Genomic features, antimicrobial susceptibility, and insights into Stenotrophomonas maltophilia in Iraqi Healthcare Settings
Abstract
Background: Stenotrophomonas maltophilia has emerged as a globally significant, intrinsically multidrug-resistant nosocomial pathogen, yet Iraqi data remain limited to phenotypic surveillance without genomic characterization. This study combined antimicrobial susceptibility testing with whole-genome sequencing (WGS) to establish a genotype-phenotype correlation for S. maltophilia in Iraqi hospitals. Methods: Sixteen clinically resistant isolates were collected from three Iraqi tertiary-care hospitals (May 2024-July 2025) and identified via VITEK®2, with susceptibility interpreted per CLSI 2025. One representative MDR isolate (6STM-Iraqi) underwent WGS (DNBSEQ-G400), with assembly, annotation, and resistome/phylogenomic analysis via Unicycler, RASTtk, and BV-BRC/PATRIC. Results: Colistin retained complete efficacy (100% susceptibility); carbapenems remained active in 75% of isolates. Complete resistance occurred to ceftriaxone and tobramycin, with high resistance to cefotaxime (87.5%) and trimethoprim-sulfamethoxazole (75%). Twelve isolates (75%) were MDR and four (25%) XDR; no PDR isolates were found. The 6STM-Iraqi genome assembled into 41 contigs (4,736,244 bp; G+C 65.3%; N50 268,582 bp), encoding 4,457 coding sequences (71.1% functionally annotated). Resistome analysis identified 114 specialty genes across nine resistance mechanisms, dominated by multidrug efflux systems and the intrinsic L1 metallo-β-lactamase. Genotype and phenotype were largely concordant for β-lactams, aminoglycosides, and fluoroquinolones, though tetracycline resistance lacked a matching genetic determinant. Phylogenetic analysis clustered 6STM-Iraqi with reference strain K279a. Conclusion: Iraqi S. maltophilia isolates revealed a high MDR/XDR burden, with colistin as the most reliable therapeutic option. WGS revealed a resistome dominated by efflux and intrinsic β-lactamase mechanisms and exposed a resistance phenotype unexplained by current AMR databases, highlighting the added value of genomic surveillance over phenotypic testing alone in this underrepresented region.