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1                                              V. cholerae acquired its cholera toxin genes by lysogeni
2                                              V. cholerae biofilms have been shown to be hyperinfectiv
3                                              V. cholerae has a characteristic curved rod morphology,
4                                              V. cholerae is a natural inhabitant of marine environmen
5                                              V. cholerae mutant strains carrying inactivated AI synth
6                                              V. cholerae serogroups O1 and O139 are responsible for c
7                                              V. cholerae was particularly vulnerable to lethal inhibi
8                                              V. cholerae was the leading pathogen in individuals abov
9                                              V. cholerae, a bacterium that utilizes linearized Ent, c
10                                              V. cholerae, the causative agent of cholera, is able to
11 diffusometry can be used to detect down to 1 V. cholerae cell in molecular-grade water in 20 minutes
12 n molecular-grade water in 20 minutes and 10 V. cholerae cells in pond water in just 35 minutes in 25
13        We probed microarrays containing 3652 V. cholerae antigens with plasma and antibody-in-lymphoc
14 re we present details of AMR profiles of 443 V. cholerae strains isolated from the stool samples of d
15 n on a smartphone, we can detect as few as 6 V. cholerae cells per reaction (0.66 aM) in just 35 minu
16                     We recently identified a V. cholerae-secreted serine protease, IvaP, that is acti
17 rs associated with the clinical outcome of a V. cholerae infection but did contain putative genomic i
18 tin utilization) to study the structure of a V. cholerae population over the course of a summer.
19 lso offer new insights into the biology of a V. cholerae serogroup that, from a genomic perspective,
20  densities, when QS autoinducers are absent, V. cholerae forms biofilms.
21 rocholate, serve as host signals to activate V. cholerae virulence through inducing the activity of t
22 ed the mechanism of how taurocholate affects V. cholerae virulence determinants.
23 opment of long-term mucosal immunity against V. cholerae O1.
24 ends upon the expression of genes that allow V. cholerae to overcome host barriers, including low pH,
25       The control of T6SS genes varies among V. cholerae strains and typically includes inputs from e
26             Rotavirus, adenovirus 40/41, and V. cholerae were the leading etiologies of infectious di
27  nutrient acquisition, biofilm assembly, and V. cholerae interactions with its host.
28 t a phage, causing bacterial infections, and V. cholerae, causing human infections, rely on the same
29 c Vibrios, including V. parahaemolyticus and V. cholerae, ToxR is required for bile resistance and vi
30 as reported that concentrations of phage and V. cholerae inversely correlate in aquatic reservoirs an
31 17 (more than 1 million suspected cases)-are V. cholerae serotype Ogawa isolates from a single sublin
32                 Here, we use 490 Argentinian V. cholerae genome sequences to characterise the variati
33 s other than O1 and O139, also designated as V. cholerae non-O1/O139 (NOVC), are not associated with
34  which, although classified serologically as V. cholerae O139, lacks the CTXphi bacteriophage and the
35                             Subsequently, as V. cholerae alkalinizes its environment in late stationa
36        Screening of all publically available V. cholerae genomes showed that numerous strains possess
37 ministration of the phages up to 24 h before V. cholerae challenge reduces colonization of the intest
38 omotes a more favourable interaction between V. cholerae and an arthropod host by reducing the nutrit
39 storing HapR expression in classical biotype V. cholerae repressed vieSAB transcription by binding to
40            We show that in classical biotype V. cholerae, LeuO cooperates with the nucleoid-associate
41 inheritance of antibiotic resistance in both V. cholerae and Streptococcus pneumoniae.
42  we show a confrontation strategy adapted by V. cholerae O1 in which it utilizes a quorum sensing (QS
43  from patients with severe cholera caused by V. cholerae O1 in Bangladesh and age-, sex-, and ABO-mat
44 s a source of iron is genetically encoded by V. cholerae(3).
45 is pathway are unlikely to be encountered by V. cholerae in aquatic reservoirs or within the human ho
46 es c-di-GMP binding and biofilm formation by V. cholerae.
47 TleV1 toxin is delivered in a T6SS manner by V. cholerae and can lyse other bacterial cells.
48 ome in human THP-1 monocytes and in PBMCs by V. cholerae varies with the biotype and is mediated by b
49 the evolution of niche-specific predation by V. cholerae-specific virulent phages, which complicates
50 (CTX), a protein complex that is secreted by V. cholerae, is required for V. cholerae to cause severe
51 domain AlmG substrate to that synthesized by V. cholerae.
