One of the diseases that is considered a health hazard to travelers
visiting certain African countries is the zoonotic, arthropodborne viral
disease Rift Valley Fever, also known as Infectious Enzootic Hepatitis of Sheep
and Cattle. Although humans are infected, mostly, by their exposure to blood,
tissues and aborted foeti of infected domestic ruminants, transmission from
animal to human by arthropod vectors plays its role as well.
The Rift Valley Fever (RVF) virus, an RNA virus in the genus
Phlebovirus (family Bunyaviridae), is found throughout most of Africa
and is endemic in southern and eastern Africa, where outbreaks occur at
irregular intervals. Epidemics have also been reported in Egypt, Saudi Arabia
and Yemen. The most recent upsurge of RVF has been observed, since December
2008, in Madagascar and its island neighbor Mayotte, off the east coast of
Africa. South Africa (Kwazulu-Natal) reported an outbreak as well. Earlier in
2008, outbreaks were reported in Kenya, Swaziland and Sudan. (A map of recent
RVF outbreaks is available on the
RVF is important in domestic ruminants, characterized by high mortality
rates in young animals and abortions in pregnant ruminants. RVF is endemic in
sub-Saharan Africa, where epidemics tend to occur at intervals, when heavy
rainfalls cause infected mosquito eggs to hatch and large numbers of
susceptible animals are present. Outbreaks are characterized by mass abortions
and high mortality in neonates. Epizootics are often accompanied by human
disease. Many human cases are caused by occupational exposure to blood and
tissues from infected animals, but mosquito-borne transmission can cause
epidemics. The most common form of the disease is a self-limiting,
influenza-like illness; however, ocular disease and rare cases of fatal
hemorrhagic fever also occur.
The disease was described in sheep since the beginning of the 20th
century in the Rift Valley area of Kenya. The identification of the causative
agent and the recognition of its zoonotic nature came in 1931. At that time it
was demonstrated that a virus, involved in the sheep disease that was initially
called enzootic hepatitis, also caused a disease in humans
resembling true dengue and yellow fever. The virus had
characteristic destructive action on hepatic cells of susceptible animals,
mainly newborn sheep and cattle, abortifacient activity and possibly mosquito
transmission. Eventually the described disease was designated as Rift
It took 19 years before RVF was diagnosed in another African country,
South Africa (1950-1951), where the diagnosis was initially done in
veterinarians engaged in the autopsy of a breeding bull; only then it became
apparent that the disease had been circulating throughout large parts of the
Union, causing losses in sheep, goat and cattle herds and infecting humans, for
several months. Since then, RVF has spread throughout the continent, reaching
Egypt in 1976 and penetrating into the Arab peninsula in the late 1980s.
RVF is transmitted by mosquitoes and is usually amplified in ruminant
hosts. In endemic regions, cases can occur sporadically or in epidemics. The
virus appears to survive in the dried eggs of Aedes mosquitoes;
epidemics are associated with the hatching of these mosquitoes during years of
heavy rainfall and localized flooding. In Africa, outbreaks typically occur in
savannah grasslands every five to 15 years and in semi-arid regions every 25 to
35 years. Once it has been amplified in animals, the RVF virus can also be
transmitted by other vectors, including many mosquito species and possibly
other biting insects such as ticks and midges. The virus can be transmitted
in utero to the fetus.
Humans do not seem to be infected by casual contact with live hosts but
can be infected by aerosols or direct contact with tissues during parturition,
necropsy, slaughter, laboratory procedures or meat preparation for cooking.
Both animals and humans theoretically have the potential to introduce
RVF into new areas by infecting mosquitoes.
Infections in animals
RVF can affect many species of animals, particularly sheep, cattle,
goats, buffalo, camels and monkeys. The primary amplifying hosts are sheep and
cattle. Experimental infections have been described in many mammals, including
adult cats, dogs, horses and some monkeys, with severe disease seen in newborn
puppies and kittens.
The incubation period can be as long as three days in sheep, cattle,
goats and dogs. In newborn lambs, it is 12 to 36 hours.
The clinical signs vary with the age, species and breed of the animal.
In endemic regions, epidemics of Rift Valley fever can be recognized by high
mortality rates (as high as 90% to 100%!) in newborn animals, and abortions in
adults, which vary from 5% to almost 100% in ewes, while in cattle typically
less than 10%. Mortality rates in calves are 10% to 70%.
