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PubMed2003

IgG-sandwich and IgM-capture enzyme-linked immunosorbent assay for the detection of antibody to Rift Valley fever virus in domestic ruminants.

The recent occurrence of the first confirmed outbreaks of Rift Valley fever in humans and livestock outside the African region, namely in the Kingdom of Saudi Arabia and Yemen, is of global medical and veterinary concern. Disadvantages of classical techniques for serological diagnosis of Rift Valley fever include health risk to laboratory personnel, restrictions for their use outside endemic areas and inability to distinguish between different classes of immunoglobulins. We report on the development and validation of sandwich and capture ELISAs (both based on inactivated antigen) for detection of IgG and IgM antibody to Rift Valley fever virus in bovine, caprine and ovine sera. Compared to virus neutralisation and haemagglutination-inhibition tests, the IgG sandwich ELISA was more sensitive in detection of the earliest immunological responses to infection or vaccination with Rift Valley fever virus. Its sensitivity and specificity derived from field data sets ranged in different ruminant species from 99.05 to 100% and from 99.1 to 99.9%, respectively. The specificity of IgM-capture ELISA varied between different species from 97.4 to 99.4%; its sensitivity was 100% in sheep tested 5-42 days post-infection. Our results in field-collected, experimental and post-vaccination sera demonstrate that these assays will be useful for epidemiological surveillance and control programmes, import/export veterinary certification, early diagnosis of infection, and for monitoring of immune response in vaccinated animals. As highly accurate and safe tests, they have the potential to replace traditional diagnostic methods, which pose biohazard risks limiting their use outside of endemic areas to high containment facilities.

Animals↗
PubMed1980

Experimental transmission and field isolation studies implicating Culex pipiens as a vector of Rift Valley fever virus in Egypt.

Attempts were made to isolate virus from wild caught mosquitoes during the 1977 and 1978 Rift Valley fever (RVF) epizootics in Egypt. Over 95% of the 55,126 mosquitoes collected from epizootic areas in the Nile Delta and Valley were Culex pipiens. Two strains of RVF virus were isolated from unengorged female C. pipiens taken in 1978. Laboratory-reared C. pipiens originating from a population sample from the Nile Delta epizootic area transmitted RVF virus. The infection rate of mosquitoes that fed on viremic hamsters was 86.7%; the transmission rate was 40.0% (46.2% based only on infected mosquitoes). From these results, it is suggested that C. pipiens was a vector of RVF virus during the 1977-1978 epizootics in Egypt.

Animals↗
PubMed1990

Pathogenesis of Rift Valley fever in rhesus monkeys: role of interferon response.

Rhesus monkeys inoculated intravenously with Rift Valley fever (RVF) virus presented clinical disease syndromes similar to human cases of RVF. All 17 infected monkeys had high-titered viremias but disease ranged from clinically inapparent to death. Three (18%) RVF virus-infected monkeys developed signs of hemorrhagic fever characterized by epistaxis, petechial to purpuric cutaneous lesions, anorexia, and vomiting prior to death. The 14 remaining monkeys survived RVF viral infection but, 7 showed clinical signs of illness characterized by diminished food intake, cutaneous petechiae, and occasional vomiting. The other 7 monkeys showed no evidence of clinical disease. All monkeys had detectable serum interferon 24-30 h after infection, but 4 of 7 monkeys that did not develop clinical illness had serum interferon titers within 12 h after infection. In lethally infected macaques, indices of hepatic function and blood coagulation were abnormal within 2 days, implicating early pathogenetic events as critical determinants of survival. Serum transferase values were elevated in proportion to severity of clinical disease and outcome of infection. Both myocardial damage and laboratory evidence consistent with disseminated intravascular coagulation were present in fatal infections. All surviving monkeys developed neutralizing antibodies to RVF virus 4-7 days after infection, and this coincided with termination of viremia. Two fatally infected monkeys were viremic until death on days 6 and 8, and the third cleared viremia on day 5 and developed antibody on day 6 but died on day 15. There was a significant correlation between a delayed interferon response and mortality, suggesting that the early appearance of interferon was influential in limiting the severity of disease.

Analysis of Variance↗
PubMed1986

Prophylaxis of Rift Valley fever with antiviral drugs, immune serum, an interferon inducer, and a macrophage activator.

