ライフサイエンスコーパス: carbapenem

1 biotic, 1-carbapen-2-em-3-carboxylic acid (a carbapenem).

2 (24%) received TZP and 141 (76%) received a carbapenem.

3 (24%) received TZP and 141 (76%) received a carbapenem.

4 ptible to chloramphenicol, azithromycin, and carbapenems.

5 oss-resistance when used in combination with carbapenems.

6 eptible to chloramphenicol, azithromycin and carbapenems.

7 paradoxically, improves binding affinity for carbapenems.

8 ffusion of both nutrients (e.g. lactose) and Carbapenems.

9 ulting in resistance to both tigecycline and carbapenems.

10 th such drugs (other active drugs [OADs]) or carbapenems.

11 tam drugs, including both cephalosporins and carbapenems.

12 genes, which confer resistance to last-line carbapenems.

13 er by the 6alpha-hydroxyethyl substituent of carbapenems.

14 inactivation method, and disk diffusion with carbapenems.

15 ics were fluoroquinolones (35%), followed by carbapenems (20%), TMP-SMX (18.5%), and ceftazidime (11%

16 terales resistant to ertapenem but not other carbapenems; (3) Enterobacterales with OXA-48-like enzym

17 l drugs was significantly more frequent with carbapenems (36/206 [17.5%]) versus ceftazidime (25/201

18 d p=0.011), and antibiotic use, particularly carbapenems (45 [9%] vs 18 [24%], adjusted p=0.002) and

19 nds apart from the current DBOs in restoring carbapenem activity against OXA-CRAB as well as SBL-carr

20 aeruginosa after patients were treated with carbapenems, along with the general preference for carba

21 leophilic serine beta-lactamases (SBLs) with carbapenems also produces beta-lactones.

22 , which interacts with the C3 carboxylate of carbapenems, also contributes strongly to the deacylatio

23 hia coli strain with resistance to colistin, carbapenem and amikacin from sewage.

24 Isolates with resistance to both carbapenem and colistin are not restricted to a given se

25 Unadjusted carbapenem and daptomycin use decreased significantly.

26 down-regulating production of gas vesicles, carbapenem and prodigiosin antibiotics, and infection in

27 Production of gas vesicles, carbapenem and prodigiosin antibiotics, and motility are

28 racillin/tazobactam (TZP) but susceptible to carbapenems and 3rd generation cephalosporins, has emerg

29 patients were included; 249 received empiric carbapenems and 86 OADs.

30 tive bacterial species that are resistant to carbapenems and other drugs.

31 (20%), and 55/344 (16%) in the ceftazidime, carbapenem, and piperacillin-tazobactam groups, respecti

32 nt (MDR) to penicillins, cephalosporins, and carbapenems, and are harboring the bla(TEM), bla(CTX), a

33 beta-lactams (penicillins, cephalosporines, carbapenems, and monobactams), by the production of beta

34 We aimed to compare ceftazidime, carbapenems, and piperacillin-tazobactam as definitive m

35 events was demonstrated between ceftazidime, carbapenems, and piperacillin-tazobactam as definitive t

36 ely drug-resistant bacteria, including ESBL, carbapenem- and colistin-resistant clinical isolates.

37 As a result, PAS8-b-PDM12 sensitizes carbapenem- and colistin-resistant GNB to multiple antib

38 Carbapenem antibiotics are poorly hydrolyzed by most bet

39 a-lactamases (MBLs), mediating resistance to carbapenem antibiotics, is a major public health problem

40 eptible to third-generation cephalosporin or carbapenem antibiotics.

41 erobacteriaceae threaten human health, since carbapenems are last resort drugs for infections by such

42 mechanisms by which beta-lactamases degrade carbapenems are still not fully understood.

43 Carbapenems are widely regarded as the antibiotics of ch

44 t in the TZP arm and 11 (8%) patients in the carbapenem arm had incident carbapenem-resistant organis

45 t in the TZP arm and 11 (8%) patients in the carbapenem arm who had incident carbapenem-resistant org

46 lysis, we selected patients receiving TZP or carbapenems as adequate empirical treatment.

