ライフサイエンスコーパス: Lyme disease

1 ergoing clinical investigation for suspected Lyme disease.

2 ity in all disease stages and OspC for early Lyme disease.

3 her deer tick-transmitted infections such as Lyme disease.

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

5 nd the erythema migrans rash associated with Lyme disease.

6 n skin transcriptional response during early Lyme disease.

7 Borrelia burgdorferi, the causative agent of Lyme disease.

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

9 useful in the laboratory diagnosis of early Lyme disease.

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

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

12 d be employed as preexposure prophylaxis for Lyme disease.

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

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

15 pediatric patients undergoing evaluation for Lyme disease.

16 ate intensity after antibiotic treatment for Lyme disease.

17 scores were other comorbidities unrelated to Lyme disease.

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

19 tools to improve the clinical management of Lyme disease.

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

21 6 months following antibiotic treatment for Lyme disease.

22 to diagnose extracutaneous manifestations of Lyme disease.

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

24 erodiagnosis for the laboratory detection of Lyme disease.

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

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

27 evelopment of vaccination strategies against Lyme disease.

28 clinicians in diagnosing and treating early Lyme disease.

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

30 a challenge for early proteomic detection of Lyme disease.

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

32 vice that specifically mentioned utility for Lyme disease.

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

34 serum samples from three patients with acute Lyme disease.

35 that marketed nonantimicrobial therapies for Lyme disease.

36 tific studies evaluating such treatments for Lyme disease.

37 orrelia burgdorferi, the aetiologic agent of Lyme disease.

38 mericanum transmits any pathogen that causes Lyme disease.

39 has limited sensitivity for detecting early Lyme disease.

40 mmonly target patients who believe they have Lyme disease.

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

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

43 btained from patients with clinically likely Lyme disease.

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

45 esis or in syndromes compatible with chronic Lyme disease.

46 is the most common clinical manifestation of Lyme disease.

47 gators developing laboratory diagnostics for Lyme disease.

48 Ixodes ticks and are the etiologic agents of Lyme disease.

49 e the test's detection sensitivity for early Lyme disease.

50 suffers from a lack of sensitivity in early Lyme disease.

51 we investigate the human immune response to Lyme disease.

52 ity of medically important zoonoses, such as Lyme disease.

53 ally reviewed to identify confirmed cases of Lyme disease.

54 er of HuMAbs that provide protection against Lyme disease.

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

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

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

58 ions for certain infectious diseases such as Lyme disease, a bacterial infection caused by Borrelia b

59 The incidence of Lyme disease, a tick-borne bacterial infection, is drama

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

61 Like the Lyme disease agent, Borrelia burgdorferi, B. miyamotoi i

62 The Lyme disease agent, Borrelia burgdorferi, colonizes the

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

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

65 Lyme disease, also known as Lyme borreliosis, is the mos

66 ient is correctly attributable to having had Lyme disease, an objective biomarker would be highly des

67 serologically defined cohort of samples from Lyme disease and control cases from areas of Lyme diseas

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

69 nically categorized case patients with early Lyme disease and healthy controls were identified (witho

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

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

72 rrelia burgdorferi is the causative agent of Lyme disease and is transmitted to vertebrate hosts by I

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

74 The emergence and spread of Lyme disease and other infections associated with black-

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

76 ycline prophylactic regimens, especially for Lyme disease and syphilis, infections that can be potent

77 two panels of serum from patients with early Lyme disease and was 100% (95% CI, 83% to 100%) for seru

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

79 The symptoms of Lyme disease are caused by inflammation induced by speci

80 A panel of multiple serological markers for Lyme disease are measured using a protein microarray sys

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

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

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

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

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

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

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

88 orrelia burgdorferi sensu lato, the agent of Lyme disease, B. miyamotoi is closely related to relapsi

89 to kill Borrelia burgdorferi, the tick-borne Lyme disease bacterial pathogen.

90 survival and persistence in the host of the Lyme disease bacterium Borrelia burgdorferi (Bb), but to

91 The Lyme disease bacterium Borrelia burgdorferi has 7-11 per

92 The Lyme disease bacterium, Borrelia burgdorferi, exemplifie

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

94 ion of Disease, Ninth Revision, diagnosis of Lyme disease between 2003 and 2013 at Children's Hospita

95 The Lyme Disease Biobank (LDB) collects samples from individ

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

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

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

99 determining the impact of climate change on Lyme disease burden has been challenging due to the comp

100 further climate change-induced increases in Lyme disease burden.

