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1 ly to have poor outcomes when treated with a carbapenem.
2 a who all received definitive therapy with a carbapenem.
3 cephalosporin who were subsequently given a carbapenem.
4 use of broad-spectrum antibiotics, including carbapenems.
5 g resistance to the last resort antibiotics, carbapenems.
6 evolved resistance to antibiotics, including carbapenems.
7 lies: penicillin/cephalosporins, clavams and carbapenems.
8 enged with escalating doses of aztreonam and carbapenems.
9 tion or other beta-lactamases that hydrolyze carbapenems.
10 tion to lower susceptibility breakpoints for carbapenems.
11 , including penicillins, cephalosporins, and carbapenems.
12 yses to compare the efficacy of cefepime and carbapenems.
13 e to tolerate quinolones, glycopeptides, and carbapenems.
14 acts specifically with PBP2, and for several carbapenems.
15 ted cross-reactivity between penicillins and carbapenems.
16 are the main mechanism of resistance against carbapenems.
17 ssociated with a worse outcome compared with carbapenems.
18 th such drugs (other active drugs [OADs]) or carbapenems.
19 d because many isolates display low MICs for carbapenems.
21 ics were fluoroquinolones (35%), followed by carbapenems (20%), TMP-SMX (18.5%), and ceftazidime (11%
22 tive skin test results to both aztreonam and carbapenems; 211 accepted challenges and tolerated them.
23 d p=0.011), and antibiotic use, particularly carbapenems (45 [9%] vs 18 [24%], adjusted p=0.002) and
28 eta-lactamase inhibitor avibactam provides a carbapenem alternative against multidrug-resistant infec
31 s with malignancy, with special attention to carbapenem and expanded-spectrum beta-lactam resistance
32 Of the savings, $54,150 (78%) was related to carbapenems and $15,274 (22%) was due to other antibioti
34 nce to all the tested antimicrobials, except carbapenems and amikacin, was observed in a proportion o
35 antibiotic treatments, and more recently to carbapenems and colistin, make UTI a prime example of th
36 revious use of beta-lactam/beta-lactamase or carbapenems and recent hospitalization were independent
37 with the highly unstable beta-lactam ring of carbapenems and that the triazole ring generated by this
39 A range of specific AMR concerns, including carbapenem- and colistin-resistant gram-negative organis
40 sp. ATCC 39006, intrinsic resistance to the carbapenem antibiotic 1-carbapen-2-em-3-carboxylic acid
41 emonstrating that a combination of AMA and a carbapenem antibiotic has therapeutic potential to addre
42 monitor the hydrolytic decomposition of the carbapenem antibiotic meropenem inside Escherichia coli
43 ve utility, the biosynthesis of the paradigm carbapenem antibiotic, thienamycin, remains largely unkn
47 (MBL) inhibitors can restore the function of carbapenem antibiotics and therefore help to treat infec
48 c beta-lactam/2-pyrrolidine precursor to all carbapenem antibiotics is biosynthesized by attachment o
55 antibiotic use and the use of moxifloxacin, carbapenems, antipseudomonal penicillins, and vancomycin
58 erobacteriaceae threaten human health, since carbapenems are last resort drugs for infections by such
68 al and Laboratory Standards Institute (CLSI) carbapenem breakpoints for Enterobacteriaceae and the la
69 tibiotics has led to a greater reliance upon carbapenems, but the expression of carbapenemases threat
73 Cox models determined that every additional carbapenem defined daily dose increased the hazard of ac
75 ests that the size of susbtituents at C-2 of carbapenem (e.g., benzoic acid of ertapenem) has signifi
78 the efficacy of active alternative drugs to carbapenems except beta-lactam/beta-lactamase inhibitors
83 The cross-reactivity between penicillins and carbapenems for IgE-mediated reactions is very low, but
86 s for the detection of intact and hydrolyzed carbapenems from an enrichment broth were developed.
89 han 2 mg/L compared with the use of colistin-carbapenem (hazard ratio, 6.93; 95% CI, 1.61-29.78; p=0.