52 e genome-encoded RecA helps CTXPhi to bypass V. cholerae immunity and allow it to replicate in the ho
53  we used classical (O395) and El Tor (C6706) V. cholerae biotypes in growth and biochemical assays.
54 surface adhesion-mediated compression causes V. cholerae biofilms to transition from a 2D branched mo
55                       HapR expression causes V. cholerae to resist VBNC induction and become dominant
56            Here, we utilize Vibrio cholerae (V. cholerae) as a proof-of-concept for our detection sys
57 ing the waterborne pathogen Vibrio cholerae (V. cholerae).
58 s the potential utility of single-chromosome V. cholerae to address fundamental questions on chromoso
59                                   A clinical V. cholerae reference strain expressing the Aux 5 cluste
60                       We show that competent V. cholerae acquire DNA fragments with a length exceedin
61 ic antibody responses to the nearly complete V. cholerae O1 protein immunome; it has identified antig
62 at ciliated protozoa release EFVs containing V. cholerae.
63                                 In contrast, V. cholerae serogroups other than O1 and O139, also desi
64 es in the gastrointestinal tract may control V. cholerae biofilm formation at physiological levels.
65 roles of the two autoinducers in controlling V. cholerae behavior.
66              We also observed that different V. cholerae O1 natural isolates with distinct QS functio
67 rst report of unique roles for the different V. cholerae autoinducers suggests that detection of kin
68 nes, we reveal and compare three-dimensional V. cholerae colonization patterns of planktonic-grown an
69 eases pathogen growth and induces a distinct V. cholerae transcriptomic signature that is indicative
70                        We sequence two dozen V. cholerae strain genomes from diverse sources and deve
71 nitially feared to represent a new, emerging V. cholerae clone that would lead to an eighth cholera p
72           We show that the genes that enable V. cholerae to obtain iron via haem and vibriobactin con
73 ent bacterial species and presumed to enable V. cholerae to assess the total bacterial cell density o
74 on within, and between, epidemic and endemic V. cholerae.
75 tulating that locally evolving environmental V. cholerae contributes to outbreaks outside Asia remain
76                     In aquatic environments, V. cholerae exists both as planktonic cells and as biofi
77  contribute to the dissemination of epidemic V. cholerae strains.
78 a, and we contrast the clonality of epidemic V. cholerae with the background diversity of local endem
79 e, using electron cryotomography, we explore V. cholerae's cytoplasmic chemoreceptor array and establ
80 dosomal trafficking induced by extracellular V. cholerae.
81     Our results suggest that EFVs facilitate V. cholerae survival in the environment, enhancing their
82 AI-1 QS pathway is activated when only a few V. cholerae cells are present, whereas the AI-2 pathway
83 bile salt-dependent virulence activation for V. cholerae The induction of TCP by murine intestinal co
84                         OhrA is critical for V. cholerae adult mouse colonization but is dispensable
85 shows that these cit genes are essential for V. cholerae growth when citrate is the sole carbon sourc
86 sent four complete, high-quality genomes for V. cholerae O139, obtained using long-read sequencing.
87 ween open and closed states is important for V. cholerae biofilm formation, as RbmA variants with swi
88 virulence regulator, ToxR, was important for V. cholerae resistance to hydrogen peroxide.
89              Our results suggest a model for V. cholerae biofilms in which Bap1 and RbmC play dominan
90 effector-immunity gene profiles observed for V. cholerae and closely related species.
91 ive by nanoliter quantitative PCR (qPCR) for V. cholerae (n = 78/849), the odds that a rapid diagnost
92           In addition, OmpR was required for V. cholerae fitness during growth under alkaline conditi
93  is secreted by V. cholerae, is required for V. cholerae to cause severe disease.
94     Here, we conducted an imaging screen for V. cholerae mutants that fail to disperse, revealing thr
95 uture peacekeeping operations: screening for V. cholerae carriage, administering prophylactic antimic
96  present in the gut is a relevant signal for V. cholerae virulence induction in vivo We further show
97              Unlike the formate channel from V. cholerae and the hydrosulphide channel from C. diffic
98 body protects the intestinal epithelium from V. cholerae infection.