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

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

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

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

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

106 ncorporated 18 years of annual, county-level Lyme disease case data in a panel data statistical model

107 ese climate-disease relationships to project Lyme disease cases using CMIP5 global climate models and

108 There was a southwestward migration of Lyme disease cases, with a shift from rural to nonrural

109 Lyme disease, caused by Borrelia burgdorferi, is an infl

110 Lyme disease, caused by some Borrelia burgdorferi sensu

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

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

113 st evolutionarily diverse genetic element in Lyme disease-causing borreliae.

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

115 for the diagnosis of central nervous system Lyme disease (CNSLD).

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

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 cents undergoing investigation for suspected Lyme disease, CTTT and MTTT results agreed in most cases

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

121 Treating Lyme disease during its initial stages with traditional

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

123 Lyme disease and control cases from areas of Lyme disease endemicity offers an additional valuable re

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 as an archetype for other areas at-risk for Lyme disease epidemics.

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

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

131 (LC), an early disseminated manifestation of Lyme disease, has important implications for patient man

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

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

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

135 recommended for the laboratory diagnosis of Lyme disease if they perform with a specificity and a se

136 urgdorferi was discovered to be the cause of Lyme disease in 1983, leading to seroassays.

137 an alternative strategy for the diagnosis of Lyme disease in adults but has not yet been evaluated in

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

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

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

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

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

143 to translate this strategy for diagnosis of Lyme disease in patients.

144 odes tick vector and increasing incidence of Lyme disease in several states, including Pennsylvania.

145 The various presentations of Lyme disease in the population suggest that differences

146 arthritis; the STT algorithm detected early Lyme disease in the same two panels of serum from patien

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 on and healthcare use patterns for pediatric Lyme disease in western Pennsylvania.

151 We find that interannual variation in Lyme disease incidence is associated with climate variat

152 redictors explained less of the variation in Lyme disease incidence than unobserved county-level hete

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

154 Conventional two-tiered testing (CTTT) for Lyme disease includes a first-tier enzyme immunoassay (E

155 An Lyme disease increased exponentially in the pediatric po

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

157 nced relationship between climate change and Lyme disease, indicating possible nonlinear responses of

158 Lyme disease is a multisystem disorder caused by the spi

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

160 Lyme disease is a tick-borne infection caused by the bac

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

162 Lyme disease is caused by the spirochete Borrelia burgdo

163 Lyme disease is diagnosed by 2-tiered serologic testing

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

165 y diagnostic testing) from three sites where Lyme disease is endemic.

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

167 Lyme disease is one of most common vector-borne diseases

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

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

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

171 Lyme disease is the most common reportable zoonotic infe

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

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

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

175 osis that is cotransmitted by ticks wherever Lyme disease is zoonotic.

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

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

178 Borrelia burgdorferi, the causative agent of Lyme disease, is internalized by macrophages and process

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

180 Borrelia burgdorferi, the causative agent of Lyme disease, is transmitted by the bite of an infected

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

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

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

184 at least two infections, West Nile virus and Lyme disease, large hosts should be more competent than

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

186 le for approximately 300,000 annual cases of Lyme disease (LD) in the United States, with increasing

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

188 Lyme disease (LD) is an increasing public health problem

189 Lyme disease (LD) is the most common tick-borne illness

190 Lyme disease (LD) is the most commonly reported vector-b

191 te change could lead to the amplification of Lyme disease (LD) risk in the future have received much

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

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

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

195 Lyme disease (LD), the most prevalent vector-borne illne

196 dorferi sensu lato is the causative agent of Lyme disease (LD).

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

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

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

200 nts with acute- and convalescent-phase early Lyme disease, Lyme arthritis, and posttreatment Lyme dis

201 or PG(Bb) in the immunopathogenesis of other Lyme disease manifestations.

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

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

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

205 Patients with Lyme disease often develop pronounced TH17 immune respon

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

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

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

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

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

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

212 miyamotoi-infected human patient, but not a Lyme disease patient.

