Rift Valley fever (RVF), an arthropod-borne viral disease, has
caused widespread epizootics in domestic animals and epidemics in
humans in sub-Saharan Africa and, in 1977 and 1978, in Egypt (1).
In
humans, RVF virus (RVFV) infection is associated with febrile
illness,
which may be complicated by encephalitis, blinding retinitis, or
fatal
hemorrhage (2). Zinga virus, originally isolated from mosquitoes
and
humans in the Central African Republic (C.A.R) (3,4), produces a
disease similiar to RVF, but was believed to be a serologically
ungrouped arthropod-borne virus. Although RVFV was previously
known
to be indigenous to Nigeria (5,6), isolations of Zinga from
mosquitoes
collected in Senegal, Madagascar, and Guinea, and from infected
humans
in Senegal, further extend the confirmed range of RVFV activity in
West Africa (7).
While testing antisera to African viruses in an enzyme-linked
immunosorbent assay using RVFV as antigen, the Yale Arbovirus
Research
Unit detected a cross-reaction between Zinga virus hyperimmune
antisera and RVFV. The relationship between RVF and Zinga viruses
was
determined using three monoclonal antibodies, each highly specific
for
different antigenic sites on three structural proteins found in all
RVFV strains that have been examined. In indirect fluorescent
antibody tests, each monoclonal antibody reacted to either RVFV or
Zinga virus antigen with identical titers. Plaque reduction
neutralization tests with reference hyperimmune antisera confirmed
that the prototype strain of Zinga virus (Institut Pasteur strain
Ar B
1976) was serologically identical to RVFV.
Because of its threat to humans and to animal production,
research
on RVFV in the United States is restricted to high containment
laboratories. During the last few years, Zinga virus has been
studied
in many laboratories in North America, Europe, and Africa, and
numerous Zinga infections have resulted from laboratory accidents
(7). Any laboratory with Zinga virus in its collection should be
aware that it is a strain of RVFV and represents a substantial
biohazard to people and animals.
Reported by JM Meegan, PhD, RE Shope MD, Yale Arbovirus Research
Unit,
Yale University School of Medicine, New Haven, Connecticut; CJ
Peters,
MD, US Army Medical Research Institute for Infectious Diseases,
Frederick, Maryland; JP Digoutte, MD, Institut Pasteur de Dakar,
Dakar, Senegal; Animal and Plant Health Inspection Svc, US Dept of
Agriculture; Special Pathogens Br, Div of Viral Diseases, Center
for
Infectious Diseases, CDC.
Editorial Note
Editorial Note: The discovery that Zinga virus cannot be
differentiated from RVFV is important to laboratorians who may have
been working with Zinga, unaware of its pathogenic potential, and
to
public health and agriculture officials concerned with RVF control
in
livestock. Documentation that the geographic range of RVF includes
much of West Africa should alert physicians to consider RVF in the
differential diagnosis of dengue-like illnesses or hemorrhagic
fever
in travelers returning from that area. Since the onset of
meningoencephalitis and retinitis may occur late in RVF, clinicians
should be aware that these complications may be the presenting
features of RVF in a returning traveler.
RVF is primarily an arthropod-borne viral disease of man,
sheep,
goats, and cattle. In epizootics, the infection results in
significant mortality among adult animals, and abortion rates and
mortality rates in young animals approach 100%. The 1977 epidemic
in
completely susceptible human populations of Egypt resulted in an
estimated 20%-30% attack rate in epidemic areas, with a
case-fatality
ratio of 3% (8). Thus, RVF has proven to be a disease of both
economic significance and public health importance.
Importation of RVF into the United States is regarded as a
threat
to the livestock industry and to human public health. Although
animals imported from areas known to have enzootic RVF are
quarantined
before entry, viremic travelers could introduce the virus, since
indigenous mosquitoes may serve as vectors. Because of these
potential threats and the many documented cases of
laboratory-acquired
RVF, work with this virus is restricted to laboratories with
high-containment facilities. The U.S. Department of Agriculture
(USDA) has developed contingency plans to respond to and control an
RVF outbreak.
Importation regulations for laboratory strains of RVF and other
exotic etiologic agents and vectors are a joint responsibility of
the
US Public Health Service and USDA. Under the Foreign Quarantine
Regulations (42CFR Section 71.156), a permit is required for
importation and subsequent domestic transport of such agents and
vectors. Adherence to these regulations rests on the good faith of
laboratorians. The potential usefulness of such regulation is
shown
in this instance in which Zinga could be traced to two laboratories
in
the United States. Other laboratories that have Zinga should
contact
the Animal and Plant Health Inspection Service of the USDA
(301-436-8017) for instructions on proper disposal.
References
Peters CJ, Meegan JM. Rift Valley fever. In: JH Steele, ed.
Handbook Series in Zoonoses, Sect. B, Vol. 1, Viral Zoonoses.
Boca
Raton, Florida: CRC Press, 1981:403-20.
Meegan JM, Shope, RE. Emerging concepts on Rift Valley fever.
Perspectives in Virology 1981;11:267-387.
Digoutte JP, Cordellier R, Robin Y, Pajot FX, Geoffroy B. Zinga
virus (Ar B 1976), a new arbovirus isolated in the Central
African
Republic. Ann Microbiol (Inst Pasteur) 1974;125B:107-18.
Digoutte JP, Jacobi JC, Robin Y, Gagnard VJ. Zinga virus
infection in man. Bull Soc Pathol Exot 1974;67:451-7.
Ferguson W. Identification of Rift Valley fever in Nigeria.
Bulletin of Epizootic Diseases of Africa 1959;7:317-8.
Fagbami AH, Tomori O, Kemp GE. A survey of Nigerian domestic
and
wild animals for neutralizing antibody to indigenous Rift Vally
fever. Nigerian Veterinary Journal 1973;2:45-8.
Digoutte JP. Viruses identified from 1963-1981. Rapport Sur
Le
Fonctionnement Technique de L'Institut Pasteur de Dakar. 1981.
El-Akkar AM. Rift Valley fever outbreak in Egypt,
October-December 1977. Journal of the Egyptian Public Health
Association 1978;53:123-128.
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