ライフサイエンスコーパス: mucoid

1 sing AlgB.D59N or H-AlgB delta1-145 remained mucoid.

2 lony morphology and phenotype referred to as mucoid.

3 s in cystic fibrosis patients are frequently mucoid.

4 ved on solid culture media is referred to as mucoid.

5 monas aeruginosa (PA) as either nonmucoid or mucoid.

6 se-negative lasB::Cm knock-out mutant in the mucoid 8821 background was constructed, and it showed a

7 aeruginosa from cystic fibrosis patients are mucoid (alginate producing) yet lack flagella.

8 Developing biofilms of the mucoid (alginate-producing) cystic fibrosis pulmonary is

9 s in Pseudomonas aeruginosa, are elevated in mucoid, alginate-producing bacteria and in response to i

10 s at least approximately 1.6-fold greater in mucoid, alginate-producing bacteria than in nonmucoid ba

11 ranscribed in response to iron limitation in mucoid, alginate-producing bacteria.

12 We demonstrate that a mucoid, alginate-producing strain of Pseudomonas aerugin

13 The resulting strain was non-mucoid and exhibited no detectable algD transcription.

14 A dominant mucoid and hypermutator mutL lineage was replaced after

15 To detect spontaneous mutations in csrRS, mucoid and large colony variants of M1 strain MGAS166 we

16 e &gland, brain, muscle, immune, metabolism, mucoid and nerve conduction.

17 ate that elastase, when overproduced in both mucoid and non-mucoid cells, stimulates alginate synthes

18 serotype A), the switching occurred between mucoid and nonmucoid colonies.

19 imary clinical B. pseudomallei isolates with mucoid and nonmucoid colony morphologies from the same s

20 table for all of the agents tested, for both mucoid and nonmucoid isolates.

21 fibrosis pulmonary isolate FRD1, as well as mucoid and nonmucoid mutant strains, were monitored by A

22 s associated with ARF in the SLC region, 964 mucoid and nonmucoid pharyngeal isolates recovered in SL

23 t in addition to being intracellular in both mucoid and nonmucoid Pseudomonas aeruginosa, Ndk is also

24 found to promote phagocytic killing of both mucoid and nonmucoid strains as well as protection again

25 As expected, a rocA mutant is mucoid and produces more transcript from the has promote

26 be difficult because the organisms are often mucoid and slow growing.

27 study, we observed that in CF isolates, the mucoid and the nonmotile phenotypes occur predominantly

28 robial susceptibilities of 48 CF strains (25 mucoid) and 50 non-CF strains to 12 anti-Pseudomonas age

29 ny size (large, medium, and small) and their mucoid appearance on blood agar.

30 sed HCN production in an alginate-producing (mucoid) background.

31 ious reports of increased algR expression in mucoid backgrounds, and RpoS additionally plays a role i

32 also are cotranscribed in both nonmucoid and mucoid backgrounds.

33 More importantly, HNO2 killed mucoid bacteria (a) in anaerobic biofilms; (b) in vitro

34 These data suggest that mucoid bacteria either are in an iron-starved state rela

35 Here we show that mucoid bacteria perish during anaerobic exposure to 15 m

36 Mucoid bacteria produced approximately twofold-higher le

37 Increased proportions of mucoid bacteria were isolated during exacerbations occur

38 bits and elicited opsonic antibodies against mucoid but not nonmucoid P. aeruginosa, but nonetheless

39 X-treated mice also had dramatically reduced mucoid cell hyperplasia, and airway responsiveness retur

40 peribronchial eosinophilic infiltration and mucoid cell hyperplasia.

