ライフサイエンスコーパス: Lyme disease

1 velopment of innate acute-phase responses in Lyme disease.

2 clinicians in diagnosing and treating early Lyme disease.

3 d be a risk factor for increased severity in Lyme disease.

4 a challenge for early proteomic detection of Lyme disease.

5 nically suffer from the tick-borne infection Lyme disease.

6 vice that specifically mentioned utility for Lyme disease.

7 n some patients with culture-confirmed early Lyme disease.

8 serum samples from three patients with acute Lyme disease.

9 that marketed nonantimicrobial therapies for Lyme disease.

10 tific studies evaluating such treatments for Lyme disease.

11 orrelia burgdorferi, the aetiologic agent of Lyme disease.

12 mericanum transmits any pathogen that causes Lyme disease.

13 has limited sensitivity for detecting early Lyme disease.

14 mmonly target patients who believe they have Lyme disease.

15 pital system in a region with little endemic Lyme disease.

16 s advertised to patients with a diagnosis of Lyme disease.

17 btained from patients with clinically likely Lyme disease.

18 ticks is correlated with a high incidence of Lyme disease.

19 esis or in syndromes compatible with chronic Lyme disease.

20 en an area of great interest in the field of Lyme disease.

21 gens like Borrelia burgdorferi, which causes Lyme disease.

22 Borrelia burgdorferi, the causative agent of Lyme disease.

23 Ixodes spp. ticks, is the causative agent of Lyme disease.

24 ctious symptoms in a subset of patients with Lyme disease.

25 e recommended for laboratory confirmation of Lyme disease.

26 responsible for the pathogenesis of chronic Lyme disease.

27 s is the first report of an association with Lyme disease.

28 ntially reduce the risk of human exposure to Lyme disease.

29 isease states that are often labeled chronic Lyme disease.

30 ive conventional antimicrobial treatment for Lyme disease.

31 nd the erythema migrans rash associated with Lyme disease.

32 ry infection, usually referred to as chronic Lyme disease.

33 orferi in patients who have been treated for Lyme disease.

34 dorferi sensu lato is the causative agent of Lyme disease.

35 tis in geographic areas that are endemic for Lyme disease.

36 d for HGA patients but not for patients with Lyme disease.

37 of the case patients may have had concurrent Lyme disease.

38 rmed HGA is a more severe illness than early Lyme disease.

39 igens, enabling a multiple vector sensor for Lyme disease.

40 e tissue damage and inflammation observed in Lyme disease.

41 ntation (P < 0.001) than patients with early Lyme disease.

42 ctors for Borrelia burgdorferi, the agent of Lyme disease.

43 n skin transcriptional response during early Lyme disease.

44 convenience sample of 62 patients with early Lyme disease.

45 infection cycle and reduce the incidences of Lyme disease.

46 omes of these polymorphisms in patients with Lyme disease.

47 outcomes were assessed in 248 patients with Lyme disease.

48 Borrelia burgdorferi, the causative agent of Lyme disease.

49 atment blood of 20 of 29 (69%) patients with Lyme disease.

50 useful in the laboratory diagnosis of early Lyme disease.

51 is has recently emerged in areas endemic for Lyme disease.

52 h a range of early to late manifestations of Lyme disease.

53 d be employed as preexposure prophylaxis for Lyme disease.

54 t in a patient with symptoms compatible with Lyme disease.

55 ) assay for the serologic diagnosis of human Lyme disease.

56 pediatric patients undergoing evaluation for Lyme disease.

57 ate intensity after antibiotic treatment for Lyme disease.

58 scores were other comorbidities unrelated to Lyme disease.

59 s scapularis, the same vector that transmits Lyme disease.

60 tools to improve the clinical management of Lyme disease.

61 ndard 2-tiered serology for the diagnosis of Lyme disease.

62 to diagnose extracutaneous manifestations of Lyme disease.

63 collected, 114 (12%) were from patients with Lyme disease.

64 erodiagnosis for the laboratory detection of Lyme disease.

65 al laboratory located in an area endemic for Lyme disease.

