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Hantavirus Pulmonary Syndrome -- Northeastern United States, 1994

On January 20, 1994, a 22-year-old Rhode Island man died of acute respiratory distress approximately 5 hours after hospitalization. This report summarizes the case investigation.

The man had sought care at an emergency department in Rhode Island on January 18 complaining of chills and diffuse myalgias and arthralgias. On evaluation in the emergency department, he had a temperature of 100.8 F (38.2 C). His complete blood count (CBC) showed a normal platelet count of 199,000/mm3, a hematocrit of 40.5%, and a white blood cell count of 3600/mm3 with 36% bands. An acute febrile illness with leukopenia was diagnosed, and he was discharged to outpatient follow-up. On January 20, he returned to the emergency department with fever (101.4 F {38.6 C}), increasing shortness of breath, and cyanosis. He was hypotensive and hypoxemic, and bilateral pulmonary infiltrates were present on chest radiograph. His CBC showed thrombocytopenia (61,000/mm3), elevated hematocrit (50.2%), and a white blood cell count of 17,400/mm3 with 41% bands. His clinical condition deteriorated rapidly, and he required mechanical ventilation for respiratory distress. He died later that day.

Because a diagnosis was not established and because the death occurred less than 24 hours after admission, the case was reported to the Rhode Island state medical examiner's office. The medical examiner's office forwarded postmortem blood specimens for evaluation for hantavirus infection to CDC. Using an enzyme-linked immunoglobulin M (IgM) capture immunosorbent assay (ELISA), elevated hantavirus IgM titers were found for the Muerto Canyon virus (MCV) (proposed to be renamed Sin Nombre virus). Postmortem tissue samples were positive for hantavirus antigens by immunohistochemistry. An MCV-like viral sequence was amplified from lung, spleen, liver, and heart tissues by reverse transcription and polymerase chain reaction (RT-PCR). A postmortem diagnosis of hantavirus pulmonary syndrome (HPS) was made. An investigation was conducted by state, county, and city health departments in New York and Rhode Island in conjunction with CDC to characterize the illness and identify the site of exposure and the local rodent reservoir for the virus.

The patient had not traveled outside the Northeast within the 2 months before his death; he had spent December 1993 and January 1994 in New York and Rhode Island. Epidemiologic and environmental investigations identified multiple possible exposure sites, including two warehouses in Queens, New York; a vacation home on Shelter Island (Long Island); and his family's residence on Long Island. These sites had a history of rodent infestation within the past 6 months but had no evidence of current rodent activity. The patient's apartment in Rhode Island had no history or evidence of rodent infestation. He had spent 2 weeks in December 1993 cleaning portions of one of the warehouses in Queens, which had been unused for more than 10 years. No other persons were involved in this activity.

Testing was conducted on serum specimens from 64 persons with exposures similar to that of the patient, including family, co-workers, and factory workers; no additional cases were identified. Rodents were captured at all suspected exposure sites (a total of 19 rodents from all suspected New York sites and 91 from Rhode Island), but none were seropositive for hantavirus. Trapping will be resumed later in 1994.

Reported by: B Mojica, MD, K Henning, MD, E Bell, New York City Dept of Health; A Greenberg, MD, R Edstrom, MD, B Smith, Nassau County Dept of Health, Mineola, Long Island; G Birkhead, MD, S Kondracki, D White, PhD, New York State Dept of Health. U Bandy, MD, E Laposata, MD, M Rittmann, W Combs, PhD, B Matyas, MD, State Epidemiologist, Rhode Island Dept of Health. Div of Vector-Borne Infectious Diseases and Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases; Div of Field Epidemiology, Epidemiology Program Office, CDC.

