Host Factors Selectively Increase Staphylococcal Adherence on Inserted Catheters: A Role for Fibronectin and Fibrinogen or Fibrin

Abstract

Intravascular catheters are prone to staphylococcal infections. To study the role in staphylococcal adherence played by fibrinogen or fibrin and fibronectin deposited on inserted catheters, 187 peripheral or central cannulae were prospectively removed from hospitalized patients. Compared with uninserted catheters, which allowed only minimal adherence, previously inserted catheters promoted significant adherence of staphylococcal isolates from patients with intravenous device infections. Adhesion-promoting properties were studied with laboratory strains having well-defined affinities for either fibronectin or fibrinogen:· adherence of Staphylococcus aureus Cowan I, which has the highest affinity for both adhesins, was more strongly promoted (10-to 50-fold) on inserted cannulae than was that of S. aureus Wood 46 (4-to lO-fold) or Staphylococcus epidermidis Rp 12 (2.2-fold), which has no affinity for fibrinogen but does for fibronectin. Although all types of cannulae contained significant amounts of fibrin, which may promote adherence of coagulase-positive staphylococci, results obtained with coagulase-negative isolates suggested that in vivo-deposited fibronectin is also a critical determinant in this process.Infectious complications associated with the use of intravascular (iv) catheters have been reported to occur in 1070-40070 of cases [1][2][3]; these devices are important causes of nosocomial sepsis (1,(3)(4)(5) and candidemia [3,5]. A major contributing factor in iv device-related infection is the transcutaneous cannula wound allowing microorganisms from the patient's skin flora to migrate across the skin barrier. The microbial colonization of the transcutaneous part of the catheter has been identified as a sensitive index of catheter-associated bacteremia [6]. The establishment of a fibrin sheath [1] surrounding the blood-exposed cannula may favor bacterial attachment and promote bacterial replication around the intravascular part of the catheter. The thrombogenicity of plastic materials plays a role in their associ- ation with device-related infections [7]; the risks of phlebitis increase with duration of insertion and severity of underlying diseases [8]. Finally, impaired host mechanisms secondary to the presence of foreign implants might playa role in catheter-associated infections as for other implants [9].Intravenous catheters are most often colonized by staphylococci [6,[10][11][12]. Staphylococcus aureus was initially considered the predominant species in cannula-related septicemia, and Staphylococcus epidermidis has recently been identified as a major pathogen of these infections [13,14]. A number of studies [15][16][17][18][19][20][21][22][23][24] have shown that most coagulasenegative strains of staphylococci infecting intravascular lines produce an extracellular fibrous matrix, designated either as slime [15][16][17][19][20][21][22] or glycocalix [18,23,24]. This material is assumed to help coagulase-negative staphylococci colonize the indwelling devices [15][16][17][18][19][20][21][22][23][24][2...

Insertional Inactivation of eap in Staphylococcus aureus Strain Newman Confers Reduced Staphylococcal Binding to Fibroblasts

“…X13404), and a 70-kDa (23) or Newman, but appear as the most prominent protein in SDS-PAGE. However, work with mutants deficient in fnbA and fnbB (13,34), as well as with mutants deficient in clfA and clfB (5) or cna (27), clearly demonstrates that the latter adhesins are the major structures pivotal for functional binding of their respective matrix ligands. In this respect, the successful construction of a ⌬eap mutant for the first time allowed us to more precisely characterize the role of Eap.…”

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).…”

Localization and characterization of the ligand-binding domain of the fibrinogen-binding protein (FgBP) of Streptococcus equi subsp. equi

“…mechanism by which streptococci resist phagocytosis remains controversial, Fg binding to M protein does appear to play a role in resistance to phagocytosis for several strains of Streptococcus pyogenes (Courtney et al, 1997 ;Kehoe, 1994 ;Navarre & Schneewind, 1999 ;Poirier et al, 1989 ;Whitnack & Beachey, 1982, 1985. On the other hand, Fg binding to Staphylococcus aureus has been shown to be important in the initiation of infections of implanted medical devices and surgical wounds by promoting bacterial attachment (Herrmann et al, 1993 ;Moreillon et al, 1995 ;Vaudaux et al, 1989Vaudaux et al, , 1995.…”