scholarly journals Prosthetic valve endocarditis caused by Pseudomonas aeruginosa with variable antibacterial resistance profiles: a diagnostic challenge

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Nicolas Gürtler ◽  
Michael Osthoff ◽  
Florian Rueter ◽  
Daniel Wüthrich ◽  
Lukas Zimmerli ◽  
...  
1992 ◽  
Vol 24 (6) ◽  
pp. 797-800 ◽  
Author(s):  
Ömrüm Uzun ◽  
H. Erdal Akalin ◽  
Serhat Ünal ◽  
Metin Demicin ◽  
A. Cem Yorgancioglu ◽  
...  

2016 ◽  
Vol 3 (4) ◽  
Author(s):  
T. Nicholas Domitrovic ◽  
Andrea M. Hujer ◽  
Federico Perez ◽  
Steven H. Marshall ◽  
Kristine M. Hujer ◽  
...  

Abstract Background.  Successful treatment of infections caused by multidrug-resistant (MDR) Pseudomonas aeruginosa is thwarted by the emergence of antibiotic resistance and biofilm formation on prosthetic devices. Our aims were to decipher the molecular basis of resistance in a unique case of prosthetic valve endocarditis (PVE) caused by MDR P. aeruginosa. Methods.  Five sequential MDR P. aeruginosa blood isolates collected during a 7-month period were recovered from a patient suffering from PVE previously exposed to β-lactam antibiotics. Minimum inhibitory concentrations (MICs) of several classes of antibiotics were used to indicate clinical resistance characteristics; relatedness of the isolates was determined using multilocus sequence typing and repetitive sequence-based polymerase chain reaction. Amplification and sequencing of regulatory and resistance genes was performed. Results.  All isolates belonged to ST 298, possessed blaPDC-16, and were resistant to fluoroquinolones and carbapenems. In the course of therapy, we observed a >2-fold increase in cephalosporin resistance (4 µg/mL to >16 µg/mL). Sequencing of the AmpC regulator, ampR, revealed a D135N point mutation in cephalosporin-resistant isolates. Common carbapenemase genes were not identified. All isolates demonstrated a premature stop codon at amino acid 79 of the outer membrane protein OprD and mutations in the quinolone resistance-determining regions of gyrA and parC. Point mutations in nalC, an efflux pump regulator, were also observed. Conclusions.  In this analysis, we chart the molecular evolution of β-lactam resistance in a case of PVE. We show that mutations in regulatory genes controlling efflux and cephalosporinase production contributed to the MDR phenotype.


2020 ◽  
Vol 33 (1) ◽  
pp. 91-94
Author(s):  
Salih Cesur ◽  
◽  
Esra Kaya Kilic ◽  
Ulku Oztoprak Siyah ◽  
Cigdem Ataman Hatipoglu ◽  
...  

2014 ◽  
Vol 62 (S 01) ◽  
Author(s):  
A. Schäfer ◽  
H. Grubitzsch ◽  
H. Reichenspurner ◽  
K.-D. Wernecke ◽  
W. Konertz

2020 ◽  
Vol 21 (12) ◽  
pp. 1140-1153 ◽  
Author(s):  
Mohammad A. Noshak ◽  
Mohammad A. Rezaee ◽  
Alka Hasani ◽  
Mehdi Mirzaii

Coagulase-negative staphylococci (CoNS) are part of the microbiota of human skin and rarely linked with soft tissue infections. In recent years, CoNS species considered as one of the major nosocomial pathogens and can cause several infections such as catheter-acquired sepsis, skin infection, urinary tract infection, endophthalmitis, central nervous system shunt infection, surgical site infections, and foreign body infection. These microorganisms have a significant impact on human life and health and, as typical opportunists, cause peritonitis in individuals undergoing peritoneal dialysis. Moreover, it is revealed that these potential pathogens are mainly related to the use of indwelling or implanted in a foreign body and cause infective endocarditis (both native valve endocarditis and prosthetic valve endocarditis) in patients. In general, approximately eight percent of all cases of native valve endocarditis is associated with CoNS species, and these organisms cause death in 25% of all native valve endocarditis cases. Moreover, it is revealed that methicillin-resistant CoNS species cause 60 % of all prosthetic valve endocarditis cases. In this review, we describe the role of the CoNS species in infective endocarditis, and we explicated the reported cases of CoNS infective endocarditis in the literature from 2000 to 2020 to determine the role of CoNS in the process of infective endocarditis.


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