A severe and often fatal respiratory disease caused by New World hantaviruses, primarily transmitted by the deer mouse (Peromyscus maniculatus) in North America and the long-tailed pygmy rice rat (Oligoryzomys longicaudatus) in South America.
Fatality Rate
38%
Regions
Americas (North, Central, and South America). Most cases reported in the United States, Argentina, Chile, Brazil, and Paraguay.
Key Symptoms
Fever and myalgia (early prodromal phase), Headache, chills, and malaise, Nausea, vomiting, and abdominal pain, Non-productive cough and tachypnea, Progressive dyspnea and hypoxemia, Pulmonary edema with bilateral infiltrates, Hypotension and cardiogenic shock, Thrombocytopenia and hemoconcentration
Hantavirus Pulmonary Syndrome is caused by several New World hantaviruses, most notably Sin Nombre virus (SNV) in North America and Andes virus (ANDV) in South America. The pathogenesis involves viral tropism for pulmonary microvascular endothelial cells. Unlike many hemorrhagic fevers, the capillary leak in HPS is not driven by direct cytopathic damage but by an exaggerated immune response: infected endothelial cells recruit CD8+ T lymphocytes and trigger a cytokine storm that increases vascular permeability in the lungs. This leads to massive non-cardiogenic pulmonary edema while simultaneously depressing myocardial function.
Epidemiologically, HPS was first recognized in 1993 during an outbreak in the Four Corners region of the United States. Since then, cases have been documented across the Americas from Canada to Patagonia. Transmission occurs primarily through inhalation of aerosolized excreta from infected rodents. Andes virus is unique among hantaviruses in that person-to-person transmission has been documented in Argentina and Chile, particularly among close household contacts during the prodromal phase. Seasonal peaks correlate with rodent population dynamics, often increasing after periods of heavy rainfall that boost food supply and rodent reproduction.
The clinical course progresses through two distinct phases. The prodromal phase lasts 3 to 6 days and presents with fever, myalgia, headache, nausea, and abdominal pain — symptoms easily mistaken for influenza or gastroenteritis. The cardiopulmonary phase follows abruptly with rapid onset of non-productive cough, tachypnea, and progressive hypoxemia. Bilateral pulmonary infiltrates develop on chest imaging, and patients may deteriorate to fulminant respiratory failure and cardiogenic shock within 24 hours. Laboratory findings typically show thrombocytopenia, leukocytosis with a left shift and immunoblasts, and elevated hematocrit due to plasma leakage.
The case fatality rate for HPS averages 38%, though early recognition and aggressive supportive care in an intensive care unit can improve outcomes. Treatment is supportive: mechanical ventilation, careful fluid management to avoid worsening pulmonary edema, and vasopressors for hemodynamic instability. Extracorporeal membrane oxygenation (ECMO) has been used successfully in severe cases. No antiviral therapy has demonstrated clear benefit in clinical trials, though intravenous ribavirin has been studied. There is currently no approved vaccine. Prevention relies on rodent control, proper ventilation when cleaning enclosed spaces, and public health education in endemic areas.