ライフサイエンスコーパス: vaginalis

1 partial draft genomes (including Trichomonas vaginalis).

2 extracellular protozoan parasite Trichomonas vaginalis.

3 is-associated bacteria including Gardnerella vaginalis.

4 virulence potential of the BV associated G. vaginalis.

5 actor in the protozoan parasite, Trichomonas vaginalis.

6 grouped into 3 subclasses, are present in T. vaginalis.

7 spp., Gardnerella vaginalis, and Trichomonas vaginalis.

8 P1 mono) from the human pathogen Trichomonas vaginalis.

9 tted infections (STIs) caused by Trichomonas vaginalis.

10 istently colonized by strains of Gardnerella vaginalis.

11 al samples tested, 6.6% were positive for T. vaginalis.

12 ification test (NAAT) were used to detect T. vaginalis.

13 extraurogenital sources, with a focus on T. vaginalis.

14 Women were also tested for Trichomonas vaginalis.

15 ernatants from growing liquid cultures of G. vaginalis.

16 ion to alpha-actinin suggests exposure to T. vaginalis.

17 nes, to genetically characterize Trichomonas vaginalis.

18 ic or symptomatic, should be screened for T. vaginalis.

19 ic diversity, and population structure of T. vaginalis.

20 d IL-8 (adjusted p = 0.0170) responses to G. vaginalis.

21 ults suggest that TVV may be commensal to T. vaginalis.

22 tiated by sexual transmission of Gardnerella vaginalis.

23 ressed inflammatory responses to Gardnerella vaginalis.

24 kbp), double-stranded RNA virus infecting T. vaginalis.

25 VCU-M1, which is also associated with T. vaginalis.

26 C trachomatis, 6.1% (4.0%-8.3%; n = 357), T vaginalis, 17.8% (12.4%-23.1%; n = 822), bacterial vagin

27 homatis, 7.1% for N gonorrhoeae, 16.1% for T vaginalis, 18.1% for bacterial vaginosis, and 8.6% for v

28 C trachomatis, 6.9% (5.1%-8.6%; n = 350), T vaginalis, 29.1% (20.9%-37.2%; n = 5502), bacterial vagi

29 The mean age of women with detectable T. vaginalis (30.6) was significantly higher than those for

30 I phenotype reflected detection of solely T. vaginalis (54.2% of all health care encounters that resu

31 te from other facilities exceeded that of T. vaginalis (7.2%; P = 0.004).

32 This rate was higher than those seen with T. vaginalis (9.0%; P = 0.005), C. trachomatis (6.2%), and

33 Gardnerella vaginalis, a facultative anaerobe, was cleared more slow

34 Trichomonas vaginalis, a flagellated protozoan, is the agent respons

35 Trichomonas vaginalis, a human-infective parasite, causes the most p

36 um supported robust outgrowth of Gardnerella vaginalis, a major sialidase producer and one of the mos

37 In Trichomonas vaginalis, a Myb1 protein was previously demonstrated to

38 Among them, Trichomonas vaginalis, a parasite adapted to the human genitourinary

39 logistic regression model that identifiedG. vaginalis,A. vaginae, andMegasphaeraphylotypes 1 and 2 a

40 vovaginal candidiasis (VVC), and Trichomonas vaginalis accounts for a significant proportion of all g

41 chomatis, Mycoplasma genitalium, Trichomonas vaginalis, adenovirus, and herpes simplex virus were abs

42 ome evidence of association with Trichomonas vaginalis (adjusted OR, 1.56; 95% CI, 1.00-2.44).

