Three hundred eighteen European cows and 115 buffaloes were vaccinated with locally prepared Smithburn vaccine, of which, 100 cows and 20 buffaloes were pregnant. Twenty-eight cows aborted within 72 days post-vaccination, buffaloes did not abort. Blood samples collected 77 days post-vaccination from aborted cows, 17 pregnant cows, 5 pregnant buffaloes, and 32 non-pregnant cows. Sera were tested by ELISA for anti-RVF IgM and IgG. All aborted cows were strongly positive for IgG. Five of 17 cows and two of five buffaloes that did not abort were IgG positive. The percentage of IgM positives in aborted cows was 25% and 0% in non-aborted cows. The percentage of IgG positives in pregnant non-aborted cows was lower than in non-pregnant cows. The percentage of IgG positives of non-pregnant cows was lower than pregnant aborted cows. Virus was isolated from one aborted fetus. The nucleotide sequence of fetus virus was compared to Smithburn of Onderstepoort, local Smithburn and virus isolates from 1993 to 1994 and 1977 RVF outbreaks. The nucleotide sequences of Onderstepoort and Egyptian Smithburn vaccines were almost identical. The sequences of 1993-1994 isolates were identical to 1977 outbreak virus. Virus from the fetus had two mutations; it is apparently a variant that is genetically distant from local Smithburn and Onderstepoort vaccines. Fetus virus was genetically distant from virus of 1993/1994 and 1977 outbreaks. In conclusion, antibody response to vaccination with local Smithburn had occurred in some, but not all the cows and buffaloes. Virus isolation from the fetus suggests in utero transmission of used vaccine virus, which resulted in high abortions in European cows.

The relative importance of arthropod-borne and other disease pathogens as the cause of an outbreak of febrile illnesses was assessed during August 1988, following severe flooding in Khartoum, Sudan. A total of 200 patients with acute febrile illness and 100 afebrile controls were enrolled in the study during October and November 1988; at the Omdurman Military Hospital, Khartoum, Sudan. Sera were tested for IgM and IgG antibodies to six arthropod-borne viruses by an enzyme-linked immunoabsorbent assay, and for similar antibodies to Lassa fever, Crimean-Congo hemorrhagic fever, and Ebola and Marburg viruses by an indirect fluorescence assay. Thick and thin blood smears were examined microscopically for malaria parasites, and fecal and blood specimens were tested for bacteria by standard culture methods. Among the acute and convalescent sera collected from 67 febrile patients, five cases were caused by sandfly fever Sicilian (SFS), six by sandfly fever Naples (SFN), and 12 by unidentified phleboviruses. Of 233 remaining unpaired, acute-phase sera collected from cases and controls, 49 (21%) had IgM antibodies to SFS or SFN, RVF, West Nile (WN), and Chikungunya (CHIK) viruses. Forty-three (22%) of 192 febrile cases and two of the 100 afebrile controls were positive for Plasmodium falciparum, and bacterial enteropathogens were associated with 25 (13%) cases and four controls. These data indicated that phleboviruses and to a lesser extent, WN, P. falciparum, and enterobacterial pathogens were causes of acute febrile illnesses following the 1988 flood in Khartoum, Sudan.

Epidemics of a malaria‐like illness affected several thousand residents of the Dam Camp, a refugee camp near Hargeysa in Somalia, during 1985, 1986, and 1987. The disease was characterized by fever, chills, sweats, headache, back and joint pains for as long as 10 days in some patients. Blood smears from acutely ill patients were negative for malaria. Of 28 acute and 10 convalescent sera tested by the indirect fluorescent antibody (IFA) and by the hemagglutination inhibition (HI) tests, all were negative for antibody to Rift Valley fever, Crimean‐Congo hemorrhagic fever, Sindbis, Chikungunya, yellow fever, and Zika viruses. However, antibody reactive to dengue 2 virus was detected by the IFA test in 39% (15/38), and 11 of 29 (38%) of the same sera were antibody positive by the HI test. Also, IgG antibody reactive to dengue 2 was demonstrated in 60% (17/28) of the same sera by the enzyme immunoassay (EIA), and 14% (4/28) were positive for IgM antibody. Of ten patients for which acute and convalescent sera were available, two developed four fold or greater rises in antibody titer evidencing infection. These data suggested that dengue virus may have been the cause of the epidemic among the Dam Camp refugees.

Nineteen street rabies virus strains, isolated in Egypt from humans (two), dogs (nine), cats (two), farm animals (two), gerbils (three), and a jackal were antigenically analyzed. The Pasteur strain used for the preparation of human rabies vaccine, the Flury high and low egg passage stains (HEP, LEP) used for animal vaccines, and the challenge virus standard (CVS) strain were also assayed. All were examined by the indirect fluorescent antibody test, using a panel of 20 monoclonal antibodies against the nucleocapsid of rabies and rabies-related viruses. The rabies isolates demonstrated patterns of reactivity with the antinucleocapsid panel different from those of the Pasteur, HEP, and CVS strains. Representative human, dog, and rodent isolates were analyzed by neutralization tests in mice, with a second panel of 19 monoclonal antibodies against rabies and Mokola envelope glycoproteins. With this panel, the isolates demonstrated patterns of reactivity different from the vaccine strains. These data indicate antigenic variation between wild virus and vaccine strains.

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