In August-September 2000, an overwhelming outbreak of Rift Valley fever (RVF) struck the southwestern part of Saudi Arabia and adjoining Yemeni territories. During the outbreak, which was the first ever to be recorded outside Africa, around 40,000 animals, mostly sheep and goats, died or aborted and 883 cases, with 124 deaths, were recorded among humans in Saudi Arabia. An additional 1328 human cases, with 166 deaths, were concurrently recorded in northwestern Yemen. Vector studies in Saudi Arabia established Aedes vexans arabiensis and Culex (culex) triteniorynchus as the biological vectors of RVF virus in the region. Both of these species and several others, which could be potential vectors of the virus, occur throughout the Kingdom. Rigorous control measures were implemented, which succeeded in curtailing the infection and preventing its spread to other parts of the country. However, the virus persisted in a cryptic form in the original area of the epizootic, resulting in intermittent diagnosis of few cases throughout the past 10 years. To date, however, no evidence was found of virus activity outside that area. This review provides, from a veterinary perspective, a brief account of the events surrounding the epizootic and its present status in Saudi Arabia and emphasizes the need for vigilance, preparedness, and regular monitoring of the disease by serosurveillance methods.

SUMMARYGroups of 1-day-old turkey poults from a parent flock free of antibodies to turkey rhinotracheitis virus (TRTV) and the pathogenic mycoplasmas, were infected by eyedrop with virulent TRTV, with Mycoplasma gallisepticum (Mg) or with both agents together. Dual infection resulted in increased morbidity compared with those groups given single infections. The presence of the Mg in the dual infection had no apparent effect on the pathogenesis of the virus, but the virus caused the Mycoplasma to be more invasive.Mg infection caused a transient depression in TRTV ELISA antibody titres at 29 days postinoculation. At 14 days post-infection Mg haemagglutination inhibition (HI) and rapid serum agglutination (RSA) titres were higher (P <0.01) in the mixed infection group compared with those infected with Mg alone, but there was no significant difference between ELISA antibody titres of these two groups.

By the end of March 2002, a collection of some 200 gazelles, kept under semi range conditions in Saudi Arabia, was hit by a highly fatal peracute disease. The morbidity rate was 51% while the case mortality rate was 100%. Clinico-pathological and virological investigations were carried out. A virus was isolated from the ailing gazelles which was identified as Peste des Petits Ruminants virus (PPRV). Epidemiology of the disease in the Arabian peninsula is discussed.

Rabbit haemorrhagic disease virus (RHDV) emerged in 1984 in China and subsequently a single strain apparently dispersed worldwide killing millions of rabbits. Two isolates that caused outbreaks in Saudi Arabia and Bahrain have been sequenced and analysed phylogenetically. The Saudi Arabian lineage is directly descended from the Chinese strain, but the Bahrain isolate occupies a distinct and more divergent lineage than the Chinese virus implying that epidemic RHDV strains have emerged at least twice during the past 20 years and are co-circulating in both domestic and wild rabbits.