C57-05 From Rats to Respiratory Failure: A Case of Hantavirus Pulmonary Syndrome in Colorado

Hantavirus pulmonary syndrome (HPS) is rare but life-threatening cardiopulmonary disease with mortality rates approaching 40%. We describe a case of HPS in a farm-dwelling patient who presented with flu-like symptoms and rapidly progressed to severe respiratory failure. A 59-year-old female with history of anxiety and tobacco use disorder who resides on a farm presented with four days of headache, fatigue, myalgias and one day of shortness of breath. On arrival, she was tachycardic and tachypneic with an oxygen saturation of 77% on room air that improved to 95% on 15L on nonrebreather mask. Physical examination was notable for diffuse rales. Laboratory results showed thrombocytopenia (platelets 69 109/L), hemoconcentration (hemoglobin 17 g/dL, hematocrit 49.4%), and positive MRSA nares. Serologic tests for COVID-19, influenza, lactate, NT-proBNP, legionella, pneumococcal, and HIV were negative. CT chest angiography was negative for pulmonary emboli and revealed bilateral pleural effusions and multifocal bilateral ground glass opacities. Broad-spectrum antibiotics, heated high-flow, and diuretics were initiated. Transthoracic echocardiography was normal, and thoracentesis yielded exudative fluid with negative gram stain, cultures, and cytology. On hospital day two, she developed worsening hypoxemia and shock requiring vasopressor support, mechanical ventilation, and proning with an arterial PO2 of 58 mmHg on an FiO2 of 100% (P:F ratio 58). Bronchoscopy was unremarkable. With new onset fevers, infectious disease was consulted and extended serologic testing for Francisella Tularensis, hantavirus, Brucella, Q fever, Yersinia Pestis, Herpes Simplex Virus (HSV), and Mycoplasma resulted positive for hantavirus, confirming the diagnosis. Hantavirus pulmonary syndrome (HPS) is a severe zoonotic disease with emerging prevalence and high mortality. This case underscores how a nonspecific viral prodrome with rapid progression to acute hypoxic respiratory failure and cardiogenic shock can obscure the diagnosis. Because symptom onset can be delayed up to four weeks after exposure, obtaining a detailed environmental and occupational history is critical. The pathogenesis of HPS is multifactorial and involves increased capillary permeability, consumptive coagulopathy, and immune-mediated hyperreactivity that explain this patient’s thrombocytopenia and rapid evolution to respiratory failure. Management remains supportive: corticosteroids may heighten infection risk, aggressive fluids may exacerbate pulmonary edema, and while reports of ECMO and ribavirin have shown occasional benefit, their efficacy has not been established in controlled trials. Providers should maintain a high index of suspicion for HPS and inquire about environmental or occupational risk factors in patients with unexplained respiratory failure and a history of farm, forestry, or rodent exposure. This abstract is funded by: None