Previously, Pseudomonas putida was considered a low-virulence pathogen and was recognized as a rare cause of bacteremia. Recently, however, multidrug-resistant and carbapenem-resistant P. putida isolates have emerged, causing difficult-to-treat nosocomial infections in seriously ill patients. Currently, the outcome of multidrug-resistant or carbapenem-resistant P. putida bacteremia remains uncertain. Here, we report 18 cases of P. putida bacteremia with high rates of carbapenem resistance and mortality. From January 2005 through December 2011, all cases of nosocomial P. putida bacteremia were identified and analyzed at Chonnam National University Hospital and Chonnam National University Hwasun Hospital. Electronic medical records were reviewed retrospectively. Four (22%) and five (23%) of 18 P. putida isolates were resistant to imipenem and meropenem, respectively. Common primary infection sites were central venous catheter (7, 39%), pneumonia (5, 28%), and cholangitis (2, 11%). Fourteen (78%) patients had indwelling devices related to the primary site of infection. The 30-day mortality rate was 39% (7/18): 40% (2/5) in patients with carbapenem-resistant P. putida bacteremia vs. 38% (5/13) in patients with carbapenem-susceptible P. putida bacteremia. Nosocomial P. putida bacteremia showed high resistance rates to most potent beta-lactams and carbapenems and was associated with high mortality rates.
Bacteremia ; beta-Lactams ; Carbapenems ; Central Venous Catheters ; Cholangitis ; Cross Infection ; Drug Resistance ; Electronic Health Records ; Humans ; Imipenem ; Pneumonia ; Pseudomonas ; Pseudomonas putida ; Retrospective Studies ; Thienamycins

OBJECTIVETo analyze the distribution of Enterobacteriaceae isolated from West China Hospital, investigate the antibiotic resistance profile of Enterobacteriaceae with decreased susceptibility to carbapenems and explore the molecular mechanism.

METHODSForty-five Enterobacteriaceae strains resistant or with reduced susceptibility to carbapenems were isolated from patients in West China Hospital. The antimicrobial susceptibility and carbapenemase-producing phenotypes of the bacteria were examined and specific PCR were performed to determine the molecular mechanism.

RESULTSOf the 45 isolates, 17, 21 and 36 were resistant or intermediate strains to imipenem, meropenem and ertapenem, respectively. The majority of these isolates showed resistance to cephalosporins. The modified Hodge test resulted in the highest positivity rate (77.8%), followed by EDTA disc test (57.8%) and PBA disc test (22.2%). BlaTEM, blaSHV and blaCTX-M were detected in 60.0%, 53.3% and 15.6% of these strains with reduced susceptibility. The rate of strains carrying 2 or more genes was 44.4%, and the detection rate of blaIMP was 48.9%. BlaKPC was identified in 4 (8.9%) high-level resistant strains and confirmed to locate on the plasmid.

CONCLUSIONProduction of carbapenemase contributes to reduced susceptibility of carbapenems in Enterobacteriaceae. The presence of blaKPC, MBL and ESBL, and their possible combinations can be the main factor contributing to carbapenem resistance or reduced susceptibility in Enterobacteriaceae. The KPC-2 carbapenemase gene located on the plasmids we found in this study can cause potential horizontal transmission across strains.

Anti-Bacterial Agents ; pharmacology ; Bacterial Proteins ; genetics ; metabolism ; Carbapenems ; pharmacology ; Cephalosporins ; pharmacology ; Enterobacteriaceae ; drug effects ; enzymology ; genetics ; Gene Amplification ; Imipenem ; pharmacology ; Microbial Sensitivity Tests ; Polymerase Chain Reaction ; Thienamycins ; pharmacology ; beta-Lactam Resistance ; beta-Lactamases ; genetics ; metabolism ; beta-Lactams ; pharmacology