91 eport a biochemical and biophysical study of carbapenem hydrolysis by the B1 enzymes NDM-1 and BcII i
93 ity (>95%) to amikacin, tigecycline, and the carbapenems (imipenem and meropenem); 90.8% of Acinetoba
96 against extended-spectrum cephalosporins and carbapenems in >90% of cases; however, against piperacil
98 ortality was similar for use of cefepime and carbapenems in adjusted regression models and propensity
99 within the Consortium on Resistance against Carbapenems in Klebsiella pneumoniae (CRACKLE) was const
100 s, CRACKLE (Consortium on Resistance Against Carbapenems in Klebsiella pneumoniae and Other Enterobac
101 tin and ceftazidime in P. aeruginosa and for carbapenems in Klebsiella species) to 3.0 (for piperacil
102 dime-avibactam as a potential alternative to carbapenems in patients with ceftazidime-resistant Enter
103 dime-avibactam as a potential alternative to carbapenems in patients with nosocomial pneumonia (inclu
106 terobacteriaceae that test as susceptible to carbapenems in vitro for the presence of carbapenemase g
107 e detection of carbapenemase production, the carbapenem inactivation method (CIM), was recently descr
109 se of this study was to develop the modified carbapenem inactivation method (mCIM) for the detection
110 escribe a two-stage evaluation of a modified carbapenem inactivation method (mCIM), in which tryptic
112 NP, the manual Blue Carba, and the modified carbapenem inactivation method for the detection of any
114 This structure of CarG is the first in the carbapenem intrinsic resistance (CIR) family of resistan
115 ty between penicillins or cephalosporins and carbapenems is anticipated as all have a beta lactam rin
117 nts with Enterobacteriaceae infection with a carbapenem MIC of 2 to 8 mg/liter were matched based on
118 ents infected with Enterobacteriaceae with a carbapenem MIC of 2, 4, or 8 mg/liter had higher mortali
119 higher 30-day mortality than the group with carbapenem MICs of </=1 mg/liter (38.9% compared to 5.6%
120 and longer ICU LOS than matched cohorts with carbapenem MICs of </=1 mg/liter, which supports CLSI's
122 am and aminoglycoside combination therapy or carbapenem monotherapy in patients with prior 3GC-R EB c
124 stic capacities, who collected the first ten carbapenem non-susceptible clinical isolates of K pneumo
128 isk) and for sequencing of DNA obtained from carbapenem-nonsusceptible isolates for carbapenemase ide
129 nation therapy as use of parenteral colistin-carbapenem or colistin-tigecycline for at least 48 hours
130 rbapenem use is not without consequence, and carbapenem overuse has contributed to the emergence of c
134 ; p = 0.0124) and time-dependent exposure to carbapenems quadrupled the hazard (hazard ratio, 4.087;
135 biotics and more importantly the last resort carbapenems, represent a major mechanism of resistance i
137 tablishes that RMDs can discriminate between carbapenem resistance and susceptibility in Acinetobacte
139 machine learning classifiers for identifying carbapenem resistance in Acinetobacter baumannii, methic
147 ses in vitro, major contributors to clinical carbapenem resistance, by removing active site zinc.
152 n sequencing (NGS) revealed that the loss of carbapenem-resistance in KpN06 was due to a 5-kb deletio
153 n of MICs, 49% (n = 98) of the isolates were carbapenem resistant (as defined by either resistance or
158 daily dose increased the hazard of acquiring carbapenem-resistant A. baumannii by 5.1% (hazard ratio,
159 ne, tigecycline, and doxycycline against 107 carbapenem-resistant A. baumannii clinical isolates.
161 The primary outcome was the acquisition of carbapenem-resistant A. baumannii on surveillance cultur
163 tients were included, of whom 49 (13.5%) had carbapenem-resistant A. baumannii on surveillance cultur
164 For minocycline susceptibility testing of carbapenem-resistant A. baumannii strains, very major er
168 epidemiology and mechanisms of resistance of carbapenem-resistant Acinetobacter baumannii (CRAB) were
170 Treatment options for infections due to carbapenem-resistant Acinetobacter baumannii are extreme
171 d to determine the effect of the presence of carbapenem-resistant Acinetobacter baumannii in accordan
172 apenem-resistant Pseudomonas aeruginosa, and carbapenem-resistant Acinetobacter baumannii in the pedi
173 e of colistin methansulfonate (CMS) to treat carbapenem-resistant Acinetobacter baumannii infections,
176 er baumannii and Pseudomonas aeruginosa, and carbapenem-resistant and third-generation cephalosporin-
177 e, beta-lactam specificity and metal content.Carbapenem-resistant bacteria pose a major health threat
179 gs and farmers, providing direct evidence of carbapenem-resistant E. coli transmission and environmen
180 rgence and spread of carbapenemase-producing carbapenem-resistant Enterobacteriaceae (CP-CRE) are a s
181 s to reliably detect carbapenemase-producing carbapenem-resistant Enterobacteriaceae (CP-CRE) is an i
182 he design of fluorogenic probes specific for carbapenem-resistant Enterobacteriaceae (CRE) and they w
190 we found that the 32-month delay in changing carbapenem-resistant Enterobacteriaceae (CRE) breakpoint
192 DC standard methodology for the isolation of carbapenem-resistant Enterobacteriaceae (CRE) from 300 r
194 nation ceftazidime-avibactam (CAZ-AVI) among carbapenem-resistant Enterobacteriaceae (CRE) has infreq
196 ribing risk factors and clinical outcomes of carbapenem-resistant Enterobacteriaceae (CRE) in sentine
202 Here we quantified fecal coliforms (FC), carbapenem-resistant Enterobacteriaceae (CRE), blaNDM-1,
204 tervention aimed at containing the spread of carbapenem-resistant Enterobacteriaceae (CRE), primarily
207 tic resistance and virulence determinants in carbapenem-resistant Enterobacteriaceae and enterohemorr
208 nt for the treatment of infections caused by carbapenem-resistant Enterobacteriaceae and Pseudomonas
214 Ceftazidime/avibactam is also active against carbapenem-resistant Enterobacteriaceae that produce Kle
216 domonas aeruginosa, Acinetobacter baumannii, carbapenem-resistant Enterobacteriaceae, and Candida spe
217 inhibitors, multidrug resistant strains and carbapenem-resistant Enterobacteriaceae, and most anaero
218 ms, AmpC beta-lactamase-producing organisms, carbapenem-resistant Enterobacteriaceae, carbapenem-resi
220 re system faced an unprecedented outbreak of carbapenem-resistant Enterobacteriaceae, primarily invol
229 methicillin-resistant Staphylococcus aureus, carbapenem-resistant Escherichia coli, and extended-spec
231 npatients with invasive infections caused by carbapenem-resistant gram-negative bacteria treated with
232 echanisms may underestimate the incidence of carbapenem-resistant gram-negative infections (CRGNIs).
