There is a stranger in my house: mixed-species biofilms in relation to medical devices and human health

So far we have only discussed biofilms comprised by a single species, because the majority of what is known about biofilm formation and development has largely been determined by studying single-species communities in vitro. These studies have provided detailed information on the mechanisms underlying community development for the species touched upon in this chapter. For some bacterial species, such as UPEC that form clonally expanded single-species biofilm-like intracellular bacterial communities (IBCs) during bladder infection (Anderson et al., 2003, 2004a; Martinez et al.,

2000), the analysis of single-species communities provides great insights into the role of biofilm formation in pathogenesis. However, the majority of biofilms relevant to human health or associated with medical devices are not comprised of just a single bacterial species; most biofilm communities are polymicrobial in nature, comprising diverse bacterial species that interact with one another in a multitude of ways. These complex interactions must be considered in order to fully understand medical deviceassociated biofilm-formation pathways and their interactions with the host.

Polymicrobial biofilms are largely symbiotic relationships between the bacterial species involved. This symbiosis offers further advantages beyond those typically provided by the ability to form biofilms. One advantage to polymicrobial biofilms is that the environment allows for increased interspecies interactions. This can result in an increased chance for horizontal gene transfer, which can support transfer of antibiotic resistance genes from one bacterial species to another (Marsh et al., 2011; Marsh, 2005; Hannan et al., 2010; Roberts and Mullany, 2010). One study on polymicrobial biofilms isolated from a patient nephrostomy tube found alarming numbers of vancomycin-resistant S. aureus strains within the community (Weigel et al., 2007). Others have shown the transfer of antibiotic resistance between Streptococcs gordonii and E. faecalis in an ex vivo model of biofilms associated with a root canal (Sedgley et al.,

2008). The ability to exchange antibiotic-resistance genes within a polymicrobial community contributes to the emergence of new antibiotic-resistant strains and further complicates treatment of infection, increasing the risk for chronic infection and sepsis.

Another advantage to polymicrobial biofilms is that, in some cases, polymicrobial interactions allow for surface adherence and biofilm formation for bacterial species that are incapable of attaching and forming a biofilm on their own. One of the best-studied examples comes from studies of oral biofilms. Oral biofilms are almost always polymicrobial in nature, and a complex interplay between the interacting bacteria involved leads to colonization and biofilm formation (Kolenbrander, 2000; Zijnge et al., 2010; Jakubovics and Kolenbrander, 2010). Oral biofilm formation begins with the attachment of initial colonizing bacteria to the dental surface (Kolenbrander et al., 2010; Li et al., 2004). These initial colonizers can consist of Streptococcus spp. (S gordonii, S. mitis, S. oralis, S. sanguinis, and so on) or other bacterial species that bind to receptors on the coating surrounding the tooth surface (Kolenbrander et al.,

2010). Adherence of the founding species to the surface serves as a foundation for further attachment by early and late colonizing bacteria that cannot interact directly with the dental surface (Periasamy and Kolenbrander, 2009; Kolenbrander et al., 2002). These early and late colonizing bacteria bind specifically to already adherent bacteria, or can bind broadly to all dental bacterial species (Kolenbrander et al., 2010). The end result of this polymicrobial biofilm formation is dental plaque, which can lead to asymptomatic colonization or tooth decay (Sbordone and Bortolaia, 2003; Marsh et al., 2011; Marsh, 2005). Dispersal from dental biofilms has been linked to increased risk of oral carcinoma (Nagy et al., 1998), endocarditis (Beikler and Flemmig, 2011), pulmonary infections (Paju and Scannapieco, 2007; Scannapieco, 1999, 2006), and pancreatic cancer (Michaud et al., 2012; Farrell et al., 2012). However, the underlying complexities of polymicrobial biofilms highlight why the field has been largely understudied to date and the necessities behind better understanding polymicrobial interactions within biofilms.

Throughout this chapter, we focused on bacterial biofilms; however, fungal species also form multicellular communities. In particular, biofilms formed by pathogenic fungi of the genus Candida have been shown to have substantial detrimental impacts on human health (Ramage et al., 2006; Kojic and Darouiche, 2004; Douglas, 2003). Perhaps the most well studied and documented pathogenic fungus of this genus, Candida albicans, has extensively been shown to be involved in human disease and medical device-associated biofilms (Andes et al., 2004; Kuhn et al., 2002; Chandra et al.,

2001). C. albicans can form biofilms on the vaginal mucosa (Harriott et al., 2010), dental surfaces in the mouth (Sen et al., 1997a,b; Cannon and Chaffin, 1999), and on medical devices (such as venous catheters) (Pannanusorn et al., 2013; Ramage et al., 2006; Andes et al., 2004; Douglas, 2003). Much like bacterial biofilms, C. albicans antifungal resistant persister cells emerge enhancing persistence and complicating treatment (LaFleur et al., 2006). More alarmingly, C. albicans has been found in polymicrobial biofilms along with bacteria such as S. aureus and has subsequently been shown to support the growth of anaerobic bacteria within the hypoxic center of its biomass (Harriott and Noverr, 2009, 2011; Shirtliff et al., 2009; Morales and Hogan, 2010; Fox et al., 2014; Peters and Noverr, 2013; Peters et al., 2013). These examples highlight the complexity of interkingdom interactions that can occur within biofilms and can promote/enhance pathogenesis.

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