Research shows mobile ‘jumping genes’ reshape hospital pathogens in transplant patients

Dr. Ami Bhatt, an oncologist and genomic researcher at Stanford University, described genomic evidence that the gut often acts as a reservoir for pathogens that later cause bloodstream infections in immunocompromised patients. "By the numbers, we found that approximately 40 percent of bloodstream infections in these transplant patients are traceable to the gut," Bhatt said, summarizing strain-tracking work that compares stool metagenomes and blood isolates.

Bhatt presented comparative analyses of thousands of genomes showing Enterococcus faecium has unusually high insertion-sequence (IS) density—about 47.4 copies per megabase in the dataset she showed—and highlighted a specific element, ISL3, that rose from roughly 17 copies per genome to about 35 copies by the 2010s. In one patient example, an ISL3 insertion landed upstream of the folT folate-transporter gene between two time points and the gene became the most upregulated in the later sample, which Bhatt said "metabolically rewires Enterococcus faecium to succeed in a very, very difficult environment." She proposed that blocking IS-based adaptation could be a therapeutic strategy but noted that this remains conceptual.

Bhatt cautioned that these structural changes are one of several mutational pathways: SNPs and other variations also contribute to outbreaks. She urged broader longitudinal sampling (including skin and environmental sites) and cross-disciplinary research to determine how common IS-driven adaptation is in different pathogens and settings.