Localized Multidrug-Resistant Morganella morganii Urinary Tract Infection in a Dapagliflozin-Treated Man with Bladder Outlet Obstruction and Incomplete Ureteral Duplication: A Case Report

Background and Clinical Significance: Sodium–glucose cotransporter-2 (SGLT2) inhibitors cause persistent glucosuria, which has been hypothesized to facilitate urinary tract infection (UTI) when urinary stasis or anatomic variants coexist; causality, however, remains unproven and almost certainly multifactorial. Case Presentation: A 72-year-old man treated with dapagliflozin 10 mg/day for 4 months presented with 3 days of dysuria and nocturia, without fever or systemic signs. One month before SGLT2 inhibitor initiation, urological work-up had been unremarkable: prostate ~50 cm3, post-void residual (PVR) 0 mL, and a negative midstream culture. At presentation we obtained a midstream clean-catch specimen before antibiotics. Dipstick showed glucose 2+ (~100 mg/dL, as expected with SGLT2 inhibition), leukocyte esterase 3+ and nitrites negative; microscopy revealed 45 leukocytes/high-power field with pronounced bacteriuria. Quantitative culture grew Morganella morganii at 1 × 105 CFU/mL in pure culture. Antimicrobial susceptibility (VITEK® 2 Compact, EUCAST v14.0, 2024) demonstrated resistance to ampicillin, amoxicillin–clavulanate, ampicillin–sulbactam, ceftriaxone, ceftazidime, gentamicin and trimethoprim–sulfamethoxazole, with susceptibility (S) retained only to piperacillin–tazobactam, levofloxacin/norfloxacin, cefepime and carbapenems (ertapenem, meropenem). Imaging revealed a right duplicated ureter with distal fusion (single bladder insertion, no dilatation or obstruction) and benign prostatic hyperplasia with PVR ~100 mL; renal function was preserved, two blood culture sets (pre-antibiotic) were negative, and repeat urine culture on day 7 was sterile. Management/outcome: The episode was classified as a localized (cystitis-range) UTI per European Association of Urology (EAU) criteria (no fever, flank pain or bacteremia). Meropenem 1 g intravenously every 8 h (3 g/day) was given for 10 days after urology/infectious-disease review. Dapagliflozin was held at presentation and not restarted during the 3-month follow-up period; reintroduction was planned only after full urological reassessment with cardiology input. Transurethral resection of the prostate (TUR-P) was performed 18 days after completing antibiotics (28 days after presentation) for bladder outlet obstruction refractory to tamsulosin 0.4 mg daily, with complete resolution of symptoms, normalization of inflammatory markers and PVR 0 mL. No recurrence occurred during 3 months of follow-up after TUR-P. Conclusions: This single case illustrates a temporal association—not proven causation—between SGLT2-related glucosuria, incomplete emptying and a non-obstructive duplicated ureter that likely created a permissive milieu for opportunistic Morganella UTI. The narrative is hypothesis-generating; urinary stasis was the dominant modifiable factor. Culture-guided therapy, individualized decisions on SGLT2 continuation, and definitive correction of outlet obstruction are the practical takeaways.