Hantavirus Pulmonary Syndrome Acquired in New York State

1Brigham and Women's Hospital, Boston, MA

Meeting: Hospital Medicine 2011, May 10-13, Dallas, Texas.

Abstract number: 243

Case Presentation:

A healthy 44‐year‐old man presented with a 4 day history of myalgia, cough, fever, and dyspnea after a hiking expedition. Two weeks prior to admission he had traveled to the Catskill Mountains, sleeping on the floor of a lean‐to hut where he heard mice scuttling about during the night. Four days before admission he developed myalgias, fever, and anorexia. He returned to Boston, where these symptoms improved, but exertional dyspnea developed, and he sought medical evaluation. Physical examination showed a nontoxic‐appearing man with normal vital signs and no rash, peripheral adenopathy, cardiopulmonary findings, or hepatosplenomegaly. Laboratory evaluation was notable for white blood cell count 8.0 × 103/ mm3 (46% PMNs, 30% band forms, 7% lymphocytes, 6% atypical lymphocytes), hematocrit 50%, platelet count 45 × 103/mm3. Tests of coagulation and renal function were normal; hepatic transaminases were mildly elevated. Electrocardiogram was normal; a chest x‐ray showed diffuse interstitial edema. On the second hospital day his atypical lymphocytosis increased to 16%. He developed an oxygen requirement of 3 L/min by nasal cannula to maintain O2 saturation > 95%, which resolved over the ensuing 48 hours. Subsequently, results of IgG and IgM antibody testing for hantavirus by ELISA returned markedly positive at 2.35 and 8.2210, respectively, (normal < 1.10).

Discussion:

Hantavirus species are rodent pathogens producing zoonotic infections in humans through inhalation of aerosolized excreta, especially urine. In North America, infection presents as hantavirus pulmonary syndrome (HPS), first described in a 1993 outbreak in the Four Corners area of the Southwest. Of 465 cases reported through March 2007, 18 cases were acquired east of the Mississippi River and only 3 in New York State. The clinical features suggesting HPS in this case were a compatible incubation period, a systemic prodrome followed by the emergence of dyspnea with noncardiogenic pulmonary edema on chest x‐ray, and characteristic laboratory abnormalities. Noncardiogenic pulmonary edema in HPS is thought to be mediated by the T‐cell response to viral microvascular pulmonary endothelial infection. Hematologic findings of thrombocytopenia, leukopenia, a left‐shifted granulocyte series without toxic granulations, atypical lymphocytosis >10%, and hemoconcentration are typical of HPS. They have been used as diagnostic criteria in high‐prevalence rural areas to triage suspected patients for transport to intensive care.

Conclusions:

The purpose of reporting this case is to highlight that, although HPS has receded from the media limelight, cases still occur in areas of low endemicity and should be considered when a suggestive epidemiologic and clinical history is associated with characteristic laboratory abnormalities.

Disclosures:

R. Blair ‐ none

To cite this abstract:

Blair R. Hantavirus Pulmonary Syndrome Acquired in New York State. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 243. Journal of Hospital Medicine. 2011; 6 (suppl 2). https://www.shmabstracts.com/abstract/hantavirus-pulmonary-syndrome-acquired-in-new-york-state/. Accessed July 19, 2019.

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