43 The T. vaginalis alpha-actinin amino acid sequence and the sequ

44 Comparison of the T. vaginalis alpha-actinin epitopes with proteins in data b

45 Cytokine secretion in response to VLY and G. vaginalis also depended on the polarity of exposure.

46 ver, first-void urine detection rates for T. vaginalis and C. trachomatis within this age demographic

47 s, but recently an emended description of G. vaginalis and descriptions of three new species - Gardne

48 cs and BV, enrichment of vaginal Gardnerella vaginalis and Lactobacillus iners was associated with in

49 and complex interactions between Gardnerella vaginalis and Lactobacillus involved in efficacy, here w

50 s regarding colonization of the vagina by G. vaginalis and may suggest an explanation for the lack of

51 Additional Trichomonas vaginalis and Mycoplasma genitalium screening found 17.4

52 on the influence of biofilm formation by G. vaginalis and other anaerobes, from the time of their in

53 cillus women, negatively correlating with G. vaginalis and other anaerobic bacteria, which depleted t

54 Ts and specific bacterial phyla (Gardnerella vaginalis and Prevotella bivia) were strongly associated

55 ired STIs included chlamydia, gonorrhoea, T. vaginalis and syphilis with rapid plasma reagin >/=1:8.

56 primary sources of sialidase activity in G. vaginalis and that these two enzymes can account for the

57 jensenii, 2 L. crispatus, 1 L. mucosae, 1 L. vaginalis and the L. acidophilus probiotic.

58 Trichomonas vaginalis and viral pathogens (herpes simplex virus type

59 es, enabling comparison of the effects of G. vaginalis and VLY following exposure to either side.

60 tive polymerase chain reaction (qPCR) for G. vaginalis and/or Atopobium vaginae above a threshold.

61 al organs (testicles, spermatic cord, tunica vaginalis) and is characterized by pain, swelling and hy

62 chomatis, Neisseria gonorrhoeae, Trichomonas vaginalis) and the E6/E7 mRNA of human papillomavirus (H

63 gonorrhoeae, 26 (5.2%) were positive for T. vaginalis, and 47 (9.5%) were positive for M. genitalium

64 , Parvimonas micra, Megasphaera, Gardnerella vaginalis, and Atopobium vaginae and decreased frequenci

65 alactiae, Chlamydia trachomatis, Trichomonas vaginalis, and Candida spp., as well as their interactio

66 Associated Bacterium 2 (BVAB-2), Gardnerella vaginalis, and Megasphaera-1--and a single organism (Lac

67 cteria: Lactobacillus crispatus, Gardnerella vaginalis, and Neisseria gonorrhoeae All vaginal microbi

68 inal pathogens Candida albicans, Gardnerella vaginalis, and Neisseria gonorrhoeae, as well as to toxi

69 as detected between the leaves of the tunica vaginalis, and rupture from the lower pole was diagnosed

70 nic protozoa Giardia lamblia and Trichomonas vaginalis, and the bacterial pathogens Helicobacter pylo

71 gilis, Pentatrichomonas hominis, Trichomonas vaginalis, and Trichomonas tenax.

72 mpling devices for Candida spp., Gardnerella vaginalis, and Trichomonas vaginalis.

73 e interaction between vaginal epithelium, G. vaginalis, and VLY using EpiVaginal tissues from MatTek.

74 els were lower in females with a positive T. vaginalis antigen test result, a vaginal pH >4.5, vagina

75 C. trachomatis (AOR, 1.43; P = .247), and T. vaginalis (AOR, 1.60; P = .120) independently increased

76 Apical tissue challenge by G. vaginalis appeared to dampen the inflammatory response,

77 G. vaginalis appears to include four nonrecombining groups/

78 haera, Prevotella timonensis and Gardnerella vaginalis are associated with CIN2 persistence and slowe

79 High vaginal loads of A. vaginae and G. vaginalis are associated with late miscarriage and prema

80 lamblia, Leishmania species, and Trichomonas vaginalis are persistently infected with dsRNA viruses,

81 Biofilms of G. vaginalis are present in human infections and are implic

82 Sera from patients infected with T. vaginalis are reactive to TvMIF, especially in males.

83 Studies have implicated Gardnerella vaginalis as an important etiological agent in bacterial

84 nters on the roles of virulent strains of G. vaginalis, as well as Prevotella bivia and Atopobium vag

85 alis prevalence using the Aptima Trichomonas vaginalis assay (ATV; Gen-Probe) and the prevalence of C

