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PubMed1982

Marburg, Ebola and Rift Valley Fever virus antibodies in East African primates.

Sera from 464 primates held at four institutes in Kenya were tested by indirect immunofluorescence for the presence of antibodies against Marburg, Ebola, Congo haemorrhagic fever, Rift Valley fever and Lassa viruses. Four of 136 vervet monkeys were positive for Marburg virus antibodies and three of 184 baboons had antibodies against Ebola virus. One baboon was positive for Marburg virus antibodies. Two vervet monkeys, three baboons and one grivet monkey (of 56 tested) had antibodies against Rift Valley fever virus. No Congo or Lassa virus antibodies were detected. A sample of 88 sera of more arboreal primates (Sykes, blue and colobus monkeys) were negative against all five antigens, as were sera from 58 staff members of the institutes who worked with or near the animals.

Animals↗
PubMed1993

Recurrence of Rift Valley fever in Egypt.

Rift Valley fever (RVF) has been recorded in man and in domestic animals in Egypt after a 12-year absence. Human infections were first noted in the Aswan Governorate in late May, 1993. Only cases of ocular disease, an infrequent and late manifestation, were reported. Of 41 cases, 35 were tested serologically and 27 (77%) had RVF virus-specific IgM antibodies. An estimated 600-1500 infections occurred in the region. Abortions in cattle and buffalo were seen concurrently and antibodies to RVFV were present in 39% of domestic livestock, presumably unvaccinated. RVFV was isolated from an aborted water buffalo fetus.

Abortion, Veterinary↗
PubMed2004

Exposure of sheep to mosquito bites: possible consequences for the transmission risk of Rift Valley Fever in Senegal.

Rift Valley Fever (RVF) is a growing health problem in West Africa. In northern Senegal, the candidate vectors of this arbovirosis are Aedes (Aedimorphus) vexans Meigen and Culex (Culex) poicilipes Theobald (Diptera: Culicidae). Domestic ruminants are the reservoirs of the virus. A study was undertaken during the 2002 rainy season to assess spatial and temporal variations in exposure to mosquito bites in sheep herds, and to evaluate the possible consequences on the risk of RVF transmission to sheep. Mosquitoes were collected with sheep-baited traps. The number of Ae. vexans females (the predominant species during the 2002 rainy season) trapped per trap-night was the dependent variable in statistical analyses. The trapping periods were divided into six series of two to five consecutive days, from July to November 2002. Three temporary ponds were selected according to their ecological features: depth, bank slope, size and vegetation cover. Traps were laid on the pond bank and in the nearest available compound, close to the sheep night pen. Data were analysed using mixed-effects Poisson models. The explanatory variables were the trapping period, the pond, and the capture site. The exposure to mosquito bites varied according to the pond type, suggesting that the risk of transmission was spatially heterogeneous. However, there was no obvious trend in transmission risk due to the effect of the distance from the compound to the pond. The period with the highest exposure was in October, i.e. when transhumant herds left the Ferlo to relocate to their dry-season settlement. It is thus hypothesized that transhumance, the seasonal movements of herds, plays a significant role in the dissemination of RVF virus in the region.

Aedes↗
PubMed1995

Antibodies to hemorrhagic fever viruses in domestic livestock in Niger: Rift Valley fever and Crimean-Congo hemorrhagic fever.

A repository of domestic animal sera collected in Niger between 1984 and 1988 was assayed for antibody against two zoonotic hemorrhagic fever viruses known to be present in the West African Sahel. A total of 2,540 serum samples from 2,324 cattle, sheep, goats, and camels were tested by an IgG-specific enzyme-linked immunosorbent assay (ELISA) and the 80% plaque reduction neutralization test (PRNT80) for Rift Valley fever (RVF) virus antibody. Of the 2,540 sera tested for RVF-specific IgG antibody, 1,676 sera from cattle, sheep, and goats were examined for RVF-specific IgM antibody by ELISA. A subset of 2,263 sera were examined for evidence of Crimean-Congo hemorrhagic fever (CCHF) virus antibody by an IgG-specific ELISA. Antibody against CCHF virus was found to be most prevalent in adult cattle (422 of 732 or 57.7% positive) sampled at nine locations in the Niamey area. The highest prevalence for RVF neutralizing antibodies was found in camels from the Agadez Department with 67 (47.5%) of 141 positive. The results indicate that both CCHF and RVF viruses are circulating in Niger and are potential zoonotic health risks.