99 esent the dodecameric structure of SpeG from V. cholerae in a ligand-free form in three different con
100 SBP of the sialic acid TRAP transporter from V. cholerae.
101  study provides mechanistic insight into how V. cholerae can acquire phosphate from extracellular DNA
102             Furthermore, these data show how V. cholerae MARTX toxin suppresses intestinal inflammati
103                Identification of immunogenic V. cholerae antigens could lead to a better understandin
104    Overall, we identified 608 immunoreactive V. cholerae antigens in our screening, 59 of which had h
105                                           In V. cholerae, mutation of the G4 motif, responsible for h
106 tory pathways that control its activation in V. cholerae.
107 ted serine protease, IvaP, that is active in V. cholerae-infected rabbits and human choleric stool.
108            Antimicrobial resistance (AMR) in V. cholerae has become a global concern.
109 eported that the virulence activator AphB in V. cholerae is involved in ROS resistance.
110  role in shaping the biofilm architecture in V. cholerae biofilms, and this growth pattern is control
111   This unusual two-chromosome arrangement in V. cholerae has sparked considerable research interest s
112 ethod and identify new T6SS gene clusters in V. cholerae.
113 decuple mutant of 12 diguanylate cyclases in V. cholerae.
114 n fatty acid biosynthesis and degradation in V. cholerae Our results provide the molecular basis for
115 ize CrvA, the first curvature determinant in V. cholerae.
116  the occurrence of cellular filamentation in V. cholerae, with variable propensity to filament among
117 e, bile resistance, and biofilm formation in V. cholerae Here, we investigated the function of ToxR a
118 protein necessary for curvature formation in V. cholerae.
119 tic elements linked with resistance genes in V. cholerae Here we present details of AMR profiles of 4
120 tive anaerobic citrate fermentation genes in V. cholerae, consisting of citCDEFXG, citS-oadGAB, and t
121 de the molecular basis for studies on Hfq in V. cholerae and highlight the importance of a previously
122           However, the RNA ligands of Hfq in V. cholerae are currently unknown.
123 study, we identified another OxyR homolog in V. cholerae, which we named OxyR2, and we renamed the pr
124 porter of nucleotides has been identified in V. cholerae, suggesting that in order for the organism t
125 ound that indole repressed genes involved in V. cholerae pathogenesis, including the ToxR virulence r
126 y by wHTH TFs: for example, ToxR and LeuO in V. cholerae; HilA, LeuO, SlyA and OmpR in S.
127  further investigate the function of OmpR in V. cholerae biology by defining the OmpR regulon through
128 regulator aphB; however, the role of OmpR in V. cholerae biology outside virulence regulation remaine
129 namic activity of type IV competence pili in V. cholerae as a model system.
130 ce gene expression and biofilm production in V. cholerae.
131                       Cobamide remodeling in V. cholerae is distinct from the canonical pathway requi
132 cing) analysis to identify Hfq-bound RNAs in V. cholerae Our work revealed 603 coding and 85 noncodin
133 his LPS modification plays a pivotal role in V. cholerae resistance to antimicrobial peptides, weapon
134            We demonstrate that cell shape in V. cholerae is regulated by the bacterial second messeng
135 ransduction pathway that is nearly silent in V. cholerae of the El Tor biotype.
136 tation of the transcriptional start sites in V. cholerae and highlight the importance of posttranscri
137        In this work, cobamide specificity in V. cholerae is demonstrated by remodeling of pseudocobal
138 ted with the transition to the VBNC state in V. cholerae.
139 e an overview of the chemosensory systems in V. cholerae and the advances toward understanding their
140 thways controlling cell shape transitions in V. cholerae and the benefits of switching between rod an
141 , we systematically dissect PTS transport in V. cholerae.
142 nto the mechanism by which bile salts induce V. cholerae virulence but also suggest a means by which
143  monovalent 2D6 Fab fragments also inhibited V. cholerae motility, demonstrating that antibody-mediat
144 own of 37 predicted essential genes inhibits V. cholerae viability, thus validating the products of t
145 rmine acts as an exogenous cue that inhibits V. cholerae biofilm formation through the NspS-MbaA sign
146 t IvaP plays a role in modulating intelectin-V. cholerae interactions.
147 dynamics of individual TcpP proteins in live V. cholerae cells with < 40 nm spatial resolution on a 5
148                       In particular, a major V. cholerae lineage occasionally grows to large numbers
149 nella enterica subsp. arizonae This modified V. cholerae strain was able to kill its parent using its
150 sion and retraction dynamics, and modulating V. cholerae surface attachment and colonization.
151 ndwork for interventions aimed at modulating V. cholerae biofilm dispersal to ameliorate disease.
