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Published on: March 26, 2018
Staphylococcus epidermidis in Acute Myeloid Leukemia: A Comparative Genomic Study Against Non-AML Isolates.
Stephanie McMahon1, Samantha Franklin1, Maliha Batool1
1Laboratory of Jessica Galloway-Peña, Interdisciplinary Genetics Program, Department of Veterinary Pathobiology, Texas A&M University, College Station, TX 77843, USA.
Genomic analysis reveals that Staphylococcus epidermidis causing bloodstream infections in acute myeloid leukemia patients differs from colonizing strains. Infectious strains possess more resistance genes, contributing to pathogenicity in immunocompromised hosts.
Area of Science:
- Microbiology
- Genomics
- Infectious Diseases
Background:
- Bloodstream infections (BSIs) are a significant cause of illness and death in acute myeloid leukemia (AML) patients receiving chemotherapy.
- Staphylococcus epidermidis, usually a harmless skin bacterium, is emerging as a key pathogen in these vulnerable patients.
Purpose of the Study:
- To investigate genomic distinctions between infectious and gastrointestinal colonizing S. epidermidis isolates from AML patients.
- To compare these isolates with colonizing and infectious strains from other patient groups and locations.
Main Methods:
- Analysis of 114 S. epidermidis isolates (44 from AML patients, 70 from public datasets).
- 16S rRNA sequencing and culture for identifying gut colonization.
- Whole-genome sequencing and comparative genomic profiling (Roary, Scoary, Phyre2, InterProScan).
Main Results:
- Infectious and colonizing S. epidermidis from AML patients were phylogenetically similar but genomically distinct.
- Infectious AML isolates showed enrichment in antibiotic resistance genes (e.g., mecA) and the biofilm gene icaA.
- AML infectious isolates had more resistance genes and mobile elements than non-AML strains, but lacked common virulence factors.
Conclusions:
- S. epidermidis pathogenicity in immunocompromised individuals like AML patients is linked to genomic adaptability and antibiotic tolerance.
- Genomic differences, not traditional virulence factors, likely drive S. epidermidis infections in vulnerable hosts.
