Infectivity of Lactobacillus rhamnosus and Lactobacillus paracasei isolates in a rat model of experimental endocarditis.
The potential pathogenicity of selected (potentially) probiotic and clinical isolates of Lactobacillus rhamnosus and Lactobacillus paracasei 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(90)) of the L. rhamnosus endocarditis isolates varied between 10(6) and 10(7) c.f.u., whereas four of the six (potentially) probiotic L. rhamnosus isolates showed an ID(90) that was at least 10-fold higher (10(8) c.f.u.) (P<0.001). In contrast, the two other probiotic L. rhamnosus isolates exhibited an ID(90) (10(6) and 10(7) c.f.u.) comparable to the ID(90) of the clinical isolates of this species investigated (P>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(90) (10(6) c.f.u.). L. paracasei tended to have a lower infectivity than L. rhamnosus (ID(90) of 10(7) to > or =10(8) c.f.u.). All isolates had comparable bacterial counts in cardiac vegetations (P>0.05). Except for one L. paracasei 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 L. rhamnosus 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.
Vankerckhoven
Vanessa
V
Laboratory of Medical Microbiology, University of Antwerp, Belgium.
Moreillon
Philippe
P
Department of Fundamental Microbiology, University of Lausanne, Switzerland.
Piu
Stéphane
S
Department of Fundamental Microbiology, University of Lausanne, Switzerland.
Giddey
Marlyse
M
Department of Fundamental Microbiology, University of Lausanne, Switzerland.
Huys
Geert
G
Laboratory of Microbiology, Ghent University, Ghent, Belgium.
Vancanneyt
Marc
M
BCCM/LMG Bacteria Collection, Ghent University, Ghent, Belgium.
Goossens
Herman
H
LUMC, Department of Medical Microbiology, Leiden, The Netherlands.|Laboratory of Medical Microbiology, University of Antwerp, Belgium.
Entenza
José M
JM
Department of Fundamental Microbiology, University of Lausanne, Switzerland.
D000818:Animals; D001422:Bacterial Adhesion / Q000187:drug effects; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004697:Endocarditis, Bacterial / Q000382:microbiology*; D005260:Female; D005344:Fibrinopeptide A / Q000494:pharmacology; D006801:Humans; D007778:Lactobacillus / Q000187:drug effects / Q000472:pathogenicity* / Q000502:physiology; D052201:Lacticaseibacillus rhamnosus / Q000187:drug effects / Q000472:pathogenicity / Q000502:physiology; D010455:Peptides / Q000276:immunology / Q000494:pharmacology; D019936:Probiotics; D051381:Rats; D017208:Rats, Wistar; D013045:Species Specificity; D014774:Virulence
D010455:Peptides; D005344:Fibrinopeptide A; C009862:connective tissue-activating peptide