ライフサイエンスコーパス: toxic shock

1 yndecan-1-null mice undergoing Gram-positive toxic shock.

2 ells, which can result in potentially lethal toxic shock.

3 ice and were also protected from SEB-induced toxic shock.

4 as a leading cause of food-borne disease and toxic shock.

5 and protective efficacy in a mouse model of toxic shock.

6 including sepsis, necrotizing fasciitis and toxic shock.

7 be key effector cells in the pathogenesis of toxic shock.

8 sociated with severe systemic infections and toxic shock.

9 -induced lymphocyte proliferation and lethal toxic shock.

10 t attempt to associate toxin production with toxic shock.

11 ock and multiorgan failure characteristic of toxic shock.

12 ring on the pathophysiology of streptococcal toxic shock.

13 e for IL-18/IL-18Ralpha in Ehrlichia-induced toxic shock.

14 ering a potential approach in the therapy of toxic shock.

15 ller (NK) and NKT cells in Ehrlichia-induced toxic shock.

16 ting inflammatory responses in Gram-positive toxic shock, a systemic disease that is a significant ca

17 oning, is also a superantigen that can cause toxic shock after traumatic or surgical staphylococcal w

18 MyD88(-/-) mice were resistant to SEA or SEB toxic shock and displayed reduced levels of pro-inflamma

19 These enterotoxins, which cause both toxic shock and food poisoning, bind in an identical way

20 Staphylococcal enterotoxin B induces toxic shock and is a major virulence factor of staphyloc

21 inflammation, permanent airway destruction, toxic shock, and mortality.

22 an diseases including pharyngitis, impetigo, toxic shock, and necrotizing fasciitis, as well as the p

23 lethal in two animal models of streptococcal toxic shock, and SpeM was lethal in one model.

24 ar to WT mice, they did not develop signs of toxic shock, as shown by elevated bacterial burdens, low

25 sm that protects the host from Gram-positive toxic shock by inhibiting the dysregulation and amplific

26 in, rescued syndecan-1-null mice from lethal toxic shock by suppressing the production of TNFalpha an

27 ing in myriad disorders, such as dermatitis, toxic shock, cardiovascular disease, acute pelvic and ar

28 hich is known to mediate immunopathology and toxic shock in a murine model of fatal ehrlichiosis.

29 EABs have recently been proposed to monitor toxic shocks in oxic solutions that are poor or devoid o

30 ctivation and cytokine production as well as toxic shock induced by staphylococcal enterotoxin B (SEB

31 omplications characteristic of streptococcal toxic shock-like syndrome (TSLS).

32 infection with IOE resulted in acute, severe toxic shock-like syndrome and severe multifocal hepatic

33 of CD1d-restricted NKT cells in induction of toxic shock-like syndrome caused by gram-negative, lipop

34 otropic Ehrlichia strains results in a fatal toxic shock-like syndrome characterized by a decreased n

35 virulent Ehrlichia strain (IOE) results in a toxic shock-like syndrome characterized by severe liver

36 uis arthroplasty infection and streptococcal toxic shock-like syndrome due to an nonencapsulated sero

37 [IOE]) results in CD8+ T-cell-mediated fatal toxic shock-like syndrome marked by apoptosis of CD4+ T

38 ls mediate Ehrlichia-induced T-cell-mediated toxic shock-like syndrome, most likely via cognate and n

39 HME disease can range from mild to a fatal, toxic shock-like syndrome, yet the mechanisms regulating

40 ng adult respiratory distress syndrome and a toxic shock-like syndrome.

41 ologies as well as severe conditions such as toxic shock-like syndrome.

42 racellular bacterium that causes acute fatal toxic shock-like syndrome.

43 man monocytic ehrlichiosis (HME) that mimics toxic-shock-like syndrome in immunocompetent hosts.

44 oup A Streptococcus, is sufficient to induce toxic-shock-like vascular leakage and tissue injury.

