Hostname: page-component-cd9895bd7-8ctnn Total loading time: 0 Render date: 2024-12-22T15:04:06.415Z Has data issue: false hasContentIssue false
  • English
  • Français

Virulence of Staphylococcus epidermidis in a mouse model: significance of extracellular slime

Published online by Cambridge University Press:  15 May 2009

M. A. Deighton ,
R. Borland  and
J. A. Capstick
M. A. Deighton
Affiliation:
Department of Applied Biology and Biotechnology
R. Borland
Affiliation:
Faculty of Biomedical and Health Sciences, Royal Melbourne Institute of Technology, 124 LaTrobe St, Melbourne 3000, Australia
J. A. Capstick
Affiliation:
Department of Applied Biology and Biotechnology
Rights & Permissions [Opens in a new window]

Summary

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

The ability to produce large quantities of bioflim on solid surfaces in vitro is believed to distinguish potentially pathogenic strains of Staphylococcus epidermidis from commensals. Bioflim consists of staphylococcal cells encased in a matrix of extracellular polysaccharide (also referred to as slime), firmly adherent to each other and to the underlying surface structure. The association of slime with colonization of catheter surfaces in vivo has been examined extensively. Less attention has been paid to the contribution of slime to infections that occur in the absence of an inserted device. In a mouse model of subcutaneous infection without an implanted device 10 S. epidermidis strains (5 slime-positive, 5 slime-negative) produced abscesses; thus a foreign body is not essential for the expression of virulence by S. epidermidis. Biofilm-positive strains produced significantly more abscesses, that persisted longer than biofilm-negative strains. In these chronic infections, large numbers of staphylococci were associated with macrophages and viable staphylococci were cultured from specimens of pus collected at autopsy. Thus slime or components of slime appear to delay the clearance of S. epidermidis from host tissues, possibly by interfering with intracellular killing mechanisms. However, differences in the capacity to produce abscesses, within both the slime-positive and slime-negative groups, indicate that other factors also contribute to the virulence of S. epidermidis.

Type
Research Article
Information
Epidemiology & Infection , Volume 117 , Issue 2 , October 1996 , pp. 267 - 280
Copyright
Copyright © Cambridge University Press 1996