152 tagged allele of VcPilQ purified from native V. cholerae cells to determine the cryoEM structure of t
153  the diversity of GIs circulating in natural V. cholerae populations and identifies GIs with VPI-1 re
154 nscriptomic studies with RND efflux-negative V. cholerae suggested that RND-mediated efflux was requi
155 bility to perform genomic analyses of non-O1 V. cholerae in the future.
156      The El Tor and classical biotypes of O1 V. cholerae show striking differences in their resistanc
157 ave been pivotal in the evolution of O1/O139 V. cholerae.
158             We show that the 26 co-occurring V. cholerae lineages continuously compete for limited sp
159 phosphoethanolamine (pEtN) to the lipid A of V. cholerae El Tor that is not functional in the classic
160 heme-independent mechanism for activation of V. cholerae H-NOX that implicates this protein as a dual
161 tiated almost immediately after adherence of V. cholerae to intestinal cells.
162 s observed within 30 minutes of adherence of V. cholerae to the intestinal cell line INT 407, and a m
163                          Genetic analysis of V. cholerae suggested that pathogen growth was dependent
164  by specifically binding to the O-antigen of V. cholerae We demonstrate that the bivalent structure o
165                      The major components of V. cholerae biofilms include Vibrio polysaccharide (VPS)
166                 This toxigenic conversion of V. cholerae has evident implication in both genome plast
167         Reflecting the complex life cycle of V. cholerae, this organism has three different chemosens
168 latform for rapid and sensitive detection of V. cholerae at the point of use.
169 nsitive and reliable method for detection of V. cholerae in natural samples.
170 s method with former report for detection of V. cholerae published in 2006.
171 martphone-based PD platform for detection of V. cholerae.
172 eflect the structure and complex dynamics of V. cholerae populations and provide a scalable high-thro
173 c reservoirs as well as ongoing evolution of V. cholerae isolates from aquatic sites.
174 in about long-term survival and evolution of V. cholerae strains within these aquatic environmental r
175 drolase CbiZ, and heterologous expression of V. cholerae CobS was sufficient for remodeling.
176 trated in vivo by heterologous expression of V. cholerae pathway enzymes in a specially engineered Es
177 gative bacteria essential for the fitness of V. cholerae in its natural environment.
178                       While the formation of V. cholerae biofilms has been well studied, little is kn
179                     Furthermore, function of V. cholerae cobamide-dependent methionine synthase MetH
180 T-dependent cholera toxin synthesis genes of V. cholerae c2-HDA significantly repressed invasion gene
181 acterial genome, we engineered the genome of V. cholerae and examined in vitro and in vivo stability
182             We also engineered the genome of V. cholerae to monitor the importance of the autonomousl
183          This study engineered the genome of V. cholerae to remove all of the GIs, ICEs, and prophage
184 onstrate that RpoS is required for growth of V. cholerae on insoluble chitin.
185 ut, which selectively promotes the growth of V. cholerae through the acquisition of host-derived haem
186                        The identification of V. cholerae O1 strains in the Haitian environment, which
187                    Notably, the inability of V. cholerae to produce and utilize pseudocobalamin contr
188 ti-TcpB antibodies block CTXphi infection of V. cholerae Finally, we show that CTXphi uptake requires
189                Recently, natural isolates of V. cholerae with chromosomal fusion have been found.
190 ulation networks among different isolates of V. cholerae.
191 e notion that the environmental lifestyle of V. cholerae fosters the exchange of genetic material wit
192 eloped a mixed-transmission dynamic model of V. cholerae, where aquatic reservoirs actively contribut
193                                  A number of V. cholerae iron acquisition systems have been identifie
194                         The lowest number of V. cholerae O1 in food sample with and without the enric
195 hitectures that separate the major phases of V. cholerae biofilm growth.
196 , evidence is lacking for phage predation of V. cholerae in aquatic environments.
197 igen (a bacterial outer-membrane protein) of V. cholerae was expressed and purified and raising of po
198 stream trisaccharide fragment of the O-PS of V. cholerae O139.
199 ation interface mutants (N381A and R385A) of V. cholerae DAPDC.
200                    The genetic regulation of V. cholerae entering its VBNC state is not well understo
201 ential use in reducing aquatic reservoirs of V. cholerae in endemic areas.