45 role for these cytokines in the treatment of toxic shock merits further investigation.

46 by proinflammatory nucleic acids in an acute toxic shock model in mice.

47 for their therapeutic efficacy in the mouse toxic shock model using different challenge doses of SEB

48 on molecule 1 have a negligible role in this toxic shock model.

49 athology in situations such as gram-positive toxic shock or Mycobacterium infection.

50 activated innate immunity: endotoxin-induced toxic shock, PMA-induced contact dermatitis and lipopoly

51 ly protected mice from lethal challenge in a toxic shock post-exposure model.

52 was 11% but was much higher in patients with toxic shock syndrome (55%) and necrotizing fasciitis (58

53 the intensive care unit (ICU) for menstrual toxic shock syndrome (m-TSS) are lacking.

54 Menstrual toxic shock syndrome (mTSS) is a life-threatening diseas

55 Menstrual toxic shock syndrome (mTSS) is a rare but severe disorde

56 Menstrual toxic shock syndrome (mTSS) is thought to be associated

57 (n = 1132), KD shock syndrome (n = 45), and toxic shock syndrome (n = 37) who had been admitted to h

58 Streptococcal toxic shock syndrome (strep TSS) with associated necroti

59 Streptococcal toxic shock syndrome (StrepTSS) is an invasive infection

60 tic cases have been defined as streptococcal toxic shock syndrome (StrepTSS).

61 e from severe cases, including streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (N

62 S) isolates from patients with streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (N

63 Streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis ar

64 n A) is highly associated with streptococcal toxic shock syndrome (STSS) and other invasive streptoco

65 s associated with outbreaks of streptococcal toxic shock syndrome (STSS) in the United States and Eur

66 Streptococcal toxic shock syndrome (STSS) is a highly lethal, acute-on

67 Streptococcal toxic shock syndrome (STSS) is a rapidly progressing, li

68 nd is strongly associated with streptococcal toxic shock syndrome (STSS), a severe and often fatal il

69 sult in the recently described streptococcal toxic shock syndrome (STSS), which is characterized by r

70 ave been implicated in causing streptococcal toxic shock syndrome (STSS).

71 necrotizing fasciitis (NF) or streptococcal toxic shock syndrome (STSS).

72 OR, 8.64; 95% CI, 5.50-13.55), streptococcal toxic shock syndrome (STSS; OR, 11.71; 95% CI, 4.39-31.1

73 e of inflammatory cytokines that can lead to toxic shock syndrome (TSS) and death.

74 Toxic shock syndrome (TSS) and other superantigen-mediat

75 erantigens (PTSAgs) that are associated with toxic shock syndrome (TSS) and staphylococcal food poiso

76 creted virulence factors sufficient to cause toxic shock syndrome (TSS) in the animals.

77 Toxic shock syndrome (TSS) is a clinical consequence of

78 Toxic shock syndrome (TSS) is a multi system disorder re

79 Toxic shock syndrome (TSS) is an acute onset illness cha

80 Toxic shock syndrome (TSS) is caused by staphylococcal a

81 Toxic shock syndrome (TSS) may be mediated by superantig

82 Lethal toxic shock syndrome (TSS) results from the MHC class II

83 uced by concentrations of the staphylococcal toxic shock syndrome (TSS) toxin 1 (TSST-1) and the stre

84 Despite knowledge of the effects of toxic shock syndrome (TSS) toxin 1 (TSST-1) on the adapt

85 During toxic shock syndrome (TSS), bacterial superantigens trig

86 G) is sometimes administered for presumptive toxic shock syndrome (TSS), but its frequency of use and

87 icated in several serious diseases including toxic shock syndrome (TSS), Kawasaki disease, and sepsis

88 Many cases of neonatal toxic shock syndrome (TSS)-like exanthematous disease bu

89 of inflammatory molecules and potentially to toxic shock syndrome (TSS).