41 -kDa Ndk-Scs complex specifically present in mucoid cell predominantly synthesizes GTP and UTP but no

42 omplex media but is greatly reduced when the mucoid cells are grown in mineral salts media or in pres

43 osa is greatly reduced in alginate-secreting mucoid cells isolated from the lungs of cystic fibrosis

44 In mucoid cells of P. aeruginosa, Ndk is also known to exis

45 22) P. aeruginosa strains were compared, the mucoid cells were cleared several-fold less efficiently

46 se, when overproduced in both mucoid and non-mucoid cells, stimulates alginate synthesis.

47 We sequenced algK from the mucoid CF isolate FRD1 and expressed it in Escherichia c

48 otype of an DeltaalgL mutation in the highly mucoid CF isolate FRD1.

49 algZ deletion mutant was constructed in the mucoid CF isolate FRD1.

50 the secretion is triggered primarily in the mucoid CF isolate of strain 8821M (or in strain FRD1) bu

51 A typical mucoid CF isolate, FRD1, and its isogenic mutants were t

52 The overall frequency of mucA alterations in mucoid CF isolates was 84%.

53 The mucA22 allele is common in mucoid CF isolates.

54 90% reduction in alginate production in the mucoid, CF isolate, P. aeruginosa FRD1.

55 ariner transposon library using CF149, a non-mucoid clinical isolate with a misssense mutation in alg

56 r, the average amount of cyanide produced by mucoid clinical isolates was 4.7 +/- 0.85 micromol of HC

57 increase in bacterial hyaluronan production (mucoid colonies 200 mug per CFU and no detectable capsul

58 tified as csrR, caused the strain to produce mucoid colonies and to increase transcription of hasA, t

59 ive ("flesh-eating") infection often grow as mucoid colonies on primary culture but lose this colony

60 no detectable capsule production in the non-mucoid colonies).

61 between small, dry, compact and larger, more mucoid colonies.

62 ooth colony (SM) switches to a more virulent mucoid colony (MC) variant.

63 23.7%) isolates lacked the typical button or mucoid colony appearance of S. pneumoniae.

64 syrA was identified by its ability to confer mucoid colony morphology and by its ability to suppress

65 solates from these patients typically have a mucoid colony morphology due to overproduction of the ex

66 3 produced a transconjugant that exhibited a mucoid colony morphology, reflecting increased hyaluroni

67 the exopolysaccharide alginate resulting in mucoid colony morphology.

68 The hldD, hldE, and waaF mutants exhibited a mucoid colony phenotype due to production of a colanic a

69 Organisms with a mucoid colony phenotype when grown on blood agar plates

70 lymer poly-gamma-glutamate (PGA) to confer a mucoid colony phenotype.

71 a usually undergoes a phenotypic switch to a mucoid colony, which is characterized by the overproduct

72 h cells from smooth-colony variants (SM) and mucoid-colony variants (MC) arising from phenotypic swit

73 These results suggest that mucoid conversion and inhibition of invasive virulence d

74 However, the mucoid conversion can occur in wt mucA strains via the d

75 These observations suggested that mucoid conversion in CF may be driven by a selection for

76 that reducing activity of RpoD is linked to mucoid conversion in CF149.

77 omoter caused the overexpression of MucE and mucoid conversion in P. aeruginosa strains PAO1 and PA14

78 ion of the exopolysaccharide alginate causes mucoid conversion in Pseudomonas aeruginosa and is a poo

79 coid isolation, increased exacerbations, and mucoid conversion in vivo.

80 Mucoid conversion is indicative of overproduction of a c

81 In this study we hypothesized that mucoid conversion may be part of a larger response that

82 Estradiol and estriol induced mucoid conversion of P. aeruginosa in women with cystic

83 th cystic fibrosis are at increased risk for mucoid conversion of Pseudomonas aeruginosa, which contr

84 e C terminus of MucE (WVF) were required for mucoid conversion via two predicted proteases AlgW (DegS

85 Thus, even though dsbA is coregulated with mucoid conversion, it was not required for alginate prod

86 n cystic fibrosis patients typically undergo mucoid conversion.

87 order to identify protein levels enhanced by mucoid conversion.

