1,721,058 research outputs found
Presence of fibrinogen-binding adhesin gene in Staphylococcus epidermidis isolates from central venous catheters-associated and orthopaedic implant-associated infections.
No full textBiomaterials. 2004 Aug;25(19):4825-9.
Presence of fibrinogen-binding adhesin gene in Staphylococcus epidermidis isolates from central venous catheters-associated and orthopaedic implant-associated infections.
Arciola CR, Campoccia D, Gamberini S, Donati ME, Montanaro L.
Research Laboratory on Biocompatibility of Implant Materials, Rizzoli Orthopedic Institute, Via di Barbiano, 1/10, Bologna 40136, Italy.
Attention has recently been paid to identify and elucidate those pathogenetic mechanisms, which play a significant role in sustaining the early phases of Staphylococcus epidermidis colonisation and infection development. Several analogies with the physiology of Staphylococcus aureus, a more thoroughly investigated pathogen, have lead to carefully consider all bacterial surface components that mediate cell adhesion. This study aimed at investigating the presence of the fbe gene encoding for a fibrinogen-binding protein in a collection of 107 S. epidermidis strains isolated from orthopaedic infections and 67 from central venous catheter-associated infections. The strains isolated
from orthopaedic infections were in large part associated to four different classes of orthopaedic devices, respectively: internal fixation devices, external fixation devices, knee arthroprostheses and hip arthroprostheses. The molecular epidemiology analysis performed by PCR enlightened a statistically significant difference in the prevalence of this adhesion mechanism between orthopaedic infections and catheter-related infections, respectively, of 78% and 91%. The prevalence of fbe ranged from 67% to 91%, suggesting that, even though this adhesin is not strictly necessary for the development of infection, nevertheless it represents a rather common characteristic of strains causing
clinical infections, this independently on the presence or the absence of implant materials
Prevalence of cna, fnbA and fnbB adhesin genes among Staphylococcus aureus isolates from orthopedic infections associated to different types of implant.
No full textFEMS Microbiol Lett. 2005 May 1;246(1):81-6.
Prevalence of cna, fnbA and fnbB adhesin genes among Staphylococcus aureus isolates from orthopedic infections associated to different types of implant.
Arciola CR, Campoccia D, Gamberini S, Baldassarri L, Montanaro L.
Research Unit on Implant Infections, Rizzoli Orthopedic Institute, Via di Barbiano 1/10, 40136 Bologna, Italy. [email protected]
Here are reported data on virulence determinants of Staphylococcus aureus from orthopedic surgical infections, emphasizing on the genes encoding fibronectin (fnbA, fnbB) and collagen (cna) adhesins. 191 S. aureus strains from orthopedic
infections (53 from internal fixation devices, 29 external fixation devices, 15 knee arthroprostheses, 30 hip arthroprostheses, 45 surgical reconstruction and 19 non-associated to medical devices) were investigated for the presence of the genes of the collagen-binding protein Cna and of the two fibronectin-binding
proteins, FnbA and FnbB. 87 (46%) strains were found to be cna+ without significant variations across the different surgical categories considered. Conversely, the fnbA and the fnbB genes were almost always present in all surgical categories. The finding that, among the investigated adhesins, fibronectin-adhesins are present in the majority of the implant associated S. aureus clinical isolates encourages the development of strategies to specifically block the interaction of bacteria with matrix fibronectin by antagonist ligands
No genotoxicity of a new nickel-free stainless steel
No full textInt J Artif Organs. 2005 Jan;28(1):58-65.
No genotoxicity of a new nickel-free stainless steel.
Montanaro L, Cervellati M, Campoccia D, Prati C, Breschi L, Arciola CR.