No abstract available.
Carbapenems* ; Korea*

No abstract available.
Carbapenems* ; Korea*

OBJECTIVE:This study was performed to compare the in vitro antimicrobial activities of prepenem (PRPM) with those of imipenem (IMPM) and meropenem (MRPM) against several clinical isolates of Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Streptococcus pneumoniae. METHODS: We tested the in vitro antimicrobial activities of PRPM, IMPM, and MRPM against total 300 clinical isolates of E. coli, K. pneumoniae, and P. aeruginosa and 134 chinical isolated of S. pneumoniae (41 penicillin-susceptible, 93 penicillin-resistant strains) collected in 5 different university hospitals (March to June, 2002). According to NCCLS guidelines, MICs of PRPM, IMPM, MRPM, and/or ceftazidime were determined. RESULTS: MIC90s of E. coli to IMPM, PRPM, and MRPM were 1, 1, and 0.125 microgram/mL, respectively. Those of K. pneumoniae were 1, 0.5, and 0.125 microgram/mL, respectively. In case of P. aeruginosa, MIC90s to IMPM, PRPM, MRPM, and ceftazidime were 16, 32, 8, and 64 microgram/mL, respectively. In penicillin-susceptible S. pneumoniae, MIC90s to IMPM, PRPM, MRPM were 0.25, 0.25, 0.5 microgram/mL, while those of penicillin-nonsusceptible strains were 1, 1, and 2 microgram/mL, respectively. IMPM and PRPM showed similar pattern of distribution of MIC to various bacterial species. CONCLUSION: E. coli, K. pneumoniae, and S. pneumonia were susceptible to PRPM, which had a pattern similar to IMPM. The antimicrobial activity of PRPM to P. aeruginosa was also comparable to that of IMPM. PRPM could be potentially useful drugs for treatment of infections caused by E. coli, K. pneumoniae, P. aeruginosa and S. pneumoniae.
Carbapenems* ; Ceftazidime ; Escherichia coli ; Hospitals, University ; Imipenem ; Klebsiella pneumoniae ; Korea* ; Pneumonia ; Pseudomonas aeruginosa ; Streptococcus pneumoniae

OBJECTIVE:This study was performed to compare the in vitro antimicrobial activities of prepenem (PRPM) with those of imipenem (IMPM) and meropenem (MRPM) against several clinical isolates of Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Streptococcus pneumoniae. METHODS: We tested the in vitro antimicrobial activities of PRPM, IMPM, and MRPM against total 300 clinical isolates of E. coli, K. pneumoniae, and P. aeruginosa and 134 chinical isolated of S. pneumoniae (41 penicillin-susceptible, 93 penicillin-resistant strains) collected in 5 different university hospitals (March to June, 2002). According to NCCLS guidelines, MICs of PRPM, IMPM, MRPM, and/or ceftazidime were determined. RESULTS: MIC90s of E. coli to IMPM, PRPM, and MRPM were 1, 1, and 0.125 microgram/mL, respectively. Those of K. pneumoniae were 1, 0.5, and 0.125 microgram/mL, respectively. In case of P. aeruginosa, MIC90s to IMPM, PRPM, MRPM, and ceftazidime were 16, 32, 8, and 64 microgram/mL, respectively. In penicillin-susceptible S. pneumoniae, MIC90s to IMPM, PRPM, MRPM were 0.25, 0.25, 0.5 microgram/mL, while those of penicillin-nonsusceptible strains were 1, 1, and 2 microgram/mL, respectively. IMPM and PRPM showed similar pattern of distribution of MIC to various bacterial species. CONCLUSION: E. coli, K. pneumoniae, and S. pneumonia were susceptible to PRPM, which had a pattern similar to IMPM. The antimicrobial activity of PRPM to P. aeruginosa was also comparable to that of IMPM. PRPM could be potentially useful drugs for treatment of infections caused by E. coli, K. pneumoniae, P. aeruginosa and S. pneumoniae.
Carbapenems* ; Ceftazidime ; Escherichia coli ; Hospitals, University ; Imipenem ; Klebsiella pneumoniae ; Korea* ; Pneumonia ; Pseudomonas aeruginosa ; Streptococcus pneumoniae

