viruses, and virus-infected cells. Springer Seminarsin Immunopathology, 6,327-347.
Cooper, N. R., Jensen, F. C., Welsh, R. M. & Oldstone, M. B. A. (1976). Lysis of RNA tumor viruses by human serum: direct antibody independent triggering of the classical complement pathway. Journal of Experimental Medicine, 144, 970-984. Halstead, S. B., O’Rourke, E. J. & Allison, A. C. (1977). Dengue viruses and mononuclear phagocytes. II. Identity of blood andtissueleukoc tessupportingin vitro infection.Journal of ExperimentalMe z.rcme, 146,218-229.
Klerx, J. P. A. M., Beukelman,C. J., Van Dijk, H. & Willers, J. M. N. (1983). Microassay for calorimetric estimation of complement activity in guinea pig, human and mouse serum.
Journal of Immunological Methods, 63,215-220.
Kuberski, T. T., Rosen, L., Reed, D. & Mataika, J. (1977). Clinical and laboratory observations on patients with primary and secondarydenguetype 1 infections with hemorrhagic manifestations in Fiji. American 3oumal of Tropical Medicine and Hygiene, 26,775-783.
Ruangjirachuporn, W., Boonpuch’navig, S. & Nimmannitya,
S. (1979). Circulating immune complexes in serum from patiets with denaue haemorrhaeic fever. Clinical and Extwrimental Immunolo&, 36,46-53.
Russell, P. K., Intavivat, A. & Kanchanapilant, S. (1969). Antidengue immunoglobulins and serum St c/a globulin levels in &;p,, shock syndrome. Journal of Immunology, 102, 412-
Rymzo,W. T., jr, Cline, B. L., Kemp, G. E., Sather,G. E. &
Craven, P. C. (1976). Dengue outbreaks in Gu’anica-Ensenadaand Villalba, Puerto Rico, 1972-1973. AmericanJournal
and Hygiene, 25,136-145.
Singh, V. K. & Tingle, A. J. (1982). Detection of circulating immune complexes by a Clq-microplate ELBA system. Journal of Immunological Methods, 50, lo%1 14. WHO (1973). Pathogenetic mechanisms in dengue haemorrhagic fever: report of an international collaboration study. Bulletin of the World Health Organization, 48, 117-133. Received accepted
1991; revised 5 Februay 19 Februa y I992
TRANSACTIONS OF THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE (1992) 86, 675
were sequentially resampled during the following 6 months.
Duration of immunoglobulin M antibodies against Rift Valley fever virus in cattle after natural infection J. Morvan*y P. E. Rollin*, S. Laventurel and J. Roux1 ‘Unite’ de Recherche sur k-s Arbovirus, Institut Pasteur de Madagascar, Antananarivq, Madagascar; *Laboratoire des Fikvres Ht%norragi$ues Vtrales, Institut Pasteur, Paris, France
IFA continued to reveal IgG in all the animals during the entire follow-up period. IgM antibodies detectable by ELISA decreased rapidly during the survey period (Table): only 27% of the cattle remained positive 2 Table. Enzyme-lied immunosorbent assay capture IgM results in cattle after natural Rift Valley fever infection in Madagascar
Months after infection s
During Rift Valley fever (RVF) outbreaks, virus isolation is often unsuccessful becauseof the short duration of viraemia and late sampling. Late diagnosis often depends on serological assays.RVF virus infection is generally associated with a high and early humoral response. Detection of immunoglobulin (Ig) G and IgM by enzymelinked immunorbent assay (ELISA) is often done on a single serum sample and the resence of IgM is usually interpreted as an indication o4 recent infection. We lack solid documentation of the duration of detectable IgM following infection with RVF virus, but limited data suggest that the IgM antibodies are likely to become undetectable less than one year following infection (KSIAZEK et al., 1989). A study done in sheep vaccinated with the attenuated strain MP-12 of RVF virus showed that IgM antibodies were undetectable after 60 d (M. Guillaud et al., unpublished data). The recent RVF outbreak in Madagascar (MORVANet al., 1991a), occurring in state farms with individuallyidentified animals, offered a unique opportunity to follow IgM persistence in cattle. The outbreak was first clinically identified by an unusual number of abortions in a short period of time, then confirmed by successful RVF virus isolations from aborted foetuses and dead calves. Specific antibody detection was done by IgM capture ELISAand/or IgG immunofluorescent assay(IFA) on infected spot slides as previously described (KSIAZEK et al., 1989; MORVAN et al., 1991b). 195 serologically positive animals (37 of which were recently aborting females)
Cattle ~~~~s.~pecificIgM Aborted animals Total females 37 158 13 2 7
months after the acute infection, and all were negative after 6 months. No significant difference (life-table analysis) was found in the decreaseof antibody between the recently aborting animals and the others. This report appears to be the first sequential follow-up of IgM antibody to RVF virus in naturally infected animals and confiis the previous suggestion that IgM detection in serosurveysis evidence of recent infection. References Ksiazek, T. G., Jouan, A., Meegan, J. M., Le Guenno, B., Wilson, M. L., Peters, C. J., Digoutte, J. P., Guillaud, M., Merzoug, N. 0. & Touray, E. M. (1989). Rift valley fever among domestic animals in the recent West African outbreak. Research in Virology, 140,67-77. Morvan, J., Rollin, P. E., Laventure, S., Rakotoarivony, I:, Coudrier, D. & Roux, J. (1991a). Rift valley fever epizoouc in the central highlands of Madagascar. 40th Annual Meeting of the American Society of Tropical Medicine and Hygiene, Boston, December l-5, abstract no. 135.
Morvan, J., Saluzzo, J. F., Fontenille, D., Rollin, P. E. & Coulanges, P. (1991b). Rift valley fever in the east-coastof Madagascar.Research in Virology, 142,475-482. Received 26 February 1992; accepted for publication March 1992