Overview of the Microbiology

Introduction

In his 1920 commentary in the British Journal of Surgery , Lord Berkeley Moynihan commented, “Every operation in surgery is an experiment in bacteriology.” What the renowned surgeon was implying was the fact that all surgical wounds are in fact contaminated by bacteria. These bacteria may be harmless flora with minimal threat of infection or they may be dangerous virulent pathogens that can jeopardize the success of a procedure. Moynihan’s statement continues to hold merit even in the modern world of medicine, because in many instances we remain uncertain as to why surgical infections occur. Nonetheless, substantial developments in microbiology as well as improvements in safety and control in the operating room have led surgical procedures to become much less of the “experiment” they once were.

From a microbiologic viewpoint, true infection after surgery occurs when the dose of a given bacteria with its innate virulence factors is able to overcome the host defenses in place to prevent the infection. These host defenses are highly variable from person to person, and in part this explains why some patients are able to use immune factors to withstand clinical infection whereas others end up with failed surgical outcomes. Additionally, we are just beginning to recognize that not all infections may be considered the same. In combination with patient factors and immune status, varying bacteriologic properties across and even within a microorganism species affect the potential for infection after any type of surgical procedure.

Infection of joint replacement prostheses is a highly studied yet persistent and devastating complication of total joint arthroplasty (TJA). This chapter discusses properties of biofilm formation on prosthetic implants, common microorganisms responsible for periprosthetic joint infection (PJI), emergence of antibiotic resistance, and the effect that microbiology ultimately has on treatment options.

Biofilm

Deep infection of the joint is an extraordinarily difficult complication after TJA. Years of research on the pathogenesis of PJI have led to the idea of the bacterial “biofilm” to explain why these infections are so persistent and difficult to treat after orthopedic procedures. Although biofilm formation is undoubtedly not unique to infection of orthopedic implants, by now it is a well-accepted concept used to elucidate the resilience of bacterial virulence mechanisms in PJI.

In basic science research models, bacterial adherence to implant material serves as the basis of biofilm formation. In general, bacteria may use both host proteins and their own virulence factors to promote adhesion of quickly aggregating pathogens, which, when encased in a matrix of polysaccharides and proteins, form the thick, slimy layer known as a biofilm.

It is out of the scope of this chapter to delve deeply into the specific cell proteins and polysaccharides that assist with bacterial virulence and pathogenicity. Even so, it should be noted that in recent decades the boom in genomic and then proteomic scientific research endeavors has led to discovery of many genes and proteins responsible for the invasive, fibrinolytic, and adhesive properties of infectious bacteria. Scanning electron microscopy has allowed detection of both the adherence phase, during which rapidly layering bacteria attach to polymer material, and the subsequent accumulation phase, during which bacteria proliferate and form multilayered clusters embedded in extracellular material. By creating this environment within the joint and around the implant, bacteria are ostensibly able to switch their metabolism from free-floating planktonic to sessile surface growth via quorum-sensing signals.

The important clinical role of the biofilm is in its promotion of insidious bacterial growth as well as the more dangerous resistance to cellular, humoral, and antibacterial insults. It has been shown repeatedly now that biofilm bacteria are 1000 times more resistant to antibiotic administration than their planktonic counterparts, as shown by their much higher minimal inhibitory concentrations in vitro. In particular, Staphylococcus strains are able to form some of the most resistant biofilms. Not only are biofilm bacteria more difficult to treat, but their adhesive property makes them much more difficult to detect, frequently yielding negative Gram stain and culture results despite clinical signs of infection. Further, these slimy layers may even persist as a nidus for sporadic infection from which recurrent exacerbations of infection can arise in the future ( Fig. 32.1 ).

Although several studies have replicated biofilm formation in vitro, only a few studies have definitively demonstrated the existence of bacterial biofilm directly on freshly removed implant surfaces. Some scientists now say that biofilms can form not only on polymer surfaces of foreign materials but also on surrounding bone cement and innate host tissue as a potential reservoir for future infection. Regardless of the area of biofilm formation deep within the joint, the stark reality currently is that prosthetic infection will not clear without removal of the implants, thorough irrigation and débridement of surrounding tissues, and administration of antibiotics. The future of PJI will surely center on preventing bacterial biofilm formation, and exciting research on topics such as quorum-sensing inhibition is already under way.