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Rodenticide-induced signs simulating Rift Valley fever in sheep and goats in Egypt.

Epidemic Rift Valley fever is generally recognised when a higher than expected frequency of abortions and haemorrhages occurs in sheep and other livestock. Other infectious agents can cause similar clinical signs. In Egypt, an outbreak of abortions and haemorrhages in sheep and goats in 1982 was traced to intoxication with the rodenticide brodifacoum. The epidemic lasted for three weeks and resulted in 120 deaths. The end of the epidemic coincided with a heavy rainstorm. This outbreak demonstrates the need for the strict control of the use of rodenticides and widens the differential diagnosis of epidemic abortion in sheep and goats.

4-Hydroxycoumarins↗

Isolation of Rift Valley fever virus from mosquitoes (Diptera: Culicidae) collected during an outbreak in domestic animals in Kenya.

During an outbreak of Rift Valley fever (RVF) in livestock near Lake Naivasha, Rift Valley Province, Kenya, 61,347 mosquitoes (1,287 pools) collected in CO2-baited light traps yielded seven viral isolates. Five isolates of RVF virus were recovered from 18,831 Culex zombaensis Theobald and one from 14,439 Mansonia africana (Theobald). One isolate of a Bunyamwera group virus was recovered from 1,175 Aedes quasiunivittatus (Theobald).

Animals↗

[Epidemiology of Rift Valley fever in western Africa. I. Serologic survey in domestic ruminants of Burkina Faso].

A serosurvey of Rift valley fever virus infection has been conducted among 2,410 domestic ruminants (sheep, goats and cattle) from Burkina Faso in 1985, 1986 and 1987. An active circulation of virus was demonstrated and 26.7% of the total animal tested had Rift valley fever virus reacting antibodies. An epizootic was demonstrated retrospectively for 1987 and appears to correspond to the RVF outbreak observed in the same type of sahelian environment during the same year in Mauritania. Analogous ecoclimatic and environmental risk factors are discussed. Others phleboviruses such as Arumowot, Gordil, Saint-Floris, Gabek Forest and Odrenisrou seem to be active in some areas but no evidence of pathogenesis for domestic ruminants was demonstrated.

Animals↗

Rift Valley fever: an uninvited zoonosis in the Arabian peninsula.

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.

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Immunogenicity of an inactivated Rift Valley fever vaccine in humans: a 12-year experience.

Rift Valley fever (RVF) virus causes serious and fatal disease in animals and man. To protect personnel who work with RVF virus in the laboratory, or troops who may be exposed to this virus, the US Army successfully developed an improved version of inactivated RVF vaccine, TSI-GSD-200. From early 1986 to late 1997, 598 at-risk workers at the US Army Medical Research Institute of Infectious Diseases (USAMRIID) were vaccinated as part of an occupational safety and health program. The subjects of this study received three subcutaneous doses (0, 7 and 28 days) of 0.5 ml of TSI-GSD-200. A total of 540 vaccinees (90.3%) initially responded (group A) with an 80% plaque-reduction neutralization antibody titer (PRNT80) of > or =1:40; whereas 58 subjects (9.7%) were initial nonresponders (group B) failing to achieve this titer. Volunteers who either failed to respond or who achieved a titer of > or =1:40 but whose titer waned below 1:40 were boosted 1-4 times with the same vaccine. Among 247 group A subjects who received the first recall injection, 242 (98%) were successfully boosted, achieving a PRNT80 > or =1:40. Thirty-three of 44 (75%) initial nonresponders were converted to responder status after the first booster, which is a lower rate than that of group A (P < 0.001). After the primary series and the first booster, Kaplan-Meier analysis showed 50% probability of group A members maintaining a titer of > or =1:40 for approximately eight years; whereas group B had a 50% probability of maintaining a titer for only 204 days. Group A immune response rates to boosts 1-4 ranged from 87 to 100% with geometric mean titers (GMTs) ranging from 80 to 916. Boosts 1-4 immune response rates of group B volunteers ranged from 67 to 79% with GMTs ranging from 90 to 177. Minor side effects to TSI-GSD-200 were noted in 2.7% of all vaccinees after primaries and 3.5% of all vaccinees who had primaries and up to four boosters. We conclude that the use of TSI-GSD-200 is safe and provides good long-term immunity in humans when the primary series and one boost are administered.

Adolescent↗

Rift Valley fever epidemic in Saudi Arabia: epidemiological, clinical, and laboratory characteristics.