66 pathology associated with late disseminated Lyme disease (12 to 13 months after tick inoculation) in

67 rvical cancer $4.7 billion) even in the USA (Lyme disease $2.5 billion), where Chagas disease has not

68 e sclerosis (3 cases), sepsis (3 cases), and Lyme disease (2 cases).

69 fidence interval, 9%-28%) were found to have Lyme disease (6 with documented travel to endemic region

70 Borrelia burgdorferi, the etiologic agent of Lyme disease, adapts to the mammalian hosts by different

71 The Lyme disease agent, Borrelia burgdorferi, colonizes the

72 Borrelia burgdorferi, a Lyme disease agent, makes different major outer surface

73 life-history traits and transmission of the Lyme disease agent.

74 gnificantly more symptoms than patients with Lyme disease alone P < .05.

75 tients have more symptoms than patients with Lyme disease alone.

76 IA as a first-tier test for the diagnosis of Lyme disease and has been suggested as a stand-alone dia

77 of early to late objective manifestations of Lyme disease and in individuals with post-treatment Lyme

78 e useful in identification of early signs of Lyme disease and inflammatory responses; we used this in

79 select a biosignature for classifying early Lyme disease and non-Lyme disease patients.

80 ive on the evolution of serologic assays for Lyme disease and provides a summary of the performance c

81 ensitivity of xenodiagnosis in patients with Lyme disease and the significance of a positive result.

82 t the entities referred to as "posttreatment Lyme disease" and "chronic Lyme disease" may not actuall

83 e of interleukin 17 (IL-17) in patients with Lyme disease, and several murine studies have suggested

84 nd host, which is illustrated by bluetongue, Lyme disease, and West Nile virus, and it is also emergi

85 ) to use as a fast and accurate sensor for a Lyme disease antigen.

86 Borrelia burgdorferi, the causative agent of Lyme disease, are known or expected to contain multiple

87 uding immuno-PCR and metabolic profiling for Lyme disease, are outlined.

88 nical syndromes compatible with disseminated Lyme disease (arthritis, cranial neuropathy, or meningit

89 We defined a case of Lyme disease as either a clinician-diagnosed erythema mi

90 ollected sera from patients at all stages of Lyme disease, as well as healthy donors and patients wit

91 undergoing conventional 2-tiered testing for Lyme disease at a single hospital-based clinical laborat

92 , there is a need to improve diagnostics for Lyme disease at the early stage, when antibiotic treatme

93 using microfluidics to aid the diagnosis of Lyme disease at the point of care.

94 The Lyme disease bacterium, Borrelia burgdorferi, exemplifie

95 tly serve as the best experimental model for Lyme disease because of their close genetic homology wit

96 elia duttonii and B. recurrentis, but not in Lyme disease Borrelia species.

97 chpin in multiple aspects of infections with Lyme disease borrelia, providing a link between the micr

98 The Lyme disease (Borrelia burgdorferi) and relapsing-fever

99 The spirochetes that cause Lyme disease (Borrelia burgdorferi) and syphilis (Trepon

100 ible for several serious diseases, including Lyme disease (Borrelia burgdorferi), syphilis (Treponema

101 The causative agent of Lyme disease, Borrelia burgdorferi, possesses a segmente

102 ed in early localized and early disseminated Lyme disease but not in the later stages of active infec

103 r study period 4723 patients were tested for Lyme disease, but only 76 (1.6%) had positive results by

104 (ADCLS) patients-individuals diagnosed with Lyme disease by testing from private Lyme specialty labo

105 f-concept that metabolic profiling for early Lyme disease can achieve significantly greater (P < .000

106 subset of patients reporting a diagnosis of Lyme disease can be described as having alternatively di

107 Borrelia burgdorferi, the causative agent of Lyme disease, can be recovered from different organs of

108 se for neighborhood control recruitment in a Lyme disease case-control study in Connecticut during 20

109 Lyme disease, caused by Borrelia burgdorferi, is the mos

110 Lyme disease, caused by Borrelia burgdorferi, is the mos

111 Lyme disease, caused by the spirochete Borrelia burgdorf

112 for trafficking TLR2 purified ligands or the Lyme disease causing bacterium, Borrelia burgdorferi, to

