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1 arious diseases including food poisoning and toxic shock syndrome.
2 ins (SEs) that cause both food poisoning and toxic shock syndrome.
3 se ranging from pharyngitis to streptococcal toxic shock syndrome.
4 rotoxins (SEs) that cause food poisoning and toxic shock syndrome.
5 m isolated from a patient with streptococcal toxic shock syndrome.
6 h as necrotizing fasciitis and streptococcal toxic shock syndrome.
7 llin-resistant strains and organisms causing toxic shock syndrome.
8 profound shock associated with streptococcal toxic shock syndrome.
9 me identified in patients with streptococcal toxic shock syndrome.
10 rldwide, including necrotizing fasciitis and toxic shock syndrome.
11 produce disease, such as food poisoning and toxic shock syndrome.
12 d as major virulence factors responsible for toxic shock syndrome.
13 sponses in the pathogenesis of streptococcal toxic shock syndrome.
14 ed with the recently described streptococcal toxic shock syndrome.
15 multiorgan failure define the streptococcal toxic shock syndrome.
16 l bacteremia that mimics human Streptococcal toxic shock syndrome.
17 ditions, including necrotizing fasciitis and toxic shock syndrome.
18 an penetrate the vaginal epithelium to cause toxic shock syndrome.
19 o life-threatening necrotizing fasciitis and toxic shock syndrome.
20 alleles significantly increase the risk for toxic shock syndrome.
21 indings that death was due to tampon-related toxic shock syndrome.
22 7-year-old female who died of tampon-related toxic shock syndrome.
23 o mediate the symptoms collectively known as toxic shock syndrome.
24 inal mucosa, induce interleukin-8, and cause toxic shock syndrome.
25 rwhelming cytokine production, which lead to toxic shock syndrome.
26 ections to life-threatening endocarditis and toxic shock syndrome.
27 ndrome toxin-1 is a major cause of menstrual toxic shock syndrome.
28 teract with underlying immune cells to cause toxic shock syndrome.
29 class II allelic variation in streptococcal toxic shock syndrome.
30 ections, including necrotizing fasciitis and toxic shock syndrome.
31 th GAS myonecrosis who died of streptococcal toxic shock syndrome.
32 ections, including necrotizing fasciitis and toxic shock syndrome.
33 nes, ultimately causing a condition known as toxic shock syndrome.
34 e outcomes such as necrotizing fasciitis and toxic shock syndrome.
35 n humans including necrotizing fasciitis and toxic shock syndrome.
36 ion of CD14 by LPS can cause the often fatal toxic-shock syndrome.
37 evere systemic conditions such as septic and toxic shock syndromes.
38 on of bacterial superantigens, most commonly toxic shock syndrome-1 (TSST-1), to specific TCR Vbeta-b
39 was 11% but was much higher in patients with toxic shock syndrome (55%) and necrotizing fasciitis (58
40 obic, Gram-positive bacterium that can cause toxic shock syndrome after gynecological procedures.
41 nkeys manifested a T cell activation-related toxic shock syndrome and a profound depletion of CD4+ ly
42 xin B (SEB) is a potent toxin that can cause toxic shock syndrome and act as a lethal and incapacitat
49 aureus group-III strains are responsible for toxic shock syndrome and have been underestimated in oth
50 auses a variety of human diseases, including toxic shock syndrome and necrotizing fasciitis, which ar
53 irulence factors and are responsible for the toxic shock syndrome and other superantigen-related dise
55 bacteremia, septic arthritis, streptococcal toxic shock syndrome, and necrotizing fasciitis) caused
56 TNF release during acute TSST1-precipitated toxic shock syndrome, and the C-terminal domain to stimu
57 rious diseases, including food poisoning and toxic shock syndrome, are termed superantigens (SAgs).