Research Laboratory on Biocompatibility of Implant Materials, Rizzoli Orthopedic Institute, Bologna, Italy. [email protected]
Stainless steel is a metallic alloy largely employed in orthopedics,
maxillofacial surgery and orthodontic therapy. However, the presence in its composition of a high quantity of nickel, an agent known to trigger toxic, allergic and cancerogenous responses in humans, is cause of some concern. In this study, we have investigated the in vitro mutagenicity and genotoxicity of a
new nickel-free stainless steel, namely P558, in comparison to the conventional stainless steel AISI 316L. The cytogenetic effects were evaluated by studying the frequency of Sister Chromatid Exchanges (SCE) and chromosomal aberrations. Ames test was performed to detect the mutagenic activity. Both P558 and AISI
316L did not cause any significant increase in the average number of SCE and in chromosomal aberrations, either with or without metabolic activation. Furthermore, the Ames test showed that the extracts of both P558 and of AISI 316L are not mutagenic. Overall, these findings prove that P558 is devoid of genotoxicity and mutagenicity. The present results, together with other previous
interesting observations that P558 promotes osseointegration, suggest that this new nickel-free stainless steel can represent a better alternative to other conventional steel alloys
A multiplex PCR method for the detection of all five individual genes of ica locus in Staphylococcus epidermidis. A survey on 400 clinical isolates from prosthesis-associated infections
No full textJ Biomed Mater Res A.
A multiplex PCR method for the detection of all five individual genes of ica locus in Staphylococcus epidermidis. A survey on 400 clinical isolates from prosthesis-associated infections.
Arciola CR, Gamberini S, Campoccia D, Visai L, Speziale P, Baldassarri L, Montanaro L.
Research Unit on Implant Infections, Rizzoli Orthopedic Institute, Via di Barbiano, 1/10, 40136 Bologna, Italy.
[email protected]
In Staphylococcus epidermidis, ica locus encodes for the synthesis of a polysaccharide intercellular adhesin (slime or biofilm). A multiplex polymerase chain reaction (PCR) for the detection of the five individual genes of ica locus was developed, with the aim to probe the set of genes in a large collection of Staphylococcus epidermidis clinical isolates. Single representative fragments
for icaR, icaA, icaD, icaB, and icaC genes were selected. Multiplex PCR was applied to two reference Staphylococcus epidermidis strains [the non-biofilm-forming ATCC 12228 and the biofilm-forming ATCC 35984 (RP62A)] and to 400 clinical isolates of Staphylococcus epidermidis from orthopedic prosthesis associated infections. The gene profile was compared with the phenotypic biofilm-forming ability, evaluated by means of an optimized Congo red agar (CRA) plate test. Among the clinical isolates, 228 (57%) turned out completely ica positive and were biofilm producing. Among the 172 non-biofilm-forming strains (43%), 164 (41%) were completely ica negative and 8 strains (2%) harbored all five ica genes. The ica locus thus proves to be a cluster of strictly linked genes, without any evidence of single gene deletion.
(c) 2005 Wiley Periodicals, Inc. J Biomed Mater Res, 2005
Antibiotic resistance in exopolysaccharide-forming Staphylococcus epidermidis clinical isolates from orthopaedic implant infections
No full textBiomaterials. 2005 Nov;26(33):6530-5.
Antibiotic resistance in exopolysaccharide-forming Staphylococcus epidermidis clinical isolates from orthopaedic implant infections.
Arciola CR, Campoccia D, Gamberini S, Donati ME, Pirini V, Visai L, Speziale P, Montanaro L.
