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Nosocomial bloodstream infection and the emerging carbapenem-resistant pathogen Ralstonia insidiosa.

ABSTRACT: BACKGROUND:Ralstonia picketti, Ralstonia mannitolilytica, and Ralstonia insidiosa have recently been regarded as emerging pathogens of infectious diseases, in particular as the pathogens responsible for nosocomial infection in immunocompromised patients. R. insidiosa differs from R. picketti and R. mannitolilytica, and its related infections are rarely reported. METHODS:Clinical data from two nosocomial bloodstream infection cases were extracted and analyzed. The causable isolates were identified by the VITEK 2 Compact system, matrix assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS), and molecular identification methods using PCR with universal and species-specific primers. Antimicrobial susceptibility testing was performed using the broth microdilution method. Both of the isolates were subjected to whole genome sequencing using a HiSeq X10 Sequencer. Antimicrobial resistance genes, virulence factors, and plasmid replicons were identified from assembled genomes. A real-time RT-PCR experiment and a cloning experiment were conducted to explore the related class D ?-lactamase-encoding genes. RESULTS:Both patients recovered under therapy with antibiotics. Isolates were initially misidentified as R. mannitolilytica by the VITEK 2 Compact system rather than R. insidiosa, as identified by both MALDI-TOF MS and 16S rRNA gene sequencing. Both isolates were resistant to aminoglycosides, ?-lactams, and polymyxin B. One isolate harboring blaOXA-570 was resistant to carbapenems. The whole genome sequencing data confirmed species identification based on average nucleotide identity (ANI) and revealed two variants of class D ?-lactamase-encoding gene blaOXA (blaOXA-573 and blaOXA-574). The real-time RT-PCR experiment showed no difference in gene expression between blaOXA-570 and blaOXA-573 in our strains. The cloning experiment showed that variant OXA-573 had no carbapenem hydrolase activity. CONCLUSIONS:We described two cases of nosocomial bloodstream infection caused by R. insidiosa strains. MALDI-TOF MS was cost-effective for rapid species identification. Clinicians should be aware that R. insidiosa can be resistant to commonly used antibiotics, even carbapenems.

SUBMITTER: Fang Q

PROVIDER: S-EPMC6480722 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Nosocomial bloodstream infection and the emerging carbapenem-resistant pathogen Ralstonia insidiosa.

Fang Qingqing Q Feng Yu Y Feng Ping P Wang Xiaohui X Zong Zhiyong Z

BMC infectious diseases 20190423 1

<h4>Background</h4>Ralstonia picketti, Ralstonia mannitolilytica, and Ralstonia insidiosa have recently been regarded as emerging pathogens of infectious diseases, in particular as the pathogens responsible for nosocomial infection in immunocompromised patients. R. insidiosa differs from R. picketti and R. mannitolilytica, and its related infections are rarely reported.<h4>Methods</h4>Clinical data from two nosocomial bloodstream infection cases were extracted and analyzed. The causable isolates ...[more]

