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1                                              A. baumannii encodes a type VI secretion system (T6SS),
2                                              A. baumannii encodes for the transport protein AceI, whi
3                                              A. baumannii expresses a variety of virulence factors, i
4                                              A. baumannii has become the Gram-negative bacterium with
5                                              A. baumannii is an increasing threat to public health du
6                                              A. baumannii isolates carrying cas5 or combinations of t
7                   Upon exposure to H(2)O(2), A. baumannii differentially transcribes several hundred
8 esistant to polymyxin B and colistin, and 20 A. baumannii worldwide isolates from 2016 and 2017 with
9                          We investigated 230 A. baumannii strains using 17 lytic A. baumannii phages
10                  Thirty P. aeruginosa and 30 A. baumannii isolates previously characterized by whole-
11 results from Raman spectroscopic data for 31 A. baumannii clinical isolates labeled according to thei
12 exposure quadrupled the hazards of acquiring A. baumannii even after controlling for severity of illn
13                                 In addition, A. baumannii OMVs increased the release of several chemo
14             The CA values for P. aeruginosa, A. baumannii, and S. maltophilia were 94.1%, 92.7%, and
15 ssential agreement values for P. aeruginosa, A. baumannii, and S. maltophilia were 99.5%, 99.2%, and
16 rs that are effective as antibiotics against A. baumannii were identified using an in vitro DHFR acti
17 d for further antibiotic development against A. baumannii.
18 cterial activity of cycloviolacin O2 against A. baumannii.
19 sults demonstrate that the Znu system allows A. baumannii to subvert host nutritional immunity and ac
20 inct arrangement and is well conserved among A. baumannii strains.
21 etoxify hydrogen peroxide is abolished in an A. baumannii strain in which the transcriptional regulat
22  from lethal infections of P. aeruginosa and A. baumannii and enhanced the activity of colistin in vi
23 more capable of disrupting P. aeruginosa and A. baumannii biofilms when compared to conventional anti
24 apenemase production among P. aeruginosa and A. baumannii Ten testing sites then evaluated the mCIM u
25 ting of Enterobacterales, P. aeruginosa, and A. baumannii complex isolates with limited category erro
26 ed using an in vitro DHFR activity assay and A. baumannii growth inhibition.
27 verall, the sensitivity for A. baumannii and A. baumannii complex identification was 100% (73/73) and
28  Last, we show that both A. nosocomialis and A. baumannii produce functioning CDI systems that mediat
29 an open-source Pathogen Box library for anti-A. baumannii compounds.
30 O is a candidate for the development of anti-A. baumannii drugs.
31 y drug-resistant A. baumannii was defined as A. baumannii (genospecies 2) nonsusceptible to all drug
32 d 7 mM HOCl completely eradicated S. aureus, A. baumannii, and P. aeruginosa biofilms after 3 hours,
33 rom the extensively drug-resistant bacteria, A. baumannii.
34                     Acinetobacter baumannii (A. baumannii) strains are common nosocomial pathogens th
35  coli (E. coli) and Acinetobacter baumannii (A. baumannii).
36 remic patients with pneumonia (PP) caused by A. baumannii (13 from the unicenter and 23 from the mult
37  antibiotic resistance, infections caused by A. baumannii have become extremely difficult to treat, u
38 ups: (1) isolates from patients colonized by A. baumannii (16 from the unicenter and 20 from the mult
39 the primary resistance mechanism employed by A. baumannii.
40                     The lipid A expressed by A. baumannii is hepta-acylated and contains 2-hydroxylau
41 e model, the minimum lethal dose required by A. baumannii ATCC 17978 DeltapstS was lower compared to
42  shown to contribute to protein secretion by A. baumannii and other pathogenic species of Acinetobact
43 -hydroxylation of the laurate transferred by A. baumannii LpxL.
44             The biological processes used by A. baumannii to cause disease are not well defined, but
45 important to discover the mechanisms used by A. baumannii to survive stresses encountered during infe
46 i from other members of the A. calcoaceticus-A. baumannii complex and to detect antimicrobial resista
47 , and WGS on 148 Acinetobacter calcoaceticus-A. baumannii complex bloodstream isolates collected from
48      We assessed the capacity of 15 clinical A. baumannii isolates including 9 recent clinical isolat
49            In this study, we used a clinical A. baumannii strain (LAC-4) that is hypervirulent to imm
50 that contribute to MDR phenotype of clinical A. baumannii isolates.
