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1 terium Salmonella enterica serovar Typhi (S. Typhi).
2 lymerase chain reaction [PCR] for Salmonella Typhi).
3 nic typhoid toxin deletion mutant (TN) of S. Typhi.
4 robial-resistant Salmonella enterica serovar Typhi.
5 lmonella (NTS) serotypes, and 126 Salmonella Typhi.
6 ecruited were culture or PCR positive for S. Typhi.
7 gent, ezetimibe, reduced susceptibility to S Typhi.
8 ng an established human infection model of S Typhi.
9 ella enterica isolates that are not serotype Typhi.
10 memory CD4+ T-cells following exposure to S. Typhi.
11 nd how they impact on the pathogenesis of S. Typhi.
12 predominance of Salmonella enterica serovar Typhi.
13 nd compared to other available genomes of S. Typhi.
14 etect 1 colony-forming unit/mL of Salmonella Typhi.
15 ted outbreak, the first of ESBL-producing S. Typhi.
16 ainst the intracellular bacterium Salmonella Typhi.
17 arly chromatin modifications modulated by S. Typhi.
18 all were extensively drug resistant (XDR) S. Typhi.
19 infection, reduces onward transmission of S. Typhi.
20 ticipants challenged with wild-type or TN S. Typhi (15 out of 21 (71%) versus 15 out of 19 (79%); P =
22 human-adapted bacterial pathogen Salmonella Typhi (6,7) , the cause of typhoid fever in humans (8-12
28 allenge with a small inoculum of virulent S. Typhi administered in bicarbonate solution can be perfor
30 rculosis MgtC is highly homologous to its S. Typhi analogue, there does not appear to be an Mtb homol
34 6 (10.1%) had positive blood cultures for S. Typhi and 297 (1.4%) had positive cultures for S. Paraty
37 YGH, we identified 33 (4.9%) with Salmonella Typhi and 9 (1.3%) with Salmonella Paratyphi A bloodstre
39 those for animals infected with wild-type R. typhi and develop comparable pathology and bacterial loa
40 ficant transmission mechanism for Salmonella typhi and dysentery-causing pathogens in this urban popu
42 the microbiological landscape of Salmonella Typhi and invasive nontyphoidal Salmonella (iNTS) in the
44 Salmonella enterica including Salmonella Typhi and nontyphoidal Salmonella (NTS) are the predomin
46 to hospital-based surveillance of Salmonella Typhi and Paratyphi A bloodstream infections from 5 Octo
47 crobial susceptibility results of Salmonella Typhi and Paratyphi A isolates sent for testing by parti
48 tion caused by Salmonella enterica serotypes Typhi and Paratyphi A, frequently presents as a nonlocal
49 fever caused by Salmonella enterica serovars Typhi and Paratyphi is substantial and has high impact i
50 erica serovar Typhimurium, the genomes of S. Typhi and S. Paratyphi A are characterized by inactivati
51 t, together with Salmonella enterica serovar Typhi and Salmonella enterica serovar Sendai, causes ent
52 -pathogen interactions induced by Salmonella Typhi and Salmonella Paratyphi A during enteric fever ar
53 reaction (qPCR) method to detect Salmonella Typhi and Salmonella Paratyphi A simultaneously in blood
54 e set was able to detect clinical Salmonella Typhi and Salmonella Paratyphi A strains and also diarrh
57 lmonellosis (infections caused by Salmonella Typhi and Salmonella Paratyphi), this disorder remains a
60 Two major serovars of Salmonella enterica, Typhi and Typhimurium, have evolved a two-component regu
62 4, 135 Salmonella enterica serotype Typhi (S Typhi) and 94 iNTS isolates were cultured from the blood
63 terica subspecies enterica serovar Typhi (S. Typhi) and can lead to systemic illness and complication
64 amushi), murine typhus (caused by Rickettsia typhi), and leptospirosis are common causes of febrile i
66 ne on 76 cases; 8 (11%) were positive for S. Typhi, and all were extensively drug resistant (XDR) S.
