Staphylococcus aureus CC30 Lineage and Absence of sed , j , r -Harboring Plasmid Predict Embolism in Infective Endocarditis

• Published in: Frontiers in cellular and infection microbiology 2018-06, Vol.8, p.187-187
• Main Authors: Rasigade, Jean-Philippe, Leclère, Amélie, Alla, François, Tessier, Adrien, Bes, Michèle, Lechiche, Catherine, Vernet-Garnier, Véronique, Laouénan, Cédric, Vandenesch, François, Leport, Catherine
• Format: Article
• Language: English
• Subjects: Bacteriology; CC30; enterotoxin; Immunology; infective endocarditis; Life Sciences; Microbiology; Microbiology and Parasitology; MRSA; S. aureus; stroke; Virology
• ISSN: 2235-2988; 2235-2988
• DOI: 10.3389/fcimb.2018.00187

induces severe infective endocarditis (IE) where embolic complications are a major cause of death. Risk factors for embolism have been reported such as a younger age or larger IE vegetations, while methicillin resistance conferred by the gene appeared as a protective factor. It is unclear, however, whether embolism is influenced by other characteristics such as clonal complex (CC) or virulence pattern. We examined clinical and microbiological predictors of embolism in a prospective multicentric cohort of 98 French patients with monomicrobial IE. The genomic contents of causative isolates were characterized using DNA array. To preserve statistical power, genotypic predictors were restricted to CC, secreted virulence factors and virulence regulators. Multivariate regularized logistic regression identified three independent predictors of embolism. Patients at higher risk were younger than the cohort median age of 62.5 y (adjusted odds ratio [OR] 0.14; 95% confidence interval [CI] 0.05-0.36). characteristics predicting embolism were a CC30 genetic background (adjusted OR 9.734; 95% CI 1.53-192.8) and the absence of pIB485-like plasmid-borne enterotoxin-encoding genes , and ( ; adjusted OR 0.07; 95% CI 0.004-0.457). CC30 has been repeatedly reported to exhibit enhanced fitness in bloodstream infections, which might impact its ability to cause embolism. -encoded enterotoxins, whose superantigenic activity is unlikely to protect against embolism, possibly acted as a proxy to others genes of the pIB485-like plasmid found in genetically unrelated isolates from mostly embolism-free patients. did not independently predict embolism but was strongly associated with . This - association might have driven previous reports of a negative association of and embolism. Collectively, our results suggest that the influence of genotypic features on the risk of embolism may be stronger than previously suspected and independent of clinical risk factors.