90 nd compared with isolates from patients with toxic shock syndrome (TSS).

91 eins compared to isolates from patients with toxic shock syndrome (TSS).

92 tening consequences typically encountered in toxic shock syndrome (TSS).

93 egs) might be beneficial in diseases such as toxic shock syndrome (TSS).

94 rome toxin-1 (TSST-1), are the main cause of toxic shock syndrome (TSS).

95 olonizer of the nose and is a major cause of toxic shock syndrome (TSS).

96 with but distinct from Kawasaki disease and toxic shock syndrome admitted to a New York City hospita

97 obic, Gram-positive bacterium that can cause toxic shock syndrome after gynecological procedures.

98 nts (three with hydronephrosis), and five of toxic shock syndrome after use of the menstrual cup.

99 nkeys manifested a T cell activation-related toxic shock syndrome and a profound depletion of CD4+ ly

100 xin B (SEB) is a potent toxin that can cause toxic shock syndrome and act as a lethal and incapacitat

101 This cascade can ultimately result in toxic shock syndrome and death.

102 e of inflammatory cytokines that can lead to toxic shock syndrome and death.

103 ens (SAg) as dangerous toxins that may cause toxic shock syndrome and death.

104 d underlying medical conditions; 4 developed toxic shock syndrome and died (case fatality, 57%).

105 SAGs have been implicated in toxic shock syndrome and food poisoning, and they may al

106 important causative agents in staphylococcal toxic shock syndrome and food poisoning.

107 aureus group-III strains are responsible for toxic shock syndrome and have been underestimated in oth

108 auses a variety of human diseases, including toxic shock syndrome and necrotizing fasciitis, which ar

109 e disease in humans, including streptococcal toxic shock syndrome and necrotizing fasciitis.

110 rom pharyngitis to severe infections such as toxic shock syndrome and necrotizing fasciitis.

111 irulence factors and are responsible for the toxic shock syndrome and other superantigen-related dise

112 duce a massive release of cytokines, causing toxic shock syndrome and possibly death.

113 describe four deaths due to endometritis and toxic shock syndrome associated with C. sordellii that o

114 Endometritis and toxic shock syndrome associated with Clostridium sordell

115 with necrotizing fasciitis or streptococcal toxic shock syndrome between January 1, 2013, and Decemb

116 e GAS infections, including 11 streptococcal toxic shock syndrome cases and one necrotizing fasciitis

117 he 1980s, and the incidence of streptococcal toxic shock syndrome cases continues to rise.

118 ylococcus aureus is a causative agent of the toxic shock syndrome disease.

119 ria that cause fatal ehrlichiosis, mimicking toxic shock syndrome in humans and mice.

120 en exotoxins that mediate food poisoning and toxic shock syndrome in humans.

121 The cause of death is a syndrome much like toxic shock syndrome in humans.

122 partial thromboplastin time in streptococcal toxic shock syndrome is associated with activation of th

123 Streptococcal toxic shock syndrome occurred in 29 children (5.8%), nec

124 ease that can have manifestations similar to toxic shock syndrome or Kawasaki disease.

125 (GAS) necrotizing soft tissue infections and toxic shock syndrome remain high-mortality conditions.

126 sis of necrotizing soft-tissue infection and toxic shock syndrome resulting from Streptococcus pyogen

127 The epidemic of toxic shock syndrome that occurred in the 1970s was caus

128 s described that specifically promote either toxic shock syndrome toxin (TSST) 1 or staphylococcal en

129 (lukMF) genes, while 44.4% were positive for toxic shock syndrome toxin (tsst) gene.

130 on of staphylococcal enterotoxin A (SEA) and toxic shock syndrome toxin (TSST) in neat milk without s

131 us, staphylococcal enterotoxins (SE) A-E and toxic shock syndrome toxin (TSST)-1, which are associate

132 ncluding the staphylococcal enterotoxins and toxic shock syndrome toxin (TSST).

