Yellow fever in the Gambia, 1978--1979: epidemiologic aspects with observations on the occurrence of orungo virus infections
Monath, T.P.; Craven, R.B.; Adjukiewicz, A.; Germain, M.; Francy, D.B.; Ferrara, L.; Samba, E.M.; N'Jie, H.; Cham, K.; Fitzgerald, S.A.; Crippen, P.H.; Simpson, D.I.; Bowen, E.T.; Fabiyi, A.; Salaun, J.J.
American Journal of Tropical Medicine and Hygiene 29(5): 912-928
1980
ISSN/ISBN: 0002-9637 PMID: 7435793 Document Number: 167236
An epidemic of yellow fever occurred in the Gambia between May 1978 and January 1979. Retrospective case-finding methods and active surveillance led to the identification of 271 clinically suspected cases. A confirmatory or presumptive laboratory diagnosis was established in 94 cases. The earliest serologically documented case occurred in June 1978, at the extreme east of the Gambia. Small numbers of cases occurred in August and September. The epidemic peaked in October, and cases continued to occur at a diminishing rate until January, when a mass vaccination campaign was completed. The outbreak was largely confined to the eastern half of the county (MacCarthy Island and Upper River Divisions). In nine survey villages in this area (total population 1531), the attack rate was 2.6-4.4%, with a mortality rate of 0.8%, and a case-fatality rate of 19.4%. If these villages are representative of the total affected region, there may have been as many as 8400 cases and 1600 deaths during the outbreak. The disease incidence was highest in the 0- to 9-year age group (6.7%) and decreased with advancing age to 1.7% in persons over 40 years. Overall, 32.6% of survey village inhabitants had yellow fever complement-fixing (CF) antibodies. The prevalence of antibody patterns indicating primary yellow fever infection decreased with age, in concert with the disease incidence. The overall inapparent:apparent infection ratio was 12:1. In persons with serological responses indicating flaviviral superinfection, the inapparent:apparent infection ratio was 10 times higher than in persons with primary yellow fever infection. Sylvatic vectors of yellow fever virus, principally mosquitoes of the group of Aedes furcifer (Edw.) and A. taylori Edw. and A. luteocephalus (Newst.) are believed to have been responsible for transmission, at least at the beginning of the outbreak. Eighty-four per cent. of wild monkeys shot in January 1979 had yellow fever neutralising antibodies, and 32% had complement-fixing antibodies. Domestic adults of A. aegypti (L.) were absent or present at very low indices in many severely affected villages. In January, however, A. aegypti-borne yellow fever 2.5 months into the dry season was documented by the isolation of yellow fever virus from a sick man and from this vector species in the absence of sylvatic vectors. Thus, in villages where the classical urban vector was abundant, interhuman transmission by A. aegypti occurred and continued into the dry season. A mass vaccination campaign, begun in December, was completed on 25 January, with over 95% coverage of the Gambian population. A seroconversion rate of 93% was determined in a group of vaccines. This outbreak emphasises the continuing public health importance of yellow fever in West Africa and points out the need for inclusion of 17D yellow fever vaccination in future programmes of multiple immunisation.