67 on 86 patients; 3 (3%) were positive for S. Typhi, and all were XDR S. Typhi, out of 86 samples test
68 IMD pathway could minimize the spread of R. typhi, and potentially other human pathogens, vectored b
70 ic depolymerase enzyme missing in S enterica Typhi, and we exploited this enzyme to isolate acylated
71 lla enterica and Salmonella enterica serovar Typhi, and Yersinia pestis), and 3 protozoa (Leishmania
72 identified several immunoreactive Salmonella Typhi antigens that seem promising for possible inclusio
76 degrees C or higher for 12 h or longer or S Typhi bacteraemia, following oral challenge administered
77 was immunogenic and effective in reducing S. Typhi bacteremia in children 9 months to 16 years of age
78 n (fever >=38 degrees C for >=12 h and/or S. Typhi bacteremia) between participants challenged with w
79 enome sequence, little is known regarding R. typhi biology in flea vectors that, importantly, do not
80 ade (2007-2017) of hospital-based Salmonella Typhi bloodstream infection (BSI) surveillance in the De
81 yphoid epidemic, using temporal trends in S. Typhi bloodstream infection and perforated abdominal vis
82 kettsia prowazekii and PKMT2 from Rickettsia typhi, both the apo form and in complex with its cofacto
84 he IMD pathway as a critical regulator of R. typhi burden in C. felis These data suggest that targeti
85 the intracellular human pathogen Salmonella Typhi, but its potential broader role in antimicrobial d
87 f typhoid fever, Salmonella enterica serovar Typhi, can partially subvert this critical innate immune
88 n of culture-proven ceftriaxone-resistant S. Typhi cases, suspected cases from the households or neig
94 he crystal structure of DHQ1 from Salmonella typhi chemically modified by this ammonium derivative re
96 t of iNTS vaccines and the introduction of S Typhi conjugate vaccines should be considered for high-i
98 out of 130 Phage and 36 HEGs in S. enterica Typhi CT18, which shows that it is more efficient in det
99 ealed differences in the ability of these S. Typhi derivatives to invade cells or induce cellular res
100 has increased in Salmonella enterica serovar Typhi, driven in part by the emergence of successful gen
103 ilure was associated with the emergence of S Typhi exhibiting resistance against fluoroquinolones, re
104 creased the odds of seroconversion of IgG S. Typhi flagella antibody (adjusted OR 6.4, 95% CI, 1.3-31
106 fferences in the phenotypic properties of S. Typhi flagella variation and how they impact on the path
107 role during infection, we constructed an S. Typhi fliC mutant and otherwise isogenic S. Typhi strain
109 mice with live typhoidal serovar, Salmonella Typhi, generates cross-reactive immune responses, which
114 ecific restimulation of spleen cells from R. typhi(GFPuv)-infected BALB/c mice elicits gamma interfer
115 he transcontinental spread of the Salmonella Typhi H58 haplotype, improved estimates of the burden of
116 confirmed cases of ceftriaxone-resistant S. Typhi had been reported in 4 months with the first case
120 sistant Salmonella enterica serovar Typhi (S Typhi) has been the main cause of enteric fever, but now
121 ear epidemics of Salmonella enterica serovar Typhi have been reported from countries across eastern a
123 1,832 Salmonella enterica serovar Typhi (S. Typhi) identifies a single dominant MDR lineage, H58, th
125 usative pathogen Salmonella enterica serovar Typhi implicated in many outbreaks through history.
126 th kinetics similar to those of wild-type R. typhi in cell culture, and stably maintain the plasmid a
128 outbreak of ceftriaxone-resistant Salmonella Typhi in Hyderabad, Pakistan, through antimicrobial resi
129 activity against E. coli, S. aureus, and S. typhi in in vitro antimicrobial tests, followed closely
134 a serovar Typhimurium, the murine model of S Typhi, in which various ECM genes were deleted or added,
135 here was widespread drug resistance among S. Typhi, including FQ non-susceptibility and the emergence
138 exchange factor BLOC-3 are permissive to S. Typhi infection and exhibit increased susceptibility to
140 ereas the cellular mechanisms involved in S. Typhi infection have been intensively studied, very litt
141 Knockdown of Relish and Imd increased R. typhi infection levels, implicating the IMD pathway as a
142 nt, with chronic Salmonella enterica serovar Typhi infection reported as a significant risk factor.