This cohort descriptive study summarizes the epidemiological, clinical, and laboratory characteristics of the Rift Valley fever (RVF) epidemic that occurred in Saudi Arabia from 26 August 2000 through 22 September 2001. A total of 886 cases were reported. Of 834 reported cases for which laboratory results were available, 81.9% were laboratory confirmed, of which 51.1% were positive for only RVF immunoglobulin M, 35.7% were positive for only RVF antigen, and 13.2% were positive for both. The mean age (+/- standard deviation) was 46.9+/-19.4 years, and the ratio of male to female patients was 4:1. Clinical and laboratory features included fever (92.6% of patients), nausea (59.4%), vomiting (52.6%), abdominal pain (38.0%), diarrhea (22.1%), jaundice (18.1%), neurological manifestations (17.1%), hemorrhagic manifestations (7.1%), vision loss or scotomas (1.5%), elevated liver enzyme levels (98%), elevated lactate dehydrogenase level (60.2%), thrombocytopenia (38.4%), leukopenia (39.7%), renal impairment or failure (27.8%), elevated creatine kinase level (27.3%), and severe anemia (15.1%). The mortality rate was 13.9%. Bleeding, neurological manifestations, and jaundice were independently associated with a high mortality rate. Patients with leukopenia had significantly a lower mortality rate than did those with a normal or high leukocyte count (2.3% vs. 27.9%; odds ratio, 0.09; 95% confidence interval, 0.01-0.63).

Adolescent↗

Induction of severe disease in hamsters by two sandfly fever group viruses, Punta toro and Gabek Forest (Phlebovirus, Bunyaviridae), similar to that caused by Rift Valley fever virus.

Adult golden hamsters inoculated subcutaneously with either of two sandfly fever group viruses, Punta Toro and Gabek Forest (Phlebovirus, Bunyaviridae), developed a fulminating fatal illness characterized by hepatic and splenic necrosis and interstitial pneumonitis. Most animals died within three days after infection; this was accompanied by high levels of viremia. Necropsy and histopathologic examination of the infected animals revealed pathologic changes involving multiple organs that resembled those described in Rift Valley fever. These two hamster-phlebovirus systems may serve as alternative animal models for Rift Valley fever and should be useful in studying the pathogenesis of severe phlebovirus infection and for testing potential therapeutic agents.

Animals↗

The pathology of Rift Valley fever. II. Lesions occurring in field cases in adult cattle, calves and aborted foetuses.

Since the original description of Rift Valley fever in sheep, cattle and man in the Rift Valley in Kenya in 1931, very little has been published on the disease in cattle. This report deals with the macroscopic and microscopic pathology of field cases of Rift Valley fever in 22 adult cattle, 8 calves and 8 aborted foetuses. The microscopic liver lesions in 13 adult cattle were characterized by marked centri- and midzonal eosinophilic necrosis, involving almost 2/3 of the lobules, and accompanied by sparsely distributed primary foci of necrosis. In 3 animals, however, the hepatic lesions were more focal in nature, while a massive hepatic necrosis was evident in 6 others. In calves, the lesions in the liver ranged from cases showing numerous haphazardly scattered primary foci of necrosis to cases where the latter were accompanied by eosinophilic necrosis of the remaining hepatocytes in the lobules. Vascular lesions, thrombosis and sinusoidal fibrin deposits were sometimes seen in the livers of both calves and adult cattle. Although the aborted foetuses were in a fairly advanced state of autolysis, it was still possible to make a diagnosis of Rift Valley fever from the characteristic lesions which were similar to those reported for new-born lambs. Other noteworthy lesions in adult cattle and calves included pyknosis and karyorrhexis of lymphocytes in the spleen and lymph nodes, widespread serosal and visceral haemorrhages which were sometimes accompanied by copious free blood in the gastrointestinal tract, and a nephrosis.

Animals↗

An epidemic of Rift Valley fever in Egypt. 2. Isolation of the virus from animals.

During the epidemic of Rift Valley fever (RVF) that occurred in Egypt and other areas of North Africa in 1977, the virus was isolated from various species of domestic animal and rats (Rattus rattus frugivorus) as well as man. The highest number of RVF virus isolates were obtained from sheep; only one isolate was recovered from each of the other species tested, viz. cow, camel, goat, horse, and rat. RVF virus was reisolated from both camel and horse sera, apparently for the first time.