Other symptoms that may occur in adult sheep include fever, weakness, a
mucopurulent nasal discharge, melena, hemorrhagic diarrhea, and vomiting.
Icterus may also be seen, particularly in cattle. Similar but milder infections
occur in goats.
No specific treatment, other than supportive care, is available.
The most consistent post-mortem lesion is hepatic necrosis, which is
more extensive and severe in younger animals. The liver lesions are usually
less severe in adult animals. Additional lesions may include jaundice,
widespread cutaneous, gastric and intestinal hemorrhages, and fluid in the body
cavities. Petechial and ecchymotic hemorrhages may be seen on the surface of
other internal organs. Microscopically, hepatic necrosis is the most prominent
RVF can be diagnosed by isolation of the virus from the blood of febrile
animals and from the tissues of dead animals and aborted fetuses; the liver,
spleen and brain are generally used. This virus can be grown in numerous cell
lines. Hamsters, adult or suckling mice, embryonated chicken eggs or
two-day-old lambs can also be used.
Viral titers in tissues are often high, and a rapid diagnosis can
sometimes be made with CFT, neutralization or agar gel diffusion tests on
tissue suspensions. Viral antigens can also be detected by immunofluorescent
staining of impression smears from the liver, spleen or brain. Enzyme
immunoassays and immunodiffusion tests can identify virus in the blood. RT-PCR
testing can detect viral RNA.
Commonly used serologic tests include virus neutralization, ELISA and
hemagglutination inhibition tests. Immunofluorescence, CF, radioimmunoassay and
immunodiffusion are used less frequently. Cross-reactions with other
phleboviruses can occur in serologic tests other than virus neutralization.
Similar techniques are applied for the diagnosis of RVF in humans.
Prevention in animals
Vaccines are generally used to protect animals in endemic regions and
prevent their infecting people. Attenuated and inactivated RVF vaccines are
both available. Attenuated vaccines produce better immunity; however, abortions
and birth defects can occur in pregnant animals. Subunit vaccines are in
The movement of animals from endemic areas to RVF-free regions can
result in epidemics.
Infections in humans
Humans are highly susceptible to RVF. Most infections involve animal
breeders, abattoir workers, veterinarians, and others who work closely with
blood and tissue samples from animals. During outbreaks in animals, mosquitoes
may spread the virus to humans and cause epidemics.
Infection with the RVF virus usually results in an asymptomatic
infection or a mild to moderate, nonfatal, influenza-like illness with fever
and liver abnormalities. The symptoms of uncomplicated infections may include
fever, headache, generalized weakness, dizziness, weight loss, myalgia and back
pain. Some patients also have stiffness of the neck, photophobia and vomiting.
Most people recover spontaneously within two days to a week. The incubation
period is two to six days.
Complications, including hemorrhagic fever, meningoencephalitis or
ocular disease, occur in a small percentage of patients. Hemorrhagic fever
usually develops two to four days after the initial symptoms. The symptoms may
include jaundice, hematemesis, melena, a purpuric rash, petechiae and bleeding
from the gums. Hemorrhagic fever frequently progresses to frank hemorrhages,
shock and death (case fatality rate of up to 50%).
Ocular disease and meningoencephalitis are usually seen one to three
weeks after the initial symptoms. The ocular form, seen in approximately 0.5%
to 2% of cases, is characterized by retinal lesions and may result in some
degree of permanent visual impairment. Death rarely occurs. The overall case
fatality rate for all patients with RVF is less than 1%.
Prevention in humans
Conventional arthropod control measures should be used to prevent
transmission by mosquitoes and other potential insect vectors. During
epidemics, vaccination of susceptible animals can prevent amplification of the
virus and protect people as well as animals. Exposure to aerosols produced
during the slaughter of animals should be avoided. A human vaccine has been
developed, but it has limited availability. Additional vaccines are under
Arnon Shimshony, DVM, is Associate Professor at the Koret School of
Veterinary Medicine Hebrew University of Jerusalem, Rehovot, and is the
ProMED-mail Animal Diseases Zoonoses Moderator. Dr. Shimshony was Chief
Veterinary Officer, State of Israel, from 1974 to 1999.