145 gical association between GBC and Salmonella Typhi infection, we show that Salmonella enterica induce
152 We reviewed Salmonella enterica serotype Typhi infections reported to the Centers for Disease Con
154 to R. typhi Initially, we determined that R. typhi infects Drosophila cells and increases antimicrobi
155 phalides felis) innate immune response to R. typhi Initially, we determined that R. typhi infects Dro
157 and help identify recent introductions of S. Typhi into new or previously endemic locations, providin
165 n the main cause of enteric fever, but now S Typhi is being displaced by infections with drug-resista
171 ubspecies enterica serovar Typhi (Salmonella Typhi) is the cause of typhoid fever and a human host-re
172 Murine typhus, or infection with Rickettsia typhi, is a global but neglected disease without randomi
173 fever, caused by Salmonella enterica serovar Typhi, is an important public health problem in resource
174 ever case with a Salmonella enterica serovar Typhi isolate showing extended spectrum beta-lactamase (
177 n (CDC) and antimicrobial-resistance data on Typhi isolates in CDC's National Antimicrobial Resistanc
178 ses of typhoid fever were diagnosed and 5004 Typhi isolates tested for antimicrobial susceptibility.
181 e (multidrug resistant [MDR]) was limited to Typhi isolates, primarily acquired in southern Asia (13%
183 essful Orientia tsutsugamushi and Rickettsia typhi isolations from this laboratory over a period of 6
185 in E (HlyE), cytolethal distending toxin, S. Typhi lipopolysaccharide (LPS), and S. Typhi membrane pr
187 Here we discuss the evolution of the S. Typhi MDR phenotype and consider options for management.
191 SCV environment, as toxin produced by an S. Typhi mutant with impaired trafficking is not properly s
193 between both pathogens is the presence in S. Typhi of TviA, a regulatory protein that shuts down flag
194 ntification of extensively drug resistant S. Typhi only highlights the dangers of ignoring this threa
198 monella enterica subspecies enterica serovar Typhi or Salmonella enterica subspecies enterica serovar
199 gnosis of enteric fever caused by Salmonella Typhi or Salmonella Paratyphi A or B is bone marrow cult
200 es positive for Salmonella enterica serotype Typhi, or Paratyphi A, B, or C) on day 8; or relapse or
201 e positive for S. Typhi, and all were XDR S. Typhi, out of 86 samples tested for histopathology 4 (5%
204 C-42 degrees C) Salmonella enterica serovars Typhi, Paratyphi A, and Sendai significantly attenuate t
211 ow designated genotype 4.3.1), the global S. Typhi population is highly structured and includes dozen
212 ted here can be used to interrogate local S. Typhi populations and help identify recent introductions
213 In conclusion, repeated vaccination with S. Typhi porins programs type I T follicular helper cell re
215 eport that upon infection of human cells, S. Typhi produces two forms of typhoid toxin that have dist
218 atient had a positive O. tsutsugamushi or R. typhi rapid diagnostic test (RDT), serology, or PCR.