113 in a blood meal from mice infected with the Lyme disease-causing bacteria Borrelia burgdorferi, lead

114 Phagocytosis of the Lyme disease-causing pathogen Borrelia burgdorferi has b

115 Borrelia burgdorferi, the agent of Lyme disease, codes for a single HtrA homolog.

116 relia burgdorferi, the spirochaetal agent of Lyme disease, codes for a single HtrA protein, HtrABb (B

117 Tick-borne diseases, such as Lyme disease, continue to increase, or, in the case of t

118 ack of an accurate laboratory test for early Lyme disease contributes to misconceptions about diagnos

119 The Lyme disease controversy can be largely linked to the mi

120 g possible mechanisms by which posttreatment Lyme disease could occur.

121 ific VlsE sequences with different phases of Lyme disease, demonstrating the potential use of detaile

122 ates suggest that patients treated for early Lyme disease develop protective immunity that is strain

123 ients with persistent symptoms attributed to Lyme disease--either related temporally to proven Lyme d

124 (QOL) measures in a cohort of patients with Lyme disease enrolled in a natural history study at the

125 of 100 subjects with culture-confirmed early Lyme disease enrolled in a prospective study with annual

126 sera from patients with both early and late Lyme disease establish that BbHtrA is expressed during h

127 This issue provides a clinical overview of Lyme disease, focusing on prevention, diagnosis, treatme

128 LDS in patients with culture-confirmed early Lyme disease followed for >10 years.

129 for studies of vector-borne disease, such as Lyme disease, for which risk is intrinsically linked to

130 at how HGA is defined in patients with early Lyme disease has an impact on the apparent rate of coinf

131 xicillin, and cefuroxime axetil for treating Lyme disease has been established in multiple trials.

132 of individual proteins during the course of Lyme disease has not been examined.

133 The laboratory mouse model of Lyme disease has revealed that Borrelia burgdorferi diff

134 relia burgdorferi, the bacterium that causes Lyme disease, has a unique segmented genome consisting o

135 Borrelia burgdorferi, the causative agent of Lyme disease, has three cheW homologues (cheW(1) , cheW(

136 e pathogenesis, ecology, and epidemiology of Lyme disease have been well described, and antimicrobial

137 the diagnosis, treatment, and prevention of Lyme disease, HGA, and babesiosis.

138 Lyme disease, human granulocytic anaplasmosis (HGA), and

139 is (Say), which vectors pathogens that cause Lyme disease, human granulocytic anaplasmosis, babesiosi

140 day course for treatment of early neurologic Lyme disease in ambulatory patients.

141 rse of oral doxycycline for early neurologic Lyme disease in ambulatory patients.

142 Case studies for heatwaves, Lyme disease in Canada, and Vibrio emergence in northern

143 M lesions from untreated adult patients with Lyme disease in comparison to controls.

144 eri sensu lato, of which three species cause Lyme disease in humans, originated from a rapid species

145 ectively predict the spatial distribution of Lyme disease in New York.

146 The causal agents of Lyme disease in North America, Borrelia burgdorferi and

147 current standard for laboratory diagnosis of Lyme disease in the United States is serologic detection

148 Borrelia burgdorferi, the causative agent of Lyme disease in the United States, is able to persist in

149 h Borrelia burgdorferi, the primary cause of Lyme disease in the United States.

150 In British Columbia, a setting with low Lyme disease incidence, ADCLS patients have a similar ph

151 atial correlation between deer abundance and Lyme disease incidence, but coyote abundance and fox rar

152 Many patients treated for early Lyme disease incur another infection in subsequent years

153 Lyme disease is a multisystemic disorder caused by Borre

154 commended laboratory diagnostic approach for Lyme disease is a standard two-tiered testing (STTT) alg

155 Control of Lyme disease is attributed predominantly to innate and a

156 Lyme disease is caused by spirochetes of the Borrelia bu

157 Lyme disease is diagnosed by 2-tiered serologic testing

158 Currently, diagnostic testing for Lyme disease is done by determination of the serologic r

159 here is no evidence to indicate that chronic Lyme disease is due to a persistent infection and that e

160 cause of disease, especially in sites where Lyme disease is endemic.