OBJECTIVE: To explore the clinical characteristics of hospitalized patients with hematologic diseases complicated with carbapenem-resistant organisms (CRO) infection and analyze the risk factors of 30-day all-cause mortality. METHODS: The clinical data and laboratory test data of 77 hospitalized patients with hematologic diseases complicated with CRO infection in department of hematology of the Third Hospital of Shanxi Medical University from January 2015 to December 2020 were retrospectively analysed, the risk factors of 30-day all-cause mortality after CRO infection were analyzed by multivariate logistic regression. RESULTS: Among the total of 77 patients with hematologic diseases complicated with CRO infection, 29 died and 48 survived within 30 days of infection, with a case fatality rate of 37.66%. A total of 93 strains of CRO were isolated from these patients, of which Acinetobacter baumannii had the highest detection rate (25.81%, 24/93), followed by Pseudomonas aeruginosa (18.28%, 17/93). The lung was the most common site of CRO infection. The detected pathogens were highly resistant to carbapenems, and 64.52% (60/93) of the pathogens were resistant to imipenem with minimum inhibitory concentration (MIC)≥16 μg/ml. The results of the univariate analysis showed that albumin concentration <25 g/L (P =0.048), serum creatinine concentration≥120 μmol/L (P =0.023), age-adjusted Charlson comorbidity index (ACCI) (P =0.037) and primary treatments (supportive treatment, immunosuppressive therapy, chemotherapy, HSCT) (P =0.048) were significantly associated with 30-day all-cause mortality after infection. The results of multivariate logistic regression analysis showed that when CRO infection confirmed, albumin concentration <25 g/L (P =0.014, OR=6.171), serum creatinine concentration≥120 μmol/L (P =0.009, OR=10.867) were independent risk factors for 30-day mortality of patients with hematologic diseases complicated with CRO infection. CONCLUSION The mortality rate of CRO-infected patients with hematologic diseases is high. The detected pathogenic bacteria are highly resistant to imipenem. The albumin concentration <25 g/L and the serum creatinine concentration≥ 120 μmol/L at diagnosis of CRO infection were independent risk factors for 30-day mortality of the patients with hematologic diseases.
Humans ; Carbapenems/pharmacology* ; Retrospective Studies ; Creatinine ; Hematologic Diseases ; Risk Factors ; Imipenem ; Albumins

Valproic acid (VPA) is a commonly prescribed anticonvulsant drug for the treatment of various forms of epilepsy. Concomitant administration of VPA and carbapenem antibiotics such as panipenem/ betamipron and meropenem has been reported to decrease the serum level of VPA. We observed seven cases which showed a decrease in serum levels of VPA due to concomitant use of VPA and carbapenem from January 2002 to October 2006 in a 750-bed university hospital, the average decrease of 70.4% was observed. Carbapenem antibiotics administrated concomitantly with VPA were panipenem (1 case), meropenem (3 cases), and imipenem (2 cases), and in one other case imipenem and meropenem were used sequentially. We found the VPA serum levels were significantly decreased with meropenem (n=4) more than with other carbapenem antibiotics (n=4, 89.3% vs. 51.5% decrease, P=0.03). Clinicians should be aware of this potential interaction, pay attention to the failure of seizure control due to decreased serum VPA levels with concomitant use of carbapenem antibiotics, and monitor VPA serum levels for those cases.
Adult ; Aged ; Aged, 80 and over ; Anti-Bacterial Agents/administration & dosage/*therapeutic use ; Anticonvulsants/administration & dosage/*blood/therapeutic use ; Carbapenems/administration & dosage/*therapeutic use ; Drug Interactions ; Drug Therapy, Combination ; Epilepsy/*drug therapy ; Female ; Humans ; Imipenem/therapeutic use ; Male ; Middle Aged ; Thienamycins/therapeutic use ; Valproic Acid/administration & dosage/*blood/therapeutic use