Research Unit on Implant Infections, Rizzoli Orthopaedic Institute, Via di Barbiano 1/10, 40136 Bologna, Italy. [email protected]
The opportunistic pathogen Staphylococcus epidermidis is able to produce biofilm and to frequently cause implant infections. In recent years, it has also exhibited an increasing antimicrobial drug resistance. Here, the resistance to a panel of 16 different antibiotics in 342 clinical strains of S. epidermidis from orthopaedic implant infections has been investigated. The isolates were pheno- and genotyped for extracellular polysaccharide production, relevant to staphylococcal biofilm formation, in order to ascertain possible associations with antibiotic resistance. Approximately 10% of the isolates were found to be sensitive to all screened antibiotics. In all, 37-38% were resistant to beta-lactams such as oxacillin and imipenem, while the resistance to penicillin, ampicillin, cefazolin, cefamandole, was consistently observed in over 80% of the
strains. Erythromycin- and clindamycin- resistant strains were approximately 41% and 16%, respectively. Of the isolates, 10% was resistant to chloramphenicol, 23% to sulfamethoxazole and 26% to ciprofloxacin. Resistance to vancomycin was never observed. Interestingly, exopolysaccharide-producing strains exhibited a significantly higher prevalence in the resistance to the four aminoglycosides (gentamicin, amikacin, netilmicin, tobramycin), to sulfamethoxazole and to ciprofloxacin with respect to non-producing isolates. Moreover, multiple resistance to antibiotics was more frequent among exopolysaccharide-forming strains
Evaluation of bacterial adhesion of Streptococcus mutans on dental restorative materials.
No full textBiomaterials. 2004 Aug;25(18):4457-63.
Evaluation of bacterial adhesion of Streptococcus mutans on dental restorative materials.
Montanaro L, Campoccia D, Rizzi S, Donati ME, Breschi L, Prati C, Arciola CR.
Research Laboratory on Biocompatibility of Implant Materials, Rizzoli
Orthopaedic Institute, and Experimental Pathology Department, University of Bologna, Italy. [email protected]
Bacterial adhesion to the surface of composite resins and other dental restorative materials is an important parameter in the aetiology of secondary caries formation. The aim of the present study was to investigate the adhesion of a Streptococcus mutans strain (ATCC 25175) on the surface of different restorative materials. The test materials examined included three flowable
composites (Filtek Flow, Tetric Flow, and Arabesk Flow), three microhybrid composites (Clearfil APX, Solitaire 2, and Z250), two glass-ionomers (Fuji IX, Fuji IX fast), a compomer (F2000), an ormocer (Admira), and a control reference material (tissue culture grade, surface treated polystyrene). The adhesion tests
were carried out in 24-well plates. Quantitative turbidimetric measurements were finally performed in order to indirectly evaluate the amount of bacteria retained on the material surface after in vitro exposure to the bacteria suspension. Under these conditions, with the exception of the Admira ormocer and the Fuji IX fast glass ionomer, which were found to be more adhesive, all the other material surfaces showed a similar susceptibility to bacterial adhesion, exhibiting values not significantly different than the reference polystyrene control. Furthermore, the release of fluoride from some of the test surfaces did not appear capable to reduce early bacterial adhesion
Search for the insertion element IS256 within the ica locus of Staphylococcus epidermidis clinical isolates collected from biomaterial-associated infections.
No full textBiomaterials. 2004 Aug;25(18):4117-25.
Search for the insertion element IS256 within the ica locus of Staphylococcus epidermidis clinical isolates collected from biomaterial-associated infections.
Arciola CR, Campoccia D, Gamberini S, Rizzi S, Donati ME, Baldassarri L, Montanaro L.