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Antigenic analysis of Rift Valley fever virus isolates: monoclonal antibodies distinguish between wild-type and neurotropic virus strains.

Rift Valley fever virus (RVFV) isolates from southern Africa were analysed for possible strain variation using monoclonal antibodies prepared against the South African prototype RVF 1830 strain. By the indirect immunofluorescence antibody assay and neutralization tests, the wild type southern African isolates were found to be antigenically similar to RVFV strains from other parts of Africa. In contrast, differences in several biologically important neutralizing and haemagglutination epitopes on both the G1 and G2 glycoproteins of the attenuated Onderstepoort veterinary vaccine and the Smithburn neurotropic strain were identified.

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Comparison of techniques for demonstrating antibodies to Rift Valley fever virus.

Nine serological techniques were compared by monitoring the response to infection with Rift Valley fever (RVF) virus in three sheep. Antibodies were monitored daily for the first 14 days after infection, then weekly and later fortnightly up to week 24. The earliest antibody response was detected in one sheep on day 3 by a plaque reduction neutralization test, and by day 6 antibodies were demonstrable in all three sheep by haemagglutination-inhibition, reversed passive haemagglutination-inhibition, immunodiffusion, indirect immunofluorescence (IF), enzyme-linked immunosorbent assay and neutralization of cytopathic effect in cell cultures. Antibodies were demonstrable by complement fixation on day 8 at the earliest. IF and the two neutralization techniques produced the highest titres, but all tests could be used satisfactorily for the serological diagnosis of RVF. Inactivated antigen could be used for all except the neutralization tests. A radioimmunoassay technique using 125I-labelled staphylococcal protein A detected antibodies on day 8 at the earliest and produced lower mean titres than some of the other techniques. This was probably because sheep immunoglobulins bind protein A poorly.

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Isolation of the Rift Valley fever virus by inoculation into Aedes pseudoscutellaris cells: comparison with other diagnostic methods.

The Rift Valley fever epidemic, which arose in the south of Mauritania beginning on October 15, 1987, enabled a comparative study of different diagnostic methods among humans. During the first two weeks of the epidemic, four parallel methods were used: inoculation into Aedes pseudoscutellaris cells, inoculation intracerebrally into suckling mice, tests by immunocapture of the circulating antigen and detection of type IgM gammaglobulins. Of 370 examined sera, 181 showed at least one marker of recent infection. Inoculation into A. pseudoscutellaris cells was by far the most sensitive and easiest method to use. Detection of the antigen by immunocapture was also a useful technique, since it allowed quick aetiological diagnosis or examination of sera conserved under poor conditions. However, its sensitivity was weak, as it could only detect 26% of positive cases. Vero cells used on a limited scale, in this particular case seemed less sensitive than A. pseudoscutellaris cells. Of a total of 991 sera, 221 diagnoses were reported by discovery of the virus and 271 by detection of specific IgM. In every case, A. pseudoscutellaris cells seemed most appropriate as the system of reference.

Aedes↗

Rift Valley fever virus: a seroepidemiologic study of small terrestrial vertebrates in South Africa.

Epizootics of Rift Valley fever (RVF) are often associated with periods of heavy rainfall, which are favorable for mosquito vectors. However, in seasons with normal or low rainfall, enzootic circulation occurs, suggesting the existence of a natural host that can act as a cryptic carrier during interepizootic periods. To confirm the role of heavy rainfall in epizootic circulation, and to identify a possible natural host of RVF virus, serum samples from small terrestrial mammals in the Free State and Northern Cape regions of South Africa were collected before and after the 1988 floods. These areas are known to support epizootic circulation of RVF virus. The samples were tested for the presence of RVF virus-specific IgG using an ELISA and positive sera were confirmed by a neutralization test. Forty-seven (15%) of 312 Aethomys namaquensis (Namaqua rock rat) had antibodies to RVF virus. Of these positive sera, nine (6%) of 141 were collected before the floods of 1988 and 38 (22%) of 171 were collected afterwards (P = 0.001). Naive A. namaquensis were inoculated with RVF virus and developed a viremia, but no clinical symptoms, suggesting that they can act as temporary asymptomatic carriers of the virus. These results suggest a role for A. namaquensis as a cryptic carrier for RVF virus during interepizootic periods and support the results of other studies suggesting an amplifying role for heavy rainfall in the circulation of RVF virus.

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