References

1.Jarvis, WR, Martone, WJ. Predominant pathogens in hospital infections. J Antimicrob Chemother (Suppl. A) 1992; 29: 19–24.Google Scholar
2.Christensen, GD. The confusing and tenacious coagulase-negative staphylococci. Adv Intern Med 1987; 32: 177–92.Google ScholarPubMed
3.Fleer, A, Senders, RC, Visser, MR et al. Septicemia due to coagulase-negative staphylococci in a neonatal intensive care unit: clinical and bacteriological features and contaminated parenteral fluids as a source of sepsis. Pediatr Infect Dis 1983; 2: 426–31.Google Scholar
4.Christensen, GD, Simpson, WA, Bisno, AL, Beachey, EH. Adherence of slime-producing strains of Staphylococcus epidermidis to smooth surfaces. Infect Immun 1982; 37: 318–26.CrossRefGoogle ScholarPubMed
5.Peters, G, Locci, R, Pulverer, G. Adherence and growth of coagulase-negative staphylococci on surfaces of intravenous catheters. J Infect Dis 1982; 146: 479–82.CrossRefGoogle ScholarPubMed
6.Goldmann, DA, Pier, GB. Pathogenesis of infections related to intravascular catheterization. Clin Microbiol Rev 1993; 6: 176–92.CrossRefGoogle ScholarPubMed
7.Arp, LH. Bacterial infection of mucosal surfaces: an overview of cellular and molecular mechanisms. In: Roth, JA, Virulence mechanisms of bacterial pathogens. Washington DC: American Society for Microbiology. 1988: 3–27.Google Scholar
8.Peters, G. New considerations in the pathogenesis of coagulase-negative staphylococcal foreign body infections. J Antimicrob Chemother 1988; 21 (Suppl. C): 139–48.CrossRefGoogle ScholarPubMed
9.Christensen, GD, Baddour, LM, Hasty, DL, Lowrance, JH, Simpson, WA. Microbial and foreign body factors in the pathogenesis of medical device infections. In: Bisno, AL, Waldvogel, FA, eds. Infections associated with indwelling medical devices. Washington DC: American Society for Microbiology, 1989: 27–59.Google Scholar
10.Bayston, R, Rodgers, J. Production of extra-cellular slime by Staphylococcus epidermidis during stationary phase of growth: its association to adherence to implantable devices. J Clin Pathol 1990; 43: 866–70.CrossRefGoogle ScholarPubMed
11.Deighton, MA, Borland, R. Regulation of slime production in Staphylococcus epidermidis by iron. Infect Immun 1993; 61: 4473–9.CrossRefGoogle ScholarPubMed
12.Dickinson, GM, Bisno, AL. Infections associated with indwelling devices: concepts of pathogenesis; infections associated with intravascular devices. Antimicrob Agents Chemother 1989; 33: 597–601.CrossRefGoogle ScholarPubMed
13.Johnson, GM, Lee, DA, Regelmann, ED, Gray, ED. Interference with granulocyte function by Staphylococcus epidermidis slime. Infect Immun 1986; 54: 13–20.CrossRefGoogle ScholarPubMed
14.Noble, MA, Reid, PE, Park, CM, Chan, VYH. Inhibition of human neutrophil bactericidal activity by extra- cellular substance from slime-producing Staphylococcus epidermidis. Diagn Microbiol Infect Dis 1986; 4: 335–9.Google Scholar
15.Kristinsson, KG, Hastings, JGM, Spencer, RC. The role of extracelluar slime in opsonophagocytosis of Staphylococcus epidermidis. J Med Microbiol 1988; 27: 207–13.Google Scholar
16.van Bronswijk, H, Verbrugh, HA, Heezius, HCJM et al. Heterogeneity in opsonic requirements of Staphylococcus epidermidis: relative importance of surface hydrophobicity, capsules and slime, Immunology 1989; 67: 81–6.Google ScholarPubMed
17.Christensen, GD, Baddour, LM, Parisi, JT et al. Colonial morphology of staphylococci on Memphis agar: phase variation of slime production, resistance to β-lactam antibiotics, and virulence. J Infect Dis 1990; 161: 1153–69.Google Scholar
18.Myrvik, QN, Wagner, W, Barth, E., Wood, P, Gristina, AG. Effects of extracellular slime produced by Staphylococcus epidermidis on oxidative responses of rabbit alveolar macrophages. J Invest Surg 1989; 2: 381–9.CrossRefGoogle ScholarPubMed
19.Stout, RD, Ferguson, KP, Li, Y-N, Lambe, DW. Staphylococcal exopolysaccharides inhibit lymphocyte proliferative responses by activation of monocyte prostaglandin production. Infect Immun 1992; 60: 922–7.Google Scholar
20.Christensen, GD, Simpson, WA, Bisno, AL, Beachey EH. Experimental foreign body infections in mice challenged with slime-producing Staphylococcus epidermidis. Infect Immun 1983; 40: 407–10.Google Scholar
21.Christensen, GD, Baddour, LM, Simpson, WA. Phenotypic variation of Staphylococcus epidermidis slime production in vitro and in vivo. Infect Immun 1987; 55: 2870–7.CrossRefGoogle ScholarPubMed
22.Barth, E, Myrvik, QM, Wagner, W, Gristina, AG. In vitro and in vivo comparative colonization of Staphylococcus aureus and Staphylococcus epidermidis on orthopaedic implant materials. Biomaterials 1989; 10: 325–8.Google Scholar