161 icacy of these unconventional treatments for Lyme disease is not supported by scientific evidence, an

162 ic symptoms in patients who were treated for Lyme disease is poorly understood, and the validity of r

163 mendation for the laboratory confirmation of Lyme disease is serology-based diagnostics.

164 most common clinical manifestation of early Lyme disease is the erythema migrans (EM) skin lesion th

165 Lyme disease is the most common vector-borne disease in

166 An enigmatic feature of Lyme disease is the slow resolution of musculoskeletal s

167 Lyme disease is transmitted by the bite of certain Ixode

168 Lyme disease is transmitted by the bite of the Ixodes sc

169 The mainstay of laboratory diagnosis for Lyme disease is two-tiered serological testing, in which

170 Borrelia burgdorferi, the causative agent of Lyme disease, is a highly motile spirochete, and motilit

171 elia burgdorferi, the spirochete that causes Lyme disease, is a tick-transmitted pathogen that requir

172 Borrelia burgdorferi, the causative agent of Lyme disease, is found within lymph nodes, causing rapid

173 Borrelia burgdorferi, the agent of Lyme disease, is maintained in nature within an enzootic

174 Borrelia burgdorferi, the causative agent of Lyme disease, is transmitted by the tick Ixodes scapular

175 elia burgdorferi, the spirochete that causes Lyme disease, is well established.

176 During Lyme disease it is clear that macrophages are capable of

177 Current serodiagnostics for Lyme disease lack sensitivity during early disease, and

178 Most patients with Lyme disease (LD) can be treated effectively with 2-4 we

179 As the incidence of Lyme disease (LD) has increased, a number of "Lyme speci

180 t method for the serological confirmation of Lyme disease (LD) is a 2-tier method recommended by the

181 Borrelia species of relapsing fever (RF) and Lyme disease (LD) lineages have linear chromosomes and b

182 onal 2-tiered serologic testing protocol for Lyme disease (LD), an enzyme immunoassay (EIA) followed

183 In early Lyme disease (LD), serologic testing is insensitive and

184 Lyme disease (LD), the most prevalent tick-borne illness

185 pful when evaluating patients with suspected Lyme disease (LD).

186 eatment of persistent symptoms attributed to Lyme disease leads to better outcomes than does shorter-

187 Its ability to transmit pathogens causing Lyme disease-like illnesses is a subject of ongoing cont

188 ients with persistent symptoms attributed to Lyme disease, longer-term antibiotic treatment did not h

189 New approaches to combat Lyme disease may include strategies to interfere with BB

190 as "posttreatment Lyme disease" and "chronic Lyme disease" may not actually exist but rather reflect

191 gest that Borrelia burgdorferi, the agent of Lyme disease, may persist after antibiotic therapy and c

192 lthough rare, sudden cardiac death caused by Lyme disease might be an under-recognized entity and is

193 feri, the bacterial pathogen responsible for Lyme disease, modulates its gene expression profile in r

194 Borrelia burgdorferi, the causative agent of Lyme disease, must adapt to two diverse niches, an arthr

195 -eight subjects with culture-confirmed early Lyme disease, of whom 55% were male, were followed for a

196 Patients with Lyme disease often develop pronounced TH17 immune respon

197 persistent symptoms possibly associated with Lyme disease often provide a challenge for clinicians.

198 disease--either related temporally to proven Lyme disease or accompanied by a positive IgG or IgM imm

199 gdorferi in either typical manifestations of Lyme disease or in other chronic disease states that are

200 ctive serum samples from patients with early Lyme disease, other diseases, and healthy controls were

201 thiamin is dispensable for the growth of the Lyme disease pathogen Borrelia burgdorferi (Bb)(3).

202 The Lyme disease pathogen Borrelia burgdorferi represents a

203 he syphilis bacterium Treponema pallidum and Lyme disease pathogen Borrelia burgdorferi, the pertinen

204 re is a documented role of these variants in Lyme disease pathogenesis or in syndromes compatible wit

205 they relate to B. burgdorferi physiology and Lyme disease pathogenesis.