Rift Valley fever virus (RVFV), a member of the family Bunyaviridae, extended its range from sub-Saharan Africa into Egypt in 1977. Its clinical spectrum is recognized to include severe manifestations such as hemorrhagic fever and encephalitis. For these reasons, as well as the limited knowledge of specific therapy for Bunyaviridae infections, we investigated several prophylactic regimens for RVF in a mouse model. Rimantadine, thiosemicarbazone, and inosiplex were ineffective. Pretreatment with glucan was of some use, but the most encouraging results were obtained with the antiviral drug ribavirin, passive antibody, or an interferon inducer polyriboinosinic-polyribocytidylic acid complexed with poly-L-lysine and carboxymethylcellulose (poly[ICLC]). Ribavirin and poly(ICLC) were also shown to be efficacious in preventing disease in hamsters. Ribavirin (loading dose of 50 mg/kg followed by 10 mg/kg at 8-h intervals for 9 days) suppressed viremia in RVF-infected rhesus monkeys. Ribavirin also reduced virus yield in infected cell cultures; sensitivity varied markedly with cell type but not with virus strain. Immune mouse ascitic fluid, with a plaque reduction neutralization titer of 1:1024, was effective in a dose of 4 ml/kg, a volume approximately equivalent to administration of a unit of convalescent plasma to a human. Poly(ICLC) may well have functioned through interferon induction, since RVFV was shown to be sensitive to interferon in cell culture, and since another macrophage activator (glucan) was only marginally effective. These studies suggest that ribavirin, poly(ICLC), and convalescent plasma may have a role in prevention or therapy of human RVF.

Animals↗
PubMedDate not supplied

Filter paper confetti in a serological Rift Valley fever survey.

In order to collect epidemiological data about the Rift Valley fever epidemic in Mauritania, we decided to use the filter paper method. The mean recovery level of specific antibodies from filter paper, tested using an immunoenzymatic method, is around one fourth. Taking the mean haematocrit into account, we estimated the extract square with a 1/300 dilution. This method was very useful for epidemiological studies, we observed few patient refusals, but it is necessary to know the exact specificity of the antibodies.

Animals↗
PubMed2002

Use of reverse transcriptase PCR in early diagnosis of Rift Valley fever.

Reverse transcriptase PCR (RT-PCR) for diagnosis of Rift Valley fever (RVF) was evaluated by using 293 human and animal sera sampled during an RVF outbreak in Mauritania in 1998. Results of the RT-PCR diagnostic method were compared with those of virus isolation (VI) and detection of immunoglobulin M (IgM) antibodies. Our results showed that RT-PCR is a specific, sensitive tool for RVF diagnosis in the early phase of the disease and that its results do not differ significantly from those obtained by VI. Moreover, the combined results of RT-PCR and IgM antibody detection were in 100% concordance with the results of VI.

Animals↗
PubMed2002

Teratogenicity of a mutagenised Rift Valley fever virus (MVP 12) in sheep.

A 5-fluorouracil mutagenised Rift Valley fever virus strain, which was shown to be attenuated and immunogenic in cattle and sheep, was evaluated for its ability to cause teratogenic effects in pregnant sheep. A group of 50 sheep at various stages of pregnancy was inoculated with the virus and the pregnancies followed to term. There were two abortions and 14% of the lambs produced by vaccinated ewes showed teratogenic effects, the most prevalent being spinal hypoplasia, hydranencephaly, brachygnathia inferior and arthrygryposis. The foetal malformations of the central nervous and musculo-skeletal systems were mostly consistent with those observed in sheep vaccinated with the attenuated Smithburn RVF strain. The teratogenic effects of MVP12 were not seen in previous experiments by other authors as immunisation of sheep took place in the second to third trimester of pregnancy, when the foetal brain tissue has completed most of its cell division.

Abortion, Veterinary↗
PubMed1986

Rift Valley fever surveillance in mobile sheep flocks in the Nile Delta.

Rift Valley fever (RVF) surveillance was carried out in the Nile Delta by monitoring mobile and stationary sheep flocks for antibodies to RVF virus. Sheep are known to be susceptible to RVF virus infection and experienced severe morbidity in 1977 and 1978 when RVF was epidemic in Egypt. Four hundred six sheep in 32 flocks were surveyed during 1984. Twenty-four sheep from 7 flocks had antibodies to RVF virus detected by hemagglutination inhibition and plaque reduction neutralization tests. Antibodies were found primarily in sheep greater than 3 years of age, although 1- and 2-year-old sheep were included in the sample. No seroconversion was observed among 177 seronegative sheep that were bled successively for a period of 10 months. These results indicate that epizootic RVF was probably not present in the Nile Delta during 1984.