51  of A. baumannii A118 and two other clinical A. baumannii strains, revealed differences in their resp
52 exidine, an antiseptic widely used to combat A. baumannii, is effected through the proteobacterial an
53  baumannii survives on surfaces, we cultured A. baumannii in liquid media for several days and then a
54 ing the World Health Organization to declare A. baumannii a "Priority 1: Critical" pathogen, for whic
55                   E-scaffold alone decreased A. baumannii and S. aureus biofilm cell densities by (3.
56            The implications of LOS-deficient A. baumannii are far-reaching - from impacts on cell env
57             Examination of the LOS-deficient A. baumannii cell surface demonstrated that specific lip
58 lycan cell wall, was lethal to LOS-deficient A. baumannii Global transcriptomic analysis of a PBP1A-d
59 BP1A-deficient mutant and four LOS-deficient A. baumannii strains showed a concomitant increase in tr
60 g the developed method to selectively detect A. baumannii M3237 and 54149 from complex serum samples
61 ycolipid profiling was able to differentiate A. baumannii complex organisms based on their membrane l
62  current approach can be used to distinguish A. baumannii M3237 from A. baumannii 54149 by using TF2-
63  of 2,500 core SNPs accurately distinguished A. baumannii isolates from different clonal lineages.
64 )) as a stressor produced in the lung during A. baumannii infection and defined OxyR as a transcripti
65                       The metabolome of each A. baumannii strain was measured using liquid chromatogr
66 scribe a Zn uptake (Znu) system that enables A. baumannii to overcome this host-imposed Zn limitation
67                      The released Zn enables A. baumannii to combat host-imposed Zn starvation.
68 del of intraperitoneal (i.p.) mucin-enhanced A. baumannii infection, we characterized the kinetics of
69 ls and play an important role in eradicating A. baumannii infection in vivo Our findings suggest that
70  we showed that a mutation of an established A. baumannii global virulence regulator led to marked ch
71               Following an outbreak of fatal A. baumannii infections in a cohort of relatively immuno
72                         We develop the first A. baumannii catheter-associated urinary tract infection
73 odstream infections, even though one in five A. baumannii strains are isolated from urinary sites.
74 oduction of inflammatory cytokines following A. baumannii infection.
75                                          For A. baumannii, a species known to undergo rapid horizonta
76 d 100% (95% CI, 83.9 to 100; range, 100) for A. baumannii Overall, we found both the mCIM and the Car
77 evaluated, with 11 for P. aeruginosa, 14 for A. baumannii, and 2 for S. maltophilia Categorical agree
78 esting for colistin should be considered for A. baumannii identified from CMS-experienced patients.
79  We also examined the importance of CsrA for A. baumannii virulence.
80 imits of detection of the current method for A. baumannii M3237 and 54149 are ~10(5) and ~10(4) cells
81                 Overall, the sensitivity for A. baumannii and A. baumannii complex identification was
82                              Specificity for A. baumannii complex identification was 86.6% (13/15).
83 S is superior to conventional techniques for A. baumannii strain typing and outbreak analysis.
84 ound found to inhibit the growth of all four A. baumannii test strains with IC(50) of 0.6-2.7 muM, IC
85                          A total of fourteen A. baumannii isolates were isolated from the donors' pre
86                                    GPLs from A. baumannii exhibited more variability in locations of
87 resolution and compare it to homologues from A. baumannii strains ACICU and BIDMC57, which are C-term
88  used to distinguish A. baumannii M3237 from A. baumannii 54149 by using TF2-Fe(3)O(4)@Al(2)O(3) and
89  encouraging results in protecting mice from A. baumannii infection, but monoclonal anti-OMP antibodi
90                        We isolated OMVs from A. baumannii cultures and intranasally introduced the OM
91 inetobacter infections other than those from A. baumannii.
92                           To investigate how A. baumannii survives on surfaces, we cultured A. bauman
93                     AXDX reliably identified A. baumannii and predicted minocycline susceptibility re
94 need for improved surveillance to identified A. baumannii with an extensive drug resistance profile.
95 methods that can be used to rapidly identify A. baumannii from complex samples should be developed.
96  transposon insertion sequencing to identify A. baumannii mutants displaying altered susceptibility t
97 l clearance and was secondary to an impaired A. baumannii phenylacetic acid catabolism pathway, which
98   As we began to examine the role of CsrA in A. baumannii, we observed that the growth of DeltacsrA m
99 phosphate sensor PstS produced a decrease in A. baumannii pathogenesis, supporting its role as a viru
100 code the major H(2)O(2)-degrading enzymes in A. baumannii, as confirmed through measurement of promot
101  it may apply to other conserved epitopes in A. baumannii.
