Concept: Streptococcus oralis
- International journal of systematic and evolutionary microbiology
- Published over 6 years ago
Genomic, taxonomic and biochemical studies were performed on two strains of alpha-haemolytic streptococci that showed to be clustered with major members of the Streptococcus mitis group. These Gram-positive strains were isolated from tooth surfaces of caries-free humans and show the classical spherical-shape of streptococcal species growing in chains. Sequence analysis from concatenated 16S and 23S rDNA, and sodA genes showed that these strains belonged to the Mitis group, but both of them cluster into a new phylogenetic branch. The genomes of these two isolates were sequenced, and whole-genome Average Nucleotide Identity (ANI) demonstrated that these strains significantly differ from any streptococcal species, showing ANI values under 91% even when compared to their phylogenetically closest species such as Streptococcus oralis and Streptococcus mitis. Biochemically, the two isolates also showed distinct metabolic features relative to close species, like an α-galactosidase activity. From the results of the present study, the name Streptococcus dentisani sp. nov. is proposed for these new couple of strains deposited in open collection at the Spanish Type Culture Collection (CECT) and Leibniz Institute DSMZ-German Collection of Microorganism and Cell Cultures (DSMZ); being respectively identified as Streptococcus dentisani Str. 7746 (CECT 8313, DSM 27089) and Streptococcus dentisani Str. 7747 (CECT 8312T, DSM 27088T).
Viridans group streptococci (VGS) are a major cause of bacteraemia in neutropenic cancer patients, particularly those receiving fluoroquinolone prophylaxis. In this study, we sought to understand the molecular basis for fluoroquinolone resistance in VGS causing bacteraemia in cancer patients by assigning 115 VGS bloodstream isolates to specific species using multilocus sequence analysis (MLSA), by sequencing the quinolone resistance-determining regions (QRDRs) of gyrA, gyrB, parC and parE, and by testing strain susceptibility to various fluoroquinolones. Non-susceptibility to one or more fluoroquinolones was observed for 78% of isolates, however only 68.7% of patients were receiving fluoroquinolone prophylaxis. All but one of the determinative QRDR polymorphisms occurred in GyrA or ParC, yet the pattern of determinative QRDR polymorphisms was significantly associated with the fluoroquinolone prophylaxis received. By combining MLSA and QRDR data, multiple patients infected with genetically indistinguishable fluoroquinolone-resistant Streptococcus mitis or Streptococcus oralis strains were discovered. Together these data delineate the molecular mechanisms of fluoroquinolone resistance in VGS isolates causing bacteraemia and suggest possible transmission of fluoroquinolone-resistant S. mitis and S. oralis isolates among cancer patients.
- Langmuir : the ACS journal of surfaces and colloids
- Published almost 7 years ago
The mechanisms of action of fluoride have been discussed controversially for decades. The cavity-preventive effect is often traced back to effects on demineralization. However, an effect on bacterial adhesion was indicated by indirect macroscopic studies. To characterize adhesion on fluoridated samples on a single bacterial level, we used AFM force-spectroscopy with bacterial probes to measure adhesion forces directly. We tested the adhesion of Streptococcus mutans, Streptococcus oralis and Staphylococcus carnosus onto smooth, high density hydroxyapatite surfaces, pristine and after treatment with fluoride solution. All bacteria species exhibit lower adhesion forces after fluoride treatment of the surfaces. These findings suggest that the decrease of adhesion properties is a further key factor for the cariostatic effect of fluoride besides the decrease of demineralization.
Streptococcus gordonii is an early colonizer of the oral cavity. Although a variety of S. gordonii adherence mechanisms have been described, current dogma is that the major receptor for S. gordonii is sialic acid. However, as many bacterial species in the oral cavity produce neuraminidase that can cleave terminal sialic acid, it is unclear whether S. gordonii relies on sialic acid for adherence to oral surfaces or if this species has developed alternative binding strategies. Previous studies have examined adherence to immobilized glycoconjugates and identified binding to additional glycans; but no prior studies have defined the contribution of these different glycan structures in adherence to oral epithelial cells. We determined that the majority of S. gordonii strains tested did not rely on sialic acid for efficient adherence. In fact, adherence of some strains was significantly increased following neuraminidase treatment. Further investigation of representative strains that do not rely on sialic acid for adherence revealed binding not only to sialic acid via the serine-rich repeat protein GspB, but also to β-1,4-linked galactose. Adherence to this carbohydrate occurs via an unknown adhesin distinct from those utilized by Streptococcus oralis and Streptococcus pneumoniae Demonstrating the potential biological relevance of binding to this cryptic receptor, we established that S. oralis increases S. gordonii adherence in a neuraminidase-dependent manner. These data suggest that S. gordonii has evolved to simultaneously utilize both terminal and cryptic receptors in response to the production of neuraminidase by other species in the oral environment.
