Raad et al. (1992) showed that sonication improved

the efficiency of identifying catheter-related infections. A study by Yűcel et al. also suggests that biofilms on CVCs lead to catheter-related bloodstream infections, because antimicrobial-treated CVCs resulted in a reduction in these infections (Yűcel et al.,2004). It is not yet clear whether specific catheters are less likely to lead to colonization and infection (Safdar & Maki, 2005), but further investigation of the link between biofilms and device-related infection is needed. Recently dental implants have been a focus of study for oral biofilms that may eventually lead to peri-implantitis with loss of the supporting bone and ultimately failure of the implant. Organisms associated with peri-implantitis are similar to those found in Erismodegib in vivo periodontitis but also include etiological involvement of actinomycetes, S. aureus, coliforms, or Candida spp. (Pye et al., 2009; Heitz-Mayfield & Lang, 2010). So far, only a few

studies have used molecular techniques like checkerboard hybridization or pyrosequencing to study the microflora of failing implants, indicating distinct species associated with peri-implantitis (Shibli et al., 2008; Kumar et al., 2012). More systematic epidemiological studies are necessary for the development PI3K inhibitor of standardized diagnostic and therapeutic strategies. Criterion 3 indicates that BAI are localized and not systemic. Systemic signs and symptoms may occur, but they may

also be a function of planktonic cells or microbial products being shed from the biofilm at the original focus of second infection (Costerton et al., 1999; Parsek & Singh, 2003). Immune complex-mediated inflammation leading to tissue damage around biofilms also dominates in some biofilm infections such as P. aeruginosa lung infection in CF patients (Høiby et al., 1986; Bjarnsholt et al., 2009a). The fourth criterion addresses another tenet of biofilms: infections with planktonic bacteria are typically treated successfully with the appropriate antibiotics where the microorganism is found susceptible in vitro, whereas BAI are recalcitrant to antibiotic therapy or at least tolerant to higher antibiotic doses compared with planktonic cells of the same isolate. Although a BAI may show some response to conventional antibiotic therapies, it will not be eradicated and therefore recurs at a subsequent point. One example is the intermittent colonization of the lower respiratory tract with P. aeruginosa that sooner or later leads to chronic lung infection in CF. Intermittent colonization by P. aeruginosa can be eradicated by early aggressive antibiotic therapy in contrast to the chronic infection, which is treated by maintenance therapy (i.e. chronic suppressive antibiotic therapy).