A new approach to mitigate biofilm formation on totally implantable venous access ports.

Use of intravascular catheters for patient care may be associated with increased risk of central line–associated bloodstream infections. It is estimated that up to 18 000 such infections occurred in intensive care units and up to 23 000 in inpatient wards of acute care hospitals in the United States in 2009 [1]. These device-associated infections result in significant morbidity, mortality, and costs of healthcare delivery in these patient populations. The infections result when microorganisms, introduced from the skin of the patient at the catheter insertion site, from a contaminated hub or needleless connector, or from hematogenous seeding, colonize the catheter and form a biofilm. The process of biofilm formation is initiated when microbial cells attach to the surfaces of the indwelling device. Microbial attachment is a complex process, affected by the chemical and physical characteristics of the substratum, host-produced conditioning films, hydrodynamics, characteristics of the aqueous medium, and properties of the microbial cell surface [2]. A distinguishing characteristic of biofilms is the presence of an extracellular polymeric substance matrix, also known as the biofilm EPS (extracellular polymeric substance). The biofilm EPS matrix may be composed of polysaccharides, proteins, and extracellular DNA and may perform a number of important functions for the component organisms, including adhesion, aggregation, and protection from the host immune system and antimicrobial agents [3]. Inhibition of biofilm formation is preferred to eradication of an established biofilm because organisms rapidly develop tolerance to antimicrobial agents, a characteristic that worsens as the biofilm ages [4]. Biofilms on central venous catheters are difficult to eradicate, and for certain organisms (eg, Staphylococcus aureus), removal of the device may be the only option. In this issue of The Journal, Chauhan et al [5] provide a novel approach for significantly reducing bacterial adherence to silicone and titanium surfaces of a totally implantable central venous access port. Silicone septum and catheter surfaces were coated with a methylcellulose polymer nanofilm. Methylcellulose is a nonionic water soluble polysaccharide that can reduce surface hydrophobicity when applied to the surface of silicone biomaterials [6]. Mussard et al [6] demonstrated that methylcellulose coating of silicone surfaces reduced nonspecific protein adsorption, and adhesion of mammalian cells and bacteria. Titanium ports of the device were coated with polyethylene glycol (PEG), which has been shown to reduce adhesion of bacteria and eukaryotic cells, including erythrocytes, by altering the physical and chemical characteristics of the surface [7–10].Both methylcellulose and PEG coatings tend to render surfaces more hydrophilic and, therefore, less prone to bacterial attachment [2]. How relevant are these data? What is needed to translate these findings to the bedside? A myriad of experimental methods have been published for the evaluation of biofilm control strategies by clinically relevant microorganisms, ranging from simple microtiter-plate methods [11] to continuous flow biofilm reactors [12] to animal model systems [13]. Although in vitro methods tend to provide greater reproducibility, higher throughput, and lower costs, results may not predict the performance of the treated device in vivo owing to the absence of host-produced conditioning films and immune response and the physical or chemical characteristics of the bloodstream [14]. Chauhan et al [5] used a continuous flow in vitro model system to evaluate treatment efficacy against 2 important healthcare-associated pathogens, S. aureus and Pseudomonas aeruginosa. Their data suggest that coating of silicone and titanium surfaces of totally implantable venous access ports with Received 21 April 2014; accepted 23 April 2014; electronically published 1 May 2014. Correspondence: Rodney M. Donlan, PhD, Centers for Disease Control and Prevention, 1600 Clifton Rd NE, Mail Stop C16, Atlanta, GA 30333 ([email protected]). The Journal of Infectious Diseases 2014;210:1345–6 Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2014. Thiswork iswritten by (a) US Government employee(s) and is in the public domain in the US. DOI: 10.1093/infdis/jiu251