistent infection of spirochetes in ticks, these arthropods rather than mammals may be the likely host where the exchange of spirochetal DNA occurs.

scholarly journals Does Host Complement Kill Borrelia burgdorferi within Ticks?

2003 ◽  
Vol 71 (2) ◽  
pp. 822-829 ◽  
Author(s):  
Sivaprakash Rathinavelu ◽  
Anne Broadwater ◽  
Aravinda M. de Silva
Keyword(s):  
Lyme Disease ◽  
Borrelia Burgdorferi ◽  
Outer Surface ◽  
Protein A ◽  
Surface Protein ◽  
Block Transmission ◽  
Outer Surface Protein A ◽  
Tick Vector ◽  
Host Blood ◽  
Transmission Blocking Vaccine

ABSTRACT The Lyme disease spirochete, Borrelia burgdorferi, inhabits the gut lumen of the tick vector. At this location the spirochete is exposed to host blood when a tick feeds. We report here on studies that were done with normal and complement-deficient (C3-knockout) mice to determine if the host complement system killed spirochetes within the vector. We found that spirochete numbers within feeding nymphs were not influenced by complement, most likely because host complement was inactivated within the vector. The Lyme disease outer surface protein A (OspA) vaccine is a transmission-blocking vaccine that targets spirochetes in the vector. In experiments with mice hyperimmunized with OspA, complement was not required to kill spirochetes within nymphs and to block transmission from nymphs to the vaccinated host. However, host complement did enhance the ability of OspA antibody to block larvae from acquiring spirochetes. Thus, the effects of OspA antibody on nymphal transmission and larval acquisition appear to be based on different mechanisms.

scholarly journals Isolation and genetic characterization of a relapsing fever spirochete isolated from Ornithodoros puertoricensis collected in central Panama

2021 ◽  
Vol 15 (8) ◽  
pp. e0009642
Author(s):  
Sergio E. Bermúdez ◽  
Brittany A. Armstrong ◽  
Lillian Domínguez ◽  
Aparna Krishnavajhala ◽  
Alexander R. Kneubehl ◽  
...  
Keyword(s):  
Latin America ◽  
North America ◽  
Central America ◽  
Human Disease ◽  
Genetic Characterization ◽  
Relapsing Fever ◽  
Tick Vector ◽  
The City ◽  
Central Panama

Tick-borne relapsing fever (TBRF) spirochetes are likely an overlooked cause of disease in Latin America. In Panama, the pathogens were first reported to cause human disease in the early 1900s. Recent collections of Ornithodoros puertoricensis from human dwellings in Panama prompted our interest to determine whether spirochetes still circulate in the country. Ornithodoros puertoricensis ticks were collected at field sites around the City of Panama. In the laboratory, the ticks were determined to be infected with TBRF spirochetes by transmission to mice, and we report the laboratory isolation and genetic characterization of a species of TBRF spirochete from Panama. Since this was the first isolation of a species of TBRF spirochete from Central America, we propose to designate the bacteria as Borrelia puertoricensis sp. nov. This is consistent with TBRF spirochete species nomenclature from North America that are designated after their tick vector. These findings warrant further investigations to assess the threat B. puertoricensis sp. nov. may impose on human health.

scholarly journals The Spirochete Borrelia crociduraeCauses Erythrocyte Rosetting during Relapsing Fever

1998 ◽  
Vol 66 (2) ◽  
pp. 815-819 ◽  
Author(s):  
Nils Burman ◽  
Alireza Shamaei-Tousi ◽  
Sven Bergström
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Antibody Response ◽  
Immune Evasion ◽  
Antigenic Variation ◽  
Erythrocyte Aggregation ◽  
Phagocytic Cells ◽  
Relapsing Fever ◽  
Borrelia Hermsii ◽  
Variable Major Proteins