88 factor MucA is a well-accepted mechanism for mucoid conversion.

89 ationic polypeptide-depleted fluid against a mucoid cystic fibrosis isolate of P. aeruginosa.

90 we tested wild-type strains PAO1, PA14, the mucoid cystic fibrosis isolate, FRD1 (mucA22+), and the

91 show here that a null mutation in kinB in a mucoid cystic fibrosis isolate, P. aeruginosa FRD1, did

92 structure of microvessel walls, formation of mucoid cysts initiated in the proximity of damaged micro

93 The severity of mucoid degeneration and chondroid metaplasia in the ACL

94 ar appearance, pronounced vacuolization, and mucoid degeneration, appearing as Wallerian degeneration

95 e found that P. aeruginosa strain PAO1 and a mucoid derivative of strain PAO1 each grew at dissolved

96 large fraction of P. aeruginosa CF isolates mucoid, did not abrogate AlgU-MucA interactions, althoug

97 iants of Cryptococcus neoformans (smooth and mucoid) differed in their abilities to promote increased

98 ns associated with cystic fibrosis are often mucoid due to the copious production of alginate, an exo

99 lon mutants are also mucoid, due to the stabilization of another Lon substrat

100 In addition, two mucoid E. faecalis isolates from patients with chronic u

101 r (TNF)-alpha, a proinflammatory cytokine in mucoid effusion, markedly increased Muc2 mucin mRNA expr

102 The mucoid exopolysaccharide (MEP) from P. aeruginosa has be

103 he opsonic antibody activity specific to the mucoid exopolysaccharide (MEP) surface antigen.

104 than those involved in the production of the mucoid exopolysaccharide alginate, are turned on during

105 aboration of the extracellular, O-acetylated mucoid exopolysaccharide, or alginate, is a major microb

106 upon the conversion of P. aeruginosa to the mucoid, exopolysaccharide alginate-overproducing phenoty

107 The conversion to mucoid, exopolysaccharide alginate-overproducing phenoty

108 from cystic fibrosis (CF) patients is their mucoid, exopolysaccharide alginate-overproducing phenoty

109 Similar experiments were performed with mucoid films collected from the inferior conjunctival fo

110 ular surface in DED patients and abundant in mucoid films.

111 use conversion from a typical nonmucoid to a mucoid form in the CF lung.

112 ix to eight times as intense as those of the mucoid FRD1 parent strain.

113 he algT-mucABCD operon, MucD was detected in mucoid (FRD1) and nonmucoid (PAO1) parental strains and

114 Four mucoid fur mutants produced 1.7- to 2.6-fold-greater fum

115 ignal intensities and the so-called inverted mucoid impaction signal (IMIS) sign was qualitatively an

116 This type of mucoid induction requires the alternate sigma factor Rpo

117 wild-type mice challenged with an LPS-rough mucoid isolate of P. aeruginosa lacking the CFTR ligand.

118 In some instances, mucoid isolates of P. aeruginosa were recovered from lun

119 Mucoid isolates were more likely to be hypermutators.

120 ratory strains and early lung colonizing non-mucoid isolates with a wt mucA.

121 However, for mucoid isolates, correlation coefficients (r values) for

122 they were significantly less effective with mucoid isolates.

123 show greater expression of the gene than do mucoid isolates.

124 tro and were associated with selectivity for mucoid isolation, increased exacerbations, and mucoid co

125 y and proteomic analyses were performed on a mucoid kinB mutant and an isogenic nonmucoid kinB rpoN d

126 ction from laboratory isolates revealed that mucoid laboratory strains made sevenfold more HCN than t

127 gulated using isogenic S. aureus MN8 and MN8 mucoid (MN8m) strains, the latter of which constitutivel

128 atients with cystic fibrosis often display a mucoid morphology due to high levels of expression of th

129 re to estradiol, P. aeruginosa adopted early mucoid morphology, whereas short-term exposure inhibited

130 romoter of rpoH was found to be activated in mucoid mucA mutants.