102 es revealed that the aceI gene is induced in A. baumannii by the short-chain diamines cadaverine and
103 vercome a myriad of resistance mechanisms in A. baumannii.
104 oles that Toll-like receptors (TLRs) play in A. baumannii OMV-mediated pulmonary inflammation.
105                A component of an RND pump in A. baumannii, AdeT1, was previously demonstrated to enha
106 o a maximum (8.27 +/- 0.05) log reduction in A. baumannii and (4.71 +/- 0.12) log reduction in S. aur
107 te the mechanisms of polymyxin resistance in A. baumannii AB307-0294 using an in vitro dynamic model
108 ethod that identifies colistin resistance in A. baumannii complex clinical isolates, as well as other
109 r of genes essential for serum resistance in A. baumannii indicates the degree of complexity needed f
110                 Here, we studied its role in A. baumannii virulence.
111 ght additional genes identified by Tn-seq in A. baumannii resistance to killing by NHS but not by nor
112 dy highlights the important roles of TLRs in A. baumannii OMV-induced pulmonary inflammation in vivo.
113 nutrient that pathogenic bacteria, including A. baumannii, must acquire from their hosts in order to
114                            During infection, A. baumannii must acquire nutrients for replication and
115          To establish a persistent infection,A. baumannii must overcome the detrimental effects of co
116 t among DHFR inhibitors tested in inhibiting A. baumannii growth.
117 s for the first time that MMV675968 inhibits A. baumannii growth via selective inhibition of AbDHFR a
118   This study provides the first insight into A. baumannii gene expression profiles during a life-thre
119  by aiding directly in the uptake of Zn into A. baumannii cells and is important for pathogenesis in
120                            By using isogenic A. baumannii mutants lacking expression of virulence eff
121  that the combination synergistically killed A. baumannii via time-dependent inhibition of different
122  in the absence of macrophages in the lungs, A. baumannii replicates significantly, and host proinfla
123 ated 230 A. baumannii strains using 17 lytic A. baumannii phages and the phage susceptibility was 46.
124                                   Four major A. baumannii clonal lineages (as defined by MLST) circul
125  pathogenic Acinetobacter species, with many A. baumannii isolates harboring two distinct CDI systems
126 erial activity, in vivo efficacy against MDR A. baumannii infections and promising preclinical safety
127 mannii with the MBC of 2.0 mug/mL and an MDR A. baumannii with the MBC of 3.13 mug/mL.
128 nt (XDR) E. coli, XDR K. pneumoniae, and MDR A. baumannii were associated with 2-3 times higher morta
129 nificant reduction in the acquisition of MDR A. baumannii (RR, 0.28 [95% CI, .18-.43] and 0.48 [95% C
130 cquired antimicrobial-resistance mechanisms, A. baumannii isolates are commonly multidrug resistant,
131                               The ability of A. baumannii to form biofilms and resist oxidative stres
132 uced motility and biofilm-forming ability of A. baumannii.
133                   Notably, MS(3) analysis of A. baumannii 1205, an antibiotic-resistant strain, confi
134   From a previous transcriptomic analysis of A. baumannii ATCC 17978 under microaerobiosis, we know t
135 formed an in vivo transcriptomic analysis of A. baumannii isolated from a mammalian host with bactere
136                         Phenotypic assays of A. baumannii A118 and two other clinical A. baumannii st
137 little is known about the molecular basis of A. baumannii pathogenesis.
138 nd our understanding of the genetic basis of A. baumannii serum resistance, a transposon (Tn) sequenc
139 gap in knowledge on the infection biology of A. baumannii, and only a few virulence factors have been
140 e to enhance the tissue and blood burdens of A. baumannii strains of different virulence.
141 port experiments conducted in whole cells of A. baumannii and Escherichia coli and also in proteolipo
142      Here, we report the characterization of A. baumannii LpxO, which encodes the enzyme responsible
143 bacterial envelope is an important driver of A. baumannii disease, both at the level of battling agai
144 iratory secretions), and without evidence of A. baumannii infections prior to the collection of the f
145                             The evolution of A. baumannii has largely been defined by recombination,
146 s for cefiderocol AST, with the exception of A. baumannii complex isolates.
