ライフサイエンスコーパス: Lyme

1 es in patients with erythema migrans (EM) or Lyme arthritis (LA) to elucidate their role early and la

2 ribute to the development and persistence of Lyme arthritis (LA).

3 eased in patients with antibiotic-refractory Lyme arthritis and in those with post-treatment Lyme dis

4 s, leading to inflammatory sequelae, such as Lyme arthritis and Lyme carditis.

5 data also suggest that antibiotic-refractory Lyme arthritis and post-treatment Lyme disease syndrome

6 mice, BLT1(-/-) mice developed nonresolving Lyme arthritis characterized by increased neutrophils in

7 ckade revealed a unique role for IFN-beta in Lyme arthritis development in B6.C3-Bbaa1 mice.

8 ease with a sensitivity of 48.5% and 75% and Lyme arthritis in serum from patients with Lyme arthriti

9 Inhibition of myostatin in vivo suppressed Lyme arthritis in the reduced interval Bbaa1 congenic mi

10 ovial Vdelta1 gammadelta T cell clone from a Lyme arthritis patient.

11 synoviocytes tested ex vivo correlates with Lyme arthritis susceptibility.

12 solution of inflammation during experimental Lyme arthritis through the activation of PPAR-gamma.

13 d Lyme arthritis in serum from patients with Lyme arthritis with a sensitivity of 100%, and the speci

14 - and convalescent-phase early Lyme disease, Lyme arthritis, and posttreatment Lyme disease syndrome,

15 rmed the contribution of type I IFN genes to Lyme arthritis.

16 urgdorferi results in prolonged nonresolving Lyme arthritis.

17 ence of regulatory T cells and recovery from Lyme arthritis.

18 I, 83% to 100%) for serum from patients with Lyme arthritis; the STT algorithm detected early Lyme di

19 Anaplasma phagocytophilum, Babesia spp., or Lyme Borrelia spp.

20 nto the adaptive mechanisms driving host and Lyme borreliae association, which will lead to the devel

21 Lyme borreliae infect diverse vertebrate reservoirs with

22 To facilitate the evasion of complement, Lyme borreliae produce diverse proteins at different sta

23 To survive in vertebrate hosts, Lyme borreliae require the ability to escape from host d

24 nt manifestations in these animals; however, Lyme borreliae strains differ in their reservoir hosts.

25 Similarly, the ability of Lyme borreliae to colonize host tissues varies among dif

26 g the ecology and evolutionary mechanisms of Lyme borreliae-host associations driven by complement ev

27 lymorphic outer surface proteins produced by Lyme borreliae.

28 when invaded by different species/strains of Lyme borreliae.

29 patients with chronic symptoms attributed to Lyme borreliosis (LB) have LB or another disease.

30 Laboratory confirmation of early Lyme borreliosis (LB) is challenging.

31 Lyme borreliosis (LB) is the archetypal emerging zoonosi

32 s (72.2%); other objective manifestations of Lyme borreliosis (LB) were present in 11 (7.6%).

33 ers, such as depression, are associated with Lyme borreliosis (LB).

34 ri sensu lato spirochetes (Borrelia) causing Lyme borreliosis are able to disseminate from the initia

35 block pathogen spread and eventually reduce Lyme borreliosis health burden.

36 itical for accurate surveillance of TBRF and Lyme borreliosis in dogs.

37 eloped as a novel diagnostic test for active Lyme borreliosis in patients presenting disseminated per

38 to describe a novel Borrelia species causing Lyme borreliosis in the USA.

39 Lyme borreliosis is a tick-borne disease caused by the B

40 Lyme borreliosis is caused by multiple species of the sp

41 Lyme borreliosis is the most common tick-borne disease i

42 Lyme borreliosis is the most prevalent vector-borne dise

43 Lyme borreliosis is the object of numerous misconception

44 cut off of two pathogen peptides, 9/10 acute Lyme Borreliosis patients resulted positive, while we id

45 i) in the upper midwestern USA, which causes Lyme borreliosis with unusually high spirochaetaemia.

46 e causative agents of the tick-borne disease Lyme borreliosis, disseminate hematogenously from the ti

47 rrelia burgdorferi, the etiological agent of Lyme borreliosis, is that persistent infection is the ru

48 Lyme disease, also known as Lyme borreliosis, is the most common tick-transmitted di

49 The causative agents of Lyme borreliosis, spirochetes belonging to the Borrelia

50 elated to Borrelia burgdorferi, the agent of Lyme borreliosis.

51 l.) species complex are known to cause human Lyme borreliosis.

52 f the varying manifestations associated with Lyme borreliosis.

53 The diagnosis of Lyme carditis (LC), an early disseminated manifestation

54 Fatal Lyme carditis caused by the spirochete Borrelia burgdorf

55 These sudden cardiac deaths associated with Lyme carditis occurred from late summer to fall, ages ra

56 mmatory sequelae, such as Lyme arthritis and Lyme carditis.