Animals↗
PubMed1988

Experimental Rift Valley fever in rhesus macaques.

Rift Valley fever (RVF) is a major cause of human morbidity and mortality in endemic areas of sub-Saharan Africa and has the potential to cause epidemic disease in receptive areas world-wide. In this study, a RVF viral isolate from the 1977 Egyptian epidemic (ZH-501) inoculated intravenously into rhesus macaques caused a benign viremic infection in most, but resulted in the hemorrhagic fever syndrome in 20 per cent (3 of 15). Serious disease of this type has not previously been observed in nonhuman primates inoculated with RVF virus and may be a consequence of the viral strain used or the route of inoculation. Severe disease was accompanied by extensive liver necrosis, disseminated intravascular coagulation, and microangiopathic hemolytic anemia. We also attempted to prevent RVF by passive transfer of serum from vaccinated rhesus monkeys (plaque-reduction neutralization test titer 1:2,560). As little as 0.025 ml/kg prevented the development of viremia in naive rhesus monkeys after subcutaneous inoculation of virus. The monkey model should be helpful in understanding the pathogenesis and prevention of human RVF.

Animals↗
PubMed2002

Development of a diagnostic one-tube RT-PCR for the detection of Rift Valley fever virus.

Diagnosis of Rift Valley fever (RVF) is based on serology and virus isolation. The disadvantages of the former include poor sensitivity, high cost, risks associated with using infectious virus as antigen, the lengthy duration of ELISA as well as cross-reactivity with other Phleboviruses. We developed, optimised and evaluated a one-tube reverse-transcription-polymerase chain reaction (RT-PCR) for the detection of Rift Valley fever virus (RVFV) in ruminants. The PCR primers for this assay were designed to anneal to a region within the M segment of the virus genome, encoding glycoproteins G1 and G2. A PCR amplicon of 363 bp was obtained. The sensitivity of the assay was determined to be 0.25 TCID50. This test should allow for the early and rapid detection of RVFV in both serum and whole blood. In addition, it could facilitate the quantification of antigen for the manufacture of current vaccines.

Animals↗
PubMed1988

Viral determinants of virulence for Rift Valley fever (RVF) in rats.

Rift Valley fever viral strains or variants (RVFV) were compared with respect to (a) virulence for Wistar-Furth rats; (b) in vitro sensitivity to rat and human interferon; (c) ability to form plaques in primary hepatocyte cultures from genetically resistant or susceptible rat strains, and (d) replicative potential in continuous rat cell lines. Egyptian strains were highly virulent for Wistar-Furth rats; relatively resistant to rat interferon-alpha/beta; capable of producing plaques in primary hepatocyte monolayers; and, in general, replicated more rapidly than the low-virulent, sub-Saharan strains. Virtually all strains from sub-Saharan Africa were sensitive to rat interferon and did not form plaques in rat hepatocyte monolayers. An exception was the 2269/74 strain from Zimbabwe, which had characteristics of the Egyptian strains including increased virulence for Wistar-Furth rats. The relative virulence of RVFV strains for rats did not correlate with interferon sensitivity when human recombinant interferon-alpha was tested on A-549 cells. Thus, several in vitro phenotypic characteristics of RVFV strains tend to correlate with virulence for Wistar-Furth rats and with geographical origin of the viral strains.

Animals↗
PubMed1983

Reversed passive hemagglutination and inhibition with Rift Valley fever and Crimean-Congo hemorrhagic fever viruses.

