International Journal of Antimicrobial Agents 21 (2003) 153 /157

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Rift Valley fever: an uninvited zoonosis in the Arabian peninsula

Hanan H. Balkhy a,c, Ziad A. Memish b,c,*
a
Department of Pediatrics, King Fahad National Guard Hospital, Riyadh, Saudi Arabia
b
Department of Medicine, King Fahad National Guard Hospital, Riyadh, Saudi Arabia
c
Department of Infection Prevention and Control, King Fahad National Guard Hospital, P.O. Box 22490, Riyadh 11426, Saudi Arabia

Abstract

Rift Valley fever (RVF) is an acute viral disease, affecting mainly livestock but also humans. The virus is transmitted to humans
through mosquito bites or by exposure to blood and bodily fluids. Drinking raw, unpasteurized milk from infected animals can also
transmit RVF. Routine vaccination of livestock in Africa has been prohibitively expensive, leading to endemicity of RVF in most
African countries. Reports in September 2000 first documented RVF occurring outside of Africa in the Kingdom of Saudi Arabia
and Yemen. Prior to this outbreak, the potential for RVF spread into the Arabian Peninsula had already been exemplified by a 1977
Egyptian epidemic. This appearance of RVF outside the African Continent might be related to importation of infected animals from
Africa. In the most recent outbreak patients presented with a febrile haemorrhagic syndrome accompanied by liver and renal
dysfunction. By the end of the outbreak, April 2001 statistics from the Saudi Ministry of Health documented a total of 882
confirmed cases with 124 deaths. Both the severity of disease and the relatively high 14% death rate might be a consequence of
underreporting of less severe disease. Travellers to endemic areas may be at risk of acquiring the disease if exposed to animals or
their body fluids directly or through mosquito bites. Special education regarding both modes of transmission and the geographical
distribution of this disease needs to be given to travellers at risk.
# 2002 Elsevier Science B.V. and International Society of Chemotherapy. All rights reserved.

Keywords: Rift Valley fever; Traveller; Epidemiology; Prevention

1. Introduction The initial description of disease dates back to 1930,

Despite their ability to cause similar clinical syn-
dromes, the haemorrhagic fever viruses vary widely both
in their clinical course and their associated morbidities
and mortalities [1]. With the exception of the Filoviruses
(Marburg and Ebola), where the natural reservoir is
unknown, these viruses are transmitted to humans either
through mosquito bites or by exposure to blood or
bodily fluids from infected animals [2].
Rift Valley fever (RVF) is a viral zoonosis that affects
sheep, goat, buffalo and cattle [3]. This RNA virus is a
Phlebovirus, of the family Bunyaviridae. Human disease
is well known, especially during periods of intense
epizootic activity (epidemics among animals) which
occur after heavy rainfall, when increased mosquito
breeding takes place [4].
* Corresponding author. Tel.:
/966-1-252-0088x3718; fax:
/966-1-
252-0437
E-mail address: memish@ngha.med.sa (Z.A. Memish).
when animal and human disease appeared on a farm in
Lake Naivasha, in the Great Rift Valley of Kenya [5]. In
retrospect, many outbreaks in the early 1900s were
attributed to RVF. Several outbreaks of disease in
humans were associated with epizootic activity. The
1970s saw the most severe outbreaks: in South Africa in
1975 and in Egypt in 1977 [1,6].
In the countries involved, the burden of human
morbidity and mortality is only compounded by the
additive economic loss of livestock, which can be as high
as 70% of all affected animals. Unfortunately, the
countries affected are often those least able to deal
with such crises.
Recent advances in technology in the form of remote
sensing satellite techniques can now provide early
warnings of climate changes liable to support RVF
transmission. Such early detection may permit timely,
‘bilateral’ intervention, through selective animal vacci-
nation and eradication of mosquito breeding sites before
an outbreak takes root [7].

