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1 ections, including necrotizing fasciitis and toxic shock syndrome.
2 nes, ultimately causing a condition known as toxic shock syndrome.
3 n humans including necrotizing fasciitis and toxic shock syndrome.
4 arious diseases including food poisoning and toxic shock syndrome.
5 ins (SEs) that cause both food poisoning and toxic shock syndrome.
6 se ranging from pharyngitis to streptococcal toxic shock syndrome.
7 rotoxins (SEs) that cause food poisoning and toxic shock syndrome.
8 m isolated from a patient with streptococcal toxic shock syndrome.
9 h as necrotizing fasciitis and streptococcal toxic shock syndrome.
10 llin-resistant strains and organisms causing toxic shock syndrome.
11 ing food poisoning, bacterial arthritis, and toxic shock syndrome.
12 profound shock associated with streptococcal toxic shock syndrome.
13 me identified in patients with streptococcal toxic shock syndrome.
14 produce disease, such as food poisoning and toxic shock syndrome.
15 d as major virulence factors responsible for toxic shock syndrome.
16 sponses in the pathogenesis of streptococcal toxic shock syndrome.
17 ed with the recently described streptococcal toxic shock syndrome.
18 multiorgan failure define the streptococcal toxic shock syndrome.
19 with necrotizing fasciitis or streptococcal toxic shock syndrome.
20 l bacteremia that mimics human Streptococcal toxic shock syndrome.
21 with necrotizing fasciitis or streptococcal toxic shock syndrome.
22 ections, including necrotizing fasciitis and toxic shock syndrome.
23 ildren, which resembles superantigen-induced toxic shock syndrome.
24 tion of T cells and inflammation, leading to toxic shock syndrome.
25 e outcomes such as necrotizing fasciitis and toxic shock syndrome.
26 m localized skin abscess to life-threatening toxic shock syndrome.
27 rldwide, including necrotizing fasciitis and toxic shock syndrome.
28 ditions, including necrotizing fasciitis and toxic shock syndrome.
29 an penetrate the vaginal epithelium to cause toxic shock syndrome.
30 o life-threatening necrotizing fasciitis and toxic shock syndrome.
31 comes of death, limb loss, and streptococcal toxic shock syndrome.
32 alleles significantly increase the risk for toxic shock syndrome.
33 indings that death was due to tampon-related toxic shock syndrome.
34 7-year-old female who died of tampon-related toxic shock syndrome.
35 o mediate the symptoms collectively known as toxic shock syndrome.
36 inal mucosa, induce interleukin-8, and cause toxic shock syndrome.
37 rwhelming cytokine production, which lead to toxic shock syndrome.
38 ections to life-threatening endocarditis and toxic shock syndrome.
39 ndrome toxin-1 is a major cause of menstrual toxic shock syndrome.
40 teract with underlying immune cells to cause toxic shock syndrome.
41 class II allelic variation in streptococcal toxic shock syndrome.
42 th GAS myonecrosis who died of streptococcal toxic shock syndrome.
43 ion of CD14 by LPS can cause the often fatal toxic-shock syndrome.
44 evere systemic conditions such as septic and toxic shock syndromes.
45 on of bacterial superantigens, most commonly toxic shock syndrome-1 (TSST-1), to specific TCR Vbeta-b
46 was 11% but was much higher in patients with toxic shock syndrome (55%) and necrotizing fasciitis (58
47 with but distinct from Kawasaki disease and toxic shock syndrome admitted to a New York City hospita
48 obic, Gram-positive bacterium that can cause toxic shock syndrome after gynecological procedures.
49 nts (three with hydronephrosis), and five of toxic shock syndrome after use of the menstrual cup.
50 tellation of symptoms that strongly resemble toxic shock syndrome, an escalation of the cytotoxic ada
51 nkeys manifested a T cell activation-related toxic shock syndrome and a profound depletion of CD4+ ly
52 xin B (SEB) is a potent toxin that can cause toxic shock syndrome and act as a lethal and incapacitat
59 aureus group-III strains are responsible for toxic shock syndrome and have been underestimated in oth
60 auses a variety of human diseases, including toxic shock syndrome and necrotizing fasciitis, which ar
63 irulence factors and are responsible for the toxic shock syndrome and other superantigen-related dise
66 bacteremia, septic arthritis, streptococcal toxic shock syndrome, and necrotizing fasciitis) caused
67 TNF release during acute TSST1-precipitated toxic shock syndrome, and the C-terminal domain to stimu
68 rious diseases, including food poisoning and toxic shock syndrome, are termed superantigens (SAgs).
