Abstract
Rift Valley fever (RVF) was first characterized by Daubney and his co-workers, Hudson and Garnham in 1934, while working at the Veterinary Research Laboratory at Kabete in Kenya. An earlier report by Stordy, working in the same department in 1913, had described a similar disease syndrome, which may well have been RVF; it presented as an acute and highly fatal disease in the Rift Valley in exotic wool sheep, which had been imported into East Africa. An association of the disease with heavy and prolonged rainy seasons was noted. Epizootics occurred periodically in Kenya until the disease was recognized in South Africa in 1951, when humans became ill after handling dead and infected animals. Sheep and to a lesser extent cattle were the principle disease hosts in both east and southern Africa. Further epizootics were subsequently confirmed in Zimbabwe, Zambia, the Sudan, and other east African countries. In 1977 there was a major epidemic in Egypt, with 20–40,000 clinical illnesses and 600 deaths. Cattle and sheep suffered from abortions and neonatal mortality; goats, camels, and water buffalo were also affected. Subsequently, RVF was identified in West Africa in Senegal and Mauritania, where human mortality was again high. In 2000, an outbreak occurred in Saudi Arabia, the first occurrence of RVF virus (RVFV) outside Africa. The ecology there is identical with that in enzootic zones in Africa and the RVF, which circulated were the same biotopes as were seen in Africa. Today, it is generally acknowledged that RVFV is enzootic throughout the African continent and Saudi Arabia, and in many African countries, although disease has not been recognized in man nor in animals in a substantial proportion of enzootic countries. Historically, during the major epizootics, the human RVF infections have been predominantly sub-clinical; many present as a mild influenza-like syndrome, commonly attributed to malaria. More serious clinical manifestations are acute febrile syndromes accompanied by findings like severe jaundice, retinitis and other ocular lesions, and encephalitis. These have been variously described to develop in from 5% to 20% of RVFV cases in man. Highly fatal hemorrhagic syndrome (HFS) is the most serious clinical manifestation of RVF infections, and has historically been found in only 1–2% of cases. The first Egyptian (1977) and the more recent RVF epizootics in West Africa and in the East and Horn of Africa in 1997 and 2006, have been characterized by the occurrence of many (several hundred) hemorrhagic fever cases with a significantly high mortality. While occasional cases had been recognized during the many RVF epizootics in the East and South of Africa, these had constituted only 1–2% of the total number of human RVF infections identified. The more recent epizootics in these areas have suggested that HFS was the predominant presenting sign in the affected population groups, and constituted approximately 10% of the human RVF cases. The ecology of RVFV may be relevant to this observation. The RVFV activity occurs in forest and forest edge situations and the moist plains and bushed and wooded grasslands, which are found over much of Africa. Rainfall in these zones is relatively high and RVF enzootic/epizootic activity is most frequently found in these zones. The RVFV transmission in such areas has involved principally the animal disease hosts. However, retrospective studies show that often 20–30% of those humans living and working with the animals during the epizootic period, have seroconverted to RVFV, usually with no manifestation of clinical signs. Human RVF cases with HFS were extremely rarely seen. Hemorrhagic cases of RVF have occurred among human populations of the alluvial flood plain zones, which are found principally in semi-arid regions. It has been tentatively suggested that these cases constituted 10% of all the RVFV cases in the recent 2000 epizootic in the Baringo and NE districts of Kenya. In Egypt in 1977, there were also many such cases. It may be relevant to note that malaria and probably schistosomiasis, were endemic in human populations in these regions. In the semiarid zones of Senegal and Mauretania, and of Kenya and the lowlands of Somalia, where there are flood plains, malaria and probably schistosomiasis commonly occur, with the possibility also today of widespread human immunodeficiency virus (HIV) infections. It is suggested that the outcome of RVFV infection in such population groups, affected by chronic immunosuppressive diseases, may render them much more susceptible to RVF infections and result in a greater proportion of HFS cases.
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