An outbreak of multidrug-resistant Serratia marcescens: the importance of continuous monitoring of nosocomial infections

Šiširak, Maida; Hukić, Mirsada

doi:10.5644/ama2006-124.67

Cited by 22 publications

(20 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is not known if these effects are the result of AP expression, per se , or if they are coincident with the expression of AP and other Ca 2+ -regulated virulence factors. While not generally associated with the lung and CF, Serratia is often cultured from trachea and is a growing concern as a human pathogen [45], [46]. Adherence and colonization of Serratia in the trachea would putatively also be modulated by normal muco-cilliary clearance mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Modulation of the Epithelial Sodium Channel (ENaC) by Bacterial Metalloproteases and Protease Inhibitors

et al. 2014

View full text Add to dashboard Cite

The serralysin family of metalloproteases is associated with the virulence of multiple gram-negative human pathogens, including Pseudomonas aeruginosa and Serratia marcescens. The serralysin proteases share highly conserved catalytic domains and show evolutionary similarity to the mammalian matrix metalloproteases. Our previous studies demonstrated that alkaline protease (AP) from Pseudomonas aeruginosa is capable of activating the epithelial sodium channel (ENaC), leading to an increase in sodium absorption in airway epithelia. The serralysin proteases are often co-expressed with endogenous, intracellular or periplasmic inhibitors, which putatively protect the bacterium from unwanted or unregulated protease activities. To evaluate the potential use of these small protein inhibitors in regulating the serralysin induced activation of ENaC, proteases from Pseudomonas aeruginosa and Serratia marcescens were purified for characterization along with a high affinity inhibitor from Pseudomonas. Both proteases showed activity against in vitro substrates and could be blocked by near stoichiometric concentrations of the inhibitor. In addition, both proteases were capable of activating ENaC when added to the apical surfaces of multiple epithelial cells with similar slow activation kinetics. The high-affinity periplasmic inhibitor from Pseudomonas effectively blocked this activation. These data suggest that multiple metalloproteases are capable of activating ENaC. Further, the endogenous, periplasmic bacterial inhibitors may be useful for modulating the downstream effects of the serralysin virulence factors under physiological conditions.

show abstract

Section: Discussionmentioning

confidence: 99%

Modulation of the Epithelial Sodium Channel (ENaC) by Bacterial Metalloproteases and Protease Inhibitors

et al. 2014

View full text Add to dashboard Cite

show abstract

“…33 The similarity in PFGE profiles among all CAZresistant S. marcescens isolates, strongly suggests an outbreak in the oncology ward; this kind of outbreaks are often caused by cross-contamination by medical staff, 4 and have a mortality rate of 10-20%. 2,4,34 Although the number of isolates reported here is small, two of these seven isolates were related to fatal outcomes, hence a 29% mortality rate. On the other hand, CAZ-resistant K. pneumoniae isolates all had distinct PFGE profiles, but they all carry a similar-size, conjugative plasmid bearing the bla SHV-5 gene, suggesting that the plasmid has been transferred between different K. pneumoniae strains within the hospital in a manner consistent with the notion of epidemic plasmids, outlined nearly 30 years ago.…”

Section: Discussionmentioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

“…1,2 Infections caused by S. marcescens or K. pneumoniae have been linked with various hospital sources, such as medical devices, milk, topical and intravenous solutions, liquid soap and air-conditioning systems. [1][2][3] Both bacterial species often cause nosocomial outbreaks and are also commonly resistant to cephalosporins (through. the production of extended-spectrum β-lactamases, ESBLs) and aminoglycosides [2][3][4] ESBLs have a serine moiety in their active sites, and can hydrolyze the β-lactam ring of third-generation cephalosporins and monobactams; genes encoding ESBLs can be chromosomal or plasmid-borne.…”

