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991.
Lijiang Chen Yapei Zhang Jia Du Xiaolei Zhang Meimei Li Huale Chen Xiao Yu Yao Sun Tieli Zhou 《Journal of microbiology, immunology, and infection》2018,51(1):115-122
Background/Purpose
Only limited information is available about the detailed characteristics of qnrD, a plasmid-mediated quinolone resistance (PMQR) gene. This study aimed to understand the distribution of qnrD and the characterization of qnrD-carrying plasmids in Proteeae.Methods
The distribution of qnrD genes was investigated by polymerase chain reaction (PCR) amplification in 203 consecutive nonduplicate clinical isolates of Proteeae collected from inpatients at the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China. The minimum inhibitory concentrations (MICs) of antibiotics were measured by agar dilution method and other PMQR determinants were also determined by PCR. qnrD was positioned via Southern hybridization and the transferability of qnrD-carrying plasmids was achieved by conjugation experiment. The genetic environment of qnrD was investigated by sequencing, and chromosomal polymorphism for qnrD-positive strains was analyzed by pulsed-field gel electrophoresis (PFGE).Results
Forty strains carried qnrD, showing decreased fluoroquinolone susceptibility or low-level fluoroquinolone resistance. qnrD was encoded on the plasmid of about 2.7 kb or 5.2 kb in length, which cannot be transferred by liquid conjugation or filter mating, but can be successfully transferred by transduction. The transformants showed 62.5–300-fold increases in the MICs of quinolones compared with the recipient. The plasmids carrying qnrD showed a high similarity with that of Providencia spp. and Proteus vulgaris. PFGE analysis demonstrated that these isolates were divergent and not clone related.Conclusion
qnrD could have originated from Proteeae or presented in these bacteria as a reservoir; furthermore, qnrD could be transferred and spread within the same or across different bacterial species if the plasmids acquired mobile elements under antimicrobial selective pressures. 相似文献992.
Yuan-Chih Mao Chin-Lu Chang Yhu-Chering Huang Lin-Hui Su Chao-Tai Lee 《Journal of microbiology, immunology, and infection》2018,51(2):214-219
Background
Providencia stuartii survives well in natural environment and often causes opportunistic infection in residents of long-term care facilities (LTCFs). Clinical isolates of P. stuartii are usually resistant to multiple antibiotics. The bacterium is also naturally resistant to colistin and tigecycline. Treatment of infections caused by carbapenem-resistant P. stuartii is challenging.Methods
During a 15-month period in 2013–2014, four isolates (P1, P2, and P3B/P3U) of P. stuartii showing intermediate resistance to imipenem were identified at a regional hospital in southern Taiwan. They were identified from three patients (P1–P3) transferred from the same LTCF for the treatment of the infection. Pulsed-field gel electrophoresis was used to genotype the isolates. Resistance genes/plasmids and outer membrane proteins were investigated by polymerase chain reaction and sequence analysis.Results
Isolates P1 and P3B/P3U demonstrated similar pulsotypes. All isolates were found to have resistance genes (blaCMY-2, qnrD1, aac(6′)-Ib-cr) carried on nonconjugative IncA/C plasmids of different sizes. A single point mutation was identified in the chromosomal gyrA (Ser83Ile) and parC (Ser84Ile) genes of all isolates. Various point mutations and insertion/deletion changes were found in their major outer membrane protein gene ompPst1.Conclusions
Isolates of similar pulsotypes could appear after 15 months and caused urosepsis in another resident of the same LTCF. The bacterium may have persisted in the environment and caused opportunistic infection. As LTCF residents are usually vulnerable to infections, surveillance of multidrug-resistant organisms and infection control intervention that have been established in acute-care hospitals to control infections by resistant organisms are apparently as essential in LTCFs. 相似文献993.
Li-Hsin Tsao Chih-Yi Hsin Hsin-Yi Liu Han-Chuan Chuang Li-Yuan Chen Yuarn-Jang Lee 《Journal of microbiology, immunology, and infection》2018,51(3):359-366
Background/purpose
The incidence of carbapenem-resistant Pseudomonas aeruginosa (CRPA) related healthcare-associated infection (HAI) has increased in recent year worldwide. This study is to investigate the risk factors associated with CRPA infections in a university hospital setting in Taiwan to provide more information for clinician and infection control system.Methods
A retrospective cross-sectional study was conducted from January 1st, 2009 to June 30th, 2014. Patients with P. aeruginosa related HAI were included and divided into the CRPA case group and carbapenem-susceptible Pseudomonas aeruginosa (CSPA) control group. The medical records were reviewed to identify risk factors for CRPA HAI and mortality. Patients with prior use of any anti-pseudomonal carbapenems were included in subgroup analysis.Results
395 cases of P. aeruginosa infection were enrolled from total of 3263 HAI events; 63 were CRPA and 332 were CSPA. The prevalence of CRPA was 15.9% (63/395). Significant risk factors related to CRPA infection were longer time at risk, prior use of anti-pseudomonal carbapenems, and prior use of aminoglycoside (p < 0.05, 0.01, and 0.05). Furthermore, anti-pseudomonal carbapenem monotherapy did not significantly increase risk for CRPA infection.Conclusion
The worldwide CRPA prevalence has been on the raise and Taiwan has been also keeping up with the trend. Antimicrobials usage should be monitored carefully, especially with carbapenems and aminoglycoside. Clinicians should be award of and understand about the risk of CRPA infection, which increases by 1% with each hospitalization day. 相似文献994.
995.
996.
997.
Ravi M. Shah Reem Elfeky Zohreh Nademi Waseem Qasim Persis Amrolia Robert Chiesa Kanchan Rao Giovanna Lucchini Juliana M.F. Silva Austen Worth Dawn Barge David Ryan Jane Conn Andrew J. Cant Roderick Skinner Intan Juliana Abd Hamid Terence Flood Mario Abinun Mary Slatter 《The Journal of allergy and clinical immunology》2018,141(4):1417-1426.e1
998.
Hassan Abolhassani Janet Chou Wayne Bainter Craig D. Platt Mahmood Tavassoli Tooba Momen Marzieh Tavakol Mohammad Hossein Eslamian Mohammad Gharagozlou Masoud Movahedi Mohsen Ghadami Amir Ali Hamidieh Gholamreza Azizi Reza Yazdani Mohsen Afarideh Alireza Ghajar Arash Havaei Zahra Chavoshzadeh Asghar Aghamohammadi 《The Journal of allergy and clinical immunology》2018,141(4):1450-1458
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1000.