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154 H.H. Balkhy, Z.A. Memish / International Journal of Antimicrobial Agents 21 (2003) 153 /157
1.1. Rift Valley fever transmission
When compared with other viral haemorrhagic dis-
eases, such as Ebola and Marburg disease, the RVF
virus has a low mortality. Unique to this virus, however,
is its ability to be transmitted by several mosquitoes.
This lack of ‘monogamy’ in vectors ensures that RVF is
likely to become an important zoonotic disease world-
wide [8].
Additionally sheep and cattle, once infected, become
highly viraemic, thus allowing both early and highly
effective infection of the vector and hence efficient
disease transmission [9]. The transovarian transmission
of the virus is another key entomological feature.
Infected mosquito eggs can survive for years in the
soil. Once proper environmental conditions prevail, such
as heavy rainfall, which fills natural depressions in the
earth creating stagnant water (dambos) the hardy eggs
hatch, and new, infected mosquitoes start a new
epizootic cycle [8].
Areas of endemic disease may provide ‘contaminated
winds’, ripe with infected mosquitoes, as well as infected
eggs, which go on to remain dormant in previously
virgin soil for several years [10]. Other manmade
iatrogenic factors contribute to epidemic cycles of
RVF disease in animals and humans. Examples include
dam construction, which often allows for flooding of
riverbanks after heavy rain, and precipitating an in-
creased mosquito density. This was clearly observed in
1987 near Rosso, on the Senegal River, when the Diama
dam was built.
In East and South Africa, the main vector known to
transmit RVF is the Aedes mosquito, including Aedes
circumluteeolus, and Aedes micintoshi . More recently, a
group of entomologists have identified different vectors
that have been responsible for RVF virus transmission
in Western Africa, including Aedes vexans and Aedes
ochraceus [11]. Virus has also been isolated from Aedes
dalzieli .
These identified vectors from Western Africa have
similar breeding habits, and feed on cattle and sheep,
just as do those from the East and South of the African
continent. Under experimental conditions, other mos-
quito species are also capable of disease transmission
including the Anopheles and Culex mosquitoes [12].
To its advantage, the RVF virus may withstand
environmental temperatures of 25 /30 8C for approxi-
mately 80 min, enabling exposure to cooling but
contaminated body fluids of infected animals to become
a major mode of transmission. This is a particular
hazard to those exposed to contaminated blood and
abortion products in the abattoir, and areas of food
preparation in endemic regions [6]. Human-to-human
transmissions have not been reported.
1.2. Disease in humans and risk to travellers
Most cases of human RVF are asymptomatic [4,13].
After a short, 2 /5 day incubation period, patients may
experience a flu-like illness, with generalized fatigue,
low-grade fever, headache, photophobia and joint pains.
Some patients develop a faint, maculopapular rash. A
significant number of symptomatic patients will present
with hepatitis [14].
The fever usually lasts for a week. Most sponta-
neously recover and less than 5% of patients will develop
complications. Complications can be grave, including
encephalitis, retinopathy, or disseminated intravascular
coagulation leading to haemorrhage and even death
[4,15].
Today, the risk of RVF to travellers is low [16,17].
Non travellers at risk include farm workers, herdsmen,
veterinarians, and abattoir workers. Others vulnerable
to RVF include soldiers, expatriates, and adventurous
travellers, who may be at risk of disease acquisition if
bitten by infected mosquitoes or exposed to infected
animal products in endemic countries [3].
Since RVF has the potential to spread via animals
(through the trade of livestock), importing countries
may become endemic for the disease if special precau-
tions are not taken [3]. In fact, with the spread of RVF
to Egypt in 1977, it became a potential threat of
dissemination to neighbouring countries in Asia and
Europe, through the cross-border movement of goods
and animals [18].
1.3. Disease in animals
As we have seen, RVF virus infects many animals,
including sheep, goats, cattle, camels, and Asian water
buffaloes. Disease presentation in the animal is similar
and includes fever, hepatitis, and importantly abortion
(the farmer will note this perhaps before any other sign).
The adult cattle and sheep fatality rates may reach 30%,
and, in younger animals, it up to a colossal 100% [9]. In
less severe cases, animals involved may present with
injected conjunctiva, nasal discharge, weakness and
decreased milk production. As in humans, the virus is
hepatotropic, and intrahepatic viral replication leads to
massive and patchy hepatic necrosis. Improved vaccines
are under development and are a much-awaited and
important tool for disease control in animals [19,20].
2. The Saudi experience
Two simultaneous outbreaks started in the fall of
2000 in the Arabian Peninsula: one in Northern Yemen,
in the El Zuhrah district of the Hodeidah governorate
and the other in Gazan, in the southern most part of
 H.H. Balkhy, Z.A. Memish / International Journal of Antimicrobial Agents 21 (2003) 153 /157
Saudi Arabia. These outbreaks traversed the Saudi /
Yemeni border.
These outbreaks are the first-ever to be documented
outside the African Continent, in the 70 years since RVF
has been recognized [21,22].
The Saudi outbreak lasted approximately 27 weeks,
