ライフサイエンスコーパス: Lyme

1 Both Lyme and K/BxN-associated arthritis were suppressed by t

2 that contributes to the pathogenesis of both Lyme and RA.

3 Development of Lyme and rheumatoid arthritis in Gusbh-expressing mice w

4 us is a tick that transmits the pathogens of Lyme and several arboviral diseases.

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

6 discover novel autoantigens associated with Lyme arthritis (LA), we identified T-cell epitopes prese

7 ences in the inflammatory infiltrates during Lyme arthritis and carditis and demonstrate the coexiste

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

9 1 (B6.C3-Bbaa1), which developed more severe Lyme arthritis and K/BxN model of rheumatoid arthritis (

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

11 or blocking mAb reduced the severity of both Lyme arthritis and RA in B6.C3-Bbaa1 mice, formally link

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

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

14 5-LOX(-/-)) mice, which display a failure of Lyme arthritis resolution, recruited fewer F4/80(+) cell

15 i-associated locus 1 (Bbaa1), that regulates Lyme arthritis severity and includes the 15 type I IFN g

16 ix metalloproteinase 9, a known modulator of Lyme arthritis severity.

17 nt for this lipoprotein in the generation of Lyme arthritis, we utilized targeted deletion to generat

18 role for this cytokine in the development of Lyme arthritis.

19 in altered joint inflammation during murine Lyme arthritis.

20 sb as a transgene were protected from severe Lyme arthritis.

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

22 a-glucuronidase (Gusb) is a key regulator of Lyme-associated and K/BxN-induced arthritis severity.

23 the C3H Gusb allele were prone to increased Lyme-associated arthritis severity.

24 ted lysosomal enzymes, as a key regulator of Lyme-associated arthritis severity.

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

26 demic and much-debated tick-borne infection, Lyme borreliosis (LB), are unknown.

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

28 ignancy more often had signs of disseminated Lyme borreliosis and more frequently needed antibiotic r

29 of IL-17 in the development of experimental Lyme borreliosis by infecting C3H mice devoid of the com

30 naming this new South American member of the Lyme borreliosis group B. chilensis VA1 in honor of its

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

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

33 has not been studied using the experimental Lyme borreliosis model of infection of C3H mice with Bor

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

35 respectively by B. burgdorferi, the agent of Lyme borreliosis, and B. hermsii, the agent of tick-born

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

37 Borrelia burgdorferi, a causative agent of Lyme borreliosis, is a zoonotic pathogen that survives i

38 ochetes' evasion of macrophages during early Lyme borreliosis.

39 f the varying manifestations associated with Lyme borreliosis.

40 ated with sequences from 35 genomes of eight Lyme-borreliosis (LB) group Borrelia species and 7 Relap

41 Fatal Lyme carditis caused by the spirochete Borrelia burgdorf

42 hird-degree conduction block associated with Lyme carditis in the United States.

43 Lyme carditis is an uncommon manifestation of Lyme disea

44 lop third-degree heart block associated with Lyme carditis is essential to providing prompt and appro

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

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

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

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

49 Lyme diagnosis was retrospectively extracted from the pa

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

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

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

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

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

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

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

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

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

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

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

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

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

63 The Lyme disease agent, Borrelia burgdorferi, colonizes the

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

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

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

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

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

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

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

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

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

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

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

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

76 The Lyme disease bacterium, Borrelia burgdorferi, exemplifie

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 Lyme disease is diagnosed by 2-tiered serologic testing

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

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

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

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

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

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

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

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

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

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

117 Patients with Lyme disease often develop pronounced TH17 immune respon

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

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

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

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

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

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

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

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

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

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

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

129 Early Lyme disease patients often present to the clinic prior

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

131 Lyme disease patients with erythema migrans are said to

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

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

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

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

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

137 Lyme disease prevails as the most commonly transmitted t

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

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

140 calculated the positive predictive value of Lyme disease serology.

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

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

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

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

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

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

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

148 The Lyme disease spirochete Borrelia burgdorferi is dependen

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

150 The Lyme disease spirochete, Borrelia burgdorferi, controls

151 The Lyme disease spirochete, Borrelia burgdorferi, expresses

152 The Lyme disease spirochete, Borrelia burgdorferi, occupies

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

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

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

156 Lyme disease spirochetes possess a single HtrA protease

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

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

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

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

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

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

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

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

165 protein is not associated with posttreatment Lyme disease syndrome.