Animals↗
PubMed1994

Effect of the developmental stage at infection on the ability of adult Anopheles stephensi to transmit Rift Valley fever virus.

The ability of adult Anopheles stephensi to transmit Rift Valley fever virus was determined for mosquitoes inoculated at selected times during development. None of 109 female An. stephensi inoculated as adults transmitted virus to hamsters. In contrast, 83% (50 of 60) of those inoculated as larvae transmitted virus by bite to hamsters. Transmission rates decreased as the stage of the mosquito at the time of inoculation changed from larva to pupa to adult. Transmission rates for adult mosquitoes inoculated as larvae, as pupae < 4 hr after pupation, as pupae > 24 hr after pupation, or as adults were 83%, 25%, 11%, and 0%, respectively. Viral titers recovered from mosquitoes were similar for all groups tested, regardless of stage at infection (larva, pupa, or adult) or of transmission status (transmitter or nontransmitter). Thus, differences in transmission rates may have been due to site-specific (i.e., salivary gland) replication, rather than a generalized increase in viral replication in mosquitoes inoculated at an earlier age.

Animals↗
PubMed1987

Pathogenicity and immunogenicity of a mutagen-attenuated Rift Valley fever virus immunogen in pregnant ewes.

A mutagenized clone of Rift Valley fever virus (RVFV; MV P12) used in inoculation of 3 pregnant ewes was immunogenic, nonpathogenic, and nonabortogenic. In contrast, inoculation of a matched group of 3 pregnant ewes with parent RVFV induced clinical disease and abortions. Ewes given MV P12 delivered healthy lambs that had RVFV antibody titers of less than 1:10 at birth, increasing to greater than or equal to 1:80 after ingestion of colostrum. Ewes inoculated with parent RVFV developed marked viremia, followed by RVFV antibody titers greater than or equal to 1:1,280; ewes inoculated with MV P12 developed low viremia titers and RVFV antibody titers of 1:80 to 1:320. Postpartum challenge exposure of the previously MV P12-inoculated ewes with virulent Zagazig human 501 strain RVFV indicated that the ewes were protected from clinical disease. The RVFV-susceptible female Culex pipiens that fed on the MV P12-inoculated ewes failed to transmit RVFV to hamsters; mosquitoes that fed on the parent RVFV-inoculated ewes became infected and transmitted RVFV to hamsters.

Animals↗
PubMed2003

Pathogenicity and neurovirulence of a mutagen-attenuated Rift Valley fever vaccine in rhesus monkeys.

Rhesus macaques, intravenously inoculated with virulent Rift Valley fever virus, develop viremia and biochemical evidence of liver damage and serve as a model for human disease. Some of these monkeys suffer more serious disease with hemorrhagic phenomena and approximately 20% die with frank hemorrhage. Presently, the only Rift Valley fever vaccine approved for use in humans is a formalin-killed product that requires annual booster vaccinations. Efforts to produce an improved vaccine to replace the present vaccine have led to a mutagen-attenuated strain of Rift Valley fever virus that was found to be markedly attenuated for rhesus macaques and showed promise as a vaccine candidate for human use. Neurovirulence testing in rhesus monkeys showed that, while the vaccine was not completely innocuous, residual lesions were no more severe than the currently used 17D yellow fever vaccine.

Animals↗
PubMed1994

[Decrease of natural immunity against Rift Valley fever in domestic ruminants of the Senegal River basin after the epizootic outbreak of 1987].

A domestic ruminants serosurvey of Rift valley fever (RVF) neutralizing antibodies has been carried out during three years after the 1987 epidemic in the Senegal River Basin. Authors present results from the 1990 serosurvey that are matched with the preview surveys. Out of 1,225 ongulate tested, 17.2% had RVF virus antibodies. There is a global decrease in the herds immunity since the epizootic manifestation associated with the 1987 epidemic. Significant differences in seroprevalence are observed from the delta (28.5%) to the lower (17.9%) and middle valley (6.1%) of the Senegal river. Cattle are more likely to be with an higher seroprevalence than goat and sheep.

Animals↗
PubMed1988

Vector potential of selected North American mosquito species for Rift Valley fever virus.

