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1 , another spirochete pathogen and a cause of relapsing fever.
2 ered species is a causal agent of tick-borne relapsing fever.
3 sis, and B. hermsii, the agent of tick-borne relapsing fever.
4 rrelia recurrentis, the agent of louse-borne relapsing fever.
5 of several spirochete species that can cause relapsing fever.
6 s of pathogenesis and immunity of tick-borne relapsing fever.
7 rsistence of Lyme borreliosis and tick-borne relapsing fever.
8 mission and pathogenesis of Lyme disease and relapsing fever.
9 of mammalian hosts, causing Lyme disease and relapsing fever.
10 oles in the pathogenesis of Lyme disease and relapsing fever.
11 lia species associated with Lyme disease and relapsing fever.
15 proteins: VspB of B. turicatae, Vsp26 of the relapsing fever agent Borrelia hermsii, and OspC of the
16 deficiency (scid mice) and infected with the relapsing fever agent Borrelia turicatae develop manifes
20 ent mice infected with Borrelia turicatae, a relapsing fever agent, have a disorder that resembles di
21 e vector-borne bacterium Borrelia hermsii, a relapsing fever agent, switches gene expression of a sur
22 smids 180 and 170 kb in size, present in the relapsing fever agents B. hermsii and B. turicatae but n
23 llow serological confirmation of louse-borne relapsing fever and determination of disease prevalence.
24 anism previously isolated from patients with relapsing fever and from ticks in Spain that is designat
26 ochetes and help clarify the distribution of relapsing fever and Lyme disease in situations in which
28 ologic disease manifestations develop during relapsing fever and that T cells play a critical role in
29 persistent infections, such as anaplasmosis, relapsing fever, and sleeping sickness, remains untested
36 e that some Borrelia species associated with relapsing fever bind fH, but not those associated with a
37 burgdorferi, the agent of Lyme disease, and relapsing fever Borrelia in the absence of complement.
38 udies have shown that antigenic variation in relapsing fever Borrelia not only permits the evasion of
39 stigated during the course of infection of a relapsing fever Borrelia species in plasminogen-deficien
42 ular and linear plasmids of Lyme disease and relapsing fever Borrelia spirochetes carry genes for mem
44 e for the PAS in heart and brain invasion by relapsing fever Borrelia, resulting in organ injury.
45 endent bactericidal monoclonal IgM against a relapsing fever Borrelia, was constructed to investigate
51 The Lyme disease (Borrelia burgdorferi) and relapsing-fever (Borrelia hispanica) agents have distinc
55 We conclude that persistent infection with relapsing fever borrelias causes significant loss of car
57 nificant injury during experimental Lyme and relapsing fever borreliosis when the immune response is
59 pathogen load, as during peak bacteremia in relapsing fever borreliosis, IL-10 protects innate immun
61 (JHR) observed after antibiotic treatment of relapsing fever caused by Borrelia recurrentis is associ
65 on, whereas the role of adaptive immunity to relapsing fever-causing spirochetes is well documented,
66 k of disease caused by tick- and louse-borne relapsing fever due to Borrelia infection is cyclic febr
69 s, pentoxifylline treatment of patients with relapsing fever fails to prevent or diminish JHR or the
71 confirmed the presence of these genes in the relapsing fever group of spirochetes but not in B. burgd
72 B. lonestari is more closely related to the relapsing fever group spirochetes than to borreliae that
74 the Western Front reported on a soldier with relapsing fever, headache, dizziness, lumbago, and shin
75 as a human pathogen causing hard tick-borne relapsing fever (HTBRF) across the Northern Hemisphere.
76 Abs are protective against Lyme disease and relapsing fever, illnesses caused by Borrelia spirochete
78 relia hermsii, a spirochaete responsible for relapsing fever in humans, grows to high density in the
80 ations for understanding the epidemiology of relapsing fever in North America and can be applied to t
82 hermsii, an etiological agent of tick-borne relapsing fever in North America, binds host-derived ser
83 the primary etiological agent of tick-borne relapsing fever in North America, binds the complement r
89 se findings suggest that thrombocytopenia of relapsing fever is the result of platelet clearance afte
91 era from individuals with syphilis (n = 43), relapsing fever (n = 8), Lyme disease (n = 8), and lepto
95 e propose to use strain SP1, isolated from a relapsing fever patient in 1994 in southern Spain, as th
99 that Borrelia hermsii, a causative agent of relapsing fever, produces a factor H (FH) and FH-like pr
101 aracterize surface proteins expressed by the relapsing fever (RF) agent Borrelia hermsii in the blood
102 orthologous thymidylate synthase gene in the relapsing fever (RF) agent Borrelia hermsii, located it
106 ement is common in the spirochetal infection relapsing fever (RF) in both humans and experimental ani
114 previously described BBK32-like proteins in relapsing fever species, indicates that BHA007 is a memb
115 arly after infection, Borrelia crocidurae, a relapsing fever species, induced a striking loss of marg
119 esponse and contribute to the ability of the relapsing fever spirochaetes to achieve high cell densit
123 ein and enzymatic activity were found in all relapsing fever spirochaetes, but not in Lyme disease or
126 cA of B. burgdorferi, as well as RecA of the relapsing fever spirochete Borrelia hermsii and the free
130 ed with serotype A but not serotype B of the relapsing fever spirochete Borrelia turicatae, early inv
131 the Borrelia parkeri-B. turicatae tick-borne relapsing fever spirochete group with a late-term aborti
134 ted the polyclonal IgM Ab response against a relapsing fever spirochete to determine the specificity
139 urgdorferi sensu stricto strain CA4, and the relapsing-fever spirochete B. parkeri (undesignated).
140 ed characterization of the Bdr proteins in a relapsing-fever spirochete species, enhancing our unders
143 n will identify people exposed previously to relapsing fever spirochetes and help clarify the distrib
144 standing of the pathogenic mechanisms of the relapsing fever spirochetes and of the molecular nature
145 ay be involved in the pathogenicity of these relapsing fever spirochetes and provide a mechanism for
146 , and Borrelia afzelii strains as well as in relapsing fever spirochetes Borrelia hermsii and Borreli
148 infected with B. hermsii or other species of relapsing fever spirochetes contained antibodies recogni
150 s complete pathway for purine salvage in the relapsing fever spirochetes may contribute, in part, to
151 poproteins are serotype-defining antigens of relapsing fever spirochetes that undergo multiphasic ant
152 poproteins are serotype-defining antigens of relapsing fever spirochetes that undergo multiphasic ant
161 losely related sequence) is multicopy in the relapsing-fever spirochetes and is carried on variably s
162 s of borreliae demonstrated GlpQ activity in relapsing-fever spirochetes but not in Lyme disease spir
163 hern blots demonstrated glpQ and glpT in all relapsing-fever spirochetes but not in the Lyme disease
164 zation of a gene from B. turicatae and other relapsing-fever spirochetes that exhibits homology with
172 a relapse followed febrile illness caused by relapsing fever, trench fever, epidemic typhus, and Malt
174 chaetes, although similar in sequence to the relapsing fever vlp genes, has evolved a completely diff
176 Borrelia hermsii, an agent of tick-borne relapsing fever, was found to contain multiple circular
177 To develop a specific serological test for relapsing fever, we created a genomic DNA library of B.
179 s obtained from 42 patients with louse-borne relapsing fever were tested with an indirect immunofluor
180 Borrelia hermsii, agents of Lyme disease and relapsing fever, were examined by epifluorescence micros
181 ination of spirochetemia in murine models of relapsing fever, without the assistance of complement.
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