69 describe four deaths due to endometritis and toxic shock syndrome associated with C. sordellii that o
71 with necrotizing fasciitis or streptococcal toxic shock syndrome between January 1, 2013, and Decemb
72 e GAS infections, including 11 streptococcal toxic shock syndrome cases and one necrotizing fasciitis
74 ted in a number of human diseases, including toxic shock syndrome, diabetes mellitus and multiple scl
80 partial thromboplastin time in streptococcal toxic shock syndrome is associated with activation of th
82 disease in epidemics and its resemblance to toxic-shock syndrome make an infectious etiology seem mo
83 known virulence factors in scarlet fever and toxic shock syndrome, mechanisms by how SAgs contribute
87 State reported cases of Kawasaki's disease, toxic shock syndrome, myocarditis, and potential MIS-C i
88 (n = 1132), KD shock syndrome (n = 45), and toxic shock syndrome (n = 37) who had been admitted to h
89 itis, impetigo, scarlet fever, streptococcal toxic shock syndrome, necrotizing fasciitis and myositis
90 ases of severe iGAS infection (streptococcal toxic shock syndrome, necrotizing fasciitis, septic shoc
93 igens (PTSAgs) that can cause illness, e.g., toxic shock syndrome, or synergize with a number of othe
94 um sordellii, causes a rarer but often fatal toxic shock syndrome, particularly in gynecological and
95 (GAS) necrotizing soft tissue infections and toxic shock syndrome remain high-mortality conditions.
96 sis of necrotizing soft-tissue infection and toxic shock syndrome resulting from Streptococcus pyogen
100 e from severe cases, including streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (N
101 S) isolates from patients with streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (N
103 n A) is highly associated with streptococcal toxic shock syndrome (STSS) and other invasive streptoco
104 s associated with outbreaks of streptococcal toxic shock syndrome (STSS) in the United States and Eur
107 nd is strongly associated with streptococcal toxic shock syndrome (STSS), a severe and often fatal il
108 sult in the recently described streptococcal toxic shock syndrome (STSS), which is characterized by r
111 OR, 8.64; 95% CI, 5.50-13.55), streptococcal toxic shock syndrome (STSS; OR, 11.71; 95% CI, 4.39-31.1
113 een implicated in serious disease, including toxic shock syndrome, the specific pathological mechanis
114 s described that specifically promote either toxic shock syndrome toxin (TSST) 1 or staphylococcal en
116 on of staphylococcal enterotoxin A (SEA) and toxic shock syndrome toxin (TSST) in neat milk without s
117 us, staphylococcal enterotoxins (SE) A-E and toxic shock syndrome toxin (TSST)-1, which are associate
119 nicity island SaPI1 carries the gene for the toxic shock syndrome toxin (TSST-1) and can be mobilized
120 IPs to S. aureus inhibited the production of toxic shock syndrome toxin (TSST-1) and enterotoxin C3,
121 dose-dependent transcytosis in vitro, while toxic shock syndrome toxin (TSST-1) exhibited increased
122 the gram-positive model of shock mediated by toxic shock syndrome toxin (TSST-1), Mif(-/-) mice succu
123 .g., carriage of the enterotoxin A (sea) and toxic shock syndrome toxin (tst) genes and production of
124 of oxygen is necessary for the production of toxic shock syndrome toxin 1 (TSST-1) by Staphylococcus
126 he effect of O(2) and CO(2) on expression of toxic shock syndrome toxin 1 (TSST-1) by Staphylococcus
129 s with staphylococcal enterotoxin B (SEB) or toxic shock syndrome toxin 1 (TSST-1) resulted in enhanc
131 T2-I-A(b), is very inefficient at presenting toxic shock syndrome toxin 1 (TSST-1) to T cells, sugges
132 ne monoclonal antibodies (MAbs) specific for toxic shock syndrome toxin 1 (TSST-1), a bacterial super
133 there have been reports of the production of toxic shock syndrome toxin 1 (TSST-1), enterotoxin, and
135 tes production of agr RNAIII, protein A, and toxic shock syndrome toxin 1 (TSST-1), particularly unde
136 r, unlike the classical enterotoxins SEB and toxic shock syndrome toxin 1 (TSST-1), the gene for SEl-
137 ught to be associated with colonization with toxic shock syndrome toxin 1 (TSST-1)-producing Staphylo
141 g., staphylococcal enterotoxin A [SEA], SEB, toxic shock syndrome toxin 1 [TSST-1]) which act both as
142 ococcal enterotoxin A (SEA), SEB, or SEC3 or toxic shock syndrome toxin 1 and a potentiating dose of
143 study the activity of superantigens such as toxic shock syndrome toxin 1 and also found that despite
144 ant Staphylococcus aureus and genes encoding toxic shock syndrome toxin 1 and Panton-Valentine leukoc
