Staphylococcus epidermidis in Acute Myeloid Leukemia: A Comparative Genomic Study Against Non-AML Isolates

TL;DR

This study compares the genomes of Staphylococcus epidermidis from leukemia patients and finds that infection-causing strains have more antibiotic resistance genes and biofilm-related traits.

Contribution

The study reveals genomic differences in S. epidermidis from AML patients, highlighting resistance and adaptability over traditional virulence factors.

Findings

Infectious AML isolates have more resistance genes like mecA and biofilm gene icaA.

AML isolates are phylogenetically close but genomically distinct from colonizing strains.

AML strains lack classical virulence factors but show higher genomic adaptability.

Abstract

Bloodstream infections (BSIs) are a major cause of morbidity and mortality in acute myeloid leukemia (AML) patients undergoing induction chemotherapy. Staphylococcus epidermidis, typically a skin commensal, is increasingly recognized as a pathogen in these vulnerable individuals. This study investigated whether genomic differences exist between infectious and gastrointestinal colonizing S. epidermidis isolates from AML patients and how these compare to colonizing and infectious isolates from other patient groups and biogeographic sites. We analyzed 114 isolates—44 from AML patients (23 infections, 21 GI colonizers) and 70 from public datasets (34 infections, 36 colonizers). Stool samples underwent 16S rRNA sequencing and culture to identify colonization, while bloodstream isolates were sequenced and compared. Genomic profiling using Roary, Scoary, Phyre2, and InterProScan revealed that infectious and GI-colonizing AML isolates were phylogenetically close but genomically distinct. Infectious isolates from AML patients were significantly enriched for resistance genes (e.g., mecA, mecR1, mecI, ANT(4′)-Ib) and the biofilm-associated gene icaA. AML infectious isolates harbored more resistance genes and mobile elements than non-AML strains but lacked widespread classical virulence factors. These results suggest that S. epidermidis pathogenicity in immunocompromised hosts is driven by genomic adaptability and antibiotic tolerance rather than traditional virulence mechanisms.

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