Biofilms and Device-Associated Infections

Rodney M. Donlan, Centers for Disease Control and Prevention Atlanta, Georgia, USA.


Emerging Infectious Diseases. 2001;7(2) 

In This Article

Mechanical Heart Valve Biofilms

Microorganisms may attach and develop biofilms on components of mechanical heart valves and surrounding tissues of the heart, leading to a condition known as prosthetic valve endocarditis. The primary organisms responsible for this condition are S. epidermidis, S. aureus, Streptococcus spp., gram-negative bacilli, diphtheroids, enterococci, and Candida spp. These organisms may originate from the skin, other indwelling devices such as central venous catheters, or dental work[3]. The identity of the causative microorganism is related to its source: whether the contaminating organism originated at the time of surgery (early endocarditis, usually caused by S. epidermidis), from an invasive procedure such as dental work (Streptococcus spp.), or from an indwelling device (a variety of organisms). Implantation of the mechanical heart valve causes tissue damage, and circulating platelets and fibrin tend to accumulate where the valve has been attached. Microorganisms also have a greater tendency to colonize these locations[3]. The resulting biofilms more commonly develop on the tissue surrounding the prosthesis or the sewing cuff fabric used to attach the device to the tissue[22,23] than on the valve itself[24]. Antimicrobial agents are usually administered during valve replacement and whenever the patient has dental work to prevent initial attachment by killing all microorganisms introduced into the bloodstream. As with biofilms on other indwelling devices, relatively few patients can be cured of a biofilm infection by antibiotic therapy alone[25]. Illingworth et al.[22] found that a silver-coated sewing cuff on a St. Jude mechanical heart valve (St. Jude Medical Inc., St. Paul, MN) implanted into a guinea pig artificially infected with S. epidermidis produced less inflammation than did uncoated fabric. Although the number of attached organisms was not determined, the authors concluded that the degree of inflammation was proportional to the number of viable organisms. Carrel et al.[23] also found this approach was effective in in vitro studies with different organisms.


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