Abstract Streptococcus mitis, part of the viridans group streptococci, is an uncommon but recognized cause of bloodstream infection in immunocompromised hosts. In patients with acute myeloid leukemia (AML), it can trigger severe systemic inflammation and respiratory complications. A cytokine release syndrome (CRS)-like response and acute respiratory distress syndrome (ARDS) have been described in a few reports, but published data remain limited and mostly anecdotal. The role of corticosteroids in managing this inflammatory response is unclear. We describe three neutropenic patients with AML who developed S. mitis bacteremia complicated by CRS-like ARDS, each showing significant improvement after corticosteroid treatment. Three adult men with AML undergoing induction chemotherapy developed S. mitis bacteremia during periods of profound neutropenia. A 70-year-old man with AML with myelodysplasia-related changes receiving CLIA (cladribine, cytarabine, idarubicin) induction presented with fever, hypotension, and progressive hypoxemia. Computed tomography of the chest showed diffuse bilateral ground-glass opacities, and bronchoalveolar lavage revealed diffuse alveolar hemorrhage. Despite broad-spectrum antibiotics, his oxygen needs increased until high-dose intravenous corticosteroids were started, leading to marked improvement in oxygenation and imaging. A 65-year-old man with newly diagnosed AML on liposomal daunorubicin/cytarabine (Vyxeos) and venetoclax developed S. mitis/oralis bacteremia during neutropenia. Within 48 hours, he developed worsening dyspnea and bilateral infiltrates despite sterile repeat cultures and continued antibiotics. The findings were consistent with CRS-related lung injury. Corticosteroid therapy resulted in rapid clinical recovery, and he remained stable off oxygen without intubation. A 73-year-old man with relapsed AML on CLIA plus venetoclax developed S. mitis bacteremia with recurrent fevers and respiratory distress. He had improved previously with steroids for a similar inflammatory episode, and repeat corticosteroid therapy again led to partial recovery. His later course was limited by leukemia progression and cytopenias. All patients demonstrated temporal association between S. mitis bacteremia, inflammatory pulmonary decompensation, and response to corticosteroid therapy. These cases support the concept that S. mitis bacteremia may trigger a cytokine-driven inflammatory process rather than a direct infectious injury, leading to ARDS in neutropenic AML patients. In our experience, corticosteroids were associated with consistent improvement in respiratory status once infection was appropriately treated. Recognition of this pattern may allow earlier intervention and possibly better outcomes. Streptococcus mitis bacteremia can cause CRS-like lung injury and ARDS in neutropenic patients with AML. Corticosteroids may help reverse the inflammatory response and improve recovery. Given the limited and dated evidence available, further studies are needed to establish standardized treatment guidance. This abstract is funded by: None
Thakkar et al. (Fri,) studied this question.