Reversed passive hemagglutination (RPHA) tests were performed by coating glutaraldehyde-fixed and tannic acid-treated sheep erthrocytes with antibodies to Rift Valley fever (RVF) and Crimean-Congo hemorrhagic fever (CCHF) viruses. Cells coated with crude antibody, in the form of mouse immune ascitic fluid, reacted with high specificity and sensitivity in RPHA tests with live or inactivated virus antigens. In inhibition (RPHI) tests, RVF antibody titers in human and sheep sera were similar to those determined by hemagglutination inhibition test. RVF virus antigen could be detected in viremic sheep sera by the RPHA technique. RPHI antibody titers to CCHF virus in human and hare sera were similar to indirect immunofluorescence (IF) titers, but sheep and cattle sera with RPHI titers of 1:32 or less were negative in IF tests.

Animals↗
PubMed2006

Vertical transmission of fatal Rift Valley fever in a newborn.

Rift Valley Fever (RVF) is a viral disease transmitted to humans by mosquito bite and contact with animals or their infected tissues. Other modes of transmission include aerosol inhalation and possibly ingestion of raw milk from infected animals. We present a 5-day-old neonate with fatal RVF. Onset of the infant's illness on the 2nd day of life combined with positive RVF-IgM and serological evidence of maternal disease supports vertical transmission.

Adult↗
PubMed1999

Genetic reassortment of Rift Valley fever virus in nature.

Rift Valley fever virus (RVFV), a phlebovirus of the Bunyaviridae family, is an arthropod-borne virus which emerges periodically throughout Africa, emphasizing that it poses a major threat for animal and human populations. To assess the genetic variability of RVFV, several isolates from diverse localities of Africa were investigated by means of reverse transcription-PCR followed by direct sequencing of a region of the small (S), medium (M), and large (L) genomic segments. Phylogenetic analysis showed the existence of three major lineages corresponding to geographic variants from West Africa, Egypt, and Central-East Africa. However, incongruences detected between the L, M, and S phylogenies suggested that genetic exchange via reassortment occurred between strains from different lineages. This hypothesis, depicted by parallel phylogenies, was further confirmed by statistical tests. Our findings, which strongly suggest exchanges between strains from areas of endemicity in West and East Africa, strengthen the potential existence of a sylvatic cycle in the tropical rain forest. This also emphasizes the risk of generating uncontrolled chimeric viruses by using live attenuated vaccines in areas of endemicity.

Genetic Variation↗
PubMed1996

Vector competence of Egyptian mosquitoes for Rift Valley fever virus.

Reintroduction of Rift Valley fever (RVF) into Egypt in 1993 raised concerns about the potential for Egyptian mosquitoes to transmit the virus. We evaluated the ability of Aedes caspius, Culex pipiens, Cx. antennatus, Cx. perexiguus, Cx. poicilipes, and Anopheles pharoensis collected in the Aswan area and Cx. pipiens collected in the Nile Delta to transmit RVF virus. All mosquito species tested were susceptible to RVF virus infection, with An. pharoensis and Ae. caspius being the most sensitive to infection. However, none of 12 An. pharoensis, including 10 with a disseminated infection, transmitted RVF virus by bite. In contrast, nearly all Cx. pipiens (87%, n = 15) and Cx. perexiguus (90%, n = 10) with a disseminated infection transmitted virus. Overall transmission rates for mosquitoes exposed to hamsters with a viremia > or = 10(7) plaque-forming units/ml were Ae. caspius, 20% (n = 5); Cx. pipiens, 7% (n = 102); Cx. antennatus, 7% (n = 30); Cx. perexiguus, 11% (n = 9); and An. pharoensis, 0% (n = 7). Based on abundance, susceptibility to infection, ability to transmit virus, and feeding behavior, Ae. caspius appeared to be the most efficient vector of the Egyptian mosquitoes evaluated. While less susceptible than Ae. caspius, Cx. pipiens, Cx. antennatus, and Cx. perexiguus were also potential vectors during this RVF outbreak in Egypt.

Animals↗
PubMed2005

Validation of IgG-sandwich and IgM-capture ELISA for the detection of antibody to Rift Valley fever virus in humans.