234 a principle contributor to the emergence of carbapenem-resistant Gram-negative pathogens that threat
236 to investigate the predation of an important carbapenem-resistant human pathogen, Klebsiella pneumoni
237 1.3%), including seven from p019-containing, carbapenem-resistant isolates (positive predictive value
238 and D), non-carbapenemase-producing (non-CP) carbapenem-resistant isolates, and carbapenem-susceptibl
239 d detection of potentially blaKPC-containing carbapenem-resistant isolates, providing early and clini
241 as performed when 9 patients with blaOXA-232 carbapenem-resistant K. pneumoniae infections were ident
242 ately identified 17 patients with blaOxa-232 carbapenem-resistant K. pneumoniae isolates, including 9
244 nt strains, but limited activity against our carbapenem-resistant K.pneumoniae (12% susceptibility.)
245 Novel therapies are urgently needed to treat carbapenem-resistant Klebsiella pneumoniae (CR-Kp)-media
247 d evaluate an outbreak of OXA-232-expressing carbapenem-resistant Klebsiella pneumoniae (CRKP) transm
253 ifficile, vancomycin-resistant Enterococcus, carbapenem-resistant Klebsiella pneumoniae, and Escheric
255 rk together to determine the risk carried by carbapenem-resistant non-glucose-fermenting Gram-negativ
256 bs from high-risk patients were screened for carbapenem-resistant organisms (CROs) using several meth
257 last 20 years there have been 32 reports of carbapenem-resistant organisms in the hospital water env
258 etrospective study of patients infected with carbapenem-resistant Pseudomonas aeruginosa who were tre
260 ms, carbapenem-resistant Enterobacteriaceae, carbapenem-resistant Pseudomonas aeruginosa, and carbape
262 linical K. pneumoniae strains, including one carbapenem-resistant ST258 strain, are less virulent tha
267 annii (78% susceptibility), including 74% of carbapenem-resistant strains, but limited activity again
268 tients who had received CMS for treatment of carbapenem-resistant, colistin-susceptible A. baumannii
269 ravenous and/or inhaled CMS for treatment of carbapenem-resistant, colistin-susceptible A. baumannii
271 s (risk ratio, 1.78 [95% CI, 1.24-2.56]) and carbapenems (risk ratio, 2.13 [95% CI, 1.49-3.06]) durin
273 gent underwent skin tests with aztreonam and carbapenems; subjects with negative results were challen
274 t arrest at the acyl-intermediate state with carbapenem substrates but maintain catalytic competency
275 cribe a flow cytometry workflow to determine carbapenem susceptibility from bacterial cell characteri
276 rug resistant and, of 33 isolates tested for carbapenem susceptibility, 12 (36%) were resistant.
277 were prepared by seeding well-characterized carbapenem-susceptible and -nonsusceptible strains into
283 rom the first two steps shared with a simple carbapenem, the pathway sharply diverges to the more str
284 receiving empiric PTZ compared with empiric carbapenem therapy (95% confidence interval, 1.07-3.45).
286 n greater than 2 mg/L compared with colistin-carbapenem therapy for extensively drug-resistant A. bau
288 , including penicillins, cephalosporins, and carbapenems, through various mechanisms, resulting in in
289 ble models, there was no association between carbapenem use and persistent bacteremia (adjusted odds
291 rd-generation cephalosporin, macrolides, and carbapenem use, exceeding hospital population specific t
295 f any type of hypersensitivity reaction to a carbapenem was 3/12 (25%); this included 2 non-IgE-media
296 of suspected hypersensitivity reaction to a carbapenem was 36/838 (4.3%; 95% confidence interval [CI
297 strain G6809 with reduced susceptibility to carbapenems was identified from a patient in a long-term
299 gecycline versus patients receiving colistin-carbapenem were 35% versus 15% (p=0.105) and 69% versus
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