47 Overall, 119 patients received TZP or carbapenems as empirical treatment.

48 0.67-2.51, for piperacillin-tazobactam, with carbapenems as reference in propensity adjusted multivar

49 nd focus is beta-lactamase interactions with carbapenems, as carbapenem-resistant bacteria are of gra

50 Meropenem-vaborbactam (MEV) is a novel carbapenem-beta-lactamase inhibitor combination antibiot

51 The carbapenem bicyclic core consists of a beta-lactam ring

52 ming barriers to updating Enterobacteriaceae carbapenem breakpoints in Los Angeles hospitals.

53 Continued use of obsolete Enterobacteriaceae carbapenem breakpoints is common in clinical laboratorie

54 oratories, using obsolete Enterobacteriaceae carbapenem breakpoints.

55 with production of a beta-lactam antibiotic (carbapenem carboxylate) and a linear tripyrrole red anti

56 Carbapenem-colistin combination therapy did not reduce t

57 We evaluated whether carbapenem-colistin combination therapy given to patient

58 We evaluated whether carbapenem-colistin combination therapy reduces the emer

59 Carbapenem daily defined doses increased in parallel wit

60 Analysis of reported crystal structures for carbapenem-derived acyl-enzyme complexes reveals preferr

61 sed on previously established ZDs around the carbapenem disks.

62 m 4% to 10% (P = 0.03), as did daily defined carbapenem doses/1,000 patient days (6.52 to 34.5; R (2)

63 f the genes hycA, dsrB, and bolA potentiated carbapenem efficacy in CRE E. coli, whereas inhibition o

64 On multivariate analysis, prior carbapenem exposure (OR: 3.23; 95% CI: 1.67-6.25) and he

65 Patients who received carbapenems for >72 hours had significantly lower alpha-

66 Patients receiving carbapenems for >72hrs prior to neutrophil recovery had

67 TZP may be a reasonable alternative to carbapenems for the management of ESBL-producing pyelone

68 f active site alanine mutants indicates that carbapenem hydrolysis is a concerted effort involving mu

69 mase beta-lactamases, suggesting it promotes carbapenem hydrolysis only in the context of KPC-2.

70 s activity with bacterial species that carry carbapenem-hydrolyzing class D beta-lactamases (OXA-23,

71 t bacteria are of grave clinical concern and carbapenem-hydrolyzing enzymes such as KPC (class A) NDM

72 enes conferring resistance/susceptibility to carbapenems in Acinetobacter spp. were evaluated.

73 ed from the Consortium on Resistance Against Carbapenems in Klebsiella and Other Enterobacteriaceae,

74 ed value to rationalize the empirical use of carbapenems in the ICU, emphasizing the urgent need for

75 terobacteriaceae that test as susceptible to carbapenems in vitro for the presence of carbapenemase g

76 e detection of carbapenemase production, the carbapenem inactivation method (CIM), was recently descr

77 ert Carba-R assay, a molecular test, and the carbapenem inactivation method (CIM).

78 aluated the performance of the EDTA-modified carbapenem inactivation method (eCIM) in tandem with the

79 elopment and evaluation of the EDTA-modified carbapenem inactivation method (eCIM), an assay for disc

80 on method (eCIM) in tandem with the modified carbapenem inactivation method (mCIM) against a large co

81 A variant of the modified carbapenem inactivation method (mCIM) was developed to d

82 escribe a two-stage evaluation of a modified carbapenem inactivation method (mCIM), in which tryptic

83 (Cepheid, Inc., Sunnyvale, CA), the modified carbapenem inactivation method (mCIM), the EDTA-modified

84 s when used in conjunction with the modified carbapenem inactivation method (mCIM).

85 on a multicenter evaluation of the modified carbapenem inactivation method (mCIM).

