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Virulence Traits (virulence + trait)
Selected AbstractsAmoebal pathogens as emerging causal agents of pneumoniaFEMS MICROBIOLOGY REVIEWS, Issue 3 2010Frédéric Lamoth Abstract Despite using modern microbiological diagnostic approaches, the aetiological agents of pneumonia remain unidentified in about 50% of cases. Some bacteria that grow poorly or not at all in axenic media used in routine clinical bacteriology laboratory but which can develop inside amoebae may be the agents of these lower respiratory tract infections (RTIs) of unexplained aetiology. Such amoebae-resisting bacteria, which coevolved with amoebae to resist their microbicidal machinery, may have developed virulence traits that help them survive within human macrophages, i.e. the first line of innate immune defence in the lung. We review here the current evidence for the emerging pathogenic role of various amoebae-resisting microorganisms as agents of RTIs in humans. Specifically, we discuss the emerging pathogenic roles of Legionella -like amoebal pathogens, novel Chlamydiae (Parachlamydia acanthamoebae, Simkania negevensis), waterborne mycobacteria and Bradyrhizobiaceae (Bosea and Afipia spp.). [source] THE INFLUENCE OF SAE LOCUS KNOCKOUT ON EXOPROTEINS IN STAPHYLOCOCCUS AUREUSJOURNAL OF FOOD SAFETY, Issue 3 2010JUNNI TANG ABSTRACT The sae operon is a key regulator in Staphylococcus aureus, which is known as an important infective and toxigenic bacterial pathogen. For the exploration of virulence factors expressed in the secreted exoprotein fraction are being controlled by sae operon, the relationship between the sae locus and exoproteins was investigated in this study. The homologous recombination vector pBT2,sae was constructed and the sae deletion mutant strain was successfully obtained. The results showed that the sae locus played an important role in the production of thermonucleases and other exoproteins. Sodium dodecyl sulfate polyacrylamide gel electrophoresis showed different exoprotein profiles between parent strain and mutant strain, in which three bands were visibly weakened. The results revealed that sae locus was involved in the regulation on exoproteins, some of which play a known fundamental role in the virulence of S. aureus. PRACTICAL APPLICATIONS This study presents that knocking out the sae gene locus in a specific Staphylococcus aureus strain results in reduced thermonuclease action, and also in reduced levels of proteins in the vicinity of 42 and 32 kDa molecular weight in sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis (PAGE) gels, indicating that their production is dependent on the sae locus. Practically, these proteins are associated with virulence traits, and with the pathogen's response to the environment and in potential hosts, which could be helpful for understanding the pathogenicity of S. aureus and also for further studies on the role of selected genes in the pathogenicity of S. aureus. [source] 5, flanking region of var genes nucleate histone modification patterns linked to phenotypic inheritance of virulence traits in malaria parasitesMOLECULAR MICROBIOLOGY, Issue 6 2007Jose Juan Lopez-Rubio Summary In the human malaria parasite Plasmodium falciparum antigenic variation facilitates long-term chronic infection of the host. This is achieved by sequential expression of a single member of the 60-member var family. Here we show that the 5, flanking region nucleates epigenetic events strongly linked to the maintenance of mono-allelic var gene expression pattern during parasite proliferation. Tri- and dimethylation of histone H3 lysine 4 peak in the 5, upstream region of transcribed var and during the poised state (non-transcribed phase of var genes during the 48 h asexual life cycle), ,bookmarking' this member for re-activation at the onset of the next cycle. Histone H3 lysine 9 trimethylation acts as an antagonist to lysine 4 methylation to establish stably silent var gene states along the 5, flanking and coding region. Furthermore, we show that competition exists between H3K9 methylation and H3K9 acetylation in the 5, flanking region and that these marks contribute epigenetically to repressing or activating var gene expression. Our work points to a pivotal role of the histone methyl mark writing and reading machinery in the phenotypic inheritance of virulence traits in the malaria parasite. [source] Identification of protein differences between two clinical isolates of Streptococcus mutans by proteomic analysisMOLECULAR ORAL MICROBIOLOGY, Issue 2 2008L. H. Guo Introduction:,Streptococcus mutans is generally considered to be the principal etiological agent for dental caries. Different strains of S. mutans may display different virulence mechanisms, so the isolation of the differential proteins is illuminating. Methods:,S. mutans strains 9-1 and 9-2, which both colonized the same oral cavity, were selected after screening for the possession of suspected virulence traits. The soluble cellular proteins were extracted from steady-state planktonic cells of strains 9-1 and 9-2 and were analyzed using high-resolution two-dimensional gel electrophoresis. Then, replicate maps of proteins from the two strains were generated. Proteins expressed only in strain 9-1 or 9-2 were excised and digested with trypsin by using an in-gel protocol. Tryptic digests were analyzed using matrix-assisted laser desorption/ionization time of flight mass spectrometry, by which peptide mass fingerprints were generated, and these were used to assign putative functions according to their homology with the translated sequences in the S. mutans genomic database. Results:, There were 