1887

Abstract

The potential pathogenicity of selected (potentially) probiotic and clinical isolates of and was investigated in a rat model of experimental endocarditis. In addition, adhesion properties of the lactobacilli for fibrinogen, fibronectin, collagen and laminin, as well as the killing activity of the platelet-microbicidal proteins fibrinopeptide A (FP-A) and connective tissue activating peptide 3 (CTAP-3), were assessed. The 90 % infective dose (ID) of the endocarditis isolates varied between 10 and 10 c.f.u., whereas four of the six (potentially) probiotic isolates showed an ID that was at least 10-fold higher (10 c.f.u.) (<0.001). In contrast, the two other probiotic isolates exhibited an ID (10 and 10 c.f.u.) comparable to the ID of the clinical isolates of this species investigated (>0.05). Importantly, these two probiotic isolates shared the same fluorescent amplified fragment length polymorphism cluster type as the clinical isolate showing the lowest ID (10 c.f.u.). tended to have a lower infectivity than (ID of 10 to ≥10 c.f.u.). All isolates had comparable bacterial counts in cardiac vegetations (>0.05). Except for one strain adhering to all substrates, all tested lactobacilli adhered only weakly or not at all. The platelet peptide FP-A did not show any microbicidal activity against the tested lactobacilli, whereas CTAP-3 killed the majority of the isolates. In general, these results indicate that probiotic lactobacilli display a lower infectivity in experimental endocarditis compared with true endocarditis pathogens. However, the difference in infectivity between endocarditis and (potentially) probiotic isolates could not be explained by differences in adherence or platelet microbicidal protein susceptibility. Other disease-promoting factors may exist in these organisms and warrant further investigation.

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2007-08-01
2024-03-28
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