86 P, and NeoRapid Carb] and a variation of the carbapenem inactivation method [CIM] test with blood cul

87 M); the latter was comprised of the modified carbapenem inactivation method and a MIC screen for erta

88 NP, the manual Blue Carba, and the modified carbapenem inactivation method for the detection of any

89 nactivation method (mCIM), the EDTA-modified carbapenem inactivation method, and disk diffusion with

90 his commentary explores modifications to the carbapenem inactivation method-but is this the right foc

91 ll rapid chromogenic assays and the modified carbapenem inactivation method.

92 orines and acylureidopenicillins but not for carbapenems (< 2%).

93 nal readouts and potentiated activity of the carbapenem, meropenem, against a strain carrying the lar

94 6 patients received therapy >72 hours with a carbapenem, none of the patients had an infection with a

95 6 patients received therapy >72 hours with a carbapenem, none of the patients had an infection with a

96 Here we determine carbapenem nonsusceptibility rates for contemporary P. a

97 Carbapenem nonsusceptibility rates were highest in Acine

98 cutive ICU P. aeruginosa isolates collected, carbapenem nonsusceptibility was observed for 35% of the

99 In particular, carbapenem-nonsusceptible (NS) P. aeruginosa poses treme

100 Carbapenem-nonsusceptible Citrobacter spp. (CNSC) are in

101 ious and well-tolerated treatment option for carbapenem-nonsusceptible infections.

102 Most (>75%) of the carbapenem-NS isolates were susceptible to ceftazidime-a

103 In these U.S. hospital ICUs, carbapenem-NS P. aeruginosa isolates from respiratory so

104 ole in the treatment of infections caused by carbapenem-NS P. aeruginosa strains.

105 nfusion of piperacillin-tazobactam (TZP) and carbapenems on 30-day mortality of patients with liver c

106 ation cephalosporins (OR 2.38; P = .03), and carbapenems (OR 2.44; P = .03) correlated with the great

107 rbapenem use is not without consequence, and carbapenem overuse has contributed to the emergence of c

108 e and to identify gene knockdown targets for carbapenem potentiation.

109 e pancreatic necrosis should be favored (eg, carbapenems, quinolones, and metronidazole).

110 f beta-lactones from all clinically relevant carbapenems regardless of the presence or absence of a 1

111 biotics and more importantly the last resort carbapenems, represent a major mechanism of resistance i

112 Recognition of the molecular basis of carbapenem resistance allowed for successful treatment b

113 tates, recognition of the molecular basis of carbapenem resistance allowed for successful treatment b

114 which provoked carbapenem use and consequent carbapenem resistance and finally increased colistin con

115 rbapenemase acquisition is the main cause of carbapenem resistance and that it occurred across divers

116 diagnostic tests to improve the detection of carbapenem resistance and the use of large, population-b

117 isolates that may have utility in predicting carbapenem resistance and tracking hospital outbreaks of

118 and describe a novel mechanism of inducible carbapenem resistance associated with the acquisition of

119 ic resistance mechanisms, such as blaKPC and carbapenem resistance consistent with the accurate natur

120 The dissemination of carbapenem resistance in Escherichia coli has major impl

121 Carbapenem resistance in gram-negative bacteria has caus

122 Carbapenem resistance in Gram-negative bacteria is a pub

123 enhance our understanding of the drivers of carbapenem resistance in the Philippines, while also ser

124 in the repeated convergence of virulence and carbapenem resistance in the United States and Europe, d

125 Carbapenem resistance is associated with increased lengt

126 iology, genetic diversity, and mechanisms of carbapenem resistance is lacking.

127 cing bacteria as well as bacteria with other carbapenem resistance mechanisms.

128 ss than E. coli, and the association between carbapenem resistance of P. aeruginosa and colistin use

129 ed to decreased carbapenem use and decreased carbapenem resistance of P. aeruginosa but not of A. bau

130 We aimed to quantify the clinical effect of carbapenem resistance on mortality and length of hospita

131 bability weighting to estimate the effect of carbapenem resistance on probability of discharge alive

132 ae cultures were identified, with an overall carbapenem resistance rate of 24.6%.