12 proteins only expressed in strain 9-1 and three proteins only expressed in strain 9-2. They were involved in protein biosynthesis, protein folding, cell wall biosynthesis, fatty acid biosynthesis, nucleotide biosynthesis, repair of DNA damage, carbohydrate metabolism, signal transduction, and translation. Conclusion:, The identification of proteins differentially expressed between strains 9-1 and 9-2 provides new information concerning the mechanisms of cariogenesis. [source] Virulence, phenotype and genotype characteristics of endodontic Enterococcus spp.MOLECULAR ORAL MICROBIOLOGY, Issue 1 2005C. M. Sedgley Background/aims:, Enterococci have been implicated in persistent root canal infections but their role in the infection process remains unclear. This study investigated the virulence, phenotype and genotype of 33 endodontic enterococcal isolates. Methods:, Phenotypic tests were conducted for antibiotic resistance, clumping response to pheromone, and production of gelatinase, hemolysin and bacteriocin. Genotype analysis involved polymerase chain reaction amplification of virulence determinants encoding aggregation substances asa and asa373, cytolysin activator cylA, gelatinase gelE, gelatinase-negative phenotype ef1841/fsrC, adherence factors esp and ace, and endocarditis antigen efaA. Physical DNA characterization involved pulsed-field gel electrophoresis of genomic DNA, and plasmid analysis. Results:, Potential virulence traits expressed included production of gelatinase by Enterococcus faecalis (n = 23), and response to pheromones in E. faecalis culture filtrate (n = 16). Fourteen strains produced bacteriocin. Five strains were resistant to tetracycline and one to gentamicin, whereas all were susceptible to ampicillin, benzylpenicillin, chloramphenicol, erythromycin, fusidic acid, kanamycin, rifampin, streptomycin and vancomycin. Polymerase chain reaction products encoding efaA, ace, and asa were detected in all isolates; esp was detected in 20 isolates, cylA in six isolates, but asa373 was never detected. The gelatinase gene (gelE) was detected in all isolates of E. faecalis (n = 31) but not in Enterococcus faecium (n = 2); a 23.9 kb deletion sequence corresponding to the gelatinase-negative phenotype was detected in six of the eight E. faecalis isolates that did not produce gelatinase. Pulsed-field gel electrophoresis and plasmid analyses revealed genetic polymorphism with clonal types evident. Plasmid DNA was detected in 25 strains, with up to four plasmids per strain and a similar (5.1 kb) plasmid occurring in 16 isolates. Conclusions:, Phenotypic and genotypic evidence of potential virulence factors were identified in endodontic Enterococcus spp., specifically production of gelatinase and response to pheromones. [source] Quorum sensing and Candida albicansMYCOSES, Issue 1 2009Michael Kruppa Summary Candida albicans is one of the most commonly identified nosocomially acquired pathogens. This organism has a number of virulence traits including production of degrading enzymes, the ability to undergo phenotypic switching, and can rapidly undergo morphogenic switch from a blastospore (yeast) phase to that of a hyphal state. Interest in C. albicans morphogenic regulation has been the focus of a large number of studies, which have characterised transcriptional modulators of these morphologies. Recently, C. albicans has been shown to regulate its morphogenic shift through changes in cell density. It was observed that C. albicans inoculated at cell densities below 106 cells ml,1 under conditions which favour hyphal morphogenesis (pH 7.5, 37 °C), will germinate to form hyphae. However, if cells densities are greater than 106 cells ml,1, little germination will occur and cells will maintain yeast morphology. The basis for this cell-density-dependent control of morphogenesis is similar to that which is seen with bacterial cells regulating their activities via quorum sensing (QS). A number of molecules have been identified which affect the ability of C. albicans to undergo the yeast-to-hyphal shift, and three compounds have been demonstrated to be quorum-sensing molecules. The scope of this review is to bring to light what is now understood about QS in C. albicans and address the roles of these molecules in relation to virulence in the host and potential roles in cross-kingdom interactions. [source] Hydrolytic enzymes as virulence factors of Candida albicansMYCOSES, Issue 6 2005Martin Schaller Summary Candida albicans is a facultative pathogenic micro-organism that has developed several virulence traits enabling invasion of host tissues and avoidance of host defence mechanisms. Virulence factors that contribute to this process are the hydrolytic enzymes. Most of them are extracellularly secreted by the fungus. The most discussed hydrolytic enzymes produced by C. albicans are secreted aspartic proteinases (Saps). The role of these Saps for C. albicans infections was carefully evaluated in numerous studies, whereas only little is known about the physiological role of the secreted phospholipases (PL) and almost nothing about the involvement of lipases (Lip) in virulence. They may play an important role in the pathogenicity of candidosis and their hydrolytic activity probably has a number of possible functions in addition to the simple role of digesting molecules for nutrition. Saps as the best-studied member of this group of hydrolytic enzymes contribute to host tissue invasion by digesting or destroying cell membranes and by degrading host surface molecules. There is also some evidence that hydrolytic enzymes are able to attack cells and molecules of the host immune system to avoid or resist antimicrobial