Contribution of the interaction of Streptococcus mutans serotype k strains with fibrinogen to the pathogenicity of infective endocarditis

Streptococcus mutans, a pathogen responsible for dental caries, is occasionally isolated from the blood of patients with bacteremia and infective endocarditis (IE). Our previous study demonstrated that serotype k-specific bacterial DNA is frequently detected in S. mutans-positive heart valve specime...

Full description

Saved in:
Bibliographic Details
Published in:Infection and immunity 2014-12, Vol.82 (12), p.5223-5234
Main Authors: Nomura, Ryota, Otsugu, Masatoshi, Naka, Shuhei, Teramoto, Noboru, Kojima, Ayuchi, Muranaka, Yoshinori, Matsumoto-Nakano, Michiyo, Ooshima, Takashi, Nakano, Kazuhiko
Format: Article
Language:English
Subjects:
Animals
Bacterial Infections
Disease Models, Animal
Endocarditis - microbiology
Endocarditis - pathology
Fibrinogen - metabolism
Host-Pathogen Interactions
Humans
Male
Platelet Aggregation
Protein Binding
Rats, Sprague-Dawley
Serogroup
Streptococcus mutans
Streptococcus mutans - metabolism
Streptococcus mutans - pathogenicity
Virulence
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Streptococcus mutans, a pathogen responsible for dental caries, is occasionally isolated from the blood of patients with bacteremia and infective endocarditis (IE). Our previous study demonstrated that serotype k-specific bacterial DNA is frequently detected in S. mutans-positive heart valve specimens extirpated from IE patients. However, the reason for this frequent detection remains unknown. In the present study, we analyzed the virulence of IE from S. mutans strains, focusing on the characterization of serotype k strains, most of which are positive for the 120-kDa cell surface collagen-binding protein Cbm and negative for the 190-kDa protein antigen (PA) known as SpaP, P1, antigen I/II, and other designations. Fibrinogen-binding assays were performed with 85 clinical strains classified by Cbm and PA expression levels. The Cbm(+)/PA(-) group strains had significantly higher fibrinogen-binding rates than the other groups. Analysis of platelet aggregation revealed that SA31, a Cbm(+)/PA(-) strain, induced an increased level of aggregation in the presence of fibrinogen, while negligible aggregation was induced by the Cbm-defective isogenic mutant SA31CBD. A rat IE model with an artificial impairment of the aortic valve created using a catheter showed that extirpated heart valves in the SA31 group displayed a prominent vegetation mass not seen in those in the SA31CBD group. These findings could explain why Cbm(+)/PA(-) strains are highly virulent and are related to the development of IE, and the findings could also explain the frequent detection of serotype k DNA in S. mutans-positive heart valve clinical specimens.
ISSN:0019-9567
1098-5522
DOI:10.1128/IAI.02164-14