Soft, adhesive (+) alpha tocopherol phosphate planar bilayers that control oral biofilm growth through a substantive antimicrobial effect
- Nanomedicine : nanotechnology, biology, and medicine
- Published about 2 years ago
‘Soft’ nanomaterials have the potential to produce substantive antibiofilm effects. The aim of this study was to understand the oral antimicrobial activity of soft nanomaterials generated from alpha-tocopherol (α-T) and alpha-tocopherol phosphate (α-TP). (+) α-TP formed planar bilayer islands (175 ± 21 nm, -14.9 ± 3.5 mV) in a Trizma® buffer, whereas (+) α-T formed spherical liposomes (563 ± 1 nm, -10.5 ± 0.2 mV). The (+) α-TP bilayers displayed superior Streptococcus oralis biofilm growth retardation, a more substantive action, generated a superior adsorption to hydroxyapatite and showed an enhanced inhibition of multi-species bacterial saliva biofilm growth (38 ± 7μm vs 58 ± 18 μm, P ˂ 0.05) compared to (+) α-T. Atomic force microscopy data indicated that the ability of the ‘soft’ α-TP nanomaterials to transition into planar bilayer structures upon contact with interfaces facilitated their adhesive properties and substantive antimicrobial effects.
Non-mutans low pH oral streptococci are postulated to contribute to caries etiology.
This paper describes a high throughput method that relies upon a microplate reader to score coaggregation 60 minutes post mixing, and use of a high-speed real-time imaging technology to describe the rate of coaggregation over time. The results of visual, microplate, and FlowCam(™) aggregation scores for oral bacteria Streptococcus gordonii, Streptococcus oralis, and Actinomyces oris, whose ability to coaggregate are well characterized, are compared. Following mixing of all possible pairs, the top fraction of the supernatant was added to a microplate to quantify cell-density. Pairs were also passed through a flow cell within a FlowCam(™) to quantify the rate of coaggregation of each pair. Results from both the microplate and FlowCam(™) approaches correlated with corresponding visual coaggregation scores and microscopic observations. The microplate-based assay enables high throughput screening, whereas the FlowCam(™) -based assay validates and quantifies the extent that autoaggregation and coaggregation occur. Together these assays open the door for future in-depth studies of autoaggregation and coaggregation among large panels of test strains. This article is protected by copyright. All rights reserved.
Streptococcus tigurinus is a novel species of viridans streptococci, shown to cause severe invasive infections such as infective endocarditis, spondylodiscitis and meningitis. S. tigurinus belongs to the Streptococcus mitis group and is most closely related to Streptococcus mitis, Streptococcus oralis, Streptococcus pneumoniae, Streptococcus pseudopneumoniae and Streptococcus infantis. The presence of S. tigurinus in the human oral cavity has been documented, including in patients with periodontal disease. This review addresses the available scientific knowledge on S. tigurinus and its association with closely related streptococci, and discusses its putative involvement in common oral infections. While there is as yet no strong evidence on the involvement of S. tigurinus with oral infections, its presence in the oral cavity and its association with endocarditis warrants special attention for a link between oral and systemic infection.
Streptococcus spp. are important causes of infective endocarditis but challenging in species identification. This study compared identification based on sequence determination of the rnpB gene with 2 systems of matrix-assisted laser desorption ionization-time of flight mass spectrometry, MALDI Biotyper (Bruker) and VITEK MS IVD (bioMérieux). Blood culture isolates of viridans streptococci from 63 patients with infective endocarditis were tested. The 3 methods showed full agreement for all 36 isolates identified in the Anginosus, Bovis, and Mutans groups or identified as Streptococcus cristatus, Streptococcus gordonii, or Streptococcus sanguinis. None of the methods could reliably identify the 23 isolates to the species level when designated as Streptococcus mitis, Streptococcus oralis, or Streptococcus tigurinus. In 7 isolates classified to the Mitis group, the rnpB sequences deviated strikingly from all reference sequences, and additional analysis of sodA and groEL genes indicated the occurrence of yet unidentified Streptococcus spp.
Multiple studies have now shown that various species of bacteria can stimulate platelets; many in a strain and donor-dependent manner. The signalling pathways underlying this platelet activation has been the subject of scrutiny for the last decade. The best-delineated pathway is that in response to Streptococcal species, such as Streptococcus sanguinis (S. sanguinis), Streptococcus gordonii (S. gordonii) and Streptococcus oralis (S. oralis), where a pathway is initiated by the engagement of the low affinity IgG receptor, FcγRIIA. This leads to and involves the tyrosine kinase Syk, the adaptor protein Linker of Activated T Cells (LAT) and subsequently both phospholipase Cγ2 (PLCγ2) and phosphatidylinositol-3-kinase (PI-3-K). Finally, this leads to the expression of the αIIbβ3 integrin, the synthesis and release of thromboxane A2 (T × A2) and the exocytosis of PF4, each of which plays a crucial role in secondary signalling and full platelet activation. Roles for other signalling pathways in Streptococcal-induced platelet activation are less clear, although an ADP-mediated inhibition of adenylyl cyclase, a glycoprotein Ib/IX/V-mediated pathway and perhaps a complement-induced pathway have each been proposed. Platelet activation by Porphyromonas gingivalis (P. gingivalis) at least partially shares the FcγRIIA/Syk/PLCγ2/PI-3-K mechanism utilised by Streptococcal species. However, it has also been suggested that P. gingivalis activates platelets by two additional methods; stimulation of the protease-activated receptors leading to activation of phospholipase Cβ (PLCβ), and the engagement of Toll-like receptors 2 and 4 by released lipopolysaccharide leading to an ill-defined pathway which may involve PI-3-K. Consequently, it appears that bacteria can stimulate platelets by eliciting multiple signalling pathways some of which are common, and some unique, to individual species.