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Arenavirus Infection -- Connecticut, 1994On August 20, 1994, the Connecticut Department of Public Health and Addiction Services received a report of a case of acute illness in a virologist suspected to be associated with Sabia virus, a newly described arenavirus. This report presents preliminary findings from the case investigation. On August 19, 1994, the virologist presented to the Tropical Medicine Clinic at Yale-New Haven Hospital with a 4-day history of fever, malaise, backache, stiff neck, and myalgias that he attributed to a recurrence of a Plasmodium vivax infection. On evaluation at the clinic, his temperature was 99.8 F (37.6 C) on antipyretics, and he had a normal physical examination. Laboratory evaluation included a negative malaria smear, a total white blood cell count (WBC) of 2600 cells/mm3 (normal: 4000-10,000 cells/mm3), a platelet count of 138,000 cells/mm3 (normal: 150,000-350,000 cells/mm3), 2+ proteinuria, and alanine aminotransferase (ALT) of 6356 U/L (upper limit normal: 35 U/L). A history of a possible laboratory exposure to Sabia virus was obtained, and the man was hospitalized for prompt treatment with intravenous ribavirin, an antiviral drug that is effective against other arenavirus infections such as Lassa fever (1). On admission, the patient had a temperature of 103 F (39.4 C). Within 24 hours of hospitalization, his total WBC and platelet count had declined to a low of 1400 cells/mm3 and 92,000 cells/mm3, respectively. His ALT peaked at 128 U/L on the 9th day of hospitalization. No hemorrhagic manifestations of the infection were observed during hospitalization. A diagnosis of Sabia infection was confirmed on acute serum by amplification of a portion of the viral genome by polymerase chain reaction and by isolation of the virus from blood. The patient recovered and was discharged on August 26. On August 8, the virologist was apparently exposed to an aerosol of Sabia virus when a centrifuge bottle developed a crack, and tissue culture supernatant containing the virus leaked into the high-speed centrifuge. At the time of the incident, the virologist was working alone in the biosafety level-3 laboratory (negative pressure with HEPA-filtered exhaust system). He cleaned the spilled material from the centrifuge while wearing a gown, surgical mask, and gloves. Persons who came in contact with the patient or with his biological specimens in the hospital laboratories since onset of his illness were notified and enrolled in a surveillance program. None of these persons have had exposure to the patient that would suggest a high risk for secondary infection. As of August 31, none of the persons under surveillance have reported a febrile illness. Reported by: M Barry, MD, F Bia, MD, M Cullen, MD, L Dembry, MD, S Fischer, MD, D Geller, MD, W Hierholzer, MD, P McPhedran, MD, P Rainey, MD, M Russi, MD, E Snyder, MD, E Wrone, MD, Yale Univ School of Medicine and Yale-New Haven Hospital; JP Gonzalez, MD, R Rico-Hesse, PhD, R Tesh, MD, R Ryder, MD, R Shope, MD, Yale Arbovirus Research Unit, Yale Univ; WP Quinn, MPH, New Haven Health Dept; PD Galbraith, DMD, ML Cartter, MD, JL Hadler, MD, State Epidemiologist, Connecticut Dept of Public Health and Addiction Svcs. A DeMaria, Jr, MD, State Epidemiologist, Massachusetts Dept of Public Health. Div of Field Epidemiology, Epidemiology Program Office; Special Pathogens Br, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC. Editorial NoteEditorial Note: Sabia virus was isolated by scientists in Sau Paulo, Brazil, in 1990 and characterized by scientists in Belem, Brazil, and at the Yale Arbovirus Research Unit (2). Only two cases of Sabia virus infection (both in Brazil) have been reported (2). One was a naturally acquired infection in an agricultural engineer who was probably infected by exposure to an infected rodent (the natural reservoir of other known arenaviruses). The engineer died approximately 2 weeks after becoming ill. The second case was in a laboratory technician who was working with the virus. He had a severe illness characterized by 15 days of fever, chills, malaise, headache, generalized myalgia, sore throat, conjunctivitis, nausea, vomiting, diarrhea, epigastric pain, bleeding gums, and leukopenia. He recovered after hospitalization and treatment with intravenous fluids. Little is known about the modes of transmission of the Sabia virus. Based on the pathogenesis of other arenaviruses, the Sabia virus is not believed to be infectious until the patient exhibits symptoms. Other arenaviruses can be transmitted by needle-stick but do not readily spread from person to person. Persons in casual contact with persons with arenavirus infection are not at risk for disease and do not require medical follow-up. References
+------------------------------------------------------------------- ------+ | | | Erratum: Vol. 43, No. 34 | | | | SOURCE: MMWR 43(35);659 DATE: Sep 09, 1994 | | | | In the article "Arenavirus Infection -- Connecticut, 1994" on | | page 635, the last sentence of the second paragraph should read | | "Laboratory evaluation included a negative malaria smear..., and | | alanine aminotransferase (ALT) of 63 U/L (upper limit normal: 35 | | U/L). | | | +------------------------------------------------------------------- ------+ Disclaimer All MMWR HTML versions of articles are electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the electronic PDF version and/or the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices. **Questions or messages regarding errors in formatting should be addressed to mmwrq@cdc.gov.Page converted: 09/19/98 |
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