Introduction: Pulmonary hemorrhage is a condition with high morbidity that can occur as a result of multiple causes; including pulmonary vasculitis, drug toxicity, aspiration of blood, thrombocytopenia, stem-cell transplant, or sepsis. In many cases no definitive cause is identified. Here, we present an unusual pediatric case of severe pulmonary hemorrhage and respiratory failure with group A streptococcus (GAS) septicemia requiring extracorporeal membrane oxygenation (ECMO). To date, there are few case reports that describe pulmonary hemorrhage in the setting of GAS sepsis. In most published reports, patients presented with a typical prodrome of fever and sore throat that was followed by pulmonary hemorrhage and death. To our knowledge, this is the only report of a patient with pulmonary hemorrhage associated with GAS sepsis that progressed to severe hypoxemic respiratory failure requiring veno-arterial ECMO. A 5-year old boy with a history of mild-persistent asthma presented to a local emergency department with acute onset of inspiratory stridor that rapidly progressed to respiratory failure. History was not concerning for infectious symptoms, foreign body ingestion, or an anaphylactic reaction. Direct laryngoscopy revealed significant airway and vocal cord edema. Initial chest x-ray was unremarkable. The child was stable on minimal ventilatory and oxygen support, and transferred to a tertiary care facility. Nasopharyngeal PCR identified parainfluenza. Dexamethasone was administered for laryngotracheobronchitis and he was observed on positive pressure ventilation overnight. 12 hours later, he developed an episode of acute hypoxemia associated with pulmonary hemorrhage requiring high frequency oscillatory ventilation. Chest x-ray demonstrated bilateral infiltrates. He developed new leukopenia and neutropenia (white blood cell 2200, absolute neutrophil count 830) presumably due to sepsis and he was started on vancomycin and ceftriaxone. Clotting times, fibrinogen, and platelet counts were not consistent with disseminated intravascular coagulopathy. There was no laboratory evidence of autoimmune disease and vasculitis. The following day, he developed hypotension with cardiovascular dysfunction requiring a continuous infusion of epinephrine. Blood and endotracheal cultures grew GAS, and clindamycin was added for anti-toxin effects. His oxygenation continued to deteriorate (oxygenation index mid 40's, PaO2/FiO2 ratio of <75) despite a mean airway pressure of 28 cm water pressure, and he was cannulated for veno-arterial ECMO. On ECMO his lungs were recruited with airway positive release ventilation (APRV). There was no further pulmonary hemorrhage and his pulmonary compliance and native gas exchange eventually improved. He was decannulated after 9 days on ECMO and extubated 6 days later. The patient's lack of prodrome and initially negative blood culture on admission suggest that his GAS infection occurred as a superinfection of a primary viral process. V-A ECMO was successfully implemented in this case of GAS sepsis/pneumonitis with pulmonary hemorrhage and cardiorespiratory failure to provide oxygenation and hemodynamic support.