86 ercial NAA test (GenProbe Aptima Trichomonas vaginalis assay; ATV) for T. vaginalis were compared wit

87 bacterial communities containing Gardnerella vaginalis associated with vaginal drying, whereas DMPA s

88 lli and higher concentrations of Gardnerella vaginalis, Atopobium vaginae, and Prevotella bivia, at t

89 Lactobacillus iners, Gardnerella vaginalis, Atopobium vaginae, Megasphaera I, and Megasph

90 d with vaginal health or disease:Gardnerella vaginalis,Atopobium vaginae, BV-associated bacteria 2 (B

91 e tested by the TVQ assay, and the Aptima T. vaginalis (ATV) assay was performed using clinician-coll

92 on tests for C trachomatis, N gonorrhoeae, T vaginalis, bacterial vaginosis, and vulvovaginal candidi

93 hem to understand the phenotypic shift of G. vaginalis biofilm formation to BV establishment.

94 Here we demonstrate that G. vaginalis biofilms contain extracellular DNA, which is e

95 s and approaches available to interrogate T. vaginalis biology, with an emphasis on recent advances a

96 ues following intravaginal infection with T. vaginalis but were not seen in uninfected mice.

97 n tests (NAATs) for detection of Trichomonas vaginalis by vaginal swabs; NAATs for detection of Neiss

98 Overall, T. vaginalis, C. trachomatis, and N. gonorrhoeae prevalence

99 ported in females, TMA-based detection of T. vaginalis can be a routine constituent within a comprehe

100 The human-infective parasite Trichomonas vaginalis causes the most prevalent nonviral sexually tr

101 mplified the beta-fructofuranosidase from T. vaginalis cDNA and cloned it into an Escherichia coli ex

102 etect beta-fructofuranosidase activity in T. vaginalis cell lysates.

103 ehavioral practices and Nugent Score with G. vaginalis clade distribution in women who have sex with

104 Our results suggest that G. vaginalis clades have varying levels of pathogenicity in

105 Identification of 4 G. vaginalis clades raised the possibility that pathogenic

106 ssed factors associated with detection of G. vaginalis clades, and multinomial regression assessed fa

107 tic Trichomonasvirus, highly prevalent in T. vaginalis clinical isolates, is sensed by the human epit

108 In females with detectable T. vaginalis, codetection of Chlamydia trachomatis and Neis

109 is, we demonstrate >10-fold inhibition of G. vaginalis colonization by DNase.

110 s with Chlamydia trachomatis and Trichomonas vaginalis decreases the prophylactic efficacy of oral em

111 traurogenital sources into assessment for T. vaginalis detection may identify additional symptomatic

112 , 858 pharyngeal specimens yielded a 2.9% T. vaginalis detection rate compared with 2.1% for N. gonor

113 The aggregate T. vaginalis detection rate trended higher than that of the

114 The M. genitalium and T. vaginalis detection rates among 755 patients at urban em

115 Given the significant rate of T. vaginalis detection, with age distribution analogous to

116 atis, Neisseria gonorrhoeae, and Trichomonas vaginalis DNA, detected using the BD MAX CT/GC/TV assay,

117 It has been reported that T. vaginalis does not grow on sucrose.

118 Eight DRP homologues [T. vaginalis DRPs (TvDRPs)], which can be grouped into 3 su

119 G. vaginalis engaged in sialoglycan foraging in vitro, in t

120 Finally, we demonstrate that T. vaginalis EV uptake is dependent on host cell cholestero

121 We show that T. vaginalis EVs interact with glycosaminoglycans on the su

122 ied an abundant protein on the surface of T. vaginalis EVs, 4-alpha-glucanotransferase (Tv4AGT), and

123 G. vaginalis exhibited more-rapid growth in coculture with

124 , and that a subspecies clade of Gardnerella vaginalis explained the genus association with PTB.

125 n substrates supports a model in which 1) G. vaginalis extracellular sialidase hydrolyzes mucosal sia

126 Nevertheless, the T. vaginalis genome contains some 11 putative sucrose trans

127 5mC), is the main DNA methylation mark in T. vaginalis Genome-wide distribution of 6mA reveals that t

128 omal RNA gene with clustering of Gardnerella vaginalis genomic clades.