133 nicity island SaPI1 carries the gene for the toxic shock syndrome toxin (TSST-1) and can be mobilized

134 IPs to S. aureus inhibited the production of toxic shock syndrome toxin (TSST-1) and enterotoxin C3,

135 dose-dependent transcytosis in vitro, while toxic shock syndrome toxin (TSST-1) exhibited increased

136 the gram-positive model of shock mediated by toxic shock syndrome toxin (TSST-1), Mif(-/-) mice succu

137 .g., carriage of the enterotoxin A (sea) and toxic shock syndrome toxin (tst) genes and production of

138 of oxygen is necessary for the production of toxic shock syndrome toxin 1 (TSST-1) by Staphylococcus

139 The production of toxic shock syndrome toxin 1 (TSST-1) by Staphylococcus

140 he effect of O(2) and CO(2) on expression of toxic shock syndrome toxin 1 (TSST-1) by Staphylococcus

141 Toxic shock syndrome toxin 1 (TSST-1) contains a long ce

142 The superantigenic function of toxic shock syndrome toxin 1 (TSST-1) is generally regar

143 s with staphylococcal enterotoxin B (SEB) or toxic shock syndrome toxin 1 (TSST-1) resulted in enhanc

144 Administration of the superantigen toxic shock syndrome toxin 1 (TSST-1) results in the spe

145 T2-I-A(b), is very inefficient at presenting toxic shock syndrome toxin 1 (TSST-1) to T cells, sugges

146 ne monoclonal antibodies (MAbs) specific for toxic shock syndrome toxin 1 (TSST-1), a bacterial super

147 there have been reports of the production of toxic shock syndrome toxin 1 (TSST-1), enterotoxin, and

148 Superantigens, such as toxic shock syndrome toxin 1 (TSST-1), have been implica

149 tes production of agr RNAIII, protein A, and toxic shock syndrome toxin 1 (TSST-1), particularly unde

150 r, unlike the classical enterotoxins SEB and toxic shock syndrome toxin 1 (TSST-1), the gene for SEl-

151 ught to be associated with colonization with toxic shock syndrome toxin 1 (TSST-1)-producing Staphylo

152 strain and presence of the gene encoding for toxic shock syndrome toxin 1 (TSST-1).

153 tigens staphylococcal enterotoxin B (SEB) or toxic shock syndrome toxin 1 (TSST-1).

154 tum or pharynx of patients with KD, secretes toxic shock syndrome toxin 1 (TSST-1).

155 g., staphylococcal enterotoxin A [SEA], SEB, toxic shock syndrome toxin 1 [TSST-1]) which act both as

156 ococcal enterotoxin A (SEA), SEB, or SEC3 or toxic shock syndrome toxin 1 and a potentiating dose of

157 study the activity of superantigens such as toxic shock syndrome toxin 1 and also found that despite

158 ant Staphylococcus aureus and genes encoding toxic shock syndrome toxin 1 and Panton-Valentine leukoc

159 ode and disseminate the superantigen toxins, toxic shock syndrome toxin 1 and superantigen enterotoxi

160 ttenuated staphylococcal enterotoxin (SE) or toxic shock syndrome toxin 1 develop protective antibodi

161 mec type II, the enterotoxin A gene, and the toxic shock syndrome toxin 1 gene.

162 taphylococcal clone or structural variant of toxic shock syndrome toxin 1 is associated with Kawasaki

163 replication, and suboptimal stimulation with toxic shock syndrome toxin 1 leads to viral replication

164 staphylococcal enterotoxin B and C negative, toxic shock syndrome toxin 1 positive, and staphylococca

165 al samples positive for S. aureus (83%), and toxic shock syndrome toxin 1 was isolated from 66 strain

166 nced portions of the regions encoding mature toxic shock syndrome toxin 1 were identical in all six s

167 f staphylococcal enterotoxin A (SEA) to SEH, toxic shock syndrome toxin 1, and Panton-Valentine leuko

168 roliferation in response to the superantigen toxic shock syndrome toxin 1, as well as the proliferati

169 erum) against combinations of superantigens (toxic shock syndrome toxin 1, enterotoxins B and C, and

170 eukocidins (eg, Panton-Valentine leukocidin, toxic shock syndrome toxin 1, exfoliative toxins, and va

171 eus toxins (the enterotoxins A and B and the toxic shock syndrome toxin).