131 Alginate production in mucoid (MucA-defective) Pseudomonas aeruginosa is depend

132 Mucoid, mucA mutant Pseudomonas aeruginosa cause chronic

133 When isogenic nonmucoid (mucA+) and mucoid (mucA22) P. aeruginosa strains were compared, the

134 However, inactivation of algZ in a mucoid mutant P. aeruginosa strain, which had AlgU freed

135 Compared with MGAS166, these mucoid mutants are more hemolytic and cause significantl

136 Three mucoid mutants were identified with transposon insertion

137 ts showed that ectopic expression of FleQ in mucoid, nonmotile CF isolates restored flagellum biosynt

138 that AlgT inhibits flagellum biosynthesis in mucoid, nonmotile P. aeruginosa cystic fibrosis isolates

139 a repressor of fleQ, we mutated amrZ in the mucoid, nonmotile P. aeruginosa strain FRD1.

140 ntation of the mutant with amrZ restored the mucoid, nonmotile phenotype.

141 he cystic fibrosis lung frequently display a mucoid, nonmotile phenotype.

142 ibits lawn bordering and roaming behavior on mucoid nonpathogenic bacteria and loss of pathogen avoid

143 charge was frequent or very frequent in 85%, mucoid or mucopurulent in 90%, and moderate to severe in

144 hose in desert tortoises and include serous, mucoid, or purulent discharge from the nares, excessive

145 Mucoid otitis media (MOM) is characterized by viscous fl

146 CF cells sequentially infected with mucoid P. aeruginosa (MPA) and RV showed lower levels of

147 tor was also associated with reduced odds of mucoid P. aeruginosa (OR, 0.77; P = .013) and Aspergillu

148 ction chromatography of the crude extract of mucoid P. aeruginosa 8821, a CF isolate.

149 nse of cystic fibrosis and wild-type mice to mucoid P. aeruginosa administered by insufflation.

150 ntion of active elastase in the periplasm of mucoid P. aeruginosa and its role in the generation of t

151 sponse regulators activate alginate genes in mucoid P. aeruginosa appears not to be mediated by conve

152 l therapeutics directed against biofilms and mucoid P. aeruginosa are being developed.

153 it may play an important role in protecting mucoid P. aeruginosa biofilm bacteria from the human imm

154 ture and extracellular matrix composition of mucoid P. aeruginosa biofilms, through increased express

155 Thus mucoid P. aeruginosa cells elaborate enzymes that modula

156 creted into the extracellular environment by mucoid P. aeruginosa cells.

157 identified a protein(s), AlgZ, expressed in mucoid P. aeruginosa CF isolates that specifically bound

158 The calcium-induced extracellular matrix of mucoid P. aeruginosa consists primarily of the virulence

159 o the important clinical goal of eradicating mucoid P. aeruginosa from the CF airways.

160 investigated mechanisms of the emergence of mucoid P. aeruginosa in CF by analyzing the status of mu

161 The emergence of mucoid P. aeruginosa in CF is associated with increased

162 The emergence of mucoid P. aeruginosa in CF is associated with respirator

163 ing to the morbidity and mortality caused by mucoid P. aeruginosa in CF.

164 ung infections could not be established with mucoid P. aeruginosa in either cystic fibrosis or wild-t

165 fection, chronic P. aeruginosa infection and mucoid P. aeruginosa in individuals with cystic fibrosis

166 on of antibodies mediated opsonic killing of mucoid P. aeruginosa in vitro.

167 Indeed, chronic infection of the lung by mucoid P. aeruginosa is a major cause of morbidity and m

168 A mutation in the algR2 gene of mucoid P. aeruginosa is known to exhibit a nonmucoid (no

169 hesis by laboratory and clinical isolates of mucoid P. aeruginosa is necessary and sufficient to atte

170 airway epithelia to the stimuli presented by mucoid P. aeruginosa is not proinflammatory and, hence,

171 lyzing the status of mucA in a collection of mucoid P. aeruginosa isolates from 53 CF patients.

