Abstract
BACKGROUND: Melioidosis is endemic in more than 45 countries worldwide. Recent reports of locally acquired cases in previously unaffected regions, including the southern United States, highlight the expanding geographic range of Burkholderia pseudomallei [1]. Climate change, extreme weather events, and increased population mobility have been associated with rising melioidosis incidence following environmental exposure to the bacterium [1_3]. CASE DESCRIPTION: A 31‑year‑old man with no prior medical history developed acute respiratory failure 24 h after returning from a 2‑week stay in Saudi Arabia, where he had twice been received symptomatic treatment for a flu‑like illness. Shortly after arriving in France, he experienced sudden dyspnea with rapid neurological deterioration. Prehospital evaluation revealed severe hypoxemia (SpO₂ 54% on room air), confusion, and bilateral crackles, requiring immediate intubation and mechanical ventilation. On admission to the intensive care unit (ICU), he presented with severe acute respiratory distress syndrome (ARDS) (PaO₂/FiO₂ ratio <50), profound metabolic acidosis (pH 6.9), septic shock requiring norepinephrine, and a Simplified Acute Physiology Score II (SAPS II) of 84. Laboratory tests showed neutropenia, marked systemic inflammation (C-reactive protein [CRP] 501 mg/L), acute kidney injury, hyponatremia, and elevated liver enzymes. Chest computed tomography (CT) demonstrated diffuse bilateral consolidations with ground‑glass opacities and a crazy‑paving pattern.Microbiological investigations identified Burkholderia pseudomallei (B. pseudomallei) in bronchial aspirate, blood cultures, and urine using matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry, confirming severe melioidosis. The organism was susceptible to ceftazidime, carbapenems, and trimethoprim-sulfamethoxazole. Empirical antibiotics therapy was escalated to meropenem plus trimethoprim-sulfamethoxazole immediately after identification.Despite optimal management-including protective ventilation, neuromuscular blockade, prone positioning, and veno‑venous ECMO-the patient developed refractory septic shock and died 72 h after ICU admission. OUTCOME: Fatal severe ARDS due to B. pseudomallei pneumonia with complicated by septic shock. CONCLUSION: Clinicians should maintain a high index of suspicion for melioidosis, even in non-endemic regions, particularly in travelers returning from areas where the disease is emerging or under-recognized. Early recognition is essential given the potential for rapid progression and high mortality.