202  resulted in a prolonged culturable state of V. cholerae in artificial sea water at 4 degrees C, wher
203                Using a filamenting strain of V. cholerae O139, we show that cells with this morphotyp
204 nated GIVchS12) from a non-O1/O139 strain of V. cholerae that is present in the same chromosomal loca
205 teins lead to competition between strains of V. cholerae, which are thought to be protected only from
206 m largely clonal, patient-derived strains of V. cholerae.
207 sal escape response in pathogenic strains of V. cholerae.
208 or individualized preventative strategies of V. cholerae infection through modulating the structure a
209  should be valuable for the genetic study of V. cholerae and could be adapted for use in other specie
210 st is paramount to the pathogenic success of V. cholerae The transition between these two disparate e
211 ned AI synthase genes, increased survival of V. cholerae and a decrease in phage titer was observed.
212 -induced lipid wasting to extend survival of V. cholerae-infected flies.
213 ions between the type VI secretion system of V. cholerae and the microbial community of the fly.
214 , we discuss the roles played by the T6SS of V. cholerae in both natural environments and hosts.
215 persistence and the modes of transmission of V. cholerae and may further apply to other opportunistic
216 that a phospholipase T6SS effector (TseL) of V. cholerae can induce T6SS dynamic activity in P. aerug
217  study would help in better understanding of V. cholerae evolution and management of cholera disease
218 in the lumen, as well as the upregulation of V. cholerae genes that encode enzymes of the tricarboxyl
219 esh water, and only ICP1 was able to prey on V. cholerae in estuarine water due to a requirement for
220 similar to GIVchS12 were identified in other V. cholerae genomes, also containing CRISPR-Cas elements
221 ic in Yemen to global radiations of pandemic V. cholerae and show that this sublineage originated fro
222 ncreased competitive fitness to pre-pandemic V. cholerae, leading to grounding of the element in the
223  a single sublineage of the seventh pandemic V. cholerae O1 El Tor (7PET) lineage.
224 on of 1,087 isolates of the seventh pandemic V. cholerae serogroups O1 and O139 biotype El Tor(2-4).
225 on, are specific to the suspected pathogenic V. cholerae O1 and O139, but they are not specific to th
226 ctor that directly regulates the two primary V. cholerae virulence factors.
227 e ligated-ileal-loop assay, 2D6 IgA promoted V. cholerae agglutination in the intestinal lumen and li
228                   The T6SS not only promotes V. cholerae's survival during its aquatic and host life
229 ecules called autoinducers (AIs) can protect V. cholerae against predatory phages.
230          The majority of clinically relevant V. cholerae O139 isolates are closely related to serogro
231    Mutation of either oxyR2 or ahpC rendered V. cholerae more resistant to H2O2 RNA sequencing analys
232 permidine and spermidine enhance and repress V. cholerae biofilm formation, respectively.
233 intestine retards this process by repressing V. cholerae succinate uptake.
234 es in the gut and, along with other secreted V. cholerae proteases, decreases binding of intelectin,
235 ompetition experiments with matrix-secreting V. cholerae variants, whose densely packed biofilm struc
236                         Conversely, straight V. cholerae mutants have reduced swimming speed when usi
237 ens included cholera toxin B and A subunits, V. cholerae O-specific polysaccharide and lipopolysaccha
238                        None of the surviving V. cholerae colonies are resistant to all three phages.
239 ng the citrate fermentation pathway and that V. cholerae likely needs to compete with other members o
240                 Finally, we demonstrate that V. cholerae biofilms can generate sufficient mechanical
241           This result also demonstrated that V. cholerae T6SS is capable of delivering effectors that
242               This led to the discovery that V. cholerae ompR was induced at alkaline pH to repress g
243                  Recently, it was found that V. cholerae isolates from the Haiti outbreak were poorly
244                 These findings indicate that V. cholerae OmpR has evolved the ability to respond to n
245         Our collective results indicate that V. cholerae ompR is an aphB repressor and regulates the
246 evious work in our laboratory indicated that V. cholerae OmpR functioned as a virulence regulator thr
247  clinical relevance was the observation that V. cholerae in the INT 407-associated biofilms was signi
248                              We propose that V. cholerae uses CAI-1 to verify that some of its kin ar
249 ll, the studies presented here revealed that V. cholerae virulence potential can evolve and that the
250        Quantitative image analyses show that V. cholerae colonizes mainly the medial portion of the s
251   Mouse colonization experiments showed that V. cholerae can utilize citrate in vivo using the citrat
252             Our previous work suggested that V. cholerae could convert pseudocobalamin produced by cy
253                       Evidence suggests that V. cholerae O1 may activate inflammatory pathways, and a
254 ntrations of DPO, allowing VqmA to drive the V. cholerae quorum-sensing transition at high cell densi
255 hia coli FeoB, which is solely a GTPase, the V. cholerae and Helicobacter pylori FeoB proteins have b
256  acquired genes from 6 different loci in the V. cholerae chromosome and showed contribution of CTX pr
257 he efficiency of integrations of MGEs in the V. cholerae chromosome.