147                            The pan-genome of A. baumannii is open when the input genomes are normaliz
148 ding AceI is conserved in the core genome of A. baumannii, suggesting that it has an important primor
149 how that CsrA is essential for the growth of A. baumannii on host-derived substrates and is involved
150 1-Dox 35/1 protects from lethal infection of A. baumannii with an ED50 value of <2.0 mg/kg.
151 ributes to the mucin-enhanced infectivity of A. baumannii in this model.
152                 Intraperitoneal injection of A. baumannii-mucin or mucin alone induced a significant
153                   Intranasal introduction of A. baumannii OMVs mediated pulmonary inflammation, which
154                             The lethality of A. baumannii strains depends on distinct stages.
155 reening of a transposon insertion library of A. baumannii ATCC 19606T resulted in the identification
156  one of the major clinical manifestations of A. baumannii infection associated with high morbidity an
157 de a useful tool for genetic manipulation of A. baumannii.
158  urgent need to understand the mechanisms of A. baumannii pathogenesis for the future development of
159 n/doripenem combination on the metabolome of A. baumannii.
160                         In a murine model of A. baumannii pneumonia, TLR9(-/-) mice exhibit significa
161 portant for pathogenesis in murine models of A. baumannii infection.
162                          In murine models of A. baumannii pneumonia, RAGE signaling alters neither in
163 penem resistance of P. aeruginosa but not of A. baumannii.
164 targeting outer membrane protein A (OmpA) of A. baumannii Five anti-OmpA MAbs were developed using hy
165                               An outbreak of A. baumannii emerging after DCD renal transplantation wa
166 ulence differences across a diverse panel of A. baumannii clinical isolates during murine bacteremia
167                 Serial in vitro passaging of A. baumannii in the presence of C8 did not cause loss of
168 rtance of UDP-GalNAcA in the pathobiology of A. baumannii.
169  the role of the GGT in the pathogenicity of A. baumannii.
170 response and contributes to the pathology of A. baumannii infection.
171          Here, we studied the performance of A. baumannii identification and minocycline susceptibili
172 rticipants and evaluated for the presence of A. baumannii.
173 oval) and then evaluated for the presence of A. baumannii.
174                 Approximately one-quarter of A. baumannii protein coding genes were differentially ex
175      In this study, we highlight the role of A. baumannii as a uropathogen.
176 ophages would enhance sepsis and severity of A. baumannii disease.
177 ighlighting the human species specificity of A. baumannii serum resistance.
178  12 out of 15 genetically diverse strains of A. baumannii are resistant to NHS killing.
179  that several multidrug-resistant strains of A. baumannii harbor a large, self-transmissible resistan
180                                   Strains of A. baumannii lacking any individual Znu component are un
181 f the T6SS varies among different strains of A. baumannii, for which the regulatory mechanisms are un
182 eful tool for future pathogenesis studies of A. baumannii-associated septicemia and identification an
183          LpxO contributes to the survival of A. baumannii in human whole blood and is required for pa
184 ified 50 genes essential for the survival of A. baumannii in NHS, including already known serum resis
185 osa and colistin use was weaker than that of A. baumannii.
186 s allowing high efficiency transformation of A. baumannii.
187 ey functions involved in the transmission of A. baumannii in hospitals.
188 athway, plays a key role in the virulence of A. baumannii.
189 ed that GGT is required for the virulence of A. baumannii.
190 y, mechanisms of resistance and virulence of A. baumannii.
191                     Here, to gain insight on A. baumannii antibiotic resistance mechanisms, we analys
192 igated the impact of alveolar macrophages on A. baumannii pneumonia using a mouse model of infection
193 ssays to further explore the impact of PF on A. baumannii's microbial behavior and the strategies use
194   Previously, strain ATCC 19606 was the only A. baumannii strain demonstrated to subsist without lipi
195                     Here, we show that other A. baumannii strains can also survive without lipid A, b
196 shed a mouse model of intraperitoneal (i.p.) A. baumannii infection.
197 nteractions were observed among 52 patients; A. baumannii was identified from healthcare worker hands
198 pathogens collected from pediatric patients; A. baumannii and P. aeruginosa were susceptible to fewer
199                                     Previous A. baumannii pan-genomic studies used modest sample size
200 ins, with 60% of the carbapenemase-producing A. baumannii isolates producing acquired OXA-type carbap
201 OXA-23 and OXA-24/40 carbapenemase-producing A. baumannii strains (1 mug mL(-1)) and also provided go
202 apenemases among the carbapenemase-producing A. baumannii strains, with 60% of the carbapenemase-prod
203 icity in identifying carbapenemase-producing A. baumannii, no assays achieved a sensitivity of greate
204 to accurately detect carbapenemase-producing A. baumannii.