129 crobial activity with complete inhibition G. vaginalis growth within 48 h.

130 Our data suggests that Gardnerella vaginalis had the highest virulence potential, as define

131 Gardnerella vaginalis has been considered a pivotal player in the pr

132 utility of TMA for detection of Trichomonas vaginalis has recently been described.

133 T. vaginalis has the coding capacity to produce an active b

134 ania spp., Trypanosoma cruzi and Trichomonas vaginalis have genes encoding homologues of Piezo channe

135 cate a role for a TvDRP in the fission of T. vaginalis hydrogenosomes, similar to that described for

136 ect N. gonorrhoeae and C. trachomatis (or T. vaginalis if utilized), there is no US Food and Drug Adm

137 (vaginal pH of 5.0 or above) and Trichomonas vaginalis (immunoassay) regardless of symptom reporting.

138 atis, Neisseria gonorrhoeae, and Trichomonas vaginalis in liquid-based cytology specimens were 1.5, 2

139 detect Mycoplasma genitalium and Trichomonas vaginalis in men and women reporting a history of recept

140 Detection of G. vaginalis in oral cavity or anal samples and Leptotrichi

141 Currently, the role of G. vaginalis in the etiology of BV remains a matter of cont

142 and specific PCR assays for detection of T. vaginalis in urine, a noninvasive specimen, and developm

143 s warrants a more thorough review of male T. vaginalis incidence.

144 d divergence of the vaginal microbiota in T. vaginalis-infected and T. vaginalis-uninfected patients

145 s (24.7 years) was lower than that of the T. vaginalis-infected females (mean, 30.1 years; P < 0.0001

146 The average age of a T. vaginalis-infected male (39.9 years) was significantly g

147 pothesized that the vaginal microbiota in T. vaginalis-infected women differs from that in T. vaginal

148 Vaginal samples from 30 T. vaginalis-infected women were matched by Nugent score to

149 ster analysis revealed 2 unique groups of T. vaginalis-infected women.

150 g and treating females with low levels of T. vaginalis infection (before they become wet mount positi

151 ction, as well as the association between T. vaginalis infection and increased transmission of and su

152 incidence and increased the clearance of T. vaginalis infection and induced both systemic and local

153 s have been correlated with both Trichomonas vaginalis infection and poor reproductive health outcome

154 The presence of CD4(+) T cells following T. vaginalis infection can potentially increase susceptibil

155 Trichomonas vaginalis infection in males has been largely uncharacte

156 C. trachomatis and T. vaginalis infection increase the susceptibility to SHIV,

157 The prevalence of Trichomonas vaginalis infection is highest in women with intermediat

158 cantly higher than the N. gonorrhoeae and T. vaginalis infection rates.

159 the potential for a human vaccine against T. vaginalis infection that could also influence the incide

160 o the diagnosis and treatment of Trichomonas vaginalis infection, as well as the association between

161 reversible contraception usage, Trichomonas vaginalis infection, bacterial vaginosis, and incident s

162 rding conditions associated with Trichomonas vaginalis infection, including human immunodeficiency vi

163 leukocytosis, and recurrent (vs initial) T. vaginalis infection, with the lowest levels observed in

164 and Neisseria gonorrhoeae with concurrent T. vaginalis infection.

165 ations were significantly associated with T. vaginalis infection.

