Hantavirus Pulmonary Syndrome: A Clinical Description of 17 Patients with a Newly Recognized Disease
Jeffrey S. Duchin, Frederick T. Koster, C.J. Peters, Gary L. Simpson, Bruce Tempest, Sherif R. Zaki, Thomas G. Ksiazek, Pierre E. Rollin, Stuart Nichol, Edith T. Umland, Ronald L. Moolenaar, Susan E. Reef, Kurt B. Nolte, Margaret M. Gallaher, Jay C. Butler, Robert F. Breiman, for The Hantavirus Study Group
Background In May 1993 an outbreak of severe respiratory illnessoccurred in the southwestern United States. A previously unknownhantavirus was identified as the cause. In Asia hantavirusesare associated with hemorrhagic fever and renal disease. Theyhave not been known as a cause of human disease in North America.
Methods We analyzed clinical, laboratory, and autopsy data onthe first 17 persons with confirmed infection from this newlyrecognized strain of hantavirus.
Results The mean age of the patients was 32.2 years (range,13 to 64); 61 percent were women, 72 percent were Native American,22 percent white, and 6 percent Hispanic. The most common prodromalsymptoms were fever and myalgia (100 percent), cough or dyspnea(76 percent), gastrointestinal symptoms (76 percent), and headache(71 percent). The most common physical findings were tachypnea(100 percent), tachycardia (94 percent), and hypotension (50percent). The laboratory findings included leukocytosis (medianpeak cell count, 26,000 per cubic millimeter), often with myeloidprecursors, an increased hematocrit, thrombocytopenia (medianlowest platelet count, 64,000 per cubic millimeter), prolongedprothrombin and partial-thromboplastin times, an elevated serumlactate dehydrogenase concentration, decreased serum proteinconcentrations, and proteinuria. Rapidly progressive acute pulmonaryedema developed in 15 of the 17 patients (88 percent), and 13patients, all of whom had profound hypotension, died (case fatalityrate, 76 percent). Increases in the hematocrit and partial-thromboplastintime were predictive of death.
Conclusions Infection with a newly described hantavirus causesthe hantavirus pulmonary syndrome, which is characterized bya brief prodromal illness followed by rapidly progressive, noncardiogenicpulmonary edema.
Source Information
From the Centers for Disease Control and Prevention, Atlanta (J.S.D., C.J.P., S.R.Z., T.G.K., P.E.R., S.N., R.L.M., S.E.R., J.C.B., R.F.B.); the Department of Infectious Diseases, University of New Mexico Hospital, Albuquerque (F.T.K., G.L.S.); the New Mexico Department of Health, Santa Fe (G.L.S., M.M.G.); the Indian Health Service, Gallup Indian Medical Center, Gallup, N.M. (B.T.); and the Office of the Medical Investigator, Albuquerque (E.T.U., K.B.N.). The opinions expressed in this paper are those of the authors and do not necessarily reflect the views of the Indian Health Service.The members of the Hantavirus Study Group are listed in the Appendix.
Address reprint requests to Dr. Duchin at NCID, Bldg. 1, Mailstop C09, Childhood and Respiratory Diseases Branch, Bacterial and Mycotic Diseases, Centers for Disease Control and Prevention, 1600 Clifton Rd., Atlanta, GA 30333.
Hantavirus Pulmonary Syndrome in New England and Europe
Brackett L. E., Rotenberg J., Sherman C. B., Clement J., Colson P., McKenna P., Denetclaw T. H., Denetclaw W. F., Duchin J. S., Breiman R. F., Butler J. C., Peters C.J., Koster F. T., Wenzel R. P.
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N Engl J Med 1994;
331:545-548, Aug 25, 1994.
Correspondence
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