23.Patrick, CC, Plaunt, MR, Hetherington, SV, May, SM. Role of Staphylococcus epidermidis slime layer in experimental tunnel tract infections, Infect Immun 1992; 60: 1363–7.Google Scholar
24.Patrick, CC, Hetherington, SV, Roberson, PK, Henwick, S, Sloas, MM. Comparative virulence of Staphylococcus epidermidis in a murine catheter model. Pediat Res; 37: 70–4.CrossRefGoogle Scholar
25.Christensen, GD, Parisi, JT, Bisno, AL, Simpson, WA, Beachey, EH. Characterization of clinically significant strains of coagulase-negative staphylococci. J Clin Microbiol 1983; 18: 258–69.Google Scholar
26.Deighton, M, Pearson, S, Capstick, J, Spelman, D, Borland, R. Phenotypic variation of Staphylococcus epidermidis isolated from a patient with native valve endocarditis. J Clin Microbiol 1992; 30: 2385–90.CrossRefGoogle ScholarPubMed
27.Deighton, MA, Capstick, J, Borland, R. A study of phenotypic variation of Staphylococcus epidermidis using Congo red agar. Epidemiol Infect 1992; 108: 423–423.CrossRefGoogle Scholar
28.Kloos, WE, Lambe, DW. Staphylococcus. In: Balows, A, Hausler, WJ JrHerrmann, KL, Isenberg, HD, Shadomy, H, eds. Manual of clinical microbiology. Washington DC: American Society for Microbiology, 1991:222–37.Google Scholar
29.Schleifer, KH. Gram-positive cocci In: Sneath, PHA, Mair, NS, Sharpe, ME, Hold, JG, eds. Bergey's manual of systematic microbiology, Baltimore: Williams and Wilkins, 1989: 999–1103.Google Scholar
30.Hébert, GA, Hancock, GA. Synergistic hemolysis exhibited by species of staphylococci. J Clin Microbiol 1985; 22: 409–15.CrossRefGoogle ScholarPubMed
31.Nash, P.Krenz, MM. Culture media. In: Balows, A, Hausler, WJ Jr, Hermann, KL, Isenberg, HD, Shadomy, HJ. eds. Manual of Clinical Microbiology. Washington DC: American Society for Microbiology, 1991: 1226–88.Google Scholar
32.Devriese, LA, Laevens, H, Haesebrouck, F, Hommez, J. A simple identification scheme for coagulase-negative staphylococci from bovine mastitis. Res Vet Sci 1994; 57: 240–4.Google Scholar
33.Ferguson, DA, Veringa, EM, Mayberry, WR, Overbeek, BP, Lambe, DW, Verhoef, J. Bacteroides and Staphylococcus glycocalyx: chemical analysis, and the effects of chemiluminescence and chemotaxis of human polymorphonuclear leucocytes. Microbios 1992; 69: 53–65.Google ScholarPubMed
34.Cooper, GL, Schiller, AL, Hopkins, CC. Possible role of capillary action in pathogenesis of experimental catheter-associated dermal tunnel infections. J Clin Microbiol 1988; 26: 8–12.Google Scholar
35.Lambe, DW, Ferguson, KP, Keplinger, JL, Gemmell, CG, Kalbfleisch, JH. Pathogenicity of Staphylococcus lugdunensis, Staphylococcus schleiferi, and three other coagulase-negative staphylococci in a mouse model and possible virulence factors. Can J Microbiol 1990; 36: 455–63.CrossRefGoogle Scholar
36.Timmerman, CP, Fleer, A, Besnier, JM, deGraaf, L, Cremers, F, Verhoef, J. Characterization of a proteinaceous adhesin of Staphylococcus epidermidis which mediates attachment to polystyrene. Infect Immun 1991;59: 4187–92.CrossRefGoogle ScholarPubMed
37.Herrmann, M, Vaudaux, PE, Pittet, D et al. Fibronectin, fibrinogen and laminin act as mediators of adherence of clinical staphylococcal isolates to foreign material. J Infect Dis 1988; 158: 693–701.Google Scholar
38.Tojo, M, Yamashita, N, Goldmann, DA, Pier, GB. Isolation and characterization of a capsular polysaccharide adhesin from Staphylococcus epidermidis. J Infect Dis 1988; 157: 713–22.Google Scholar
39.Takeda, S, Pier, GB, Kojima, Y et al. Protection against endocarditis due to Staphylococcus epidermidis by immunization with capsular polysaccharide/adhesin. Circulation 1991; 84: 2539–46.CrossRefGoogle ScholarPubMed
40.Christensen, GD, Barker, LP, Mawhinney, TP, Baddour, LM, Simpson, WA. Identification of an antigenic marker of slime production for Staphylococcus epidermidis. Infect Immun 1990; 58: 2906–11.CrossRefGoogle ScholarPubMed
41.Mack, D, Siemssen, N, Laufs, R. Parallel induction by glucose of adherence and a polysaccharide antigen specific for plastic-adherent Staphylococcus epidermidis: evidence for functional relation to intercellular adhesion. Infect Immun 1992; 60: 2048–57.Google Scholar
42.Muller, E, Hübner, J, Gutierrez, N, Takeda, S, Goldmann, DA, Pier, GB. Isolation and characterization of transposon mutants of Staphylococcus epidermidis deficient in capsular polysacharide/adhesin and slime. Infect Immun 1993; 61: 551–8.CrossRefGoogle Scholar
43.Finlay, BB, Falkow, S. Common themes in microbial pathogenicity. Microbiol Rev 1989; 53: 210–30.CrossRefGoogle ScholarPubMed