166 Trichomonas vaginalis infections are usually asymptomatic or can res

167 oeae, Mycoplasma genitalium, and Trichomonas vaginalis infections as well as the characteristics of b

168 ogether, these data indicate that chronic T. vaginalis infections may result in TvMIF-driven inflamma

169 e presence of clinical symptoms or repeat T. vaginalis infections with TVV+ isolates (P = .14 and P =

170 mbers of C trachomatis, N gonorrhoeae, and T vaginalis infections, but much higher numbers of bacteri

171 Trichomonas vaginalis is a common sexually transmitted infection (ST

172 Trichomonas vaginalis is a common sexually transmitted parasite that

173 Trichomonas vaginalis is a highly divergent, unicellular eukaryote o

174 Trichomonas vaginalis is a parasite of the urogenital tract in men a

175 Gardnerella vaginalis is a predominant bacterial species, but BV is

176 Gardnerella vaginalis is abundant in bacterial vaginosis (BV), a con

177 However, G. vaginalis is also commonly found in asymptomatic or BV-n

178 Trichomonas vaginalis is an extracellular protozoan parasite that bi

179 Gardnerella vaginalis is associated with a spectrum of clinical cond

180 We show that 6mA in T. vaginalis is associated with silencing when present on g

181 Gardnerella vaginalis is detected in women with and without bacteria

182 However, T. vaginalis is disproportionality under studied, especiall

183 Critics of this model have iterated that G. vaginalis is found in virginal women and in sexually act

184 T. vaginalis is the most common sexually transmitted infect

185 Gardnerella vaginalis is the most common species found in bacterial

186 Trichomonas vaginalis is the most prevalent nonviral sexually transm

187 Trichomonas vaginalis is the most prevalent nonviral sexually transm

188 G. vaginalis is the pathogen responsible for the initiation

189 formed on the vaginal epithelium and that G. vaginalis is typically the predominant species.

190 better understand the differences between G. vaginalis isolated from women with a positive (BV) versu

191 virulence potential of 7 BV and 7 non-BV G. vaginalis isolates and assessed the virulence factors re

192 examine the TVV prevalence in US Trichomonas vaginalis isolates and TVV's associations with patient d

193 Archived T. vaginalis isolates from the enrollment visits of 355 wom

194 Of 355 T. vaginalis isolates tested for TVV, T. vaginalis isolates

195 355 T. vaginalis isolates tested for TVV, T. vaginalis isolates tested for TVV, the prevalence was 40

196 Among a collection of 34 G. vaginalis isolates, nanH2, nanH3, or both were present i

197 of inflammatory cytokines in response to G. vaginalis, isolates from women with non-optimal microbio

198 on quantified Atopobium vaginae, Gardnerella vaginalis, lactobacilli, Mycoplasma hominis, and the hum

199 eting 16S ribosomal RNA genes of Gardnerella vaginalis, Lactobacillus crispatus, BVAB1, BVAB2, BVAB3,

200 The SLPI level was reduced by >50% in a T. vaginalis load-dependent manner.

201 levels observed in those with the highest T. vaginalis loads.

202 und that T. vaginalis secretes a protein, T. vaginalis macrophage migration inhibitory factor (TvMIF)

203 T. vaginalis may alter the vaginal microbiota in a manner t

204 esults from this study suggest that while G. vaginalis may grow on the apical face of the vaginal epi

205 The genetic diversity of G. vaginalis may result in virulent and avirulent strains.

206 isms of pathogenicity factors of Gardnerella vaginalis, Mycoplasma genitalium, Mycoplasma hominis, Ne

207 chomatis, Neisseria gonorrhoeae, Trichomonas vaginalis, Mycoplasma hominis, Ureaplasma species, and y

208 d with Chlamydia trachomatis and Trichomonas vaginalis (n = 9) or medium (controls; n = 7) were repea

209 In vivo, G. vaginalis normally colonizes the apical face of the vagi

210 e of extragenital infection with Trichomonas vaginalis of the conjunctiva of a 32-year-old man.

211 obic BV-associated species, and levels of G. vaginalis often rebounded during treatment.

212 ed rapid point-of-care tests for Trichomonas vaginalis on self-collected vaginal swabs.

213 s of the score (ie, detection of Gardnerella vaginalis or Bacteroides spp and non-detection of Lactob

214 ntly different between women with detected G vaginalis or Bacteroides spp morphotypes and those witho

215 ominated by Lactobacillus iners, Gardnerella vaginalis or were highly diverse profiles.

216 gents) and 26.1% were solely positive for T. vaginalis (P < 0.0002 versus C. trachomatis).

