Prosthetic Joint Infection (2005)

There is no current consensus in the orthopaedic surgery or infectious diseases communities as to what constitutes definitive evidence of prosthetic joint infection. Prosthesis infection may be easy to identify, particularly if there is a sinus tract communicating with the prosthesis, if purulence is present on aspiration of the joint or at the time of surgery, or if multiple cultures taken from periprosthetic tissue or fluid yield the same microorganism. However, many prosthetic joint infections present with isolated joint pain and prosthesis failure or loosening which can be attributed to multiple etiologies, including infection.7 Even if a microorganism is grown from periprosthetic tissues, one may not be entirely certain that infection is present, because the typical pathogens that cause prosthetic joint infection are also normal skin flora (eg, coagulase-negative staphylococci) and therefore also may be intraoperative or laboratory contaminants. Furthermore, it is clear that in biofilm-associated infections such as prosthetic joint infection, the microorganisms that live within the biofilm may be difficult to identify using routinely available culturing techniques and therefore microbiologic results alone may be insufficient to rule out infection as a source of prosthesis failure.8,9 This situation makes patient treatment very difficult. An accurate diagnosis as to the reason for prosthesis failure is key to appropriate treatment strategies. Because of these current diagnostic difficulties, current definitions of prosthetic joint infection used by clinicians to diagnose and to treat prosthetic joint infection are derived from multiple sources of clinical information, none of which can be relied on as a gold standard. This information is obtained from the available history and physical examination of the patient, as well as results from the clinical and microbiology laboratory, radiographic tests and/or pathologic examination of periprosthetic tissue for evidence of infection surrounding the prosthesis.1,3,5,6,7 Some investigators have used combinations of clinical data and test results in an attempt to identify the presence of infection accurately, but none of these schemes has been prospectively validated against an agreed on gold-standard definition of infection.2,7 The realization by workshop participants of the difficulties in the diagnosis of joint prosthesis infection and the knowledge after the workshop presentations that new more sensitive and specific tools soon will be available to identify microbes associated with a biofilm on joint prostheses more accurately, convinced participants of the importance of attempting to reach consensus regarding a proposed criteria for future definitions of prosthetic joint infection. Criteria Participants were able to reach consensus on the following criteria that they think future definitions of prosthetic infection should fulfill (Table 1). Participants considered that the use of these criteria might be easy to fulfill in many clinical situations (eg, a patient with Staphylococcus aureus bacteremia, purulence surrounding a loose prosthesis, and multiple cultures of periprosthetic tissue that yield S. aureus). They thought, however, that their use will be increasingly important as more sensitive methods of identifying microbes on prostheses are validated and become routinely available and microbes are identified in clinical situations not previously associated with infection.4,8,9Table 1: Criteria for Future Definitions of Prosthetic Joint InfectionThe proposed criteria require three pieces of information. The first is that the prosthesis is dysfunctional (eg, loosening) in some way. Second, a microorganism or its associated biofilm, as detected by a diagnostic test, must be identified on the prosthesis itself or in periprosthetic tissue. Participants noted that new diagnostic techniques might include tests for identifying biofilm on the prosthesis itself, microorganisms within that biofilm, or host responses to microorganisms on the prosthesis. Because of the increasing use of these very sensitive tests participants noted that it is likely that some patients that would previously have been considered to have aseptic loosening may actually have prosthetic joint infection. This possibility was discussed in detail at the workshop by Sheila Patrick and Gregory McLorinan, who reviewed their group’s previously published work showing that, at the time of revision hip arthroplasty surgery, up to 63% of 120 hip arthroplasties at their institution had a microbe identified on the prosthesis using immunofluorescence microscopy, often without other clinical evidence to support infection.8,9 What the workshop participants, including the investigators, questioned was whether the prosthesis dysfunction that led to revision arthroplasty in their study was caused by these organisms on the prosthesis or whether the biofilm-associated organisms were “innocent bystanders.” It was noted that a patient having a functional prosthesis after revision surgery for a prolonged period of time without specific local or systemic antimicrobial therapy would not in itself prove the hypothesis that infection was the cause of the prosthesis dysfunction. The surgery itself might be therapy for the infection. This difficulty led to a discussion of the lack of data regarding the natural history of biofilms on joint prostheses and the plausibility of the hypothesis that biofilm organisms may colonize a prosthesis for long periods of time without ever leading to associated symptoms or signs of prosthesis infection. All agreed that currently available data do not answer this question definitively. The final portion of the breakout session discussion centered on the third piece of information that should be required to authoritatively state that prosthesis “infection” as opposed to asymptomatic “colonization” is present. Participants thought that the other piece of required information was evidence that the etiology of the prosthesis dysfunction was the microbe on the prosthesis creating an abnormal host response that then led to prosthesis dysfunction. Participants thought that satisfying this part of the workshop criteria would require identifying virulence factors produced by microbes in biofilms that lead to pathologic host responses that then subsequently are shown to be the etiology prosthesis dysfunction (eg, loosening). Participants agreed that additional research in this area is necessary before these criteria can be satisfied on a routine basis for all patients with potential prosthetic joint infection. Until this time, the clinical judgments of the orthopaedist and infectious-diseases physician caring for these patients will need to be relied on to distinguish prosthesis infection, colonization, and culture contamination.