206 of IgG and IgM to each in a training set of Lyme disease patient samples and controls.

207 d use of sample sets from well-characterized Lyme disease patients and controls are needed to better

208 lar features, and correctly classified early Lyme disease patients and healthy controls with a sensit

209 ing of long-term symptoms and overall QOL of Lyme disease patients and should be considered in the ev

210 molecular features that distinguished early Lyme disease patients from healthy controls.

211 Early Lyme disease patients often present to the clinic prior

212 culturing spirochetes from the serum of U.S. Lyme disease patients was recently reported by Sapi and

213 Lyme disease patients with erythema migrans are said to

214 Late stage Lyme disease patients, as well as infected mice and rabb

215 e for classifying early Lyme disease and non-Lyme disease patients.

216 assified 77%-95% of the of serology negative Lyme disease patients.

217 glycolysis-derived lactate was confirmed in Lyme disease patients.

218 anel identified a higher proportion of early-Lyme-disease patients as positive at the baseline or pos

219 Much of the controversy that surrounds Lyme disease pertains to whether it produces prolonged,

220 A case of a woman with early disseminated Lyme disease presenting with NAGU is reported.

221 Lyme disease prevails as the most commonly transmitted t

222 atients with early or late manifestations of Lyme disease, primarily in those with refractory arthrit

223 Borrelia burgdorferi, the etiologic agent of Lyme disease, produces a variety of proteins that promot

224 Agents that cause Lyme disease, relapsing fever, leptospirosis, and syphil

225 Borrelia burgdorferi, the causative agent of Lyme disease, reliably produces an infectious arthritis

226 eatment of persistent symptoms attributed to Lyme disease remains controversial.

227 eliella (Borrelia) burgdorferi, the cause of Lyme disease, represent an increasingly large public hea

228 Borrelia burgdorferi, the agent of Lyme disease, responds to numerous host-derived signals

229 small-mammal predators can sharply increase Lyme disease risk.

230 oratory testing results are now available to Lyme disease serological test users and researchers deve

231 calculated the positive predictive value of Lyme disease serology.

232 stemic infection, which are reviewed herein, Lyme disease should be considered in women presenting wi

233 ents who received conventional treatment for Lyme disease should not be attributed to persistent acti

234 HA007 and its orthologs to BBK32 proteins of Lyme disease species, as well as to previously described

235 As the Lyme disease spirochaete Borrelia burgdorferi shuttles b

236 the most common area of colonization for the Lyme disease spirochaete Borrelia burgdorferi.

237 an disease and is conserved within the major Lyme disease spirochaete species, degrades the extracell

238 mmunogenic, and conserved in the three major Lyme disease spirochaete species.

239 The Lyme disease spirochaete, Borrelia burgdorferi, causes d

240 expression is a key strategy adopted by the Lyme disease spirochaete, Borrelia burgdorferi, for adap

241 tebrates by several pathogens, including the Lyme disease spirochete bacterium, Borrelia burgdorferi.

242 tion by three distinct bacteria, that is the Lyme disease spirochete Borrelia burgdorferi and the ric

243 lycan cell-wall synthesis, we found that the Lyme disease spirochete Borrelia burgdorferi displays a

244 The Lyme disease spirochete Borrelia burgdorferi exists in n

245 As an obligate pathogen, the Lyme disease spirochete Borrelia burgdorferi has a strea

246 ogens, promotes vascular interactions of the Lyme disease spirochete Borrelia burgdorferi Here, we in

247 etect heterogeneity of ospC genotypes of the Lyme disease spirochete Borrelia burgdorferi in the tick

248 The Lyme disease spirochete Borrelia burgdorferi is dependen

249 The Lyme disease spirochete Borrelia burgdorferi lacks endog

250 The Lyme disease spirochete Borrelia burgdorferi undergoes s

251 iota of I. scapularis, a major vector of the Lyme disease spirochete Borrelia burgdorferi, influence

252 , motility, and infectious life cycle of the Lyme disease spirochete Borrelia burgdorferi.