activity. High hydrolytic activity with broad substrate specificity has been found in several Candida species, most notably in C. albicans. This activity is attributed to multigene families with at least 10 members for Saps and Lips and several members for PL B. Distinct members of these gene families are differentially regulated in various Candida infections. In future, prevention and control of Candida infections might be achieved by pharmacological or immunological tools specifically modulated to inhibit virulence factors, e.g. the family of Saps. [source] Changes of virulence factors accompanying the phenomenon of induced fluconazole resistance in Candida albicansMYCOSES, Issue 7-8 2000K. Fekete-Forgács Summary We investigated a fluconazole-sensitive (MICflu,=,5 ,g ml,1) clinical isolate and a fluconazole-resistant (MICflu >80 ,g ml,1) laboratory mutant Candida albicans strain developed from the sensitive one. We studied putative virulence factors including germination, adherence ability to either buccal epithelial cells or acrylate surface, the secreted aspartic proteinase, and the extracellular phospholipase activity of the two strains as well as their growth. The fluconazole-resistant strain proved to be superior to the original strain in all the virulence traits tested. The higher virulence of the fluconazole-resistant strain was also supported by a mouse model. These results suggest that the development of fluconazole resistance can be accompanied by serious morphological and physiological changes: several putative virulence traits, moreover the in vivo virulence can increase simultaneously. [source] Signalling pathways in the pathogenesis of CryptococcusCELLULAR MICROBIOLOGY, Issue 3 2009Lukasz Kozubowski Summary Efficient communication with the environment is critical for all living organisms. Fungi utilize complex signalling systems to sense their environments and control proliferation, development and in some cases virulence. Well-studied signalling pathways include the protein kinase A/cyclic AMP (cAMP), protein kinase C (PKC)/mitogen-activated protein kinase (MAPK), lipid signalling cascades, and the calcium,calcineurin signalling pathway. The human pathogenic basidiomycetous fungus Cryptococcus neoformans deploys sensitive signalling systems to survive in the human host, leading to life-threatening meningoencephalitis. Known virulence traits of this fungus, including the antioxidant melanin production, the antiphagocytic polysaccharide capsule and the ability to grow at 37°C, are orchestrated by complex signalling networks, whose understanding is crucial to better treat, diagnose and prevent cryptococcosis. [source] An epidemiologic analysis of staphylococcus aureus-associated keratitis in BostonACTA OPHTHALMOLOGICA, Issue 2009I BEHLAU Purpose S. aureus is a normal commensal of the human skin and nasopharynx. It is therefore of interest to determine whether S. aureus keratitis is caused by a subset of these organisms. In this study, the phenotypic and genotypic characteristics of S.aureus keratitis isolates were analyzed. Methods All S. aureus clinical isolates were prospectively collected over a 24 month period at the MEEI (2006-2008). The diagnosis of clinical keratitis and associated risk factors was by medical record review. Keratitis-associated S. aureus strains were assessed for: 1) antibiotic susceptibility, 2) biofilm robustness by gentian violet staining using an in vitro microtiter plate assay, and 3) genetic lineage by multi-locus sequence typing (MLST). Results 26 cases of keratitis were identified from the 600 S. aureus clinical isolates. Risk factors associated with S.aureus keratitis included trauma, prior surgery, soft contact lens wear, and the presence of a foreign body. Ocular surface disease does not appear to be an independent risk factor. All 26 isolates were tetracycline- and trimethoprim-sulfamethoxazole- sensitive. All the MRSA strains were found to be ciprofloxacin-resistant (10/26). Nearly one-half of all the S.aureus keratitis-associated isolates were caused by a single clone, ST5. Both methicillin sensitive and resistant S. aureus strains were represented within ST5. Conclusion These results suggest that there may be specific S.aureus lineages which possess phenotypic and genotypic characteristics that enable S. aureus to more effectively cause sight-threatening keratitis. Future work will examine their virulence traits and a comparison to commensal S.aureus strains. [source] Adhesion of Pseudomonas aeruginosa ocular isolates to mucinCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 3 2001Lina Panayiota Aristoteli BSc(Hons) ABSTRACT The purpose of this study was to compare the adhesion of Pseudomonas aeruginosa ocular isolates to mucin. An adhesion assay was developed using biotin-labelled P. aeruginosa strains (two corneal ulcer, two acute red eye, one asymptomatic and one standard strains) incubated with porcine gastric mucin immobilized on a nitrocellulose membrane. The adhesion was semiquantified using densitometry. The results showed that all P. aeruginosa strains tested were able to adhere to mucin to various extents with three strains (one corneal ulcer, one acute red eye, one asymptomatic) binding significantly greater than the negative control (P < 0.1). Results suggest that ocular strains of P. aeruginosa strains differ in their adhesion to mucin but this did not correlate with the pathogenic origin of the strain. It is concluded that the adhesion of P. aeruginosa strains to mucin alone may not be a principal determinant of pathogenesis but may be a contributing factor along with other bacterial virulence traits. [source] | |||||||||||||