205 c pathway as a key determinant in protecting A. baumannii from the bactericidal activity of NHS via t
206 O-dependent lipid A 2-hydroxylation protects A. baumannii from polymyxin B, colistin, and human beta-
207    Our work further demonstrates how rapidly A. baumannii can generate resistance to a last resort an
208 of bacteriophages AB2 and AB6, can recognize A. baumannii clinical isolates M3237 and 54149, respecti
209  results provide novel information regarding A. baumannii pathogenesis and may be important for the d
210 ignificant proportion of clinically relevant A. baumannii strains are resistant to killing by normal
211 ed killing of competing bacteria but renders A. baumannii susceptible to antibiotics.
212  of the polymyxin-susceptible and -resistant A. baumannii strains.
213 een the polymyxin-susceptible and -resistant A. baumannii strains.
214  of the polymyxin-susceptible and -resistant A. baumannii.
215 ith infection caused by carbapenem-resistant A. baumannii (CRAB) identified as colistin susceptible (
216 solates and analyzing a carbapenem-resistant A. baumannii (CRAB) outbreak.
217 se, provoking spread of carbapenem-resistant A. baumannii and consequent colistin use.
218 on recently highlighted carbapenem-resistant A. baumannii as a "critical priority" for the developmen
219 the hazard of acquiring carbapenem-resistant A. baumannii by 5.1% (hazard ratio, 1.051; 95% CI, 1.007
220 doxycycline against 107 carbapenem-resistant A. baumannii clinical isolates.
221 bsequent development of carbapenem-resistant A. baumannii infections.
222             Presence of carbapenem-resistant A. baumannii on surveillance cultures is strongly associ
223  was the acquisition of carbapenem-resistant A. baumannii on surveillance cultures.
224 sceptibility testing of carbapenem-resistant A. baumannii strains, very major errors are rare, but ma
225  = 0.0004) of acquiring carbapenem-resistant A. baumannii.
226 ) became colonized with carbapenem-resistant A. baumannii.
227 The treatment regimen for colistin-resistant A. baumannii infection associated with the lowest mortal
228 ipid A was present in all colistin-resistant A. baumannii isolates.
229                           Colistin-resistant A. baumannii occurred almost exclusively among patients
230 on or colonization due to colistin-resistant A. baumannii were identified at a hospital system in Pen
231      Twenty patients with colistin-resistant A. baumannii were identified.
232 e 176 episodes of extensively drug-resistant A. baumannii bacteremia evaluated, 55 patients with a me
233      Breakthrough extensively drug-resistant A. baumannii bacteremia under steady state concentration
234 IONS: Adults with extensively drug-resistant A. baumannii bacteremia were prospectively followed from
235  of patients with extensively drug-resistant A. baumannii bacteremia, treated with colistin-carbapene
236 penem therapy for extensively drug-resistant A. baumannii bacteremia.
237                   Extensively drug-resistant A. baumannii was defined as A. baumannii (genospecies 2)
238                          Multidrug resistant A. baumannii has risen rapidly in Vietnam, where colisti
239 mes of phage susceptible multidrug resistant A. baumannii strains from Thailand.
240 n multivariate analysis, multidrug-resistant A. baumannii (odds ratio, 4.78; 95% CI, 2.14-18.45) and
241 interaction network of a multidrug-resistant A. baumannii clinical strain (AB5075).
242                  Indeed, multidrug-resistant A. baumannii is a major cause of hospital-acquired infec
243 icrobial-susceptible and multidrug-resistant A. baumannii strains impairs growth in the presence of H
244 eat infections caused by multidrug-resistant A. baumannii.
245        Recent reports of polymyxin-resistant A. baumannii highlight the urgent need for research into
246 olymyxin-susceptible and polymyxin-resistant A. baumannii using untargeted metabolomics.
