Antimicrobial-coated CVCs were developed in an effort to mitigate risk of serious CVC-related infections. Meta-analyses have shown that chlorhexidine-silver sulfadiazine CVCs, and particularly minocycline-rifampin CVCs, reduce the risk of CRBSI in prospective, randomized trials [2–4]. We compared data regarding colonization of antimicrobial and standard CVCs with known microorganisms that can cause CRBSI with an aim to investigate any potential vulnerability in the spectrum of antimicrobial activity. We found that chlorhexidine-silver sulfadiazine CVCs may have unique activity in reducing risk of colonization by Acinetobacter species and diphtheroids, but the former finding needs to be confirmed since we detected publication bias. Single study findings suggest that the miconazole-rifampin CVC may reduce the risk of colonization by coagulase-negative staphylococci, while the silver CVC and minocycline-rifampin CVC may be more vulnerable to coliform colonization, but these observations need to be confirmed by future studies. We identified a significant increase in the proportion of Candida species colonization among colonized minocycline-rifampin CVCs. Published clinical trials have not found an increased incidence of CVC-related bloodstream infections due to Candida species but these studies are underpowered to detect such a difference.
Our findings regarding minocycline-rifampin CVC colonization with Candida species, as well as coliforms, support the observations of other investigators [22, 27–29]. Some investigators found significantly less microbial adherence of Enterobacter aerogenes, Escherichia coli, Klebsiella pneumoniae, and C. albicans to chlorhexidine-silver sulfadiazine CVCs compared to non-antimicrobial CVCs but no such difference when minocycline-rifampin CVCs or silver CVCs were tested . Additionally, they found increased microbial adherence of C. albicans to minocycline-rifampin CVCs compared to control CVCs in an in vitro model.
Our study has important limitations. We looked at CVC colonization rather than CVC-related bloodstream infection. However, as previously stated, for endemic intravascular CVC infections, CVC colonization is a prerequisite for bloodstream infection. As such, we feel that our findings have clinical relevance. We were unable to assess differences in CVC colonization based on the anatomic site of CVC insertion as this information was unavailable in the majority of the studies included in our analysis. Another potential weakness was the variable reported use of neutralizers when cultures of antimicrobial CVCs were performed.
Prospective studies and the ensuing meta-analyses have demonstrated the attributes of antimicrobial CVCs. However, we were interested in further understanding potential unintended consequences of widespread use of such devices. The data presented herein suggest that some antimicrobial CVCs may not reduce risk of CVC infections due to Candida or coliforms compared to uncoated CVCs despite showing overall benefit in clinical trials. As such, clinicians should weigh potential risks and benefits when contemplating use of specific antimicrobial CVCs in patients with prior colonization or infection due to these pathogens or when the patients are located in clinical areas where these microorganisms are endemic. Novel CVCs combining components of previously studied catheters have been demonstrated to have broader antimicrobial coverage and may well be less prone to colonization with select microorganisms as demonstrated in our investigation .