B urkholderia pseudomallei, which causes melioidosis, is a gram-negative saprophytic bacterium endemic to tropical and subtropical environments worldwide; to our knowledge, isolation from the continental United States has not been reported (1-3). The most overrepresented risk factor for melioidosis is diabetes mellitus (3,4). B. pseudomallei is resistant to many antimicrobial drugs (3). Laboratory exposures might occur without appropriate biosafety precautions (2,5). Surveillance is challenging because melioidosis is not nationally notifiable; however, B. pseudomallei is a Tier 1 overlap Select Agent (6), and the Centers for Disease Control and Prevention (CDC) receives voluntary reports (2,7). We report a case of melioidosis in a Texas resident who had no recent travel history. The Study On November 17, 2018, a 63-year-old man from Atascosa County, Texas, came to hospital A with fever, chest pain, and dyspnea of 3 days' duration. At admission, he reported congenital unilateral renal agenesis. Renal function measures were unremarkable. Increased hemoglobin A1c level and hyperglycemia (glucose >200 mg/dL) suggested undiagnosed type 2 diabetes. Computed tomography of chest and abdomen with intravenous contrast showed left lower lobe pneumonia with a small left pleural effusion. Empiric antimicrobial drug therapy with intravenous azithromycin and ceftriaxone was initiated. Blood culture yielded presumptive B. pseudomallei, which was sent for confirmation to the laboratory response network (LRN) site in Houston, Texas. On November 20, a localized, violaceous, cutaneous lesion developed on the central anterior chest wall of the patient and progressed to become purulent and ulcerated (Figure 1). The next day, he experienced respiratory failure, was emergently intubated, and was transferred to hospital B. Hospital B was not aware of the presumptive diagnosis and performed a blood and chest wound culture. Both cultures showed gram-negative rods; blood analysis showed acute kidney injury. On November 25, B. pseudomallei susceptible to trimethoprim/sulfamethoxazole and ceftazidime (Table) was identified, and treatment was switched to ceftazidime by using dosing for continuous renal replacement therapy (4). On November 26, the patient was extubated and began hemodialysis (3 ×/wk). He was discharged on December 9 and received 3 months of daily trimethoprim/sulfamethoxazole (4). Subsequent followup showed clinically recovery and resolution of z renal insufficiency.