A 62-year-old woman with osteoarthritis presents with a 7-month history of progressively worsening left hip pain radiating to the groin, 8 months after undergoing total left-hip arthroplasty. The pain has not responded to nonsteroidal antiinflammatory drugs. Physical examination reveals a sinus tract overlying her left hip. Her leukocyte count is 8000 per cubic millimeter, and the C-reactive protein (CRP) level is 15.5 mg per liter. A radiograph shows loosening of the prosthesis at the bone–cement interface. Synovial-fluid aspirate shows 15×103 cells per cubic millimeter (89% neutrophils); cultures of an aspirate from the hip grow Staphylococcus epidermidis. How should her case be managed?

Biofilm formation is a crucial step in the pathogenesis of many subacute and chronic bacterial infections, including foreign body-related infections. Biofilms are difficult to eradicate with conventional antimicrobial agents. Bacterial biofilms have several potential antimicrobial resistance mechanisms. Antimicrobial resistance mechanisms may act concurrently, and in some cases, synergistically. Persister cells play a major role in the tolerance of biofilm bacteria to antimicrobial agents. Understanding the mechanisms involved in biofilm-associated antimicrobial resistance is key to development of new therapeutic strategies.

SUMMARY Staphylococcus lugdunensis has gained recognition as an atypically virulent pathogen with a unique microbiological and clinical profile. S. lugdunensis is coagulase negative due to the lack of production of secreted coagulase, but a membrane-bound form of the enzyme present in some isolates can result in misidentification of the organism as Staphylococcus aureus in the clinical microbiology laboratory. S. lugdunensis is a skin commensal and an infrequent pathogen compared to S. aureus and S. epidermidis, but clinically, infections caused by this organism resemble those caused by S. aureus rather than those caused by other coagulase-negative staphylococci. S. lugdunensis can cause acute and highly destructive cases of native valve endocarditis that often require surgical treatment in addition to antimicrobial therapy. Other types of S. lugdunensis infections include abscess and wound infection, urinary tract infection, and infection of intravascular catheters and other implanted medical devices. S. lugdunensis is generally susceptible to antimicrobial agents and shares CLSI antimicrobial susceptibility breakpoints with S. aureus. Virulence factors contributing to this organism's heightened pathogenicity remain largely unknown. Those characterized to date suggest that the organism has the ability to bind to and interact with host cells and to form biofilms on host tissues or prosthetic surfaces.

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Biofilm formation represents a protected mode of growth that renders bacterial cells less susceptible to antimicrobials and to killing by host immune effector mechanisms and so enables the pathogens to survive in hostile environments and also to disperse and colonize new niches. Biofilm disease includes device-related infections, chronic infections in the absence of a foreign body, and even malfunction of medical devices. Areas covered: This review puts forward a new medical entity that represents a major public health issue, which we have named 'biofilm-related disease'. We highlight the characteristics of biofilm disease including its pathogenesis, microbiological features, clinical presentation, and treatment challenges. Expert commentary: The diversity of biofilm-associated infections is increasing over time and its impact may be underestimated. This peculiar form of development endows associated bacteria with a high tolerance to conventional antimicrobial agents. A small percentage of persister cells developing within the biofilm is known to be highly tolerant to antibiotics and has typically been involved in causing relapse of infections. Knowledge of the pivotal role played by biofilm-growing microorganisms in related infections will provide new treatment dynamics for this biofilm-related disease.

Vascular access for haemodialysis is key in renal patients both due to its associated morbidity and mortality and due to its impact on quality of life. The process, from the creation and maintenance of vascular access to the treatment of its complications, represents a challenge when it comes to decision-making, due to the complexity of the existing disease and the diversity of the specialities involved. With a view to finding a common approach, the Spanish Multidisciplinary Group on Vascular Access (GEMAV), which includes experts from the five scientific societies involved (nephrology [S.E.N.], vascular surgery [SEACV], vascular and interventional radiology [SERAM-SERVEI], infectious diseases [SEIMC] and nephrology nursing [SEDEN]), along with the methodological support of the Cochrane Center, has updated the Guidelines on Vascular Access for Haemodialysis, published in 2005. These guidelines maintain a similar structure, in that they review the evidence without compromising the educational aspects. However, on one hand, they provide an update to methodology development following the guidelines of the GRADE system in order to translate this systematic review of evidence into recommendations that facilitate decision-making in routine clinical practice, and, on the other hand, the guidelines establish quality indicators which make it possible to monitor the quality of healthcare.

The activity of electrical current against planktonic bacteria has previously been demonstrated. The shortterm exposure of the bacteria in biofilms to electrical current in the absence of antimicrobials has been shown to have no substantial effect; however, longer-term exposure has not been studied. A previously described in vitro model was used to determine the effect of prolonged exposure (i.e., up to 7 days) to low-intensity (i.e., 20-, 200-, and 2,000-microampere) electrical direct currents on Pseudomonas aeruginosa, Staphylococcus aureus, and Staphylococcus epidermidis biofilms. Dose-and time-dependent killing was observed. A maximum of a 6-log 10 -CFU/cm 2 reduction was observed when S. epidermidis biofilms were exposed to 2,000 microamperes for at least 2 days. A 4-to 5-log 10 -CFU/cm 2 reduction was observed when S. aureus biofilms were exposed to 2,000 microamperes for at least 2 days. Finally, a 3.5-to 5-log 10 -CFU/cm 2 reduction was observed when P. aeruginosa biofilms were exposed to electrical current for 7 days. A higher electrical current intensity correlated with greater decreases in viable bacteria at all time points studied. In conclusion, low-intensity electrical current substantially reduced the numbers of viable bacteria in staphylococcal or Pseudomonas biofilms, a phenomenon we have labeled the "electricidal effect."The pathogenesis of a wide variety of human infections, including device-related infections, is now recognized to be related to the presence of bacteria in biofilms. The biofilm mode of growth protects bacteria from host defense mechanisms and conventional antimicrobial agents. The development of biofilm-related infections begins with the adhesion of the microorganisms to the biomaterial surface, mediated by the Van der Waals forces, acid-base interactions, and electrostatic forces (28). Electrostatic forces between bacteria and surfaces are generally repulsive, since almost all biomaterials are negatively charged, as are bacteria (19). It has been proposed that these repulsive forces can be enhanced by the application of electrical current, which provokes the surface detachment of bacterial biofilms (26,34,37).The antibacterial activity of electrical current has previously been demonstrated against Staphylococcus aureus and Staphylococcus epidermidis in agar (21, 24); the normal flora on human skin (2); Escherichia coli, Proteus species, and Klebsiella pneumoniae in synthetic urine (5); E. coli, Staphylococcus aureus, and Bacillus subtilis in water (12,22,23); and E. coli in salt solutions (27). The mechanism of the antibacterial activity of electrical current has been suggested to result from toxic substances (e.g., H 2 O 2 , oxidizing radicals, and chlorine molecules) produced as a result of electrolysis (21), the oxidation of enzymes and coenzymes, membrane damage leading to the leakage of essential cytoplasmic constituents (30), and/or a decreased bacterial respiratory rate (22).The aim of the present study was to determine the effect of prolonged exposure (i.e., up to 7 d...

Although uncommon, toxoplasmosis in SOT patients causes substantial morbidity and mortality. Seronegative recipients are at high risk for developing toxoplasmosis and should be given prophylaxis and receive careful follow-up.