Fibronectin Is More Active than Fibrin or Fibrinogen in Promoting Staphylococcus aureus Adherence to Inserted Intravascular Catheters

Abstract

To further define the role offibrin(ogen) and fibronectin in Staphylococcus aureusadherence to central venous catheters, the amount, chemical integrity, and biologic activity of these proteins adsorbed on lines inserted in hospitalized patients were prospectively studied. Polyurethane cannulas promoted a significantly lower adherence of S. aureusthan polyvinyl chloride (P < .01) or Hickman (P < .001) cannulas and contained the lowest amount of immunologically assayed fibronectin but not offibrin(ogen). Fibrinogen showed an extensive loss of adherence-promoting activity on inserted cannulas, which was related to its proteolytic breakdown, as detected by SDS-PAGE and immunoblots with antifibrinogen antibodies and confirmed by in vitro studies with purified protein fragments. In contrast, either intact or fragmented fibronectin, although present in much lower amounts than fibrin(ogen), could actively promote S. aureus adherence onto intravenous catheters.Microbial colonization of intravascular devices is an important source of nosocomial infection and sepsis [1,2]. Such device-related infections are frequently due to staphylococci and represent a major risk to the patients receiving intravenous (iv) therapy [I, 2]. Several factors may explain the frequent colonization of iv devices by Staphylococcus aureus, Staphylococcus epidermidis, or other species ofcoagulase-negative staphylococci: First, the presence ofa transcutaneous cannula wound allowing skin microorganisms to migrate across the skin barrier [1,2]; second, the microbial production of mucoid exopolymeric substances enhancing the stickiness of colonizing organisms [3][4][5][6]; and third, the presence of plasma proteins adsorbed on iv devices, which might selectively promote staphylococcal attachment to their surfaces [7][8][9][10].We have reported that plasma proteins deposited on various categories of iv catheters removed from patients played a significant role in staphylococcal adherence [11]. Clinical isolates of S. aureus were more strongly promoted for adherence by cannula-adsorbed plasma proteins than clinical isolates of S. epidermidis [11]. This observation was explained in part by the more frequent occurrence ofclinical [8,12,13] 1993;167:633-41 of S. epidermidis on surface determinants recognizing some major plasma or matrix proteins, such as fibronectin [8,[10][11][12][14][15][16][17][18], fibrinogen [9,16,[19][20][21], collagen [13, 17], laminin [8, 17, 22], or vitronectin [23]. Each of these individual proteins is known to promote staphylococcal adherence when adsorbed in vitro on polymeric surfaces [8][9][10]. In our in vivo study, we also found that on cannulas inserted in patients, most of the adherence-promoting activity was mediated via surface-bound fibronectin and fibrinogen or fibrin [11]. However, the respective roles of each of these protein components in staphylococcal adherence could not be precisely evaluated [11].The objectives ofthis study were to quantify the respective content of surface-bound fibronectin versus fibrinoge...

Nonvalvular Cardiovascular Device–Related Infections

“…There are several S aureus adhesins [5][6][7][8][9] that are operative in the binding of microorganisms to extracellular and host plasma proteins that coat the surface of indwelling medical devices. These host proteins are exposed in areas where endothelium has been denuded by contact with or attachment to indwelling devices.…”

Bacterial fibronectin-binding proteins and endothelial cell surface fibronectin mediate adherence of Staphylococcus aureus to resting human endothelial cells

“…The fibrinogen-binding protein ClfA and collagen-binding protein have been shown to be important in the pathogenesis of experimental endocarditis (Moreillon et al, 1995 ;Hienz et al, 1996). The fibronectin-and fibrinogen-binding proteins of S. aureus promote bacterial attachment to plasma clots (Raja et al, 1990 ;Moreillon et al, 1995), and to plastic coated with these host proteins in vitro and ex vivo (Vaudaux et al, 1989(Vaudaux et al, , 1993Greene et al, 1995). It is possible that these observations have direct relevance to the mechanisms by which S. aureus adheres to host cells, given that endothelial cells synthesize and incorporate fibronectin into the extracellular matrix, and secrete it into the culture medium when grown in vitro (Jaffe & Mosher, 1978).…”

Tracking adhesion factors in Staphylococcus caprae strains responsible for human bone infections following implantation of orthopaedic material

“…The routine use of molecular methods to identify staphylococci at the species level (Chesneau et al, 1992(Chesneau et al, , 1993De Buyser et af., 1989 led to the detection, in our reference centre, of 10 S. caprae strains from four patients suffering from bone and joint infections following the implantation of orthopaedic material. The aim of this study was to characterize these ten strains and four unrelated S. caprae strains isolated from the milk of mastitis-free goats and, in particular, to track the adhesion factors or genes that have been shown to be implicated in the pathogenesis of staphylococci (Bedidi-Madani et al, 1998a;Christensen et al, 1983 ;Deighton et al, 1996 ;Greene et al, 1995 ;Heinz et a/., 1996;Hell et al, 1998;Moreillon et al, 1995;Patti et al, 1994;Rupp et al, 1998;Vaudaux et al, 1993).…”