Panton-Valentine leukocidin gene detected in Staphylococcus aureus strain isolated from a knee arthroprosthesis infection.

This report focuses on the molecular characterization of a Staphylococcus aureus strain isolated from a knee arthroprosthesis infection and recognized retrospectively as a carrier of the Panton-Valentine leukocidin gene. The stored microbiological isolate, which belonged to the strain collection of the Research Unit on Implant Infections of the Rizzoli Orthopaedic Institute, was retrieved for molecular analysis. Genotyping was carried out, revealing an interesting profile. In addition to the positivity for the Panton-Valentine toxin gene, the results indicated that the isolate belonged to the agr III group and was endowed with bbp and cna genes, both encoding for staphylococcal adhesins that bind bone proteins. The strain had the mecA gene for methicillin resistance, even though it was unable to resist any of the beta-lactam or other antibiotics. Its gene configuration matched that of other community-acquired methicillin-resistant and methicillin-susceptible Staphylococcus aureus(CA-MRSA and CA-MSSA) strains which have recently been reported worldwide. As far as we know,this is the first report on a PVL-positive S. aureus strain associated with an orthopedic implant (knee arthroprosthesis) infection.

Presence of fibrinogen-binding adhesin gene in Staphylococcus epidermidis isolates from central venous catheters-associated and orthopaedic implant-associated infections.

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.

Occurrence of ica genes for slime synthesis in a collection of Staphylococcus epidermidis strains from orthopedic prosthesis infections.

Staphylococcus epidermidis is a frequent pathogen in infections associated with orthopedic implants. We studied 123 S. epidermidis strains from infections related to orthopedic implants, as regards their ability to express a factor of virulence, namely the slime, an extracellular polysaccharide, which mediates adherence to implants and bacterial colonization. The slime-producing ability was determined by PCR detection of icaA and icaD genes responsible for slime synthesis, and by culture on Congo red agar plates in which slime-producing strains form black colonies, while nonslime-forming ones develop red colonies. 56% of the S. epidermidis isolates were icaA- icaD-positive and grew to become black colonies. In the evaluation of the distribution of slime-forming strains in different sites and types of implants, we found a slight, but not statistically significant, increase in slime-forming strains in total joint prostheses, where tissue compression near the articular faces can form niches in which bacteria crowd, sheltered by the slime. Our findings confirm the role of ica genes as a virulence marker in the pathogenesis of implant-associated orthopedic infections. However, they do not show the existence of a higher frequency of slime-positive strains in a specific type of implant.