Abstract

Although hantaviruses have been known to exist for over 40 years, they were thought only to be the cause of hemorrhagic fever and renal syndrome (HFRS) in Europe and Asia. Rodents are the primary hosts of hantaviruses, and humans become infected mainly by inhalation of viral particles in the rodent excreta. The United States was thought to be spared from pathologic hantaviruses until the summer of 1993, when an outbreak of acute respiratory distress syndrome occurred in the Four Corners region of the United States, which includes Colorado, New Mexico, Arizona, and Utah. Through serological studies, the etiologic agent of this respiratory disease was found to be a heretofore-unknown hantavirus that was named the Sin Nombre virus. The resulting condition was renamed Hantavirus Pulmonary Syndrome (HPS). HPS begins as a febrile prodrome and quickly progresses to a life-threatening cardiorespiratory failure. A laboratory triad of thrombocytopenia, leucocytosis with bandemia, and immunoblasts is specific to HPS, and enzyme-linked immunosorbent assay remains the gold standard for diagnosis of hantaviruses. The management of both HFRS and HPS is mainly supportive, although ribavirin has been shown to be useful for HFRS. Eliminating exposure to rodents remains the key to prevention of hantavirus infection.

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