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Dispatches Acute Sin Nombre Hantavirus Infection without Pulmonary Syndrome, United StatesPaul T. Kitsutani,* Robert W. Denton, Curtis L. Fritz, Robert A.
Murray,§ Randall L. Todd,¶# W. John Pape,**J. Wyatt Frampton, Joni C. Young,* Ali S. Khan,* Clarence J. Peters,* and
Thomas G. Ksiazek*
Hantavirus pulmonary syndrome (HPS) is an emerging infectious disease, often characterized by rapid, dramatic clinical progression and high case-fatality rates. Most cases in the United States are caused by Sin Nombre virus (SNV); like other viruses causing HPS, SNV has a single rodent host belonging to the subfamily Sigmodontinae (1). The virus is transmitted to humans through inhalation of aerosolized feces, urine, or saliva from infected rodents. Since the initial outbreak in the Four Corners region in 1993 (2), 217 cases of HPS were reported in the United States as of May 28, 1999; 32 of these occurred before May 1993. These cases have provided information on the clinical symptoms, disease progression, and laboratory characteristics of HPS. An incubation period of 2 to 3 weeks is typically followed by high fever, myalgia, headache, fatigue, and gastrointestinal symptoms (3,4). This phase is followed 4 to 6 days later by abrupt onset of dyspnea and hypoxia, typically associated with noncardiac pulmonary edema and respiratory failure, requiring hospitalization and intensive-care management (4,5). Hypotension or shock with myocardial depression is present in most patients; renal dysfunction of varying severity is sometimes observed. Common laboratory findings include elevated hematocrit, leukocytosis with left shift and immature myelocytes and immunoblasts, and thrombocytopenia (6,7). The diagnosis is confirmed by serologic testing for hantavirus SNV immunoglobulin (Ig)M and IgG, although reverse transcriptase polymerase chain reaction (RT-PCR) or immunohistochemical analysis (IHC) can also be done. In a study of the prevalence of SNV antibody in patients who had mild febrile illness during the 1993 HPS outbreak, asymptomatic and mild infections were uncommon (8). This observation contrasts with reports of hantaviruses that cause hemorrhagic fever with renal syndrome; mild disease can occur after infection with Hantaan virus and is predominately associated with Puumala virus infections (9,10). Since May 1993, five persons with mild acute HPS illness have been identified; one was a 4-year-old boy whose case has been described (11). We describe the other four cases, two of which were detected in 1998 and one in 1999. HPS is clinically defined as a febrile illness (temperature >38.3°C) with bilateral diffuse infiltrates that cause respiratory compromise requiring supplemental oxygen within 72 hours of hospitalization (12). A case may also be defined postmortem as an unexplained, fatal respiratory illness, with noncardiogenic pulmonary edema of unknown cause. Clinically suspected cases are confirmed by fulfilling one of three criteria at a reference laboratory: detection of hantavirus-specific IgM or rising titers of IgG antibodies, or hantavirus-specific RNA sequence by RT-PCR, or hantavirus antigens in tissues by IHC. These four atypical cases were identified through the National HPS Surveillance System, although they did not meet the clinical criteria for HPS. In Patients 2 and 3, infection with SNV was suspected early in the illness, and sera were tested promptly for hantavirus antibodies. Serum from Patient 1 was tested for SNV antibody retrospectively, after a friend with a common exposure history was diagnosed with HPS. Acute- and convalescent-phase sera from each patient were also tested at CDC for hantavirus IgM and IgG antibodies by using a panel of prototypic hantavirus strains (13). Cases were confirmed as acute SNV infections if there were substantial titers of anti-SNV IgM and either substantial acute-phase titers of IgG or a fourfold rise in convalescent-phase IgG titers. Case Report 1A 38-year-old previously healthy man from Nevada visited a local emergency room in October 1993 with a 3-day history of fever, headache, fatigue, malaise, dizziness, progressive myalgia, dry cough, and shortness of breath (Table). His temperature was 38.3°C, pulse 103 per minute, and blood pressure 130/77 mm Hg. His oxygen saturation was 85% on room air, improving to 94% on 2 liters of oxygen by nasal cannula. Except for frontal sinus tenderness, his physical examination was otherwise unremarkable. Approximately 2 weeks later, a friend of the patient's died of a respiratory illness diagnosed as HPS. A case investigation of all household and social contacts led retrospectively to the diagnosis of acute hantavirus infection in the patient, as demonstrated by positive SNV IgM and IgG titers. The patient and his friend had worked together at a ranch in rural Nevada, where they slept for 2 days in a rodent-infested guest house (14). Case Report 2A 36-year-old woman from California visited her physician in July 1998 with a 2-day history of fever, headache, and malaise. Her temperature was 37.5°C, pulse 130 per min, and blood pressure 90/60/mm Hg. Physical examination was unremarkable. Two days later, she visited the emergency room for the same complaints, as well as myalgia, dry cough accompanied by substernal burning and pain, sore throat, vomiting, and photophobia (Table). She was not in acute respiratory distress. An infectious mononucleosis test was positive. She was diagnosed with a viral syndrome probably secondary to mononucleosis and dehydration, treated with intravenous fluids, and discharged. Her clinical course improved without hospitalization. The patient worked as a registered nurse and lived on a ranch. She had no history of recent travel. She reported three exposures to rodent excreta in the month before becoming ill, twice while cleaning a barn and once while cleaning her mobile home. Because of this history, she was tested for SNV antibodies on day 2 of illness. This acute-phase serum, as well as a convalescent-phase serum, tested positive for both SNV IgM and IgG antibodies. Case Report 3A previously healthy 19-year-old man visited a local Colorado emergency room in June 1999 with a 2-day history of fever, chills, myalgia, nausea, and vomiting, but no shortness of breath. His vital signs included a temperature of 39.5°C, pulse of 93 per minute, blood pressure 114/71 mm Hg, and oxygen saturation of 89.9% on room air. A platelet count was 96,000/mm3. A chest X-ray was unremarkable. A diagnosis of HPS was suspected because of a history of rodent exposure in the community, with two recent fatal cases, but the patient refused hospitalization. The patient was admitted 2 days later after his initial serum specimen was noted to have SNV IgM and IgG antibodies. He felt better, although he remained febrile and had developed a slight cough. A repeat chest X-ray was initially reported as normal but was retrospectively read as having a slight left lower lobe interstitial infiltrate. His symptoms gradually resolved and he was discharged 2 days after admission.
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