BACKGROUND: Gram-negative bacilli can be stored in cystine tryptic agar (CTA) at room temperature for over 1 year, but we experienced a loss of imipenem resistance among VIM-2-producing isolates. The aims of this study were to determine the frequency of loss of IMP-1 and VIM-2 genes during storage in CTA at room temperature and to document any change in the MIC of antimicrobial agents and the location of the gene. METHODS: Bacteria were isolated from clinical specimens at Severance Hospital collected from 1995-2000. Modified Hodge and double disk synergy tests were performed for screening of MBL-production isolates, and blaIMP-1 and blaVIM-2 were detected by PCR. Loss of resistance was tested in CTA at room temperature. PFGE and hybridization using a blaVIM-2 probe were carried out to determine the location of the VIM-2 gene. RESULTS: When VIM-2- and IMP-1-producing strains of eight P. aeruginosa and two Acinetobacter spp. were stored in CTA at room temperature, some isolates lost imipenem resistance after 3 days and 90% lost resistance after 15 weeks. Loss of resistance genes resulted in a decrease of the MIC of imipenem from 32-128 mug/mL to 0.5-8 mug/mL for P. aeruginosa, and from 32 mug/mL to 0.25-4 mug/mL for Acinetobacter spp. Hybridization of I-CeuI and S1-digested and PFGE suggested that VIM-2 genes are located on approximately 50-100 kb or 400 kb plasmids. CONCLUSION: Isolates may lose resistance genes when stored in CTA at room temperature. Therefore, it is necessary for MBL-production tests including the Modified Hodge test and double disk synergy test and detection of MBL genes.
Acinetobacter ; Agar ; Anti-Infective Agents ; Bacteria ; Carbapenems ; Chimera ; Cystine ; Imipenem ; Mass Screening ; Polymerase Chain Reaction ; Sprains and Strains

BACKGROUND: Doripenem is the most recently introduced antimicrobial agent of the carbapenem class. It is a valuable therapeutic option in the context of increasing antimicrobial resistance to imipenem and meropenem among gram-negative bacilli (GNB) clinical isolates. However, clinicians are usually reluctant to prescribe doripenem, because susceptibility to doripenem is not automatically reported by most clinical laboratories and the in vitro activity of doripenem against clinically significant GNB isolates remains uncertain. MATERIALS AND METHODS: We investigated the in vitro antibacterial activity of doripenem in GNB blood isolates in a tertiary care center. Over a period of 10 months, 212 adult bacteremia cases were treated at the study hospital. Doripenem susceptibility testing was performed for the 212 blood isolates by the disk diffusion method, and clinical data were collected. RESULTS: Among the blood isolates, the rate of doripenem resistance (7.5%) was lower than that of imipenem (12.9%) or other anti-GNB antimicrobial agents, except amikacin (2.1%). Almost all imipenem-susceptible GNB blood isolates (181/182, 99.5%) were susceptible to doripenem. Whereas doripenem resistance was rarely observed in Enterobacteriaceae (2/181, 1.1%), it was frequently observed in patients with non-fermentatative GNB (12/27, 44.4%), hospital-acquired infections (7/27, 25.9%), and pneumonia (11/49, 22.4%). CONCLUSION: Doripenem exhibited more potent in vitro activity against GNB blood isolates than other anti-GNB antimicrobial agents in a tertiary care center where it was infrequently prescribed compared with other carbapenems. However, its clinical utility may be limited due to the increasing number of carbapenem-resistant non-fermentative GNB infections.
Adult ; Amikacin ; Anti-Infective Agents ; Bacteremia ; Carbapenems ; Diffusion ; Enterobacteriaceae ; Gram-Negative Bacteria ; Humans ; Imipenem ; Pneumonia ; Tertiary Care Centers* ; Tertiary Healthcare*