145 ode and disseminate the superantigen toxins, toxic shock syndrome toxin 1 and superantigen enterotoxi
146 ttenuated staphylococcal enterotoxin (SE) or toxic shock syndrome toxin 1 develop protective antibodi
148 taphylococcal clone or structural variant of toxic shock syndrome toxin 1 is associated with Kawasaki
149 replication, and suboptimal stimulation with toxic shock syndrome toxin 1 leads to viral replication
150 staphylococcal enterotoxin B and C negative, toxic shock syndrome toxin 1 positive, and staphylococca
151 al samples positive for S. aureus (83%), and toxic shock syndrome toxin 1 was isolated from 66 strain
152 nced portions of the regions encoding mature toxic shock syndrome toxin 1 were identical in all six s
153 f staphylococcal enterotoxin A (SEA) to SEH, toxic shock syndrome toxin 1, and Panton-Valentine leuko
154 roliferation in response to the superantigen toxic shock syndrome toxin 1, as well as the proliferati
155 erum) against combinations of superantigens (toxic shock syndrome toxin 1, enterotoxins B and C, and
156 eukocidins (eg, Panton-Valentine leukocidin, toxic shock syndrome toxin 1, exfoliative toxins, and va
158 ere capable of attenuating the production of toxic shock syndrome toxin-1 (also under the control of
160 as well as the staphylococcal superantigens toxic shock syndrome toxin-1 (TSST-1) and staphylococcus
161 fine the interface between the bacterial SAG toxic shock syndrome toxin-1 (TSST-1) and the TCR, we pe
162 ee-dimensional structures of five mutants of toxic shock syndrome toxin-1 (TSST-1) have been determin
164 aphylococcus aureus strains that produce the toxic shock syndrome toxin-1 (TSST-1) superantigen.
165 superantigens [staphylococcal enterotoxins, toxic shock syndrome toxin-1 (TSST-1), and streptococcal
166 Staphylococcal superantigens (SAgs), such as toxic shock syndrome toxin-1 (TSST-1), are the main caus
167 nical cases of TSS arise due to an exotoxin, toxic shock syndrome toxin-1 (TSST-1), elaborated by tox
169 ram quantities of topically applied purified toxic shock syndrome toxin-1 (TSST-1), staphylococcal en
173 We investigated whether the superantigen toxic shock syndrome toxin-1 (TSST1) could induce an ant
176 nine mutations were constructed in S. aureus toxic shock syndrome toxin-1 amino acids D120 to D130.
178 lysin streptolysin O enhanced penetration of toxic shock syndrome toxin-1 and streptococcal pyrogenic
180 d theories of Kawasaki disease etiology, the toxic shock syndrome toxin-1 hypothesis and the coronavi
183 r, a detailed structural analysis shows that toxic shock syndrome toxin-1 lacks several structural fe
187 e, 96% of the lesional isolates produced the toxic shock syndrome toxin-1 superantigen, and most of t
188 ly express BP107 conformational epitopes and toxic shock syndrome toxin-1 superantigen-binding capabi
189 ells were stimulated with the staphylococcal toxic shock syndrome toxin-1, enterotoxin A, or enteroto
190 - and beta-toxins, but not enterotoxin A and toxic shock syndrome toxin-1, rapidly potentiated sheddi
192 enough to allow for enhanced penetration of toxic shock syndrome toxin-1, whereas streptolysin O dir
193 trains of S. aureus produce the superantigen toxic shock syndrome toxin-1, which can penetrate the va
200 es (both MSSA and MRSA) carried the gene for toxic shock syndrome toxin; however, carriage of the gen
202 anton-Valentine leukocidin, alpha-toxin, and toxic-shock syndrome toxin 1 and increased toxin product
203 Immunoblot analysis of the enterotoxins, toxic-shock syndrome toxin 1, and SpeA with antiserum pr
204 n-Valentine leukocidin, alpha-hemolysin, and toxic-shock syndrome toxin 1, in both methicillin-sensit
205 lococcus aureus enterotoxins (S.E.) A-I, and toxic-shock syndrome toxin TSST-1 act as superantigens t
208 erantigens (PTSAgs) that are associated with toxic shock syndrome (TSS) and staphylococcal food poiso
216 uced by concentrations of the staphylococcal toxic shock syndrome (TSS) toxin 1 (TSST-1) and the stre
219 G) is sometimes administered for presumptive toxic shock syndrome (TSS), but its frequency of use and
220 icated in several serious diseases including toxic shock syndrome (TSS), Kawasaki disease, and sepsis
230 esis, a strain recovered from a patient with toxic shock syndrome was serially passaged for 6 weeks,
233 V-2 infection, shares clinical features with toxic shock syndrome, which is triggered by bacterial su
234 ained from seven patients with streptococcal toxic shock syndrome who received IVIG therapy, and the
235 g high-risk or protection from streptococcal toxic shock syndrome with a strong protection conferred