PMID: 31014269

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Project description:Background:We retrospectively analyzed the effect of tigecycline and cefoperazone/sulbactam therapies on the prognosis of patients with carbapenem-resistant Acinetobacter baumannii bloodstream infection (CRAB-BSI). Methods:CRAB-BSI patients receiving tigecycline therapy or cefoperazone/sulbactam therapy between January 2012 and December 2017 was enrolled, and strict exclusion criteria were followed. The 28-day mortality of patients was analyzed. The impact of cefoperazone/sulbactam therapy on prognosis was evaluated using Cox multivariate regression analysis. The 28-day mortality of patients receiving cefoperazone/sulbactam monotherapy and cefoperazone/sulbactam-based combination therapy was also compared. Results:Three hundred forty eight patients with CRAB-BSI were enrolled in the study. Two hundred ten patients were included after applying the exclusion criteria. Of these, 135 patients received tigecycline therapy and 75 patients received cefoperazone/sulbactam therapy. The 28-day mortality of patients in the latter group was, significantly lower than that of the tigecycline group [29.3% vs. 51.9%; P = 0.001]. Cox multivariate regression analysis revealed that cefoperazone/sulbactam therapy exerted a protective effect on the prognosis of patients [hazard ratio 0.566, 95% confidence interval (0.342-0.940); P = 0.028]. Kaplan-Meier survival curve analysis indicated that the 28-day mortality of patients receiving cefoperazone/sulbactam therapy was lower than that of patients receiving cefoperazone/sulbactam monotherapy, but the difference was not significant (22.2% vs. 40%; P = 0.074). However, the mortality of patients receiving cefoperazone/sulbactam with imipenem/cilastatin was significantly lower than that of patients receiving cefoperazone/sulbactam monotherapy (P = 0.048). Conclusions:Patients treated with cefoperazone/sulbactam therapy had a better clinical outcome. The mortality of patients receiving cefoperazone/sulbactam with imipenem/cilastatin seems to be the lowest.

Project description:Bloodstream infection (BSI) caused by carbapenem-resistant Klebsiella pneumoniae (CRKP) is a serious and urgent threat for hospitalized patients. This study aims to describe the clinical and molecular characteristics of CRKP causing BSI in a tertiary-care hospital in Beijing, China. A total of 146 CRKP strains and 39 carbapenem-susceptible K. pneumoniae (CSKP) strains collected in the hospital from 2017 to 2020 were sent for whole-genome sequencing. Univariate and multivariate analyses were used to evaluate risk factors for in-hospital mortality of CRKP-BSI cases. Thirty (20.5%) of 146 CRKP-BSI patients and three (7.7%) of 39 CSKP-BSI patients died at discharge (χ2 = 3.471, P = 0.062). Multivariate logistic regression analysis indicated that age and use of urinary catheters were independent risk factors for the death of CRKP-BSI. The 146 CRKP isolates belonged to 9 sequence types (STs) and 11 serotypes, while the 39 CSKP isolates belonged to 23 STs and 27 serotypes. The mechanism of carbapenem resistance for all the CRKP strains was the acquisition of carbapenemase, mainly KPC-2 (n = 127). There were 2 predominant serotypes for ST11 CRKP, namely, KL47 (n = 82) and KL64 (n = 42). Some virulent genes, including rmpA2, iucABCD and iutA, and repB gene, which was involved in plasmid replication, were detected in all ST11-KL64 strains. Evolutionary transmission analysis suggested that ST11 CRKP strains might have evolved from KL47 into KL64 and were accompanied by multiple outbreak events. This study poses an urgent need for enhancing infection control measures in the hospital, especially in the intensive care unit where the patients are at high-risk for acquiring CRKP-BSI. IMPORTANCE CRKP-BSI is demonstrated to cause high mortality. In this study, we demonstrated that ST11 CRKP strains might carry many virulent genes. Meanwhile, outbreak events occurred several times in the strains collected. Carbapenemase acquisition (mainly KPC-2 carbapenemase) was responsible for carbapenem resistance of all the 146 CRKP strains. As 2 predominant strains, all ST11-KL64 strains, but not ST11-KL47 strains, carried rmpA2, iucABCD, iutA, as well as a plasmid replication initiator (repB). Our study suggested that the occurrence of region-specific recombination events manifested by the acquisition of some virulence genes might contribute to serotype switching from ST11-KL47 to ST11-KL64. The accumulation of virulent genes in epidemic resistant strains poses a great challenge for the prevention and treatment of BSI caused by K. pneumoniae in high-risk patients.

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Nosocomial bloodstream infection and the emerging carbapenem-resistant pathogen Ralstonia insidiosa.

Publications

Nosocomial bloodstream infection and the emerging carbapenem-resistant pathogen Ralstonia insidiosa.

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