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

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

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

216 drome (PTLDS) occurs in approximately 10% of Lyme disease patients following antibiotic treatment.

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

218 Among symptomatic subjects, Lyme disease patients had a higher mean number of sympto

219 Early Lyme disease patients often present to the clinic prior

220 Immunochip identified a higher proportion of Lyme disease patients than the two-tiered testing (82.4%

221 Lyme disease patients with erythema migrans are said to

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

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

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

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

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

227 Lyme disease prevails as the most commonly transmitted t

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

229 served that more antigens became positive as Lyme disease progressed from early to late stages.

230 Lyme disease projections indicate that cases in the Nort

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

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

233 relia burgdorferi Current diagnosis of early Lyme disease relies heavily on clinical criteria, includ

234 The laboratory diagnosis of Lyme disease relies upon serologic testing.

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

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

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

238 pping studies project an overall increase in Lyme disease risk as the climate warms, such conclusions

239 calculated the positive predictive value of Lyme disease serology.

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

241 rine infectivity and tick persistence of the Lyme disease spirochete Borrelia (Borreliella) burgdorfe

242 sion increased microbial colonization by the Lyme disease spirochete Borrelia burgdorferi and the ric

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

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

245 The Lyme disease spirochete Borrelia burgdorferi exhibits dr

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

247 The Lyme disease spirochete Borrelia burgdorferi is dependen

248 arial parasite Plasmodium falciparum and the Lyme disease spirochete Borrelia burgdorferi, among othe

249 ility and flagellar filament assembly in the Lyme disease spirochete Borrelia burgdorferi.

250 The Lyme disease spirochete, Borrelia burgdorferi, controls

251 The Lyme disease spirochete, Borrelia burgdorferi, expresses

252 When the Lyme disease spirochete, Borrelia burgdorferi, transfers

253 visualize the intact flagellar motor in the Lyme disease spirochete, Borrelia burgdorferi.

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

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

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

257 e current landscape of complement evasion by Lyme disease spirochetes and provide an update on recent

258 Lyme disease spirochetes interfere with complement by pr

259 Lyme disease spirochetes possess a single HtrA protease

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

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

262 are use that can be designed to identify the Lyme disease stage.

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

264 ective symptom for >=6 months (posttreatment Lyme disease symptoms [PTLDS]).

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

266 Post-treatment Lyme disease symptoms/syndrome (PTLDS) occurs in approxi

267 rash and acute symptoms, (2) post treatment Lyme disease syndrome (PTLDS), and (3) clinical suspicio

268 ibiotics treatment are called post-treatment Lyme disease syndrome (PTLDS).

269 up to 20% of patients develop post-treatment Lyme disease syndrome (PTLDS).

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

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

272 e disease, Lyme arthritis, and posttreatment Lyme disease syndrome, as well as the necessary controls

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

274 protein is not associated with posttreatment Lyme disease syndrome.

275 caused by spirochetal microorganisms include Lyme disease, syphilis, leptospirosis, and tick-borne re

276 Positive Lyme disease test results may have little diagnostic val

277 terpret, MTTT provides a promising alternate Lyme disease testing strategy for children.

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

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

280 the development of new strategies to control Lyme disease that bypassed direct vaccination of the hum

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

282 pidemiology and healthcare use for pediatric Lyme disease, the current study may inform public health

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 Borrelia burgdorferi causes Lyme disease, the most common tick-transmitted illness i

286 necessary to evaluate its potential use for Lyme disease therapy.

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

288 ut also to cyclic dimers (Newcastle disease, Lyme disease), trimers (influenza hemagglutinins), and t

289 g for B. burgdorferi, the causative agent of Lyme disease, underscoring the need for improved serolog

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

291 7 functional scales, reference serology for Lyme disease using Centers for Disease Control and Preve

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

293 klegged tick (Ixodes pacificus), the primary Lyme disease vector in western North America, to project

294 eal the precise mechanisms of this important Lyme disease virulence factor.

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

296 At baseline, patients with Lyme disease were more likely than controls to have at l

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

298 two panels of serum from patients with early Lyme disease with a sensitivity of 48.5% and 75% and Lym

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

300 humans results in significant morbidity from Lyme disease worldwide.