Section: Introductionmentioning

confidence: 99%

“…[1][2][3] Both bacterial species often cause nosocomial outbreaks and are also commonly resistant to cephalosporins (through. the production of extended-spectrum β-lactamases, ESBLs) and aminoglycosides [2][3][4] ESBLs have a serine moiety in their active sites, and can hydrolyze the β-lactam ring of third-generation cephalosporins and monobactams; genes encoding ESBLs can be chromosomal or plasmid-borne. [5][6][7] Since their first characterization, in the 1980's and 1990's in Germany and France, ESBLs have spread worldwide.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Sulfhydryl variable-5 extended spectrum β-lactamase in nosocomial enteric bacteria causing sepsis in mexican children

et al. 2015

View full text Add to dashboard Cite

Introduction: Enteric bacteria causing nosocomial infections are often resistant to third-generation cephalosporins due to the production of extended-spectrum β-lactamases (ESBLs).Objective: To describe and characterize the ESBLs pattern present in Klebsiella pneumoniae and Serratia marcescens strains, isolated as causative of nosocomial sepsis in pediatric patients at Instituto Nacional de Pediatría (National Institute of Pediatrics). Material and methods:We analyzed 94 strains of K. pneumoniae and 7 of S. marcescens isolated from clinical specimens from 2002-2005, causative of sepsis in a children's hospital. We evaluated antibiotic susceptibility and detection of ESBL phenotypes by disk diffusion methods; ceftazidime-resistant isolates were further characterized by pulsed field gel electrophoresis (PFGE); and ESBLs were phenotypically and genotypically characterized by isoelectric focusing, polymerase chain reaction (PCR) and sequencing. We also assed for presence of conjugative plasmids bearing the ESBL gene.Results: 51/94 (54%) of K. pneumoniae isolates, and 5/7 (71%) of S. marcescens isolates were resistant to ceftazidime; all carried a bla gene. All K. pneumoniae isolates had a distinct PFGE profile, yet all carried a ~48-Kb plasmid, that was conjugatively transferable to an Escherichia coli receptor, which expressed the resistance phenotype. On the other hand, all S. marcescens isolates had a similar PFGE profile, were unable to transfer the ceftazidime-resistance phenotype, and were isolated from the same ward in a short time-span suggesting an outbreak. Conclusions:The overall prevalence of ESBL-producing enteric bacteria in this hospital is high but similar to other Latin American reports. The sulfhydryl variable-5 (SHV-5) ESBL gene appears to reside in a highly mobile plasmid, capable of spreading among different K. pneumoniae clones and perhaps even to S. marcescens.

show abstract

Microbial Composition and Antibiotic Resistance of Biofilms Recovered from Endotracheal Tubes of Mechanically Ventilated Patients

Vandecandelaere

Coenye

2014

Advances in Experimental Medicine and Biology

View full text Add to dashboard Cite

In critically ill patients, breathing is impaired and mechanical ventilation, using an endotracheal tube (ET) connected to a ventilator, is necessary. Although mechanical ventilation is a life-saving procedure, it is not without risk. Because of several reasons, a biofilm often forms at the distal end of the ET and this biofilm is a persistent source of bacteria which can infect the lungs, causing ventilator-associated pneumonia (VAP). There is a link between the microbial flora of ET biofilms and the microorganisms involved in the onset of VAP. Culture dependent and independent techniques were already used to identify the microbial flora of ET biofilms and also, the antibiotic resistance of microorganisms obtained from ET biofilms was determined. The ESKAPE pathogens play a dominant role in the onset of VAP and these organisms were frequently identified in ET biofilms. Also, antibiotic resistant microorganisms were frequently present in ET biofilms. Members of the normal oral flora were also identified in ET biofilms but it is thought that these organisms initiate ET biofilm formation and are not directly involved in the development of VAP.

show abstract

An outbreak of multidrug-resistant Serratia marcescens: the importance of continuous monitoring of nosocomial infections

Cited by 22 publications

References 20 publications

Modulation of the Epithelial Sodium Channel (ENaC) by Bacterial Metalloproteases and Protease Inhibitors

Modulation of the Epithelial Sodium Channel (ENaC) by Bacterial Metalloproteases and Protease Inhibitors

Sulfhydryl variable-5 extended spectrum β-lactamase in nosocomial enteric bacteria causing sepsis in mexican children

Microbial Composition and Antibiotic Resistance of Biofilms Recovered from Endotracheal Tubes of Mechanically Ventilated Patients

Contact Info

Product

Resources

About