247 on risk; however, having multidrug-resistant-A. baumannii and specific healthcare worker activities l
248 e advantage possessed by multidrug-resistant-A. baumannii in this environment and suggest possible ar
249  Here, we show that exogenous Mn can restore A. baumannii viability in the presence of reactive oxyge
250 mutilin derivatives against a drug sensitive A. baumannii strain, new molecules (2-4) exhibit bacteri
251 tion, we identified further mutations in six A. baumannii genes (vacJ, pldA, ttg2C, pheS and conserve
252 TF6 can be used as probes to target specific A. baumannii strains.
253 cing of the first complete genome of an ST10 A. baumannii clinical strain should accelerate our under
254 1) times the risk of developing a subsequent A. baumannii infection compared with patients who remain
255  behind the global propagation of successful A. baumannii lineages.
256 nhibited growth of both CRAB and susceptible A. baumannii (MIC 64-256 ug/mL), and also exhibited acti
257 f carbapenem-resistant, colistin-susceptible A. baumannii infection prior to identification of colist
258 f carbapenem-resistant, colistin-susceptible A. baumannii infection.
259 ycycline (1-Dox 35/1) kills drug susceptible A. baumannii with the MBC of 2.0 mug/mL and an MDR A. ba
260 -genome sequences of seven phage susceptible A. baumannii isolates revealed that six groups of antibi
261 resence of ompA gene among phage susceptible A. baumannii strains (p-value < 0.05).
262 nd biofilm formation among phage susceptible A. baumannii strains.
263  were carried by all seven phage susceptible A. baumannii.
264 esults in decreased survival during systemic A. baumannii infection that mirrors that of wild-type (W
265                           Following systemic A. baumannii infection, TLR9(-/-) mice have significantl
266            We showed that MMV675968 targeted A. baumannii dihydrofolate reductase (AbDHFR) as determi
267                             We conclude that A. baumannii's pathoadaptive responses is induced by HSA
268              Here, we show conclusively that A. baumannii mla mutants exhibit no defects in anterogra
269               These results demonstrate that A. baumannii employs several mechanisms to ensure bioava
270 ee Acinetobacter strains, demonstrating that A. baumannii subsets produce morphologically distinct ty
271                                          The A. baumannii Kdp system has a distinct arrangement and i
272                                          The A. baumannii PPA and NPA, respectively, were 97.1% (90.2
273 the Enterobacterales, P. aeruginosa, and the A. baumannii complex, respectively.
274 as 98.3% for P. aeruginosa and 91.6% for the A. baumannii complex when both the FDA and ISO criteria
275  breakpoints are currently available for the A. baumannii complex).
276                 We previously identified the A. baumannii histidine utilization (Hut) system as being
277 deABC, AdeIJK, and AdeFGH are encoded in the A. baumannii genome and are reported to contribute to an
278 immune responses by eliciting changes in the A. baumannii metabolic profile.
279 indicate that although the C terminus of the A. baumannii ATCC 19606T SecA is not essential for viabi
280 he highly variable and dynamic nature of the A. baumannii genome may be the result of its success in
281  and research results, we concluded that the A. baumannii isolates 3R1 and 3R2 was probably transmitt
282                          For the first time, A. baumannii KdpE is shown to be crucial to pneumonia on
283  for pneumonia, bacteremia, and death due to A. baumannii.
284 tor X plays a role in the immune response to A. baumannii Factor X deficiency was associated with red
285 e the role for TLR9 signaling in response to A. baumannii infection.
286 s were used as affinity probes to trap trace A. baumannii M3237 and 54149, respectively, from sample
287 y, an oxyR mutant is less fit than wild-type A. baumannii during infection of the murine lung.
288 n peroxide (H(2)O(2)) killing than wild-type A. baumannii However, mumR, which encodes the transcript
289                                Two unrelated A. baumannii clades were associated with the outbreak.
290                       The mechanism by which A. baumannii OMVs mediate inflammation is not fully defi
291 ients known to be infected or colonized with A. baumannii.
292 ands/gloves are frequently contaminated with A. baumannii after patient care.
293                      Mice were infected with A. baumannii American Type Culture Collection 17978 usin
294 t, RAGE(-/-) mice systemically infected with A. baumannii exhibit increased survival and reduced bact
295 synthesis is essential during infection with A. baumannii, K. pneumoniae and P. aeruginosa.
296 ia and that a similar phenomenon occurs with A. baumannii In the context of the pulmonary microbiome,
297 nosa isolates and less reliable for use with A. baumannii isolates.
298                   In addition, both Tet(X3) (A. baumannii) and Tet(X4) (E. coli) significantly compro
299 ing and novel mAb as therapy for lethal, XDR A. baumannii infections, and demonstrate that it synergi
300 epsis and aspiration pneumonia models of XDR A. baumannii infection.

 
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