Sabia virus article in MMWR

Ruben Donis rdonis at UNL.EDU
Mon Sep 12 19:13:24 EST 1994


DEAR NET:
In reply to:
**********************************************
>From: exb0431 at csdvax.csd.unsw.edu.au
>Newsgroups: bionet.virology
>Subject: yale disease handling error?
>Message-ID: <1994Sep6.130310.2546 at csdvax.csd.unsw.edu.au>
>Date: 6 Sep 94 13:03:10 +1000
>Organization: University of New South Wales
>Lines: 2

>For more information on the arenavirus infection in Connecticut see
>the MMWR dated 9.2.94 ie. Sabia virus
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HERE IS THE MMWR INFO REGARDING SABIA VIRUS:
Following material was taken from the electronic text from the Morbidity and
Mortality Weekly Report (MMWR), vol. 43, no. 34, dated September 2,
1994.  The MMWR is published by the U.S. Department of Health and
Human Services, Public Health Service, Centers for Disease Control
and Prevention (CDC).  Inquiries about the MMWR Series, including
material to be considered for publication, should be directed to:
Editor, MMWR Series, Mailstop C-08, Centers for Disease Control and
Prevention, Atlanta, GA 30333; telephone (404) 332-4555.

All material in the MMWR Series is in the public domain and may be
used and reprinted without special permission; citation as to
source, however, is appreciated.
-----------------------------------------------------------------STUFF DELETED
Emerging Infectious Diseases
Arenavirus Infection -- Connecticut, 1994

     On 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/cubic millimeter (normal: 4000-
10,000 cells/cubic millimeter), a platelet count of 138,000
cells/cubic millimeter (normal: 150,000-350,000 cells/cubic
millimeter), 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/cubic millimeter and
92,000 cells/cubic millimeter, 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 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
1. McCormick JB, King IJ, Webb PA, et al. Lassa fever: effective
therapy with ribavirin. N Engl J Med 1986;314:20-6.
2. Coimbra TLM, Nassar ES, Burattini MN, et al. New arenavirus
isolated in Brazil. Lancet 1994;343:391-2.
__________

Food for thought for anyone working with pathogenic viruses.
Cheers,
Ruben



Dr. Ruben Donis
Dept. of Veterinary and Biomedical Sciences
202 VBS
University of Nebraska,
Lincoln, NE 68583-0905
Phone: 402-472-6063
FAX to 402-472-9690
E-mail RDONIS at UNL.EDU





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