Rift Valley fever (RVF) virus is an important zoonotic and a potential biothreat agent. This paper describes validation of sandwich and capture enzyme-linked immunoassays (ELISA) based on gamma-irradiated antigens for the detection of RVFV-specific IgG and IgM antibody in humans. Validation data sets derived from testing field-collected sera from Africa (n=2400) were dichotomised according to the results of a virus neutralisation test. In addition, sera from laboratory workers immunized with inactivated RVF vaccine (n=93) and serial sera (n=3) from a single RVF case were used. ELISA data were expressed as percentage of high-positive control serum (PP). Cut-off values at 95% accuracy level were optimised using the misclassification cost term option of the two-graph receiver operating characteristics analysis. During the routine use of assays there was no evidence for excessive intra- and inter-plate variations within and between runs of assays. At a cut-off of 13.2 PP the sensitivity of the IgG-sandwich ELISA was 100% and specificity 99.95%, while for the IgM-capture ELISA the values were 96.47 and 99.44%, respectively, at a cut-off of 7.1 PP. Compared to the virus neutralisation test, the IgG-sandwich ELISA was more sensitive in detection of immunological responses in vaccines. Following natural infection class-specific antibodies were detected in serum taken 6 days after onset of symptoms. The results demonstrate that both assays will be useful for early diagnosis of infection, epidemiological surveillance and for monitoring of immune response after vaccination. As highly accurate, robust and safe tests, they have the potential to replace traditional diagnostic methods which are unable to distinguish between different classes of immunoglobulins, and pose health risks necessitating their use being restricted to high containment facilities outside RVF endemic areas.

Antibodies, Viral↗
PubMed1987

Reduced survival of adult Culex pipiens infected with Rift Valley fever virus.

The effect of Rift Valley fever (RVF) viral infection on the survival of female Culex pipiens was examined. In 3 experiments in which mosquitoes ingested RVF virus, there was a 44% decrease in survival to days 14-16 for transmitting vs. nontransmitting mosquitoes, and a 48% decrease in survival for individuals with disseminated vs. nondisseminated infections. These results were corroborated by other experiments in which survival of mosquitoes intrathoracically inoculated with RVF virus was compared with that of those inoculated with diluent. In both the per os and inoculation tests, uninfected mosquitoes survived significantly longer than infected mosquitoes. Even though mosquitoes with disseminated infections had a lower survival rate than did uninfected mosquitoes, dissemination and transmission rates were similar at days 7 and 14-18 after the infectious bloodmeal. This suggests that nondisseminated individuals were developing disseminated infections and becoming capable of transmitting virus between days 7 and 14-18 at approximately the same rate older transmitters were dying. The decreased survival associated with RVF viral infection should be considered in predictive models of this disease.

Animals↗
PubMed1996

Distribution of viral antigen in tissues of new-born lambs infected with Rift Valley fever virus.

The distribution of Rift Valley fever (RVF) viral antigen was studied by immunohistochemistry in the liver, spleen, prescapular lymph node, lungs and kidneys ot eight experimentally infected new-born lambs and in four new-born lambs that died of RVF during the 1974-75 RVF epidemic. The eight experimentally infected lambs were euthanazed at 6, 12, 18, 24, 30, 33, 48 and 51 h post-infection (p.i.), respectively. Immunohistochemical staining utilized polyclonal hyperimmune mouse ascites fluid to RVF virus and peroxidase-diaminobenzidine was substrate. Virus antigen was most prominent in the liver and was detected as early as 18 h p.i. in the cytoplasm of hepatocytes that were sparsely scattered throughout the lobules. At 24-33 h p.i. antigen was also present in or adjacent to small foci of hepatocellular necrosis. At 48-51 h p.i. and in one of the field cases, positive staining was widespread and most consistently present in the cytoplasm of large numbers of degenerated or necrotic hepatocytes and in a new acidophilic bodies. Immunohistochemical staining was rarely observed in hepatocyte nuclei. Almost diffuse histochemical staining was observed in disintegrated cells and in the cytoplasm of necrotic hepatocytes throughout the liver in the other three field cases with pannecrosis; only the primary foci necrosis and a narrow periportal rim of intact hepatocytes did not stain. No staining was observed in bile duct epithelium, endothelial and Kupffer cells in the initial stages of Infection, supporting the contention that hepatocytes constitute the primary site of RVF virus replication in new-born lambs. Few cells stained positively in the spleen, prescapular lymph node, lungs and kidneys.

