FimA, a major virulence factor associated with Streptococcus parasanguis endocarditis

D. Burnette-Curley, V. Wells, H. Viscount, Cindy Munro, J. C. Fenno, P. Fives- Taylor, F. L. Macrina

Research output: Contribution to journalArticle

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Abstract

Adherence of microorganisms to damaged heart tissue is a crucial event in the pathogenesis of infective endocarditis. In the present study, we investigated the role of the FimA protein as a potential virulence factor associated with Streptococcus parasanguis endocarditis. FimA is a 36-kDa surface protein that is a recognized adhesin in the oral cavity where it mediates adherence to the salivary pellicle. An insertion mutant and a deletion mutant of S. parasanguis were employed in the rat model of endocarditis to determine the relevance of FimA in endocarditis pathogenesis. Catheterized rats were infected with either the fimA deletion mutant VT929, the fimA insertion mutant VT930, or the isogenic, wild-type S. parasanguis FW213. Rats inoculated with FW213 developed endocarditis more frequently (50.9%) than animals inoculated with either the deletion mutant (2.7%) or the insertion mutant (7.6%) (P < 0.001). A series of in vitro assays were performed to explore the mechanism(s) by which FimA enhanced the infectivity of S. parasanguis. FimA did not inhibit the uptake or the subsequent killing of S. parasanguis by phagocytic granulocytes. Similarly, FimA did not play a role in the adherence to or the aggregation of platelets. Significant differences were noted between FW213 and VT929 (P < 0.05) and FW213 and VT930 (P < 0.001) in their abilities to bind to fibrin monolayers. The mean percent adherence of FW213 to fibrin monolayers (2.1%) was greater than those of VT929 (0.5%) and VT930 (0.12%). Taken together, these results indicate that FimA is a major virulence determinant associated with S. parasanguis endocarditis and further suggest that its role is associated with initial colonization of damaged heart tissue.

Original languageEnglish (US)
Pages (from-to)4669-4674
Number of pages6
JournalInfection and Immunity
Volume63
Issue number12
StatePublished - Jan 1 1995
Externally publishedYes

Fingerprint

Virulence Factors
Endocarditis
Streptococcus
Fibrin
Dental Pellicle
Platelet Aggregation
Granulocytes
Virulence
Mouth
Membrane Proteins
Proteins

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases

Cite this

Burnette-Curley, D., Wells, V., Viscount, H., Munro, C., Fenno, J. C., Fives- Taylor, P., & Macrina, F. L. (1995). FimA, a major virulence factor associated with Streptococcus parasanguis endocarditis. Infection and Immunity, 63(12), 4669-4674.

FimA, a major virulence factor associated with Streptococcus parasanguis endocarditis. / Burnette-Curley, D.; Wells, V.; Viscount, H.; Munro, Cindy; Fenno, J. C.; Fives- Taylor, P.; Macrina, F. L.

In: Infection and Immunity, Vol. 63, No. 12, 01.01.1995, p. 4669-4674.

Research output: Contribution to journalArticle

Burnette-Curley, D, Wells, V, Viscount, H, Munro, C, Fenno, JC, Fives- Taylor, P & Macrina, FL 1995, 'FimA, a major virulence factor associated with Streptococcus parasanguis endocarditis', Infection and Immunity, vol. 63, no. 12, pp. 4669-4674.
Burnette-Curley D, Wells V, Viscount H, Munro C, Fenno JC, Fives- Taylor P et al. FimA, a major virulence factor associated with Streptococcus parasanguis endocarditis. Infection and Immunity. 1995 Jan 1;63(12):4669-4674.
Burnette-Curley, D. ; Wells, V. ; Viscount, H. ; Munro, Cindy ; Fenno, J. C. ; Fives- Taylor, P. ; Macrina, F. L. / FimA, a major virulence factor associated with Streptococcus parasanguis endocarditis. In: Infection and Immunity. 1995 ; Vol. 63, No. 12. pp. 4669-4674.
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abstract = "Adherence of microorganisms to damaged heart tissue is a crucial event in the pathogenesis of infective endocarditis. In the present study, we investigated the role of the FimA protein as a potential virulence factor associated with Streptococcus parasanguis endocarditis. FimA is a 36-kDa surface protein that is a recognized adhesin in the oral cavity where it mediates adherence to the salivary pellicle. An insertion mutant and a deletion mutant of S. parasanguis were employed in the rat model of endocarditis to determine the relevance of FimA in endocarditis pathogenesis. Catheterized rats were infected with either the fimA deletion mutant VT929, the fimA insertion mutant VT930, or the isogenic, wild-type S. parasanguis FW213. Rats inoculated with FW213 developed endocarditis more frequently (50.9{\%}) than animals inoculated with either the deletion mutant (2.7{\%}) or the insertion mutant (7.6{\%}) (P < 0.001). A series of in vitro assays were performed to explore the mechanism(s) by which FimA enhanced the infectivity of S. parasanguis. FimA did not inhibit the uptake or the subsequent killing of S. parasanguis by phagocytic granulocytes. Similarly, FimA did not play a role in the adherence to or the aggregation of platelets. Significant differences were noted between FW213 and VT929 (P < 0.05) and FW213 and VT930 (P < 0.001) in their abilities to bind to fibrin monolayers. The mean percent adherence of FW213 to fibrin monolayers (2.1{\%}) was greater than those of VT929 (0.5{\%}) and VT930 (0.12{\%}). Taken together, these results indicate that FimA is a major virulence determinant associated with S. parasanguis endocarditis and further suggest that its role is associated with initial colonization of damaged heart tissue.",
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