172 ere capable of attenuating the production of toxic shock syndrome toxin-1 (also under the control of

173 Responses to toxic shock syndrome toxin-1 (TSST-1) and pokeweed mitog

174 as well as the staphylococcal superantigens toxic shock syndrome toxin-1 (TSST-1) and staphylococcus

175 fine the interface between the bacterial SAG toxic shock syndrome toxin-1 (TSST-1) and the TCR, we pe

176 ee-dimensional structures of five mutants of toxic shock syndrome toxin-1 (TSST-1) have been determin

177 The staphylococcal superantigen toxic shock syndrome toxin-1 (TSST-1) is a causative age

178 aphylococcus aureus strains that produce the toxic shock syndrome toxin-1 (TSST-1) superantigen.

179 superantigens [staphylococcal enterotoxins, toxic shock syndrome toxin-1 (TSST-1), and streptococcal

180 Staphylococcal superantigens (SAgs), such as toxic shock syndrome toxin-1 (TSST-1), are the main caus

181 nical cases of TSS arise due to an exotoxin, toxic shock syndrome toxin-1 (TSST-1), elaborated by tox

182 Tst, the gene for toxic shock syndrome toxin-1 (TSST-1), is part of a 15.2

183 ram quantities of topically applied purified toxic shock syndrome toxin-1 (TSST-1), staphylococcal en

184 A major causative agent of TSS is toxic shock syndrome toxin-1 (TSST-1), which is unique r

185 teins although they elaborate high levels of toxic shock syndrome toxin-1 (TSST-1).

186 EB), staphylococcal enterotoxin C (SEC), and toxic shock syndrome toxin-1 (TSST-1).

187 We investigated whether the superantigen toxic shock syndrome toxin-1 (TSST1) could induce an ant

188 Toxic shock syndrome toxin-1 (TSST1) is a superantigenic

189 Panton-Valentine Leukocidin toxin (PVL), and toxic shock syndrome toxin-1 (tst) genes.

190 nine mutations were constructed in S. aureus toxic shock syndrome toxin-1 amino acids D120 to D130.

191 A dodecapeptide region (toxic shock syndrome toxin-1 amino acids F119-D130), rel

192 lysin streptolysin O enhanced penetration of toxic shock syndrome toxin-1 and streptococcal pyrogenic

193 The pyrogenic toxin toxic shock syndrome toxin-1 from Staphylococcus aureus

194 d theories of Kawasaki disease etiology, the toxic shock syndrome toxin-1 hypothesis and the coronavi

195 Toxic shock syndrome toxin-1 induces interleukin-8 from

196 Staphylococcus aureus superantigen toxic shock syndrome toxin-1 is a major cause of menstru

197 r, a detailed structural analysis shows that toxic shock syndrome toxin-1 lacks several structural fe

198 Toxic shock syndrome toxin-1 producing S. aureus was int

199 bond affects S. aureus biofilm formation and toxic shock syndrome toxin-1 production.

