Şeyma Arslan, Merve Büyükkörük, Sidre Erganiş, Sıla Soylu Koçoğlu, Gözde Savaş, Kayhan Çağlar, Özge Özgen Top, Hasan Selçuk Özger
Gastrointestinal CPE colonization in patients with solid organ malignancies was primarily driven by OXA-48-producing E. coli and K. pneumoniae. Although colonization did not significantly increase the overall risk of severe infection or mortality in this cohort, further large-scale, multicenter studies are needed to identify specific high-risk subgroups.
PURPOSE: To evaluate the prevalence of carbapenemase-producing Enterobacterales (CPE) colonization in patients with solid organ malignancies and investigate its association with severe infection, infection free survival, and mortality through prospective follow-up.
METHODS: This single-center, prospective, observational study (July 2024-July 2025) included adult patients with lung, genitourinary, or gastrointestinal cancers at Gazi University Hospital. Rectal swabs were screened using chromogenic agar, and isolates were identified by MALDI-TOF MS. Meropenem susceptibility was determined via disk diffusion. Carbapenemase genes (OXA-48, NDM, KPC, VIM, IMP) were detected using an in-house multiplex PCR. All patients were followed for six months.
RESULTS: Among 269 patients, the CPE colonization prevalence was 9.7% (n=26). E. coli and K. pneumoniae were the predominant isolates (46.2% each), with OXA-48 being the most frequent gene (84.6%), followed by NDM (11.5%). No significant differences were found between CPE-colonized and non-colonized patients regarding severe infection rates (34.6% vs 35.8%, p=0.904), infection-free survival (p=0.314), or mortality at 30, 90, and 180 days (p=0.481, p=0.519, and p=0.239). Among colonized patients, the rectal colonizing strain was phenotypically concordant with the causative pathogen of subsequent severe infection in 15.4% (n=4) of the cases. The median time to infection was 12 days (IQR, 6-15 days).
CONCLUSIONS: Gastrointestinal CPE colonization in patients with solid organ malignancies was primarily driven by OXA-48-producing E. coli and K. pneumoniae. Although colonization did not significantly increase the overall risk of severe infection or mortality in this cohort, further large-scale, multicenter studies are needed to identify specific high-risk subgroups.