133 ce phenotypes that coincide with the growing carbapenem resistance rates observed since 2010.

134 Moreover, evaluating the problem of carbapenem resistance requires the consideration of both

135 Carbapenem resistance was associated with an increased l

136 Carbapenem resistance was common (57.1%).

137 Carbapenem resistance was defined by the most recent bre

138 Carbapenem resistance was mediated primarily by blaKPC-2

139 ses in vitro, major contributors to clinical carbapenem resistance, by removing active site zinc.

140 In conclusion, carbapenem resistance, colistin resistance and high-leve

141 f these agents as a function of mechanism of carbapenem resistance, the clinical data supporting thei

142 terminants that enable host adaptability and carbapenem resistance.

143 st one critical priority pathogen expressing carbapenem resistance.

144 Carbapenem-resistance in Klebsiella pneumoniae (KP) sequ

145 gative pathogens, including those with major carbapenem-resistance mechanisms, and stability against

146 n of MICs, 49% (n = 98) of the isolates were carbapenem resistant (as defined by either resistance or

147 Carbapenems resistant Enterobacteriaceae infections are

148 y emerging: hypervirulent (hvKP) strains and carbapenem-resistant (CR-KP) strains.

149 evaluated patients with infection caused by carbapenem-resistant A. baumannii (CRAB) identified as c

150 ncreased carbapenem use, provoking spread of carbapenem-resistant A. baumannii and consequent colisti

151 rld Health Organization recently highlighted carbapenem-resistant A. baumannii as a "critical priorit

152 activity of beta-lactam antibiotics against carbapenem-resistant Acinetobacter baumannii (CRAB), a W

153 g-resistant gram-negative pathogens, such as carbapenem-resistant Acinetobacter baumannii (CRAB).

154 selected antibiotics and incidence rates of carbapenem-resistant Acinetobacter baumannii (Hungary),

155 infection (from 24.15 to 15.76 per 10,000), carbapenem-resistant acinetobacter species infection (fr

156 on, carbapenem-resistant Enterobacteriaceae, carbapenem-resistant acinetobacter species, and MDR Pseu

157 a in the critical priority category, such as carbapenem-resistant Acinetobacter, Pseudomonas and Ente

158 in against Gram-negative bacteria, including carbapenem-resistant and colistin-resistant strains bear

159 ug for the treatment of infections caused by carbapenem-resistant and/or multidrug-resistant (MDR) Gr

160 -lactamase interactions with carbapenems, as carbapenem-resistant bacteria are of grave clinical conc

161 e, beta-lactam specificity and metal content.Carbapenem-resistant bacteria pose a major health threat

162 nem-susceptible Enterobacteriaceae (CSE) and carbapenem-resistant Entero-bacteriaceae (CRE) bloodstre

163 merous government and agency reports discuss carbapenem-resistant Enterobacterales (CRE) and carbapen

164 tam antibiotics, to various extents, against carbapenem-resistant Enterobacterales (CRE) carrying cla

165 Cefiderocol AST was performed on consecutive carbapenem-resistant Enterobacterales (CRE; 58 isolates)

166 an oral therapy for multidrug resistant and carbapenem-resistant Enterobacterales infections.

167 s to reliably detect carbapenemase-producing carbapenem-resistant Enterobacteriaceae (CP-CRE) is an i

168 Carbapenem-resistant Enterobacteriaceae (CRE) are a seri

169 Carbapenem-resistant Enterobacteriaceae (CRE) are among

170 Carbapenem-resistant Enterobacteriaceae (CRE) are an urg

171 Carbapenem-resistant Enterobacteriaceae (CRE) are associ

172 Carbapenem-resistant Enterobacteriaceae (CRE) are high-p

173 Carbapenem-resistant Enterobacteriaceae (CRE) are multid

174 Clinical testing detects a fraction of carbapenem-resistant Enterobacteriaceae (CRE) carriers.

175 Here, using carbapenem-resistant Enterobacteriaceae (CRE) clinical i

176 Since 2010, the incidence of carbapenem-resistant Enterobacteriaceae (CRE) has been i

177 In recent years, the prevalence of carbapenem-resistant Enterobacteriaceae (CRE) has risen

178 The rapidly increasing dissemination of carbapenem-resistant Enterobacteriaceae (CRE) in both hu

179 facilities (LTCFs) are a major reservoir of carbapenem-resistant Enterobacteriaceae (CRE) in healthc