200 Toxic shock syndrome toxin-1 residue D130 may contribute

201 e, 96% of the lesional isolates produced the toxic shock syndrome toxin-1 superantigen, and most of t

202 ly express BP107 conformational epitopes and toxic shock syndrome toxin-1 superantigen-binding capabi

203 ells were stimulated with the staphylococcal toxic shock syndrome toxin-1, enterotoxin A, or enteroto

204 - and beta-toxins, but not enterotoxin A and toxic shock syndrome toxin-1, rapidly potentiated sheddi

205 The superantigenic toxins toxic shock syndrome toxin-1, staphylococcal enterotoxin

206 enough to allow for enhanced penetration of toxic shock syndrome toxin-1, whereas streptolysin O dir

207 trains of S. aureus produce the superantigen toxic shock syndrome toxin-1, which can penetrate the va

208 Toxic shock syndrome toxin-1-neutralizing antibodies wer

209 This study shows that toxic shock syndrome toxin-1-positive S. aureus is preva

210 irements similar to that for presentation of toxic shock syndrome toxin-1.

211 is, and Neisseria gonorrhoeae, as well as to toxic shock syndrome toxin-1.

212 as inhibition of T cell proliferation due to toxic shock syndrome toxin-1.

213 era toxin, staphylococcal enterotoxin A, and toxic shock syndrome toxin.

214 es (both MSSA and MRSA) carried the gene for toxic shock syndrome toxin; however, carriage of the gen

215 One isolate possessed the gene for toxic shock syndrome toxin; none had genes for exfoliati

216 ium or serum or in vivo in a rabbit model of toxic shock syndrome using DNA microarrays.

217 esis, a strain recovered from a patient with toxic shock syndrome was serially passaged for 6 weeks,

218 ained from seven patients with streptococcal toxic shock syndrome who received IVIG therapy, and the

219 g high-risk or protection from streptococcal toxic shock syndrome with a strong protection conferred

220 tellation of symptoms that strongly resemble toxic shock syndrome, an escalation of the cytotoxic ada

221 bacteremia, septic arthritis, streptococcal toxic shock syndrome, and necrotizing fasciitis) caused

222 TNF release during acute TSST1-precipitated toxic shock syndrome, and the C-terminal domain to stimu

223 rious diseases, including food poisoning and toxic shock syndrome, are termed superantigens (SAgs).

224 ted in a number of human diseases, including toxic shock syndrome, diabetes mellitus and multiple scl

225 Most strains causing toxic shock syndrome, however, produce and secrete very

226 known virulence factors in scarlet fever and toxic shock syndrome, mechanisms by how SAgs contribute

227 State reported cases of Kawasaki's disease, toxic shock syndrome, myocarditis, and potential MIS-C i

228 itis, impetigo, scarlet fever, streptococcal toxic shock syndrome, necrotizing fasciitis and myositis

229 ases of severe iGAS infection (streptococcal toxic shock syndrome, necrotizing fasciitis, septic shoc

230 igens (PTSAgs) that can cause illness, e.g., toxic shock syndrome, or synergize with a number of othe

231 um sordellii, causes a rarer but often fatal toxic shock syndrome, particularly in gynecological and

232 een implicated in serious disease, including toxic shock syndrome, the specific pathological mechanis

233 iseases, including necrotizing fasciitis and toxic shock syndrome, were analyzed.

234 Staphylococcal superantigens cause toxic shock syndrome, which is characterized by massive

235 V-2 infection, shares clinical features with toxic shock syndrome, which is triggered by bacterial su

236 on of bacterial superantigens, most commonly toxic shock syndrome-1 (TSST-1), to specific TCR Vbeta-b

237 ections to life-threatening endocarditis and toxic shock syndrome.

238 ndrome toxin-1 is a major cause of menstrual toxic shock syndrome.

239 teract with underlying immune cells to cause toxic shock syndrome.

240 class II allelic variation in streptococcal toxic shock syndrome.

241 th GAS myonecrosis who died of streptococcal toxic shock syndrome.

242 ections, including necrotizing fasciitis and toxic shock syndrome.

243 nes, ultimately causing a condition known as toxic shock syndrome.

244 n humans including necrotizing fasciitis and toxic shock syndrome.

245 arious diseases including food poisoning and toxic shock syndrome.