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

167 Positive Lyme disease test results may have little diagnostic val

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

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

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

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

172 7 functional scales, reference serology for Lyme disease using Centers for Disease Control and Preve

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

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

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

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

177 humans results in significant morbidity from Lyme disease worldwide.

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

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

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

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

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

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

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

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

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

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

188 Lyme disease, caused by the spirochete Borrelia burgdorf

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

222 to diagnose extracutaneous manifestations of Lyme disease.

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

224 erodiagnosis for the laboratory detection of Lyme disease.

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

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

227 clinicians in diagnosing and treating early Lyme disease.

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

229 a challenge for early proteomic detection of Lyme disease.

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

231 vice that specifically mentioned utility for Lyme disease.

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

233 serum samples from three patients with acute Lyme disease.

234 that marketed nonantimicrobial therapies for Lyme disease.

235 tific studies evaluating such treatments for Lyme disease.

236 orrelia burgdorferi, the aetiologic agent of Lyme disease.

237 mericanum transmits any pathogen that causes Lyme disease.

238 has limited sensitivity for detecting early Lyme disease.

239 mmonly target patients who believe they have Lyme disease.

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

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

242 btained from patients with clinically likely Lyme disease.

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

244 esis or in syndromes compatible with chronic Lyme disease.

245 gens like Borrelia burgdorferi, which causes Lyme disease.

246 Borrelia burgdorferi, the causative agent of Lyme disease.

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

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

249 e recommended for laboratory confirmation of Lyme disease.

250 responsible for the pathogenesis of chronic Lyme disease.

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

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

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

254 isease states that are often labeled chronic Lyme disease.

255 ive conventional antimicrobial treatment for Lyme disease.

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

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

258 nd the erythema migrans rash associated with Lyme disease.

259 n skin transcriptional response during early Lyme disease.

260 Borrelia burgdorferi, the causative agent of Lyme disease.

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

262 useful in the laboratory diagnosis of early Lyme disease.

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

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

265 d be employed as preexposure prophylaxis for Lyme disease.

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

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

268 pediatric patients undergoing evaluation for Lyme disease.

269 ate intensity after antibiotic treatment for Lyme disease.

270 scores were other comorbidities unrelated to Lyme disease.

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

272 tools to improve the clinical management of Lyme disease.

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

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

275 s system Borrelia burgdorferi infection) and Lyme encephalopathy (altered nervous system function in

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

277 y Clark and colleagues reported detection of Lyme group Borrelia in A. americanum using a nested-flag

278 is that A. americanum ticks are a vector for Lyme group Borrelia infections.

279 of an independent gene region; this is not a Lyme group spirochete and is not considered zoonotic.

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

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

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

283 e assessed a causal role for inflammation in Lyme neuroborreliosis pathogenesis by evaluating the ind

284 Lyme neuroborreliosis, caused by the spirochete Borrelia

285 s a causal role in the pathogenesis of acute Lyme neuroborreliosis.

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

287 CLS patient was confirmed as having positive Lyme serology by reference laboratory testing, and there

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

289 yme disease (LD) has increased, a number of "Lyme specialty laboratories" have emerged, claiming sing

290 ed on laboratory results from a nonreference Lyme specialty laboratory using in-house criteria.

291 ositive cultures and the development of post-Lyme symptoms (P </= .02).

292 tigen were more common in patients with post-Lyme symptoms (P = .07) and were correlated directly wit

293 patients with erythema migrans, 45 with post-Lyme symptoms and 41 without symptoms, who were evaluate

294 Despite the presence of post-Lyme symptoms, all posttreatment culture results were ne

295 ctable IL-23 levels, 25 (61%) developed post-Lyme symptoms, and all 7 with IL-23 levels >/= 230 ng/mL

296 nied by autoantibodies, correlated with post-Lyme symptoms, providing a new paradigm for the study of

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

298 ed as having alternatively diagnosed chronic Lyme syndrome (ADCLS), in which diagnosis is based on la

299 samples from 37 patients with posttreatment Lyme syndrome, as well as 40 medically healthy controls

300 between alternative and reference laboratory Lyme testing results in this setting is most likely expl