ABSTRACT Several species of the genus Borrelia exhibit antigenic variation of variable major proteins on their surface during relapsing fever. We have investigated the African relapsing fever speciesBorrelia crocidurae during infections in mice and compared it with the thoroughly studied North American species Borrelia hermsii. A major difference between the two species is thatB. crocidurae can bind and become completely covered with erythrocytes. In addition, B. crocidurae causes a prolonged spirochetemia which coincides with a delayed appearance of antiborrelial antibodies. We show that the antibody response against an unrelated antigen is not delayed and that antibiotic treatment, which dissociates rosettes and inhibits the spirochetes, also leads to an early antibody response. Taken together, the erythrocyte aggregation and prolonged spirochetemia hint at a new mode of immune evasion where erythrocyte-covered spirochetes may avoid contact with the phagocytic cells and B cells of the immune system, thereby delaying the onset of a specific immune response.

scholarly journals Identification and Characterization of a Linear-Plasmid-Encoded Factor H-Binding Protein (FhbA) of the Relapsing Fever Spirochete Borrelia hermsii

2004 ◽  
Vol 186 (9) ◽  
pp. 2612-2618 ◽  
Author(s):  
Kelley M. Hovis ◽  
John V. McDowell ◽  
LaToya Griffin ◽  
Richard T. Marconi
Keyword(s):  
Molecular Mechanisms ◽  
Binding Protein ◽  
Genetic Locus ◽  
Factor H ◽  
Linear Plasmid ◽  
Relapsing Fever ◽  
Gene Encoding ◽  
Borrelia Hermsii ◽  
Identification And Characterization

ABSTRACT In North America, tick-borne relapsing fever (TBRF) is caused by the spirochete species Borrelia hermsii, Borrelia parkeri, and Borrelia turicatae. We previously demonstrated that some isolates of B. hermsii and B. parkeri are capable of binding factor H and that cell-bound factor H can participate in the factor I-mediated cleavage of C3b. Isolates that bound factor H expressed a factor H-binding protein (FHBP) that we estimated to be approximately 19 to 20 kDa in size and thus, pending further characterization, temporarily designated FHBP19. Until this report, none of the FHBPs of the TBRF spirochetes had been characterized. Here we have recovered the gene encoding the FHBP of B. hermsii YOR from a lambda ZAP II library and determined its sequence. The gene encodes a full-length protein of 22.7 kDa, which after processing is predicted to be 20.5 kDa. This protein, which we redesignate factor H-binding protein A (FhbA), is unique to B. hermsii. Two-dimensional pulsed-field gel electrophoresis and hybridization analyses revealed that the B. hermsii gene encoding FhbA is a single genetic locus that maps to a linear plasmid of approximately 220 kb. The general properties of FhbA were also assessed. The protein was found to be surface exposed and lipidated. Analysis of the antibody response to FhbA in infected mice revealed that it is antigenic during infection, indicating expression during infection. The identification and characterization of FhbA provides further insight into the molecular mechanisms of pathogenesis of the relapsing fever spirochetes.

scholarly journals Surface Protein Variation by Expression Site Switching in the Relapsing Fever Agent Borrelia hermsii

2000 ◽  
Vol 68 (12) ◽  
pp. 7114-7121 ◽  
Author(s):  
Alan G. Barbour ◽  
Carol J. Carter ◽  
Charles D. Sohaskey
Keyword(s):  
Membrane Protein ◽  
Antigenic Variation ◽  
Surface Protein ◽  
Relapsing Fever ◽  
Borrelia Hermsii ◽  
Immunodeficient Mice ◽  
Major Surface Protein ◽  
Protein Variation ◽  
Expression Site ◽  
Major Surface

