Like any foreign object orthopaedic implants are susceptible to Thioridazine hydrochloride

Like any foreign object orthopaedic implants are susceptible to Thioridazine hydrochloride infection when introduced into the human body. review we highlight the etiology and Thioridazine hydrochloride taxonomic groupings of bacteria known to cause prosthetic joint infections and examine their key mechanisms of attachment. We propose that antimicrobial strategies should focus on the most harmful bacteria taxa within the context of occurrence taxonomic diversity adhesion mechanisms and implant design. Patient-specific identification of organisms that cause prosthetic joint infections will permit assessment of their biological vulnerabilities. The latter can be targeted using a range of antimicrobial techniques that exploit different colonization mechanisms including implant surface attachment biofilm formation and/or hematogenous recruitment. We anticipate that customized strategies for each patient joint and prosthetic component will be most effective at reducing prosthetic joint infections including those caused by antibiotic-resistant and polymicrobial bacteria. is the most prevalent causative agent accounting for more than half of all cases (Table 1). Surprisingly is widely known to be very pathogenic 12 but only causes about half of (CoNS) which includes several species: species in “aseptic loosening” implants.7 Nevertheless Thioridazine hydrochloride PCR can be prone to detecting false positives and is unlikely to accurately characterize polymicrobial PJIs.7 Other factors that could obfuscate a PJI include: biofilms intracellular infections of peri-implant tissue or phenotypic reductions of bacterial colony size in situ.2 Whether undetected PJIs of an implant are primarily responsible for loosening remains the subject of considerable debate 2 yet the need for preventing bacterial adhesion to orthopaedic implants is crucial for reducing all PJI-related complications. Bacterial Adhesion to Orthopaedic Implants According to some researchers nearly 60% of PJIs occur during implantation procedures by known sources of pathogenic bacteria such as the patient’s skin or a contaminated surgical suite.26 Suboptimal surgical attire can also have generalizable effects on the prevalence of surgical wound infections.27 PJIs begin with bacterial adherence to the implant surface making necessary an accurate understanding of the specific adhesion mechanisms employed by PJI-causing bacteria to prevent their establishment. Hip and knee implant surfaces are heterogeneous with each modular component specifically designed to suit a particular function within a joint. For example the femoral stem and acetabular cup of a hip implant are designed to promote osseointegration and have therefore been subject to Thioridazine hydrochloride modifications in surface topography and chemistry. In contrast the necks liners and femoral heads of implants have a smooth composition designed to reduce friction between intercalating components. Any prosthetic component is susceptible to microbial colonization which can lead to full-onset PJI. One study Rabbit Polyclonal to SEPT7. for example found no significant difference in the preference of bacteria between knee and hip implant components 28 possibly due to the heterogeneous adhesion abilities of different species of bacteria. Others found that acetabular cups and polyethylene liners were most commonly infected.29 30 Although these studies demonstrated that all components of knee and hip implants can become infected they did not address the divergent behaviors among multiple species of bacteria. This is due at least in part to the fact that multiple components can become infected simultaneously or asynchronously which can be difficult to measure in vivo. Further complicating this issue is the observation that different species of bacteria may better infect specific implant components creating a heterogeneous surface mosaic of infected sites. This is evidenced by an apparent strong preference of for polyethylene liners 30 which is likely due to an adhesion mechanism that increases substrate suitability. Causative agents of PJI have a diverse arsenal of adherence mechanisms. For adherence to an inert surface non-specific adhesion is governed primarily by molecular chemistry (e.g. van der Waals Lewis acid/base electrostatic and hydrophobic forces).31–34 Some researchers postulate that non-specific adhesion between a microbe and its substrate can only be explained by the combined interaction of both weak (van der Waals) and stronger (electrostatic) forces.32 34 35 Lewis acid/base forces caused by the coupling.