Selected North American mosquito species were evaluated as potential vectors of Rift Valley fever virus. Field populations of Aedes canadensis, Ae. cantator, Ae. excrucians, Ae. sollicitans, Ae. taeniorhynchus, Ae. triseriatus, Anopheles bradleyi-crucians, Culex salinarius, Cx. tarsalis, and Cx. territans perorally exposed to 10(6.2)-10(7.2) plaque forming units of Rift Valley fever virus readily became infected. Infection rates ranged from 51% (65/127) for Cx. salinarius to 96% (64/67) for Ae. canadensis. Disseminated infection rates were generally greater at 14 days than at 7 days after the infectious bloodmeal, and, with the exception of An. bradleyi-crucians, they were not significantly different than the pooled rate of 59% for each species tested. Only 5/55 (9%) of the An. bradleyi-crucians developed a disseminated infection. For most of the species, about half of the mosquitoes with a disseminated infection transmitted an infectious dose of virus to hamsters. While all species, with the exception of An. bradleyi-crucians, transmitted virus, Ae. canadensis, Ae. taeniorhynchus, and Cx. tarsalis had the highest vector potential of the species tested. Following inoculation of approximately 10(1.6) plaque forming units of virus, 100% of the mosquitoes of each species became infected. For most species, transmission rates were similar for inoculated individuals and those that developed a disseminated infection following peroral infection. Viral titers of transmitting and nontransmitting-disseminated individuals were similar for all species tested. These data suggest that, if Rift Valley fever virus was introduced into North America, several mosquito species would be capable of transmitting it.

Aedes↗
PubMed2006

Risk of a rift valley fever epidemic at the haj in Mecca, Saudi Arabia.

Rift Valley fever (RVF) is a zoonotic disease that affects both humans and domestic animals. In humans, it can cause a fatal haemorrhagic fever disease. When domestic animals such as sheep, goats, camels and cattle are infected, the infection may or may not be accompanied by clinical signs of disease. Both sub-clinical and clinically affected animals present a hazard as a source of infection for humans. The risk of infection is greatest at the time of killing, when aerosols of infected blood may be generated, particularly by traditional sacrificial slaughtering practices. Every year some 10 million to 15 million small ruminants may be slaughtered during the religious festivals at Mecca. Some of these animals come from the Arabian Peninsula itself, but most are imported across the Red Sea, from countries in East Africa and the Horn of Africa, where RVF is known to be enzootic and can be greatly amplified during periods of epizootic virus activity. These animals may be transported to and arrive in Mecca within the incubation period for the disease. Rift Valley fever is also known to occur in the tihama zones of both Saudi Arabia and Yemen.

Africa↗
PubMed1989

[Development of a clinical and biological scoring system for the prognosis of Rift Valley fever].

With regard to an acute disease, Rift Valley fever, we tried to establish a prognostic score to help physicians to set prognosis and to choose a health management suitable in their context. Using clinical and biological data collected during the 1987 RVF epidemic in Southern Mauritania, we established a prognosis score card. Data analysis allows to prognosticate forms of possible severe evolution as an association of four syndromes: fever over 39 degrees, hemorrhagic syndrome, icterus and neurological signs. Using 12 clinical symptoms and 3 biological signs, it is possible to prognosticate cases with fatal evolution.

Disease Outbreaks↗
PubMed1979

The Rift Valley fever epizootic in Egypt 1977-78. 2. Ecological and entomological studies.

Epidemiological factors related to the introduction, spread and maintenance of Rift Valley fever (RVF) virus were studied during the 1977-78 epizootic in Egypt, Culex pipiens is the most ubiquitous and prevalent mosquito species in the Nile Valley and Delta. Isolation of RVF virus from unengorged C. pipiens, and demonstration of laboratory transmission of the virus by this species, strongly implicate it as the chief vector in Egypt. Virus transmission to man also occurs by contamination when handling infected meat and by inhaling natural virus aerosols. Wild rodents apparently do not serve as RVF virus reservoirs. Domestic sheep, cattle, buffaloes, camels, goats, donkeys and dogs act as amplifying hosts. Over 30% of the camels sampled at the southern border of Egypt were serologically positive for antibodies to RVF virus and it appears likely that the virus was introduced into Egypt, either by these animals or by other vehicles from the south.

Animals↗
PubMed1989

[Neurologic and neurosensory forms of Rift Valley fever in Mauritania].

During and after a Rift Valley fever epidemic in Southern Mauritania, we observed 348 patients infected by RVF virus. 17 of them had encephalitis. These belonged to 2 groups, acute febrile forms with short duration and possibility of death, and sub-acute forms, with a longer duration and with sequelae. They were pure encephalitis, without clinical or biological meningeal signs. We also noticed 5 brutal ocular attacks, running very slowly, with sequelae.

Adult↗