180 The rise in carbapenem-resistant Enterobacteriaceae (CRE) infections

181 Twenty patients with carbapenem-resistant Enterobacteriaceae (CRE) infections

182 14-day inpatient mortality in nonbacteremia carbapenem-resistant Enterobacteriaceae (CRE) infections

183 Rapid diagnosis of infections caused by carbapenem-resistant Enterobacteriaceae (CRE) is crucial

184 Two collections of carbapenem-resistant Enterobacteriaceae (CRE) isolates w

185 ta-lactamase-producing organisms (ESBL), and carbapenem-resistant Enterobacteriaceae (CRE) using nare

186 Carbapenem-resistant Enterobacteriaceae (CRE), Acinetoba

187 the management of invasive infections due to carbapenem-resistant Enterobacteriaceae (CRE), leading t

188 rry antibiotic-resistant bacteria, including carbapenem-resistant Enterobacteriaceae (CRE).

189 a cefotaxime-containing medium (OPP-C), and carbapenem-resistant Enterobacteriaceae (CRE).

190 multidrug-resistant pathogens, particularly carbapenem-resistant Enterobacteriaceae (CREs), present

191 Carbapenem-resistant Enterobacteriaceae are resistant to

192 model, parametrized via a novel analysis of carbapenem-resistant Enterobacteriaceae data reported to

193 Carbapenem-resistant Enterobacteriaceae have recently be

194 The incidence of carbapenem-resistant Enterobacteriaceae infection did no

195 Twenty patients with carbapenem-resistant Enterobacteriaceae infections were

196 Carbapenem-resistant Enterobacteriaceae threaten human h

197 health threats is the worldwide emergence of carbapenem-resistant Enterobacteriaceae(1-4), which are

198 crobials of last resort for the treatment of carbapenem-resistant Enterobacteriaceae, but resistance

199 d-spectrum beta-lactamase (ESBL) production, carbapenem-resistant Enterobacteriaceae, carbapenem-resi

200 by antibiotic-resistant bacteria, including carbapenem-resistant Enterobacteriaceae, have increased

201 ens including Mycobacterium tuberculosis and carbapenem-resistant Enterobacteriaceae.

202 extended-spectrum beta-lactamase (ESBL) and carbapenem-resistant Enterobacteriaceae.

203 ended-spectrum beta-lactamase-producing, and carbapenem-resistant Enterobacteriaceae.

204 overuse has contributed to the emergence of carbapenem-resistant Enterobacteriaceae.

205 bapenem-resistant Pseudomonas aeruginosa and carbapenem-resistant Enterobacteriaceae.

206 Carbapenem-resistant Enterobacteriacieae (CRE) isolates

207 of 88 New Delhi metallo-beta-lactamases-type carbapenem-resistant Escherichia coli (NDM-EC), includin

208 i-drug-resistant bacteria strains (including carbapenem-resistant Escherichia coli and methicillin-re

209 (s), capable of sequence-specific killing of carbapenem-resistant Escherichia coli and methicillin-re

210 amicin were combined with meropenem to treat carbapenem-resistant Escherichia coli.

211 As a case study, we multiplexed 3 carbapenem-resistant genes to show the impact of this ap

212 hod is applied to four of the most prominent carbapenem-resistant genes: bla(OXA-48), bla(NDM), bla(V

213 Carbapenem-resistant Gram-negative bacteria (CRGNB) cont

214 Carbapenem-resistant Gram-negative bacteria (GNB) are he

215 randomized controlled trial of patients with carbapenem-resistant gram-negative bacterial infections

216 ymyxins are relied upon for the treatment of carbapenem-resistant Gram-negative bacterial infections,

217 apy given to patients with infections due to carbapenem-resistant Gram-negative organisms reduces the

218 hen given to patients with infections due to carbapenem-resistant Gram-negative organisms.