58 describe four deaths due to endometritis and toxic shock syndrome associated with C. sordellii that o
60 e GAS infections, including 11 streptococcal toxic shock syndrome cases and one necrotizing fasciitis
62 ted in a number of human diseases, including toxic shock syndrome, diabetes mellitus and multiple scl
68 partial thromboplastin time in streptococcal toxic shock syndrome is associated with activation of th
69 disease in epidemics and its resemblance to toxic-shock syndrome make an infectious etiology seem mo
70 known virulence factors in scarlet fever and toxic shock syndrome, mechanisms by how SAgs contribute
72 itis, impetigo, scarlet fever, streptococcal toxic shock syndrome, necrotizing fasciitis and myositis
73 ases of severe iGAS infection (streptococcal toxic shock syndrome, necrotizing fasciitis, septic shoc
74 igens (PTSAgs) that can cause illness, e.g., toxic shock syndrome, or synergize with a number of othe
75 sis of necrotizing soft-tissue infection and toxic shock syndrome resulting from Streptococcus pyogen
79 e from severe cases, including streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (N
80 S) isolates from patients with streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (N
82 n A) is highly associated with streptococcal toxic shock syndrome (STSS) and other invasive streptoco
83 s associated with outbreaks of streptococcal toxic shock syndrome (STSS) in the United States and Eur
85 nd is strongly associated with streptococcal toxic shock syndrome (STSS), a severe and often fatal il
86 sult in the recently described streptococcal toxic shock syndrome (STSS), which is characterized by r
90 s described that specifically promote either toxic shock syndrome toxin (TSST) 1 or staphylococcal en
91 on of staphylococcal enterotoxin A (SEA) and toxic shock syndrome toxin (TSST) in neat milk without s
92 us, staphylococcal enterotoxins (SE) A-E and toxic shock syndrome toxin (TSST)-1, which are associate
94 nicity island SaPI1 carries the gene for the toxic shock syndrome toxin (TSST-1) and can be mobilized
95 IPs to S. aureus inhibited the production of toxic shock syndrome toxin (TSST-1) and enterotoxin C3,
96 dose-dependent transcytosis in vitro, while toxic shock syndrome toxin (TSST-1) exhibited increased
97 .g., carriage of the enterotoxin A (sea) and toxic shock syndrome toxin (tst) genes and production of
98 of oxygen is necessary for the production of toxic shock syndrome toxin 1 (TSST-1) by Staphylococcus
100 he effect of O(2) and CO(2) on expression of toxic shock syndrome toxin 1 (TSST-1) by Staphylococcus
103 s with staphylococcal enterotoxin B (SEB) or toxic shock syndrome toxin 1 (TSST-1) resulted in enhanc
105 T2-I-A(b), is very inefficient at presenting toxic shock syndrome toxin 1 (TSST-1) to T cells, sugges
106 ne monoclonal antibodies (MAbs) specific for toxic shock syndrome toxin 1 (TSST-1), a bacterial super
107 there have been reports of the production of toxic shock syndrome toxin 1 (TSST-1), enterotoxin, and
109 tes production of agr RNAIII, protein A, and toxic shock syndrome toxin 1 (TSST-1), particularly unde
110 r, unlike the classical enterotoxins SEB and toxic shock syndrome toxin 1 (TSST-1), the gene for SEl-
111 ught to be associated with colonization with toxic shock syndrome toxin 1 (TSST-1)-producing Staphylo
114 g., staphylococcal enterotoxin A [SEA], SEB, toxic shock syndrome toxin 1 [TSST-1]) which act both as
115 ococcal enterotoxin A (SEA), SEB, or SEC3 or toxic shock syndrome toxin 1 and a potentiating dose of
116 study the activity of superantigens such as toxic shock syndrome toxin 1 and also found that despite
117 ant Staphylococcus aureus and genes encoding toxic shock syndrome toxin 1 and Panton-Valentine leukoc
118 ttenuated staphylococcal enterotoxin (SE) or toxic shock syndrome toxin 1 develop protective antibodi