253 investigations into mechanisms by which the Lyme disease spirochete controls synthesis of its Erp su

254 The Lyme disease spirochete, Borrelia burgdorferi, controls

255 The Lyme disease spirochete, Borrelia burgdorferi, exists in

256 The Lyme disease spirochete, Borrelia burgdorferi, expresses

257 The Lyme disease spirochete, Borrelia burgdorferi, occupies

258 ion between arthropod and mammals forces the Lyme disease spirochete, Borrelia burgdorferi, to adapt

259 Borrelia burgdorferi, the Lyme disease spirochete, couples environmental sensing a

260 CsrA in differential gene expression in the Lyme disease spirochete.

261 y that is essential to the life cycle of the Lyme disease spirochete.

262 gene deletion during murine infection by the Lyme disease spirochete.

263 tion suggests a role in transmission of this Lyme disease spirochete.

264 Lyme disease spirochetes possess a single HtrA protease

265 variable metabolic requirements of different Lyme disease spirochetes within tick vectors could poten

266 The Lyme disease spirochetes, Borrelia burgdorferi (sensu la

267 In human Lyme disease, spirochetes spread from the site of a tick

268 ong-term (>/=2 years) symptoms, adjusted for Lyme disease stage and severity at diagnosis.

269 Infection of Lyme disease-susceptible C3H/HeN mice with the arp delet

270 hema migrans are said to have post-treatment Lyme disease symptoms (PTLDS) if there is persistence of

271 The causes of post-Lyme disease symptoms are unclear.

272 ese findings support the notion that chronic Lyme disease symptoms can be attributable to residual in

273 s negative in 16 patients with posttreatment Lyme disease syndrome (PTLDS) and/or high C6 antibody le

274 refractory Lyme arthritis and post-treatment Lyme disease syndrome are associated with elevated CRP r

275 sease and in individuals with post-treatment Lyme disease syndrome were compared with those in health

276 protein is not associated with posttreatment Lyme disease syndrome.

277 e arthritis and in those with post-treatment Lyme disease syndrome.

278 Positive Lyme disease test results may have little diagnostic val

279 revalence cohort, fewer than 20% of positive Lyme disease tests are obtained from patients with clini

280 a potential autoantigen in manifestations of Lyme disease that are thought to involve immune-mediated

281 yme carditis is an uncommon manifestation of Lyme disease that most commonly involves some degree of

282 en and adolescents undergoing evaluation for Lyme disease, the C6 EIA could guide initial clinical de

283 ne variation for the symptoms and outcome of Lyme disease, the factors influencing cytokine productio

284 dorferi spirochete is the causative agent of Lyme disease, the most common tick-borne disease in the

285 phology of B. burgdorferi from patients with Lyme disease, the organism was invariably described as h

286 Borrelia burgdorferi, the causative agent of Lyme disease, triggers host immune responses that affect

287 linical illness compatible with disseminated Lyme disease underwent 2-tiered serologic testing.

288 7 functional scales, reference serology for Lyme disease using Centers for Disease Control and Preve

289 highlighting use of BBI39 proteins as novel Lyme disease vaccines that can target pathogens in the h

290 Early Lyme disease was defined by the presence of erythema mig

291 False-positive serology for Lyme disease was reported in patients with acute infecti

292 date pathogen-host interactions during early Lyme disease, we developed a mathematical model that exp

293 different two-tiered testing strategies for Lyme disease were compared using the median charges for

294 , CCL1, CCL2 and CCL5) that are hallmarks of Lyme disease were induced.

295 detect HGA infection in patients with early Lyme disease who presented with erythema migrans.

296 describe 2 patients with early disseminated Lyme disease who were misdiagnosed with infectious monon

297 st-effective two-tiered testing strategy for Lyme disease with acute-phase serum samples.

298 records of patients who tested positive for Lyme disease with standardized 2-tiered serologic testin

299 blots in the two-tiered testing protocol for Lyme disease without a loss of sensitivity or specificit

300 humans results in significant morbidity from Lyme disease worldwide.