219 ria and has proven in vitro activity against carbapenem-resistant gram-negative pathogens, including

220 ad antibacterial activity, including against carbapenem-resistant gram-negative pathogens.

221 to investigate the predation of an important carbapenem-resistant human pathogen, Klebsiella pneumoni

222 and D), non-carbapenemase-producing (non-CP) carbapenem-resistant isolates, and carbapenem-susceptibl

223 Carbapenem-resistant K. pneumoniae (CR-KP) posts signifi

224 We describe an outbreak of carbapenem-resistant K. pneumoniae containing the blaOXA

225 as performed when 9 patients with blaOXA-232 carbapenem-resistant K. pneumoniae infections were ident

226 ort the global evolution of pathogenicity in carbapenem-resistant K. pneumoniae, resulting in the rep

227 The rapid emergence of carbapenem-resistant Klebsiella pneumoniae (CRKP) repres

228 Control of infections caused by carbapenem-resistant Klebsiella pneumoniae continues to

229 he incidence of nosocomial infections due to carbapenem-resistant Klebsiella pneumoniae is increasing

230 rventions to control the current epidemic of carbapenem-resistant Klebsiella pneumoniae rely on a com

231 Carbapenem-resistant Klebsiella pneumoniae sequence type

232 ancomycin-resistant Enterococcus faecium and carbapenem-resistant Klebsiella pneumoniae, emerge from

233 here is increased awareness of the impact of carbapenem-resistant nonfermenting gram-negative bacteri

234 creen for gastrointestinal colonization with carbapenem-resistant organisms (CRO) has yet to be estab

235 bapenem-resistant Enterobacterales (CRE) and carbapenem-resistant organisms (CROs).

236 datasets to capture a greater proportion of carbapenem-resistant organisms can help us gain a better

237 and accurate treatment of infections due to carbapenem-resistant organisms is facilitated by rapid d

238 and accurate treatment of infections due to carbapenem-resistant organisms is facilitated by rapid d

239 ients in the carbapenem arm who had incident carbapenem-resistant organisms isolated within 30 days (

240 patients in the carbapenem arm had incident carbapenem-resistant organisms isolated within 60 days (

241 is and may mitigate the risk of emergence of carbapenem-resistant organisms, compared with carbapenem

242 emergence in patients with infections due to carbapenem-resistant organisms.

243 , ST258 and ST512, which are associated with carbapenem-resistant outbreaks in China and the US, incl

244 Twenty-eight patients infected with carbapenem-resistant P. aeruginosa isolates susceptible

245 Carbapenem-resistant P. aeruginosa NCTC 13437 and an unr

246 hat are the ultimate line of defense against carbapenem-resistant pathogens in clinical settings.

247 st influence on hospital-endemic species and carbapenem-resistant pathogens.

248 6.2% of Pseudomonas aeruginosa isolates were carbapenem-resistant preimplementation compared with 25.

249 Carbapenem-resistant Pseudomonas aeruginosa (CRPA) colon

250 d diversity of carbapenemase producers among carbapenem-resistant Pseudomonas aeruginosa (CRPA) isola

251 activity of beta-lactam antibiotics against carbapenem-resistant Pseudomonas aeruginosa and carbapen

252 The prevalence of carbapenem-resistant Pseudomonas aeruginosa is increasin

253 etrospective study of patients infected with carbapenem-resistant Pseudomonas aeruginosa who were tre

254 To address this issue, we studied a carbapenem-resistant ST-15 K. pneumoniae isolate (Kp3380

255 In the United States and Europe, carbapenem-resistant strains of the Klebsiella pneumonia

256 tamase, methicillin-resistant S. aureus, and carbapenem-resistant strains was also observed.

257 enem and meropenem against highly pathogenic carbapenem-resistant strains, such as Acinetobacter baum

258 ivity against multidrug-resistant (including carbapenem-resistant) Enterobacteriaceae.