Editorial Note

Editorial Note: As of July 28, 1994, a total of 83 cases of HPS have been identified in the United States; 45 (54%) of these patients have died. Ninety-six percent of these cases have been identified west of the Mississippi River, where Peromyscus maniculatus (deer mouse) is the primary reservoir of MCV (1-3). The range of P. maniculatus includes all of the United States, except the southeast and the Atlantic seaboard. Infected rodents have no signs of infection; however, they shed virus in their saliva, urine, and feces. Humans exposed to infected rodent excreta can develop HPS. The patient in Rhode Island had a history of exposure to a previously closed space with rodent infestation; such exposures have been associated with HPS (1). The small number of rodents caught at suspected exposure sites in New York probably was attributed to excessively cold weather.

Four cases of HPS have been identified outside the range of P. maniculatus, one each in eastern Texas, Louisiana, Florida, and Rhode Island. In Florida, a new but related virus (recently named Black Creek Canal virus {BCCV}) isolated from Sigmodon hispidus (cotton rat) is genetically distinct from MCV (4) and from sequences demonstrated by RT-PCR in lung tissues from a person who died of HPS in Louisiana (5). Initial serologic testing at CDC of an acute-phase serum sample from the Florida patient demonstrated the presence of only immunoglobulin G to MCV by direct ELISA, although IgM to MCV was detected by the Western blot assay performed at the University of New Mexico (S. Jenison and B. Hjelle, University of New Mexico, Albuquerque, personal communication, 1994) (6). However, repeat serologic testing at CDC using BCCV antigens showed IgM antibodies. Sequence analysis of the RT-PCR fragment from lung tissue of the patient in this report suggests the presence of a variant of MCV or a new, related virus. Taxonomic assessment of the infecting agent probably will require identification of the reservoir host and additional sequence information from viruses in the northeastern United States.

Although the overall incidence of HPS is unknown, the syndrome appears to be widespread geographically. Recognition of HPS during its early stages is difficult because of the nonspecificity of symptoms; later in the syndrome, tachypnea, hemoconcentration, thrombocytopenia, leukocytosis with a high proportion of bands, and other features are suggestive of HPS (7,8). Prompt control of hypoxia (which can rapidly worsen), avoidance of excessive fluid administration, and the early use of ino-tropic and pressor drugs appear particularly important in treating HPS (7,8).

CDC has provided intravenous ribavirin for investigational open-label use in treating HPS since June 1993. On July 19 and 20, 1994, eight experts from outside of CDC reviewed the results of the open-label ribavirin protocol. Ribavirin was generally well tolerated in patients with HPS but had no clearly positive influence on outcome. As a result, enrollment under this protocol will close September 1, 1994. No controlled studies of this agent have been conducted in patients with HPS.

Clinicians and public health officials should remain alert for persons who have unexplained febrile illness with bilateral interstitial infiltrates, and appropriate specimens should be collected for serologic and tissue diagnostic assays. Suspected cases of HPS should be reported to CDC through state health departments.


  1. CDC. Hantavirus infection -- southwestern United States: interim recommendations for risk reduction. MMWR 1993;42(no. RR-11).

  2. CDC. Hantavirus pulmonary syndrome -- United States, 1993. MMWR 1994;43:45-8.

  3. Childs JE, Ksiazek TG, Spiropoulou CF, et al. Serologic and genetic identification of Peromyscus maniculatus as the primary rodent reservoir for a new hantavirus in the Southwestern United States. J Infect Dis 1994;169:1271-80.

  4. CDC. Newly identified hantavirus -- Florida, 1994. MMWR 1994;43:99,105.

  5. CDC. Update: hantavirus disease -- United States, 1993. MMWR 1993;42:612-4.

  6. Jenison S, Yamada T, Morris C, et al. Characterization of human antibody responses to Four Corners hantavirus infections among patients with hantavirus pulmonary syndrome. J Virol 1994;68:3000-7.

  7. CDC. Update: hantavirus pulmonary syndrome -- United States, 1993. MMWR 1993;42:816-20.

  8. Duchin JS, Koster FT, Peters CJ, et al. Hantavirus pulmonary syndrome: a clinical description of 17 patients with a newly recognized disease. New Engl J Med 1994;330:949-55.

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