246 ins (SEs) that cause both food poisoning and toxic shock syndrome.

247 se ranging from pharyngitis to streptococcal toxic shock syndrome.

248 rotoxins (SEs) that cause food poisoning and toxic shock syndrome.

249 m isolated from a patient with streptococcal toxic shock syndrome.

250 h as necrotizing fasciitis and streptococcal toxic shock syndrome.

251 llin-resistant strains and organisms causing toxic shock syndrome.

252 ing food poisoning, bacterial arthritis, and toxic shock syndrome.

253 profound shock associated with streptococcal toxic shock syndrome.

254 me identified in patients with streptococcal toxic shock syndrome.

255 with necrotizing fasciitis or streptococcal toxic shock syndrome.

256 produce disease, such as food poisoning and toxic shock syndrome.

257 d as major virulence factors responsible for toxic shock syndrome.

258 sponses in the pathogenesis of streptococcal toxic shock syndrome.

259 ed with the recently described streptococcal toxic shock syndrome.

260 multiorgan failure define the streptococcal toxic shock syndrome.

261 l bacteremia that mimics human Streptococcal toxic shock syndrome.

262 ections, including necrotizing fasciitis and toxic shock syndrome.

263 with necrotizing fasciitis or streptococcal toxic shock syndrome.

264 ildren, which resembles superantigen-induced toxic shock syndrome.

265 tion of T cells and inflammation, leading to toxic shock syndrome.

266 m localized skin abscess to life-threatening toxic shock syndrome.

267 e outcomes such as necrotizing fasciitis and toxic shock syndrome.

268 rldwide, including necrotizing fasciitis and toxic shock syndrome.

269 ditions, including necrotizing fasciitis and toxic shock syndrome.

270 comes of death, limb loss, and streptococcal toxic shock syndrome.

271 an penetrate the vaginal epithelium to cause toxic shock syndrome.

272 o life-threatening necrotizing fasciitis and toxic shock syndrome.

273 alleles significantly increase the risk for toxic shock syndrome.

274 indings that death was due to tampon-related toxic shock syndrome.

275 7-year-old female who died of tampon-related toxic shock syndrome.

276 o mediate the symptoms collectively known as toxic shock syndrome.

277 inal mucosa, induce interleukin-8, and cause toxic shock syndrome.

278 rwhelming cytokine production, which lead to toxic shock syndrome.

279 has features that overlap with myocarditis, toxic-shock syndrome and Kawasaki disease.

280 disease in epidemics and its resemblance to toxic-shock syndrome make an infectious etiology seem mo

281 anton-Valentine leukocidin, alpha-toxin, and toxic-shock syndrome toxin 1 and increased toxin product

282 Immunoblot analysis of the enterotoxins, toxic-shock syndrome toxin 1, and SpeA with antiserum pr

283 n-Valentine leukocidin, alpha-hemolysin, and toxic-shock syndrome toxin 1, in both methicillin-sensit

284 lococcus aureus enterotoxins (S.E.) A-I, and toxic-shock syndrome toxin TSST-1 act as superantigens t

285 ion of CD14 by LPS can cause the often fatal toxic-shock syndrome.

286 evere systemic conditions such as septic and toxic shock syndromes.

287 microbial cathodes may be more sensitive to toxic shocks than anodic, heterotrophic EABs.

288 The Staphylococcus aureus gene for toxic shock toxin (tst) is carried by a 15 kb mobile pat

289 cline, and vancomycin resistance, as well as toxic shock toxin and Panton-Valentine leukocidin.

290 k, we reported that the staphylococcal toxin toxic shock toxin-1 (TSST-1), a prototypic superantigen,

291 Surprisingly, 6 of 16 strains were the same toxic shock toxin-1 (TSST-1)-positive clone, designated

292 ich CD8(+) T cells mediate Ehrlichia-induced toxic shock, which is associated with IL-10 overproducti