217 lls perform trogocytosis to kill Trichomonas vaginalis parasites.

218 All T. vaginalis pharyngeal detections were confirmed by TMA-ba

219 gens, as well as protozoa, e.g., Trichomonas vaginalis, Plasmodium berghei, and sporozoites and blood

220 and phylogenetic analyses determined that T. vaginalis population structure is strongly influenced by

221 A total of 85.7% of males with T. vaginalis-positive pharyngeal collections indicated stri

222 A total of 38.1% of T. vaginalis-positive pharyngeal specimens were derived fro

223 llus (59.2%) and the other where Gardnerella vaginalis predominated with other anaerobic bacteria (40

224 Gardnerella vaginalis predominates in bacterial vaginosis.

225 e evaluated with more-sensitive tests for T. vaginalis, preferably NAATs, if microscopy is negative.

226 T. vaginalis prevalence differed by race/ethnicity, with th

227 High T. vaginalis prevalence in all age groups suggests that wom

228 alth care system was performed to address T. vaginalis prevalence in males.

229 Higher T. vaginalis prevalence in women of >40 years is probably a

230 T. vaginalis prevalence ranged from 5.4% in family planning

231 Our aim was to determine Trichomonas vaginalis prevalence using the Aptima Trichomonas vagina

232 The highest T. vaginalis prevalence was in women >/= 40 years old (>11%

233 ed in vitro by the catalytic subunit of a T. vaginalis protein kinase A, TvPKAc.

234 we describe the performance of the new BD T. vaginalis Qx (TVQ) amplified DNA assay, which can be per

235 T. vaginalis research entered the age of genomics with the

236 Trichomonas vaginalis results were concordant between the BD MAX Vag

237 care professionals can consider TMA-based T. vaginalis screening for a wide age range of patients; in

238 tandard for clinical culture for Trichomonas vaginalis screening.

239 We have found that T. vaginalis secretes a protein, T. vaginalis macrophage mi

240 for C. glabrata; and 96.5% and 95.1% for T. vaginalis Sensitivities and specificities were similar i

241 oeae sensitivity 66.0%, specificity 45.2%; T vaginalis sensitivity 60.4%, specificity 45.6%; bacteria

242 VVC due to Candida glabrata, and 10% for T. vaginalis Sensitivity and specificity estimates for the

243 (sensitivity 76.0%, specificity 100%), and T vaginalis (sensitivity 68.5%, specificity 97.4%), high s

244 atis, Neisseria gonorrhoeae, and Trichomonas vaginalis Sequencing was used to assess macrolide antibi

245 , BLAST searches predicted two additional G. vaginalis sialidases, NanH2 and NanH3.

246 specimens were analyzed using established G. vaginalis species-specific and clade-typing polymerase c

247 Similarly, G. vaginalis strains encoding NanH2 cleaved and foraged sig

248 study, we examined the propensities of 26 T. vaginalis strains to bind to and lyse prostate (BPH-1) a

249 asure, the degree of difference among the G. vaginalis strains was the highest observed among 23 path

250 of pathogenic properties among different T. vaginalis strains, all strains show strict contact-depen

251 ture of BV and is produced by a subset of G. vaginalis strains.

252 The InPouch Trichomonas vaginalis test is the gold standard for clinical culture

253 e compared with the Affirm VPIII Trichomonas vaginalis test.

254 , and a composite of NAAT and culture for T. vaginalis The prevalences of infection were similar for

255 Gardnerella vaginalis, the bacterial species most frequently isolate

256 m assay includes a DNA probe for Gardnerella vaginalis, the Hologic transcription-mediated amplificat

257 s for C. trachomatis, N. gonorrhoeae, and T. vaginalis TMA screening.

258 ermore, we also determined the ability of G. vaginalis to displace lactobacilli previously adhered to

259 oniasis results from adhesion of Trichomonas vaginalis to the mucous membrane of the urethra or vagin

260 syphilis, chlamydia, gonorrhoea, Trichomonas vaginalis (together defined as 'any STI') and HIV-1.

