Search bioRxiv⌕ Search

Biology subjects

Garcia-de-la-Maria, C.

Publications and source records attributed to Garcia-de-la-Maria, C..

2 recordsLinked to original sources

Widespread occurrence of ampicillin-susceptible Enterococcus faecium and Enterococcus lactis clinical isolates with low MICs to cephalosporins from Spain and Portugal

Reduced cephalosporin resistance in Enterococcus faecium has traditionally been reported in laboratory mutants and, more recently, in a single clinical ampicillin-susceptible (AmpS) isolate. Herein, we investigated whether this phenotype is widespread by analysing 95 clinical enterococcal isolates (78 AmpS and 17 ampicillin resistant [AmpR]) collected from three hospitals in Spain and Portugal (2009-2025). Low ceftriaxone MICs ([≤]4 mg/L) were detected in 19/51 (37.3%) AmpS E. faecium and 7/27 (25.9%) E. lactis but in none of the AmpR isolates. Low ceftriaxone MICs were associated with older patient age in both species and with prior ampicillin therapy in E. faecium, but not with other clinical or epidemiological variables. Ceftaroline MICs were consistently low among AmpS isolates, while ceftriaxone and cefotaxime showed greater variability. Low-MIC isolates were distributed across multiple clonal lineages and hospitals and did not share a distinctive resistance or virulence gene profile. PBP5 phylogeny and variation at the psr-pbp5 region separated AmpS from AmpR E. faecium but did not explain variability in ceftriaxone MICs. Five AmpS isolates with reduced ceftriaxone MICs carried chromosomal deletions that included the psr-pbp5 region and genes with diverse cellular functions. Variation in other candidate resistance genes (pbpA, ponA, pbpF, croRS, stpA/stk and murAA) did not consistently explain the MIC differences. These results reveal unexpected heterogeneity in intrinsic cephalosporin resistance in clinical E. faecium and E. lactis and suggest that additional genetic or regulatory mechanisms underlie reduced susceptibility.

microbiology↗

Comparative mortality of dominant Staphylococcus aureus lineages in human bacteremia and animal infection models

Staphylococcus aureus is a major cause of severe infections including infective endocarditis, but lineage-specific virulence determinants remain unclear. We analyzed 77 S. aureus bacteremic isolates from major lineages using phenotypic assays, infection models, and transcriptomics. Our results revealed significant heterogeneity in S. aureus pathogenicity. ST398 isolates exhibited heightened virulence, characterized by increased hemolysin production, whereas CC30 strains showed reduced growth, biofilm formation, and infectivity. Notably, the ST398 agrC mutant Sau7 exhibited unique phenotypic behavior, with high biofilm production and decreased virulence in Galleria mellonella larvae model. Infection studies in the rabbit experimental endocarditis model showed increased vegetation size and bacterial load in Sau7-infected animals, highlighting the role of agr system in S. aureus colonization and biofilm formation. Transcriptomic analysis identified key pathways, including quorum sensing systems and hemolysins, driving virulence in ST398 strains. These findings provide insights into the lineage-specific virulence mechanisms and the multifaceted nature of S. aureus pathogenicity.

microbiology↗