A49-14 A Rash Decision - Legionella Pneumonia Complicated by Purpura Fulminans

Abstract Introduction Purpura fulminans is an acute condition characterized by microvascular thrombosis and hemorrhagic necrosis of the skin, most commonly associated with infectious etiologies. It is a dermatologic emergency due to its association with sepsis, disseminated intravascular coagulation, and circulatory collapse. Although typically linked to meningococcemia or streptococcus pneumonaie, purpura fulminans can rarely complicate severe Legionella pneumophila pneumonia, the causative agent of Legionnaires’ disease. With very few documented cases, we report a case of Legionella pneumonia associated with a purpuric rash. Description A 57-year-old woman with hypertension and obesity presented with dyspnea and abdominal pain. Initial evaluation revealed leukocytosis, lactic acidosis, and diffuse pulmonary opacities on chest X-ray. She rapidly progressed to respiratory failure, requiring intubation, vasopressor support, and medical ICU admission. Broad-spectrum antibiotics (vancomycin, meropenem, azithromycin) and dexamethasone were initiated for pneumonia and acute respiratory distress syndrome. She subsequently developed oliguria and severe acidosis, necessitating continuous renal replacement therapy (CRRT). Respiratory cultures grew Legionella pneumophila, prompting an attempt to narrow antibiotic therapy to azithromycin. Despite weaning off vasopressors, she then developed a purpuric rash with central hemorrhagic necrosis and bullae on her upper abdomen and right arm, as well as associated digital ischemia. Skin biopsy revealed full-thickness epidermal and dermal necrosis, consistent with ischemic necrosis and suggestive of purpura fulminans. Associated labs demonstrated decreased antithrombin III, while extensive autoimmune and infectious serologies were negative. A new fever prompted the broadening of antibiotics back to include meropenem and vancomycin. Patient went back into septic shock and was restarted on vasopressors. Her lactic acidosis worsened despite multiple vasopressors and escalating CRRT. She succumbed to cardiac arrest within 24 hours. Discussion This rare case of Legionella pneumophila pneumonia complicated by purpura fulminans underscores the potential for severe, atypical manifestations in Legionnaires’ disease. It also highlights the difficulty of recognizing the signs and symptoms of purpura fulminans with the use vasopressors, as it can coincide with vasopressor-induced ischemia. Infectious purpura fulminans can be due to the consumption of protein C, protein S, and antithrombin III in the setting of severe bacterial infection and is often a fatal subtype of disseminated intravascular coagulation (DIC). The patient’s rapid deterioration despite aggressive interventions highlights the critical need for early recognition and management of such complications. Further research into the pathophysiology and treatment of purpura fulminans in Legionella infections is essential to improve outcomes in these rare but lethal cases. This abstract is funded by: None