120 taphylococcal clone or structural variant of toxic shock syndrome toxin 1 is associated with Kawasaki
121 replication, and suboptimal stimulation with toxic shock syndrome toxin 1 leads to viral replication
122 staphylococcal enterotoxin B and C negative, toxic shock syndrome toxin 1 positive, and staphylococca
123 nced portions of the regions encoding mature toxic shock syndrome toxin 1 were identical in all six s
124 f staphylococcal enterotoxin A (SEA) to SEH, toxic shock syndrome toxin 1, and Panton-Valentine leuko
125 roliferation in response to the superantigen toxic shock syndrome toxin 1, as well as the proliferati
126 erum) against combinations of superantigens (toxic shock syndrome toxin 1, enterotoxins B and C, and
128 ere capable of attenuating the production of toxic shock syndrome toxin-1 (also under the control of
130 as well as the staphylococcal superantigens toxic shock syndrome toxin-1 (TSST-1) and staphylococcus
131 fine the interface between the bacterial SAG toxic shock syndrome toxin-1 (TSST-1) and the TCR, we pe
132 ee-dimensional structures of five mutants of toxic shock syndrome toxin-1 (TSST-1) have been determin
134 superantigens [staphylococcal enterotoxins, toxic shock syndrome toxin-1 (TSST-1), and streptococcal
135 Staphylococcal superantigens (SAgs), such as toxic shock syndrome toxin-1 (TSST-1), are the main caus
136 nical cases of TSS arise due to an exotoxin, toxic shock syndrome toxin-1 (TSST-1), elaborated by tox
138 ram quantities of topically applied purified toxic shock syndrome toxin-1 (TSST-1), staphylococcal en
142 We investigated whether the superantigen toxic shock syndrome toxin-1 (TSST1) could induce an ant
145 nine mutations were constructed in S. aureus toxic shock syndrome toxin-1 amino acids D120 to D130.
147 lysin streptolysin O enhanced penetration of toxic shock syndrome toxin-1 and streptococcal pyrogenic
149 d theories of Kawasaki disease etiology, the toxic shock syndrome toxin-1 hypothesis and the coronavi
152 r, a detailed structural analysis shows that toxic shock syndrome toxin-1 lacks several structural fe
155 ly express BP107 conformational epitopes and toxic shock syndrome toxin-1 superantigen-binding capabi
156 ells were stimulated with the staphylococcal toxic shock syndrome toxin-1, enterotoxin A, or enteroto
157 - and beta-toxins, but not enterotoxin A and toxic shock syndrome toxin-1, rapidly potentiated sheddi
159 enough to allow for enhanced penetration of toxic shock syndrome toxin-1, whereas streptolysin O dir
160 trains of S. aureus produce the superantigen toxic shock syndrome toxin-1, which can penetrate the va
165 es (both MSSA and MRSA) carried the gene for toxic shock syndrome toxin; however, carriage of the gen
167 anton-Valentine leukocidin, alpha-toxin, and toxic-shock syndrome toxin 1 and increased toxin product
168 Immunoblot analysis of the enterotoxins, toxic-shock syndrome toxin 1, and SpeA with antiserum pr
169 n-Valentine leukocidin, alpha-hemolysin, and toxic-shock syndrome toxin 1, in both methicillin-sensit
170 lococcus aureus enterotoxins (S.E.) A-I, and toxic-shock syndrome toxin TSST-1 act as superantigens t
173 erantigens (PTSAgs) that are associated with toxic shock syndrome (TSS) and staphylococcal food poiso
181 uced by concentrations of the staphylococcal toxic shock syndrome (TSS) toxin 1 (TSST-1) and the stre
184 G) is sometimes administered for presumptive toxic shock syndrome (TSS), but its frequency of use and
185 icated in several serious diseases including toxic shock syndrome (TSS), Kawasaki disease, and sepsis
195 esis, a strain recovered from a patient with toxic shock syndrome was serially passaged for 6 weeks,
198 ained from seven patients with streptococcal toxic shock syndrome who received IVIG therapy, and the
199 g high-risk or protection from streptococcal toxic shock syndrome with a strong protection conferred
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