Animals↗
PubMed1982

The spread of Rift Valley fever and approaches to its control.

Rift Valley fever (RVF) is primarily a disease of sheep, cattle, other domestic animals, and man; it was believed to be relatively benign for man until 1977 when it spread to Egypt. There it caused enormous losses of sheep and cattle, and thousands of human cases occurred, with nearly 600 reported deaths. Although mosquitos are known to transmit RVF virus in epizootics and epidemics, the reservoir and means of inter-epizootic maintenance are not known. RVF epizootics can be recognized by a combination of observations: abortions and neonatal death in sheep and cattle at times when mosquitos are abundant, accompanied by cases of fever in man, which are complicated in a minority of patients by haemorrhagic fever, encephalitis, and retinitis with blindness. Vaccination of livestock with available killed or live attenuated vaccines should prevent transmission to both human subjects and animals. Although routine quarantine of animals is not deemed a practical measure, movement of animals should be restricted when an epizootic is in progress. Since it is possible that RVF may spread from Africa in the future, serological surveillance in man and animals is recommended in potentially receptive countries of the Mediterranean Basin and South-West Asia to establish baseline data and to familiarize staff with the methods of RVF diagnosis.

Africa↗
PubMed1975

Observations on the epidemiology of Rift Valley fever in Kenya.

The epizootic range of Rift Valley fever in Kenya is defined from the results of virus isolations during epizootics, and form an extensive serological survey of cattle which were exposed during an epizootic. A study of the sera from a wide range of wild bovidae sampled immediately after the epizootic, showed that they did not act as reservoir or amplifying hosts for RVF. Virus isolation attempts from a variety of rodents proved negative. Rift Valley fever did not persist between epizootics by producing symptomless abortions in cattle in areas within its epizootic range. A sentinel herd sampled annually after an epizootic in 1968 revealed not one single seroconversion from 1969 to 1974. Certain forest and forest edge situations were postulated as enzootic for Rift Valley fever, and a small percentage of seroconversions were detected in cattle in these areas, born four years after the last epizootic. This has been the only evidence for the persistence of the virus in Kenya since 1968, and may be a part of the interepizootic maintenance cycle for Rift Valley fever in Kenya, which otherwise remains unknown.

Abortion, Veterinary↗
PubMed2006

Descriptive and spatial epidemiology of Rift valley fever outbreak in Yemen 2000-2001.

Rift valley fever (RVF) is an arboviral disease produced by a bunyavirus belonging to the genus Phlebovirus. Several species of Aedes and Culex are the vectors of this virus that affects sheep, goats, buffalos, cattle, camels and human beings. The human disease is well known, especially during periods of intense epizootic activity. The initial description of the disease dates back to 1930, when animals and human outbreaks appeared on a farm in Lake Naivasha, in the Great Rift Valley of Kenya. Until 2000, this disease was only described in Africa, and then outbreaks were also declared in the Kingdom of Saudi Arabia (2000-2001 and 2004) and in Yemen (2000-2001). Animal and human cases were recorded. This work presents a retrospective summary of the data collected on animal RVF cases during this epidemic in Yemen. Results from several RVF surveys were gathered from the Yemeni vet services and FAO experts. Geographical data (topographic maps and data freely available on internet) were used for the location of outbreaks. After cleaning and standardization of location names, all the data were introduced into a GIS database. The spatial distribution of outbreaks was then studied at two scales: at the national level and at a local scale in the particular area of Wadi Mawr in the Tihama plain, Western coast of Yemen.

Animals↗