Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl
Preferences help
enabled [disable] Abstract
Number of results

Results found: 5

Number of results on page
first rewind previous Page / 1 next fast forward last

Search results

Search:
in the keywords:  virulence factors
help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
EN
Klebsiella pneumoniae, known as a major threat to public health, is the most common factor of nosocomial and community acquired infections. In this study, 50 K. pneumoniae clinical specimens isolated from bronchial, urea, blood, catheter, rectal, bile, tracheal and wound cultures were collected. These isolates were identified and carbapenem resistance was determined via an automated system, CHROMagar Orientation and CHROMagar KPC. The carbapenemase gene regions (blaIMP, blaVIM, blaOXA, blaNDM and blaKPC) and presence of virulence factors (magA, k2A, rmpA, wabG, uge, allS, entB, ycfM, kpn, wcaG, fimH, mrkD, iutA, iroN, hly ve cnf-1) of these isolates were determined by using Multiplex-PCR. The OXA-48 carbapenemase gene regions were determined in 33 of 50 K. pneumoniae strains. In addition, NDM-1 resistance in one, OXA-48 and NDM-1 resistance in four unusual K. pneumoniae isolates were detected. Virulence gene regions that were encountered among K. pneumoniae isolates were 88% wabG, 86% uge, 80% ycfM and 72% entB, related with capsule, capsule lipoprotein and external membrane protein, responsible for enterobactin production, respectively. Even though there was no significant difference between resistant and sensitive strains due to the virulence gene regions (P≥0.05), virulence factors in carbapenem resistant isolates were found to be more diverse. This study is important for both, to prevent the spread of carbapenem resistant infections and to plan for developing effective treatments. Moreover, this study is the first detailed study of the carbapenem resistance and virulence factors in K. pneumoniae strains.
EN
Staphylococcus aureus is a widespread, opportunistic pathogen that causes community and hospital acquired infections. Its high pathogenicity is driven by multifactorial and complex mechanisms determined by the ability of the bacterium to express a wide variety of virulence factors. The proteome secreted into extracellular milieu is a rich reservoir of such factors which include mainly nonenzymatic toxins and enzymes. Simultaneously, membrane proteins, membrane-cell wall interface proteins and cell wall-associated proteins also strongly influence staphylococcal virulence. Proteomics shows a great potential in exploring the role of the extracellular proteome in cell physiology, including the pathogenic potential of particular strains of staphylococci. In turn, understanding the bacterial physiology including the interconnections of particular factors within the extracellular proteomes is a key to the development of the ever needed, novel antibacterial strategies. Here, we briefly overview the latest applications of gel-based and gel-free proteomic techniques in the identification of the virulence factors within S. aureus secretome and surfacome. Such studies are of utmost importance in understanding the host-pathogen interactions, analysis of the role of staphylococcal regulatory systems and also the detection of posttranslational modifications emerging as important modifiers of the infection process.
EN
The frequency of severe systemic fungal diseases has increased in the last few decades. The clinical use of antibacterial drugs, immunosuppressive agents after organ transplantation, cancer chemotherapy, and advances in surgery are associated with increasing risk of fungal infections. Opportunistic pathogens from the genera Candida and Aspergillus as well as pathogenic fungi from the genus Cryptococcus can invade human organism and may lead to mucosal and skin infections or to deep-seated mycoses of almost all inner organs, especially in immunocompromised patients. Nowadays, there are some effective antifungal agents, but, unfortunately, some of the pathogenic species show increasing resistance. The identification of fungal virulence factors and recognition of mechanisms of pathogenesis may lead to development of new efficient antifungal therapies. This review is focused on major virulence factors of the most common fungal pathogens of humans: Candida albicans, Aspergillus fumigatus and Cryptococcus neoformans. The adherence to host cells and tissues, secretion of hydrolytic enzymes, phenotypic switching and morphological dimorphism contribute to C. albicans virulence. The ability to grow at 37°C, capsule synthesis and melanin formation are important virulence factors of C. neoformans. The putative virulence factors of A. fumigatus include production of pigments, adhesion molecules present on the cell surface and secretion of hydrolytic enzymes and toxins.
EN
Introduction: The development of resistance to multiple antimicrobial agents in pathogenic bacteria has become a threat to public health. Multidrug-resistant strains that are particularly dangerous include MDR, XDR and PDR strains. Material and methods: Aspirate material from paranasal sinuses, obtained from patients with chronic sinusitis undergoing functional endoscopic sinus surgery (FESS) in Medical Center MML in Warsaw, was subjected to bacteriologic analysis. The isolated strains were identified to the species level and tested for antibiotic resistance. Then, minimal inhibitory concentration (MIC) was determined. R esults: The isolated strains of coagulase-negative staphylococci were resistant mainly to macrolides, aminoglycosides and tetracycline. Nine of the isolated strains exhibited multidrug-resistance. Discussion: Bacteria causing chronic sinusitis are becoming increasingly resistant to antimicrobial agents. The diagnostic process for coagulase-negative staphylococci (CNS) is often limited to the identification of species, or even genus of the bacteria. The CNS strains are considered to be non-pathogenic and they are not subject to eradication. This may lead to erroneous therapeutic decisions and, consequently, to the development of antibiotic resistance. CNS infections are classified as nosocomial and therefore, appropriate epidemiological procedures have to be followed. The authors highlight the necessity to determine MIC values for antibiotics and to introduce personalized treatment.
EN
Introduction: The development of resistance to multiple antimicrobial agents in pathogenic bacteria has become a threat to public health. Multidrug-resistant strains that are particularly dangerous include MDR, XDR and PDR strains. Material and methods: Aspirate material from paranasal sinuses, obtained from patients with chronic sinusitis undergoing functional endoscopic sinus surgery (FESS) in Medical Center MML in Warsaw, was subjected to bacteriologic analysis. The isolated strains were identified to the species level and tested for antibiotic resistance. Then, minimal inhibitory concentration (MIC) was determined. R esults: The isolated strains of coagulase-negative staphylococci were resistant mainly to macrolides, aminoglycosides and tetracycline. Nine of the isolated strains exhibited multidrug-resistance. Discussion: Bacteria causing chronic sinusitis are becoming increasingly resistant to antimicrobial agents. The diagnostic process for coagulase-negative staphylococci (CNS) is often limited to the identification of species, or even genus of the bacteria. The CNS strains are considered to be non-pathogenic and they are not subject to eradication. This may lead to erroneous therapeutic decisions and, consequently, to the development of antibiotic resistance. CNS infections are classified as nosocomial and therefore, appropriate epidemiological procedures have to be followed. The authors highlight the necessity to determine MIC values for antibiotics and to introduce personalized treatment.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.