258 ication mechanism that only functions in the V. cholerae El Tor biotype.
259  7 predicted endochitinase-like genes in the V. cholerae genome.
260 t OxyR2 and AhpC play important roles in the V. cholerae oxidative stress response.
261 ion, allowing the phage to be drawn into the V. cholerae periplasm as an extension of the pilus filam
262 ortant GI involved in cholera disease is the V. cholerae pathogenicity island 1 (VPI-1).
263 omic differences between these isolates, the V. cholerae O1 reference strain N16961, and the prototyp
264 endent of primary secreted components of the V. cholerae biofilm matrix; instead, filamentous biofilm
265 crease the negatively charged surface of the V. cholerae outer membrane.
266 e autoinducer AI-2 that sets the pace of the V. cholerae QS program.
267 stinal tract and which are substrates of the V. cholerae RND efflux systems.
268 porin, VcChiP, from the cell envelope of the V. cholerae type strain O1.
269     Here, we have expressed and purified the V. cholerae HisKa (HnoK) and H-NOX in its heme-bound (ho
270                     Our data showed that the V. cholerae gene VC2714, encoding a homolog of Escherich
271                 Our findings reveal that the V. cholerae PTS is an additional modulator of the ToxT r
272 iple copies at the phage tip, to bind to the V. cholerae toxin-coregulated pilus (TCP).
273                      Although related, these V. cholerae serogroups differ in several fundamental way
274 , this biosensor was successfully applied to V. cholerae detection in environmental samples with no s
275 ectin, which inhibited intelectin binding to V. cholerae These results suggest that IvaP plays a role
276 es the expression of ohrA and contributes to V. cholerae's ability to survive in a variety of environ
277 onsive regulatory genes for contributions to V. cholerae virulence factor production.
278  intestinal carbohydrate-binding protein, to V. cholerae in vivo IvaP bears homology to subtilisin-li
279 tal introductions of seventh pandemic El Tor V. cholerae and that at least seven lineages local to th
280            The almEFG operon found in El Tor V. cholerae confers >100-fold resistance to antimicrobia
281 sely related to serogroup O1, biotype El Tor V. cholerae, and comprise a single sublineage of the sev
282 raphy of both clinical and aquatic toxigenic V. cholerae O1 isolates and show robust evidence of the
283  colony-forming units/ml) for both toxigenic V. cholerae serogroups.
284         Indole is also produced by toxigenic V. cholerae strains in the human intestine, but its sign
285 c environments, with environmental toxigenic V. cholerae O1 strains serving as a source for recurrent
286  Three of these sequences are from toxigenic V. cholerae, and one is from a bacterium which, although
287  The single-source introduction of toxigenic V. cholerae O1 in Haiti, one of the largest outbreaks oc
288 estigated the effects of indole on toxigenic V. cholerae O1 El Tor during growth under virulence indu
289                                      The two V. cholerae autoinducers funnel information into a share
290      During microcolony formation, wild-type V. cholerae cells tended to exist as straight rods, whil
291 ted approximately 1 x 10(5) CFU of wild-type V. cholerae O1 El Tor Inaba strain N16961 10 days or 3 m
292                             Unlike wild-type V. cholerae, mutants lacking wigR fail to recover follow
293 These effects are relevant for understanding V. cholerae pathogenicity and are mediated through the p
294  barriers to infection and showed unexpected V. cholerae migration counter to intestinal flow.
295 kling mice from oral challenge with virulent V. cholerae O395.
296 atients enrolled, 6.2% (n = 1604) cases were V. cholerae O1.
297                 Intestinal colonization with V. cholerae results in expenditure of host lipid stores
298 dicating that cell shape is coregulated with V. cholerae's induction of sessility.
299 d did not (for ciprofloxacin) correlate with V. cholerae suppression.
300 t (MDR) and extensively drug-resistant (XDR) V. cholerae to identify AMR genes and genomic elements t

 
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