Clinical Pearls & Morning Reports
Published April 15, 2020
Hantaviruses are murine viruses associated with two severe clinical presentations: the hemorrhagic fever with renal syndrome and hantavirus cardiopulmonary syndrome. Read the Case Records of the Massachusetts General Hospital here.
Q: What virus is the most common cause of hantavirus cardiopulmonary syndrome in the United States?
A: Hantavirus cardiopulmonary syndrome was first described in 1993 during an outbreak of unexplained fever and the acute respiratory distress syndrome among members of the Navajo tribe at the northern border between New Mexico and Arizona. Since 1993, a total of 728 cases have been reported by the Centers for Disease Control and Prevention. Sin Nombre virus is the most common cause of hantavirus cardiopulmonary syndrome in the United States, and the natural host is the deer mouse. Exposure to Sin Nombre virus can occur through inhalation of aerosolized particles from contaminated feces, urine, or saliva or through direct inoculation from an animal bite.
Q: What are some of the clinical and laboratory features of hantavirus cardiopulmonary syndrome?
A: The incubation period is 2 to 4 weeks and is followed by a prodromal phase that lasts 3 to 5 days. This phase is characterized by high-grade fever, myalgias, malaise, severe headache with neck pain, abdominal pain associated with nausea and vomiting, and occasionally diarrhea. Severe leukocytosis with bandemia and thrombocytopenia also develops. There is typically minimal or no involvement of the liver or kidneys. The prodromal phase is followed by an abrupt progression to the cardiopulmonary phase, which is characterized by productive cough with nonpurulent secretions and dyspnea with severe respiratory distress. Myocardial depression with increased peripheral vascular resistance is also common.
A: Serologic testing, nucleic acid testing, and immunohistochemical staining are all acceptable methods for diagnostic confirmation of hantavirus cardiopulmonary syndrome. Serologic testing for hantavirus-specific IgM is the most commonly performed diagnostic test, because almost all infected persons will have hantavirus-specific IgM at the onset of clinical symptoms. Hantavirus-specific IgG is often also present in the blood shortly after the onset of illness and can persist for months to years after the acute illness has occurred; the detection of rising titers of hantavirus-specific IgG in serial samples can also be used for diagnostic confirmation. Nucleic acid testing for the detection of hantavirus viremia can be a useful diagnostic tool only if it is performed early in the course of the acute illness, since blood levels of the virus decrease quickly after the onset of symptoms. Immunohistochemical staining for hantaviral antigens directly on tissue can also be performed.
A: Treatment of hantavirus cardiopulmonary syndrome is largely supportive care, and mortality approaches 40%. Although the antiviral ribavirin has in vitro efficacy against hantavirus species, clinical data regarding its efficacy are mixed, and toxic effects from this medication are common. As such, use of this agent for the treatment of hantavirus cardiopulmonary syndrome is not recommended.