172 Comparison of paired nonmucoid and mucoid P. aeruginosa isolates from three CF patients ind

173 Interestingly, mucoid P. aeruginosa isolates from urinary tract infecti

174 enance of biofilms produced by nonmucoid and mucoid P. aeruginosa isolates.

175 rogated AIgU-dependent rpoH transcription in mucoid P. aeruginosa laboratory isolates and CF isolates

176 pared with wild-type controls in the face of mucoid P. aeruginosa lung infection.

177 in CF is the result of a global induction in mucoid P. aeruginosa of lipoproteins that act as proinfl

178 Our data indicate that (i) mucoid P. aeruginosa regardless of their origin (laborat

179 Transcriptional profiling analyses comparing mucoid P. aeruginosa strains to their isogenic algR dele

180 tibility testing of CF strains, particularly mucoid P. aeruginosa strains, is unknown.

181 ere similar in mice exposed to nonmucoid and mucoid P. aeruginosa throughout the infection.

182 tion of alginate maximizes the resistance of mucoid P. aeruginosa to antibody-independent opsonic kil

183 te plays an important role in the ability of mucoid P. aeruginosa to form biofilms and to resist comp

184 is the molecular basis for the resistance of mucoid P. aeruginosa to normally nonopsonic but alginate

185 ds or beads containing a clinical isolate of mucoid P. aeruginosa were instilled in the right lung of

186 We have previously reported that in mucoid P. aeruginosa, an intracellular protease cleaves

187 The recognition of genes induced in mucoid P. aeruginosa, other than those associated with a

188 ng that AlgR activates hcnA transcription in mucoid P. aeruginosa.

189 lobal responses to infection with motile and mucoid P. aeruginosa.

190 when the bulk of alginate is synthesized by mucoid P. aeruginosa.

191 Elastase is secreted in non-mucoid P. aeruginosa.

192 patients, encounters alginate elaborated by mucoid P. aeruginosa.

193 isk factors, only respiratory infection with mucoid PA correlated significantly with bronchiectasis (

194 isolates were more likely to be infected by mucoid PA, and they showed a narrow T-cell epitope respo

195 cantly related to respiratory infection with mucoid PA; attempts to prevent bronchiectasis should inc

196 Disruption of dsbA in the mucoid PDO300 background did not affect alginate product

197 Overexpression of algW in PAO1 resulted in a mucoid phenotype and alginate production, even in the ab

198 tion of phpA was found to correlate with the mucoid phenotype and an increase in algD transcription i

199 system that, when inactivated, results in a mucoid phenotype and enhanced virulence in mouse infecti

200 biofilms and the selection of mutants with a mucoid phenotype are major adaptations that allow its pe

201 conversion of Pseudomonas aeruginosa to the mucoid phenotype coincides with the establishment of chr

202 ion of invasive virulence factors and have a mucoid phenotype due to the production of an alginate ca

203 The conversion to mucoid phenotype in Pseudomonas aeruginosa during chroni

204 The mucoid phenotype indicates alginate overproduction and i

205 The mucoid phenotype is due to abundant production of the hy

206 well-studied mechanism for transition to the mucoid phenotype is mutation of mucA, leading to loss of

207 regulator of both sigma(22) activity and the mucoid phenotype is the cognate anti-sigma factor MucA.

208 we demonstrated that in vivo switching to a mucoid phenotype occurred in two mice strains and was as

209 ere identified as positive regulators of the mucoid phenotype on PIAAMV.