259 the treatment of severe infections caused by carbapenem-resistant, colistin-susceptible Gram-negative

260 the treatment of severe infections caused by carbapenem-resistant, colistin-susceptible Gram-negative

261 ibute to high morbidity/mortality rates with carbapenem-resistant, Gram-negative bacterial infections

262 ,882 (10%) isolates from 4,038 patients were carbapenem-resistant.

263 r bacterial resistance to cephalosporins and carbapenems, respectively.

264 These findings suggest modifications of the carbapenem scaffold to avoid hydrolysis by KPC-2 beta-la

265 a large tertiary refferential center, use of carbapenems seems necessary to achieve a high antibiotic

266 enems, along with the general preference for carbapenem-sparing regimens, suggests using ceftazidime

267 logical data, subgroups for highly effective carbapenem-sparing therapy can be defined.

268 cribe a flow cytometry workflow to determine carbapenem susceptibility from bacterial cell characteri

269 rug resistant and, of 33 isolates tested for carbapenem susceptibility, 12 (36%) were resistant.

270 esistance whereby isolates that appear to be carbapenem susceptible on initial testing can develop in

271 erales with OXA-48-like enzymes that remain "carbapenem susceptible" at breakpoint; and (4) Pseudomon

272 were prepared by seeding well-characterized carbapenem-susceptible and -nonsusceptible strains into

273 CNSC genomes were compared with genomes of carbapenem-susceptible Citrobacter spp. from UPMC and wi

274 uiting consecutively diagnosed patients with carbapenem-susceptible Enterobacteriaceae (CSE) and carb

275 (non-CP) carbapenem-resistant isolates, and carbapenem-susceptible isolates.

276 se (KPC) is a widespread SBL that hydrolyzes carbapenems, the most potent beta-lactams; known KPC var

277 arbapenem-resistant organisms, compared with carbapenem therapy.

278 ird- and fourth-generation cephalosporins or carbapenems, there was a 2.1% and 2.9% increase in HO-CD

279 PNA was then tested in combination with each carbapenem to assess its effect on the antibiotics' mini

280 IM-1, BcII, CphA, and L1) tested all degrade carbapenems to preferentially give the Delta(2) (enamine

281 nappropriate treatment (IAT) and unnecessary carbapenem use (UCU).

282 ing cephalosporin resistance, which provoked carbapenem use and consequent carbapenem resistance and

283 Colistin use led to decreased carbapenem use and decreased carbapenem resistance of P.

284 In interrupted time-series analysis, carbapenem use decreased by -230 days of therapy (DOT)/1

285 e appear protective against infection, while carbapenem use is associated with consequences to the mi

286 However, indiscriminant carbapenem use is not without consequence, and carbapene

287 alosporin-resistant Klebsiella spp. provoked carbapenem use less than E. coli, and the association be

288 Impact on carbapenem use was assessed at several cut-off points.

289 This led to increased carbapenem use, provoking spread of carbapenem-resistant

290 for febrile neutropenia effectively reduced carbapenem use, which may have resulted in decreased VRE

291 roducing pyelonephritis receiving TZP versus carbapenems using an inverse probability of treatment we

292 pyelonephritis who were receiving TZP versus carbapenems, using an inverse probability of treatment w

293 ous selective pressure imposed by widespread Carbapenem utilisation in hospital settings drives the e

294 These MbetaLs hydrolyse carbapenems via a similar mechanism, with accumulation o

295 ving C/EI or intermittent infusion of TZP or carbapenems was assessed with Kaplan-Meier curves, Cox-r

296 who received empiric treatment with OADs or carbapenems was performed.

297 er spp., or Klebsiella spp. resistant to >=1 carbapenem were reported from residents.

298 baumannii) resistant to cephalosporins or to carbapenems were analyzed using VAR models.

299 es are a major threat to the clinical use of carbapenems, which are often antibiotics of last resort.

300 al testing can develop in vivo resistance to carbapenems with repeated exposure.