terminating in April 2001. By this time, a total of 882
cases were identified through serological testing: 747
(85%) were Saudi nationals and 113 (13%) Yemeni. The
majority, 98%, were from Gazan and Asir and had
repeated mosquito exposure. In addition, 66% had
direct contact with animals. People living in these areas
are mainly farmers and rely on farming as the sole
source of income. The living accommodation is very
poor and most of the areas they live in do not have
electricity. Most of the houses have animals in very close
proximity. This coupled with the habit of sleeping
outdoor due to the hot weather make it ideal for the
RVF disease cycle to be complete (Fig. 1).
Noteworthy, in this first Arabian outbreak, is the
exceptionally high case fatality rate, which was 14% and
much higher than previously described in other RVF
outbreaks. This could be partly explained by the under-
reporting of many mild or a symptomatic cases at the
time of the outbreak.
During the outbreak, aerial surveys and satellite
images revealed areas along the Southwest coast of the
Peninsula highly suitable for RVF transmission as they
had an increased vegetation index due to the heavy
rainfall in the proceeding year.
Intense and highly collaborative governmental efforts
by both the Saudi and Yemeni authorities curtailed this
Fig. 1. The life cycle for Rift Valley Fever.
155
epidemic, through vigorous vector control, restricting
(cross border) animal movement, and widespread edu-
cational campaigns [23].
Whether future outbreaks could recur, under suitable
environmental conditions, is yet to be seen.
2.1. Disease outbreaks
RVF has been widely distributed in sub-Saharan
Africa, with epizootic activity affecting animals in
Kenya, Tanzania, Zambia, and Uganda (Fig. 2)
[1,7,11,18,24 /26]. In 1977 and 1978 widespread RVF
epizootic activity was seen in areas of Egypt. Unlike
previous RVF outbreaks, the Egyptian outbreaks were
distinguished by an extensive human contribution to
their genesis. These outbreaks followed the construction
of the Aswan Dam, and more than 18 000 cases were
reported to be involved with RVF resulting in close to
600 deaths. Building the dam was followed by flooding
and overflowing riverbanks after heavy rain and this
precipitated an increased mosquito’s density.
Fifteen years later, in 1993, a second outbreak
occurred in Egypt. The spread of RVF was not a
surprise; in fact, it had been expected, since livestock
trade occurred between many African nations within the
continent and also transcontinentally, between Africa
and other nations. The continuing movement of live-
stock from endemic countries in Africa to Egypt has
been postulated as the source of the second outbreak.
Finally, in a 1979 retrospective study Meegan and co-
workers were able to detect RVF antibodies in eight
Swedish soldiers and a single Bedouin all from Sinai,
156 H.H. Balkhy, Z.A. Memish / International Journal of Antimicrobial Agents 21 (2003) 153 /157
Fig. 2. Documented haemorrhagic RVF outbreaks.
prior to the 1977 outbreak, who were known not to have
crossed the Suez Canal. This indicates the potential of
the RVF virus to spread to neighboring areas, probably
years before the occurrence of an outbreak [27].
2.2. Diagnosis
Once an outbreak is recognized and early cases are
proven, it becomes much easier to diagnose further cases
of RVF. The most popular method of laboratory
diagnosis uses serology to detect antibodies, either
IgM antibodies in a single serum sample, or by detecting
a rising titre of IgG antibody in acute and convalescent
serum samples [14]. In patients with encephalitis,
cerebrospinal fluid may be tested for locally produced
IgM. With the presence of equipped virological labora-
tories, RVF virus can be isolated from blood in the
acute phase of illness. Finally, PCR detects the viral
nucleic acid sequence of the RVF virus both in serum
and tissue [28].
2.3. Treatment
Treatment is entirely supportive: for mild to moderate
cases of RVF simple analgesia and fluids can be
administered and the prognosis should be favorable.
For those who develop severe disease, including en-
cephalitis, and hemorrhage, early recognition and ag-
gressive critical care, including assisted ventilation and
blood product transfusion is essential, for any hope of
survival [4,13].
2.4. Prevention and advice to the international traveller
Intensified mosquito control methods must be im-
plemented in areas of epizootic and human RVF
activity. An increased awareness of RVF among both
residents and visitors to endemic areas is paramount to
the future control and prevention of outbreaks. Educa-
tion regarding modes of disease transmission and
necessary precautions, especially protection against
mosquito bites is vital [29,30]. Protective clothing such
as shirts with long sleeves and trousers, the use of
insecticide-impregnated mosquito bed-nets and avoiding
sleeping outdoors are all simple yet important protective
measures.
The protection of high-risk travellers, such as soldiers,
has prompted vaccine development. Pittman et al. in
their evaluation of the long-term immunogenicity of an
inactivated RVF vaccine have proved it to be safe and
immunogenic [31]. No vaccine has yet been recom-
mended for those who live in endemic areas or for
regular travellers [32].
 H.H. Balkhy, Z.A. Memish / International Journal of Antimicrobial Agents 21 (2003) 153 /157
Acknowledgements
The authors would like to acknowledge Dr Qanta A.
Ahmed for her review of the manuscript and valuable
comments.
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