210 Conversion of Pseudomonas aeruginosa to the mucoid phenotype plays a major role in the pathogenesis

211 The mucoid phenotype results from loss-of-function mutations

212 The alginate-overproducing (Alg(+)) mucoid phenotype seen in the CF isolates is extremely un

213 rity, and in the concomitant appearance of a mucoid phenotype that is reminiscent of cells in the ear

214 y have negative effects on expression of the mucoid phenotype under the conditions tested.

215 Reversion to the mucoid phenotype was associated with reversion of the mu

216 The algXDelta::Gm mutant was restored to the mucoid phenotype with wild-type P. aeruginosa algX provi

217 opolysaccharide abundance (contributing to a mucoid phenotype).

218 riant was experimentally proven to cause the mucoid phenotype, and corresponding resistance to phagoc

219 tic susceptibility, capsule composition, and mucoid phenotype.

220 s, P. aeruginosa undergoes a conversion to a mucoid phenotype.

221 saccharide, alginate, giving these strains a mucoid phenotype.

222 ause alginate overproduction, resulting in a mucoid phenotype.

223 lginate, an exopolysaccharide that confers a mucoid phenotype.

224 ss of O-antigen synthesis alternating with a mucoid phenotype.

225 kground was constructed, and it showed a non-mucoid phenotype.

226 classic feature of CF airway isolates is the mucoid phenotype.

227 the host immune system, and conversion to a mucoid phenotype.

228 P. aeruginosa strains PAO1 and PA14 are non-mucoid, producing minimal amounts of alginate.

229 enBank database with only weak similarity to mucoid protein sequences.

230 In conclusion, mucoid Pseudomonas adapted to the CF-lung remained able

231 [FEV(1)]) of the CFTR gene genotype, gender, mucoid Pseudomonas aeruginosa (MPA) infection status, pr

232 Mucoid Pseudomonas aeruginosa (n = 12; 15%) and nontuber

233 iated with chronic pulmonary infections with mucoid Pseudomonas aeruginosa (PA).

234 tics, tobramycin and ciprofloxacin, into non-mucoid Pseudomonas aeruginosa biofilms.

235 fficacy of azithromycin in a murine model of mucoid Pseudomonas aeruginosa endobronchial infection.

236 maintenance of chronic lung infections with mucoid Pseudomonas aeruginosa in patients with cystic fi

237 The exopolysaccharide alginate, produced by mucoid Pseudomonas aeruginosa in the lungs of cystic fib

238 tible to chronic pulmonary disease caused by mucoid Pseudomonas aeruginosa strains that overproduce t

239 In non-mucoid Pseudomonas aeruginosa strains, the Pel and Psl p

240 ciated with chronic pulmonary infection with mucoid Pseudomonas aeruginosa.

241 c bacteria and loss of pathogen avoidance on mucoid Pseudomonas aeruginosa.

242 tors in nontypeable, alginate overproducing (mucoid) Pseudomonas aeruginosa strains isolated from cys

243 we screened a transposon library in the non-mucoid reference strain PAO1, and identified a mutant th

244 were found to display phenotypes which were mucoid relative to the phenotype of the parental algB st

245 s been attributed to accumulation of viscous mucoid secretions in intrahepatic bile ducts.

246 hrough viscoelastic cervical mucus and other mucoid secretions to reach the site of fertilization.

247 By using a representative strain of the mucoid serotype 3 clone, rough phase variants with a div

248 ations were found to be strain specific: the mucoid strain 18A experienced mutations in alginate prod

249 ies from isogenic nonmucoid strain 4095a and mucoid strain 4095c were further investigated.

250 whether these proteins were enhanced in the mucoid strain due to increased transcription.

251 genesis of nonmucoid algB derivatives of the mucoid strain FRD1 was employed.