57 cluded adult patients who visited a tertiary Lyme center between January 2008 and December 2014.

58 subgroups of patients referred to a tertiary Lyme center, to investigate whether depressive symptoms

59 be used to discriminate for LB in a tertiary Lyme center.

60 Lyme diagnosis was retrospectively extracted from the pa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 The Lyme disease agent, Borrelia burgdorferi, colonizes the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Treating Lyme disease during its initial stages with traditional

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 An Lyme disease increased exponentially in the pediatric po

133 Lyme disease is a multisystem disorder caused by the spi

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

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

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

137 Lyme disease is caused by the spirochete Borrelia burgdo

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

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

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

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

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

143 Lyme disease is the most common reportable zoonotic infe

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

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

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

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

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

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

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

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

152 Patients with Lyme disease often develop pronounced TH17 immune respon

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

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

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

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

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

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

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

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

161 Lyme disease prevails as the most commonly transmitted t

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

163 Lyme disease projections indicate that cases in the Nort

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

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

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

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

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

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

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

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

172 The Lyme disease spirochete Borrelia burgdorferi exhibits dr

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

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

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

176 When the Lyme disease spirochete, Borrelia burgdorferi, transfers

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

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

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

180 Lyme disease spirochetes interfere with complement by pr

181 Lyme disease spirochetes possess a single HtrA protease

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 humans results in significant morbidity from Lyme disease worldwide.

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

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

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

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

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

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

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

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

214 Lyme disease, caused by some Borrelia burgdorferi sensu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 ally reviewed to identify confirmed cases of Lyme disease.

246 er of HuMAbs that provide protection against Lyme disease.

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

248 ergoing clinical investigation for suspected Lyme disease.

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

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

251 nd the erythema migrans rash associated with Lyme disease.

252 n skin transcriptional response during early Lyme disease.

253 Borrelia burgdorferi, the causative agent of Lyme disease.

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

255 useful in the laboratory diagnosis of early Lyme disease.

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

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

258 d be employed as preexposure prophylaxis for Lyme disease.

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

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

261 pediatric patients undergoing evaluation for Lyme disease.

262 ate intensity after antibiotic treatment for Lyme disease.

263 scores were other comorbidities unrelated to Lyme disease.

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

265 tools to improve the clinical management of Lyme disease.

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

267 to diagnose extracutaneous manifestations of Lyme disease.

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

269 erodiagnosis for the laboratory detection of Lyme disease.

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

271 evelopment of vaccination strategies against Lyme disease.

272 6 months following antibiotic treatment for Lyme disease.

273 is the most common clinical manifestation of Lyme disease.

274 gators developing laboratory diagnostics for Lyme disease.

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

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

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

278 we investigate the human immune response to Lyme disease.

279 The commercially-available C6 Lyme enzyme immunoassay (EIA) has been approved to repla

280 western Pennsylvania from a Lyme-naive to a Lyme-epidemic area, highlighting changes in clinical pre

281 its dissociated first-tier tests, the Vidas Lyme IgM II (LYM) and IgG II (LYG) EIAs, which use purif

282 ation cohort (n = 90) acquired from CDC, the Lyme Immunochip identified a higher proportion of Lyme d

283 measured using a protein microarray system, Lyme Immunochip, in a single step but interpreted adheri

284 he new assay is able to readily detect early Lyme infection in patient samples from outside North Ame

285 ate of seropositivity in patients with early Lyme infection.

286 he conversion of western Pennsylvania from a Lyme-naive to a Lyme-epidemic area, highlighting changes

287 Lyme neuroborreliosis (LNB) caused by the tick-borne spi

288 Lyme neuroborreliosis (LNB), caused by the tick-borne sp

289 lay and sequelae are common in patients with Lyme neuroborreliosis (LNB).

290 on the course and outcome of early European Lyme neuroborreliosis is limited.

291 Stroke, as a manifestation of Lyme neuroborreliosis, is considered in the context of o

292 IA using samples from 471 well-characterized Lyme patients and controls.

293 ures in PTLDS and clinically cured non-PTLDS Lyme patients.

294 among a well-characterized CDC Premarketing Lyme serum panel.

295 ed with Lyme disease by testing from private Lyme specialty laboratories but who test negative by ref

296 nly proves that exposure of an individual to Lyme spirochetes had occurred.

297 patients and alternatively diagnosed chronic Lyme syndrome (ADCLS) patients-individuals diagnosed wit

298 The Lyme Total assay also performs well under a modified two

299 ntibodies to B. burgdorferi The BioPlex 2200 Lyme Total assay exhibits an improved rate of seropositi

300 to this result was the observation that the Lyme Total assay retained a high first-tier specificity