Research Laboratory on Biocompatibility of Implant Materials, Rizzoli
Orthopaedic Institute, and Experimental Pathology Department, University of Bologna, Italy. [email protected]
Staphylococcus epidermidis biofilm-forming strains produce a polysaccharide intercellular adhesin (PIA), which mediates bacterial cell aggregation and favours the colonisation on prosthetic implants. PIA synthesis is regulated by the icaADBC locus. In vitro, by repeated subcultures of a biofilm-producing strain, the loss of the ability to produce biofilm appears associated with the
insertion of the IS256 element into the ica locus. This study was aimed (i) to investigate if the five genes of ica locus are always all present in different strains of S. epidermidis, and (ii) to search if IS256 insertion naturally occurs in ica locus without making recourse to the experimental procedure of repeated subcultures of strains. 120 S. epidermidis clinical isolates from peri-prosthesis infections were investigated both by an original multiplex PCR
analysis of the ica genes and by PCR amplification of the IS256 element. Also two reference strains (the biofilm-negative S. epidermidis ATCC 12228 and the biofilm-forming ATCC 35984 [RP62A]) and two biofilm-negative RP62A-derived acriflavin mutants (D9 and HAM892) were analysed. D9 e HAM892 were for the first time shown to contain in ica locus, at the base 3319, a 1300-bp insertion with a DNA sequence corresponding to IS256. Among the 120 clinical isolates, 51 (43%) turned out completely ica-positive, 69 completely ica-negative (57%). The genes of the ica locus appear, in all cases of the present collection, strictly linked
each other, so they are either all present or all absent. In this collection, IS256 was present in eight out of the 69 ica-negative strains and in 34 out of the 51 ica-positive strains. IS256, also when present in bacterial genomic DNA, was never found inside the ica locus, thus suggesting that insertion/excision of this element is not a natural occurring mechanism for off/on switching of
biofilm production
Nanostructured materials for inhibition of bacterial adhesion in orthopedic implants: A minireview
No full textOrthopedic implants may fail owing to different reasons: poor osseointegration at the tissue-implant interface, generation of wear debris, stress and strain imbalance between implant and surrounding tissues, and infections. To ensure success in orthopedics, implant materials must not evoke an undesirable inflammatory response, they must be habitable by bone-forming cells (favoring adhesion of osteoblasts), hinder formation of soft connective tissue (hindering adhesion of fibroblasts), and be anti-infective (discouraging bacterial adhesion). Recent studies have suggested that nanophase materials have a better efficacy as bone implants in favoring osseointegration compared to conventional orthopedic implant materials. This minireview discusses studies on nanophase materials as bone implants, focusing on the effect of these materials in inhibiting bacterial adhesion forthe prevention of implant infections
Advancements in molecular epidemiology of implant infections and future perspectives
No full textImplant infection remains the major and often irreducible complication in clinical use of biomaterials, demanding new therapeutic and preventive strategies. Etio-pathogenesis of biomaterials-related infections is being more and more studied, and various virulence bacterial factors have progressively been identified, but little is still known about the weight of the distinct molecules in the context of specific peri-implant infection sites. Molecular epidemiology has become recently integrated into the research on implant infections. What distinguishes molecular epidemiology from the simple molecular biology is that the use of molecular techniques is applied to the study of the distribution and prevalence of virulence and resistance genes in collections of bacterial clinical isolates from implant infections. Here, the authors comment on the range of molecular techniques available, reviewing the various applications of molecular epidemiology to the study of implant infections and providing some experimental examples related to the field of orthopaedic implant infections. They highlight the new opportunities arising from molecular epidemiology of designing measures useful to prevent and treat implant infections. The knowledge of the relative weight of virulence factors and of their regulatory mechanisms at molecular level can open the way to new strategies also including gene therapies aimed at silencing or knocking out crucial genes responsible for the aggressive tools (adhesins, biofilm production, antibiotic resistance) of the aetiological agents of implant-related infections
Tracing the origins of extracellular DNA in bacterial biofilms: story of death and predation to community benefit
Full text linkExtracellular DNA (eDNA) is a macromolecule copiously found in various natural microenvironments, but its origin and significance still remain partly mysterious phenomena. Here, the multifaceted origins of eDNA in bacterial biofilms are explored. The release of eDNA can follow a suicidal programmed bacterial apoptosis or a fratricide-induced death, under the control of quorum sensing systems or triggered by specific stressors. eDNA can be released into the extracellular space or as a free macromolecule or enclosed within membrane vesicles or even through an explosion of bubbles. eDNA can also be derived from host tissue cells through bacterial cytolytic/proapoptotic toxins or stolen from neutrophil extracellular traps (NETs). eDNA can alternatively be produced by lysis-independent mechanisms. Sub-inhibitory doses of antibiotics, by killing a fraction of bacteria, result in stimulating the release of eDNA. Even phages appear to play a role in favoring eDNA release. Unveiling the origins of eDNA is critical to correctly address biofilm-associated infections
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