223 tsutsugamushi) and murine typhus (Rickettsia typhi) research to provide an evidence base for biosafet
224 zae, S suis) and O tsutsugamushi, Rickettsia typhi/Rickettsia spp, and Leptospira spp infections in b
225 lity (236/876 [27%]), with 18% (13/71) for R typhi/Rickettsia spp, O tsutsugamushi, and Leptospira sp
228 n 31, 2014, 135 Salmonella enterica serotype Typhi (S Typhi) and 94 iNTS isolates were cultured from
229 tidrug-resistant Salmonella enterica serovar Typhi (S Typhi) has been the main cause of enteric fever
232 monella enterica subspecies enterica serovar Typhi (S. Typhi) and can lead to systemic illness and co
234 nalysis of 1,832 Salmonella enterica serovar Typhi (S. Typhi) identifies a single dominant MDR lineag
236 he population of Salmonella enterica serovar Typhi (S. Typhi), the causative agent of typhoid fever,
238 ight into the molecular bases for Salmonella Typhi's host specificity and may help the development of
239 We designed primers for genes specific to S. Typhi, S. Paratyphi A, and genes conserved among Salmone
240 ablished that the human-adapted typhoidal S. Typhi, S. Paratyphi A, and S. Sendai are all noticeably
241 Blood samples spiked with in vitro grown S. Typhi, S. Paratyphi A, S. Typhimurium, and E. coli were
242 n error was 22%, which was mainly due to non-Typhi Salmonella (NTS) diagnoses being misclassified as
243 monella enterica subspecies enterica serovar Typhi (Salmonella Typhi) is the cause of typhoid fever a
248 live attenuated Salmonella enterica serovar Typhi strain to create a bivalent mucosal plague vaccine
249 vaccination with live-attenuated Salmonella Typhi strain Ty21a is modestly efficacious, but the mech
250 al ileum exposed ex vivo to the wild-type S. Typhi strain were stained with a 33-metal-labeled antibo
251 monella enterica subspecies enterica serovar Typhi strain with resistance against beta-lactams, cepha
252 Typhi fliC mutant and otherwise isogenic S. Typhi strains expressing the Hj, Hd, Hz66 flagella antig
254 e data safety and monitoring board because S Typhi strains with high-level resistance to ciprofloxaci
256 appear dispensable in the replication of S. Typhi, supporting findings from a recent human challenge
259 asing antimicrobial resistance in Salmonella Typhi that have served to increase interest in typhoid e
260 xin, a unique virulence factor of Salmonella Typhi (the cause of typhoid fever), recapitulates in an
261 ion of Salmonella enterica serovar Typhi (S. Typhi), the causative agent of typhoid fever, exhibits l
263 ulence factor of Salmonella enterica serovar Typhi, the causative agent of typhoid fever, and is thou
269 e regulation of virulence factors enables S. Typhi to evade innate immune recognition by concealing a
270 We also compared the clinical features of S. Typhi to S. Paratyphi A among both outpatients and inpat
271 , Enterococcus, P. aeruginosa and Salmonella typhi) to antibiotics such as ampicillin and kanamycin.
273 In this study, we use a high-density S. Typhi transposon library in hu-SRC-SCID mice to identify
275 etabolic changes of the typhoidal Salmonella Typhi Ty2, the nontyphoidal Salmonella Typhimurium LT2,
277 n factors (Arfs), is critical for Rickettsia typhi (typhus group rickettsiae) entry but pseudogenized
284 We show how evolutionary divergence in S. Typhi was driven by rising global antibiotic use and by
286 (ESBL)-producing Salmonella enterica serovar Typhi was identified, whole-genome sequence typed, among
289 ical patients presenting to QECH; Salmonella Typhi was isolated on 2054 occasions (1.2%) and nontypho
292 ense, invasive NTS was common and Salmonella Typhi was uncommon, whereas the inverse was observed at
293 ts experimentally infected with wild-type S. Typhi, we detected significant cytokine responses within
295 4% (21/152) were Salmonella enterica serovar Typhi, whereas 86% (131/152) were serovars other than Ty
296 t pathogenic Salmonella including Salmonella Typhi which causes systemic infection, typhoid, in human
297 yphimurium from 2002 to 2008, and Salmonella Typhi, which began in 2011 and was ongoing in 2014.
299 for the first time the transformation of R. typhi with the pRAM18dRGA plasmid that originally derive
300 d in vivo culture of O. tsutsugamushi and R. typhi would require that only high-risk activities (anim