261 s reported increased accuracy of Trichomonas vaginalis transcription-mediated amplification (TMA)-bas

262 nt visits of 355 women participating in a T. vaginalis treatment trial in Birmingham, Alabama, were t

263 ciated with an increased risk of Trichomonas vaginalis (TV) acquisition, it is unknown whether other

264 t and persistent infections with Trichomonas vaginalis (TV) are common.

265 Mycoplasma genitalium (MG), and Trichomonas vaginalis (TV) are sexually transmitted infections (STIs

266 nodeficiency virus transmission, Trichomonas vaginalis (TV) infection constitutes an important public

267 Trichomonas vaginalis (TV) is the most common nonviral sexually tran

268 urealyticum biovar 2 (UU-2), and Trichomonas vaginalis (TV) using nucleic acid amplification tests.

269 lvovaginal candidiasis (VVC), or Trichomonas vaginalis (TV), were randomly assigned to receive vagina

270 sed the performance of the cobas Trichomonas vaginalis (TV)/MG assay (cobas) for the detection of M.

271 l microbiota in T. vaginalis-infected and T. vaginalis-uninfected patients among women with normal an

272 nalis-infected women differs from that in T. vaginalis-uninfected women.

273 matched by Nugent score to those from 30 T. vaginalis-uninfected women.

274 that the BV-associated bacterium Gardnerella vaginalis uses sialidase to break down and deplete siali

275 Taken together, these studies show that G. vaginalis utilizes sialidase to support the degradation,

276 aluminum hydroxide-adjuvanted whole-cell T. vaginalis vaccine for efficacy in a BALB/c mouse model o

277 A whole-cell T. vaginalis vaccine was administered subcutaneously to BAL

278 gnificant proportion of healthy women and G. vaginalis vaginal colonization does not always lead to B

279 rus 2 infection, genital ulcers, Trichomonas vaginalis, vaginitis or cervicitis, and male circumcisio

280 atis, Neisseria gonorrhoeae, and Trichomonas vaginalis via commercial transcription-mediated amplific

281 Trichomonas vaginalis virus (TVV) is a non-segmented, 4.5-5.5 kilo-b

282 to be more thermoresistant than Trichomonas vaginalis virus 1, but no specific protein machinery to

283 uding Leishmania RNA viruses and Trichomonas vaginalis viruses.

284 he BD MAX CT/GC/TV assay for detection of T. vaginalis was determined.

285 i in the presence and absence of Gardnerella vaginalis was measured using Luminex.

286 T. vaginalis was more prevalent than C. trachomatis or N. g

287 G. vaginalis was the only recognized species in its genus f

288 T. vaginalis was the predominant sexually transmitted agent

289 ing primers against pfoB gene of Trichomonas vaginalis, was developed and evaluated using dry ectocer

290 new murine vaginal colonization model for G. vaginalis, we demonstrate >10-fold inhibition of G. vagi

291 lium, C. trachomatis, N. gonorrhoeae, and T. vaginalis were 100, 70, 67, and 20%, respectively.

292 antly, we demonstrated that BV associated G. vaginalis were able to displace pre-coated vaginal prote

293 loads of either or both of A. vaginae and G. vaginalis were associated with preterm birth (hazard rat

294 ima Trichomonas vaginalis assay; ATV) for T. vaginalis were compared with the Affirm VPIII Trichomona

295 oeae, Chlamydia trachomatis, and Trichomonas vaginalis were performed.

296 y-eight historical and recent isolates of T. vaginalis were sampled from the American Type Culture Co

297 838 women, 116 of whom were infected with T. vaginalis, were analyzed.

298 ed by the sexual transmission of Gardnerella vaginalis, which has the appropriate virulence factors t

299 against the primary BV pathogen Gardnerella vaginalis with a minimum inhibitory concentration (MIC)

300 l swab and first-void urine screening for T. vaginalis within a regional health care system was perfo

301 nd cervical specimen-derived detection of T. vaginalis within African American majority geographical