Defect of cell wall construction may shield oral bacteria's survival in bloodstream and cause infective endocarditis

Infective endocarditis (IE) is a rare but life-threatening infection. Bacteremia with organisms known to cause IE occurs commonly in association with invasive dental origin. Despite daily oral activities as well as professional dental treatments inducing bacteremia and the dental bacteremia as a risk factor of IE, the details of dental bacteria in the pathogenesis of IE are far from elucidation to date. How do a few microorganisms survive host defenses or escape from antibiotic attacking to seed target organs and cause distant infections? Why are Gram-positive bacteria more frequently detected than Gram-negative bacteria in IE? Cell wall-deficient bacteria (CWDB) were traditionally defined as bacteria with altered morphology and consistent with damaged or absent cell wall structures identified by EM. A number of case reports and laboratory studies suggest that CWDB may be found in the peripheral blood of patients with IE, and may also be demonstrated in vegetations on the valves of patients with IE. CWDB, in vitro, are resistant to antibiotics that act on cell wall biosynthesis. Recent studies indicate that the Streptococcus mutans (S. mutans) strains, the major cariogenic bacterium, isolated from the infected valve were deficient in some wall-associated proteins which are main cariogenic virulence of S. mutans, and the deficient stains exhibited less susceptible to antibiotics that act on cell wall biosynthesis. Further, the cloned deficient mutans were less susceptible to phagocytosis by human polymorphonuclear leukocytes but to possess higher platelet aggregation properties than their parent strains. As outlined above, we hypothesize that defect of cell wall construction may shield oral bacteria's survival in bloodstream and cause IE.