ABSTRACT Borrelia hermsii, an agent of relapsing fever, undergoes antigenic variation of serotype-specifying membrane proteins during mammalian infections. When B. hermsii is cultivated in broth medium, one serotype, 33, eventually predominates in the population. Serotype 33 has also been found to be dominant in ticks but not in mammalian hosts. We investigated the biology and genetics of two independently derived clonal populations of serotype 33 of B. hermsii. Both isolates infected immunodeficient mice, but serotype 33 cells were limited in number and were only transiently present in the blood. Probes for vsp33, which encodes the serotype-specifying Vsp33 outer membrane protein, revealed that the gene was located on a 53-kb linear plasmid and that there was only one locus for the gene in serotype 33. The vsp33 probe and probes for other variable membrane protein genes showed that expression of Vsp33 was determined at the level of transcription and that when thevsp33 expression site was active, an expression site for other variable proteins was silent. The study confirmed that serotype 33 is distinct from other serotypes of B. hermsii in its biology and demonstrated that B. hermsii can change its major surface protein through switching between two expression sites.

Transmission Of Borreua Hermsii, The Agent Of Relapsing Fever, By The Tick Vector Ornithodoros Hermsi

1999 ◽  
Vol 5 (S2) ◽  
pp. 1220-1221
Author(s):  
Elizabeth R. Fischer ◽  
Tom G. Schwan
Keyword(s):  
Salivary Glands ◽  
Soft Tick ◽  
Relapsing Fever ◽  
Tick Feeding ◽  
Infected Tick ◽  
Borrelia Hermsii ◽  
Tick Vector ◽  
Functional Relationships ◽  
Ornithodoros Hermsi ◽  
Tick Midgut

Relapsing fever, a disease characterized by recurrent episodes of high fevers, is caused by geographically distinct spirochetes of the genus Borrelia,transmitted by ticks of the genus Ornithodoros. In the Northwestern United States, the soft tick Ornithodoros hermsi has been identified as the vector for the spirochete Borrelia hermsii. The life cycle of O.hermsi includes larval and multiple nymphal stages prior to full maturation into an adult male or female (Fig.1). Progression into each stage requires a blood-meal typically provided by squirrels and chipmunks, and incidentally humans. Feeding is rapid, lasting 10-60 minutes, and during this time an infected tick can transmit the agent of relapsing fever, B. hermsii. Following ingestion, spirochetes are initially found in the tick midgut. Within 1-3 weeks, they are found in other organs, including the central ganglion and salivary glands. Since saliva is the primary mode of transmission of these bacteria during tick feeding, we assessed by electron microscopy the structural and functional relationships between the spirochetes and the salivary glands.

scholarly journals A Novel Surface Antigen of Relapsing Fever Spirochetes Can Discriminate between Relapsing Fever and Lyme Borreliosis

2010 ◽  
Vol 17 (4) ◽  
pp. 564-571 ◽  
Author(s):  
Job E. Lopez ◽  
Merry E. Schrumpf ◽  
Vijayaraj Nagarajan ◽  
Sandra J. Raffel ◽  
Brandi N. McCoy ◽  
...  
Keyword(s):  
North America ◽  
Recombinant Protein ◽  
Protein A ◽  
Hypothetical Protein ◽  
Western North America ◽  
Immunogenic Protein ◽  
Relapsing Fever ◽  
Serum Samples ◽  
Borrelia Hermsii ◽  
Protein Serum

ABSTRACT In a previous immunoproteome analysis of Borrelia hermsii, candidate antigens that bound IgM antibodies from mice and patients infected with relapsing fever spirochetes were identified. One candidate that was identified is a hypothetical protein with a molecular mass of 57 kDa that we have designated Borrelia immunogenic protein A (BipA). This protein was further investigated as a potential diagnostic antigen for B. hermsii given that it is absent from the Borrelia burgdorferi genome. The bipA locus was amplified and sequenced from 39 isolates of B. hermsii that had been acquired from western North America. bipA was also expressed as a recombinant fusion protein. Serum samples from mice and patients infected with B. hermsii or B. burgdorferi were used to confirm the immunogenicity of the recombinant protein in patients infected with relapsing fever spirochetes. Lastly, in silico and experimental analysis indicated that BipA is a surface-exposed lipoprotein in B. hermsii. These findings enhance the capabilities of diagnosing infection with relapsing fever spirochetes.

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