252 gG activity, a mutant was constructed in the mucoid strain FRD1 with a defined non-polar deletion of

253 Herein we show that a highly mucoid strain of E. coli K-12 ligates CA repeats to a si

254 on the eradication of biofilms formed by the mucoid strain of Pseudomonas aeruginosa and investigated

255 FU of group B streptococci or 10(7) CFU of a mucoid strain of Pseudomonas aeruginosa by intratracheal

256 For mucoid strain P. aeruginosa FRD1, calcium addition (1.0

257 eatment with S-nitrosoglutathione, while the mucoid strain PAO578II showed no further upregulation ab

258 pted agar bead murine model using a clinical mucoid strain that demonstrates the key features of tran

259 teins that were clearly more abundant in the mucoid strain were observed.

260 However, the mucoid strains can revert to nonmucoidy in vitro through

261 Non-mucoid strains can use either Pel or Psl as the primary

262 tions are cleared but chronic infection with mucoid strains ensues in the majority of CF patients and

263 Here, we show that mucoid strains of bacteria that produce an exopolysaccha

264 In the presence of mucoid strains of bacteria, the C. elegans laboratory wi

265 However, certain clinical mucoid strains of P. aeruginosa have a wild-type (wt) mu

266 odies broadly cross-reactive to heterologous mucoid strains of P. aeruginosa.

267 an extracellular polysaccharide produced by mucoid strains of Pseudomonas aeruginosa that are typica

268 The second were the mucoid strains Smith diffuse and M, both of which encode

269 on resulted in suppression of mucoidy in all mucoid strains tested, indicating that sigma factor comp

270 ent promoter (PssrA ) was more active in non-mucoid strains than in isogenic mucoid variants.

271 l), is required for biofilm formation in non-mucoid strains that do not rely on alginate as the princ

272 uggests that the reduced CBC observed in the mucoid strains was due to masking of the collagen adhesi

273 ) of nonmucoid strains and 40% (24 of 60) of mucoid strains were definitively identified as Pseudomon

274 n were non-CF strains (P < 0.0001), although mucoid strains were not more likely to have serious disc

275 Mucoid strains with mucA mutations predominantly populat

276 enhanced or reduced formation of alginate in mucoid strains, respectively.

277 ved from Pseudomonas lipoproteins induced in mucoid strains.

278 d the presence of mucA mutations only in the mucoid strains.

279 tL lineage was replaced after 11 days by non-mucoid strains.

280 MAb-reactive (nonmucoid) and nonreactive (mucoid) strains from the same patient exhibited identica

281 onic acid capsule on highly encapsulated, or mucoid, strains.

282 Selection of both pre-existing non-mucoid subpopulations and of novel phenotypic traits sug

283 Similar to cells of the mucoid switch variant, all1Delta cells produced a larger

284 und to be downregulated in the hypervirulent mucoid switch variant, both during logarithmic growth an

285 mimicked the hypervirulent phenotype of the mucoid switch variant, which is characterized by decreas

286 hese mutants ranged from being only slightly mucoid to being indistinguishable from that of the origi

287 One of the particularly mucoid transposon mutants was chosen for further study.

288 erotype 19 gives rise to variants (the small mucoid variant [SMV] and the acapsular small-colony vari

289 Rats infected with the mucoid variant developed increased ICP, whereas rats inf

290 The large mucoid variant formed flat unstructured biofilms, failed

291 brain fungal burdens were comparable between mucoid variant- and smooth parent-infected rats.

292 cerebrospinal fluid (CSF) fungal burden for mucoid variant-infected rats, although brain fungal burd

293 intensity over the surfaces of the brains of mucoid variant-infected rats.

294 charide accumulated in the CSF and brains of mucoid variant-infected rats.

295 tic inflammatory response in the meninges of mucoid variant-infected rats.

296 Mucoid variants appeared at later biofilm developmental

297 Mucoid variants of the opportunistic pathogen Pseudomona

298 Low oxygen tension growth of mucoid variants readily selects for nonmucoid variants.

299 ctive in non-mucoid strains than in isogenic mucoid variants.

300 In contrast, the mucoid wild-type strain produced only polymerized uronic