VIR VHF EC 84.6 Eng.Pdf (1.858
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WORLD HEALTH ORGANIZATION VIR/VHF/EC/84.6 ORGANISATION MONDIALE DE LA SANTE ENGLISH ONLY INDE/ EXPERT COMMITTEE ON VIRAL HAEMORRHAGIC FEVER Geneva, 19-23 March 1984 Draft agenda item 3.1 EPIDEMIOLOGICAL, CLINICAL AND PHYSIOPATHOLOGICAL DESCRIPTION OF YELLOW FEVER IN AFRICA by ' f^-- c Dr P. Brès Institut Pasteur, Paris Although the first epidemic which could reasonably be attributed to yellow fever was described in Senegal in 1778, it is certain that this disease was well established in the African continent before that time, and was particularly feared by European sailors, troops and traders. Several large outbreaks periodically decimated the expatriate populations on the West Coast, but the disease was well known to occur in the Africans as well. In 1972, during one of the periodical outbreaks of the disease, the virus was isolated simultaneously by the Rockefeller Foundation Mission at Accra, Ghana, from the blood of an African patient named Asibi, and by workers at the Pasteur Institute, Dakar, Senegal, from the blood of a Lebanese, by inoculation of the susceptible Indian rhesus monkey. The strain from the Pasteur Institute was further adapted to mouse brain by M. Theiler and became known as the French Neurotropic Virus. Apart from a different degree in neurotropism, both strains are identical but they show a slight antigenic difference compared with the South-American strains and with the 17D vaccine substrain derived from the Asibi strain and which was not passaged in mouse brain. The molecular structure of yellow fever virus has recently been studied ana found somewhat similar to that of other viruses of the Flavivirus genus of the Togaviridae family. In spite of similarities with the American virus, the epidemiology of yellow fever is somewhat different in Africa. The clinical pattern of classical severe forms of the disease has not changed since the first descriptions by Dutrouleau in 1858, but mild cases have been more frequently recognized since 1930 owing to the progress in laboratory diagnostic methods. However, there has been little opportunity in Africa recently to add to the classical descriptions and improve the knowledge available ot the physiopathology of the disease. The issue of this document does not constitute Ce document ne constitue pas une publication. formal publication. It should not b« reviewed, Il ne doit faire l'objet d'aucun compte rendu ou abstracted or quoted without the agreement of résumé ni d'aucune citation sans l'autorisation de the World Health Organization. Authors alone l'Organisation mondiale de la Santé. Les opinions are responsible for views expressed in signed exprimées dans les articles signés n'engagent que articles. leurs auteurs. VIR/VHF/EC/84.6 Page 2 1. EPIDEMIOLOGY 1.1 Geographical Distribution The endemic, zone for yellow fever defined by the International Health Regulations lies between the 15th parallel North and the 10th South and includes totally or partially 28 countries. This zone has been delimited on the basis of neutralization tests in a serological survey carried out in these countries in the 193ÛS under the Rockefeller Foundation auspices. 1.2 Virus Transmission Chains The first data on the virus transmission chains in Africa were obtained by the Rockefeller Mission in Bwamba County, Uganda, in the 1930s. It was proved that the virus was transmitted between monkeys in the forest canopy by the Aedes africanus mosquito (sylvatic yellow fever). Monkeys infected in the forest may raid banana plantations in nearby villages and are bitten by Aedes simpsoni mosquitoes which breed in plant axils and afterwards can bite man (jungle yellow fever). In villages, the virus can be transmitted from person to person by Aedes aegypti; if present, or by Aedes simpsoni (so called "urban" yellow fever). This pattern, typical of East Africa, was observed in Ethiopia during the large epidemic of 1960-1962 which caused about 100,000 cases, of which 30,000 died out of a population of one million inhabitants. The attack rate was lower in the Didessa valley, where man was infected by Aedes africanus on entering the forest, than in the Omo valley where man was infected by Aedes simpsoni in villages. A slightly different transmission pattern has been found recently in West Africa involving other mosquito species (table 1). Although Aedes simpsoni is also present in Africa west of the Cameroons, it does not bite man. Studies carried out by the Institut Pasteur and the Oftice de la Recherche scientifique et technique Outre-mer have shown the same enzootic basic maintenance cycle of monkey-to-monkey transmission in the western strip of the Congolese Guinean rain forest by Aedes africanus mosquitoes. This causes exceptionally a few sporadic human cases (sylvatic yellow fever). From the forest cycle, the virus can irradiate periodically along riverine forests which penetrate into the surrounding savanna zone and is transmitted by different vector mosquito species according to the type of savanna, humid (Guinean) or dry (Sundanese): this is the "emergency zone" (table 1). Sporadic human cases reflect an enzootic situation, or circumscribed outbreaks reflect an epizootic situation in monkeys. Man-to-man transmission may also be caused by these mosquitoes, which play the same role as Aedes simpsoni in the East (jungle yellow fever). It has been shown that the density of mosquitoes in riverine forests increases during the second half of the rainy season, first for Aedes luteocephalus and soon after Aedes furciier and Aedes taylori. The proportion of infected mosquitoes also increases rapidly. Male mosquitoes have been found naturally infected with yellow fever virus which proves the "vertical" (transovarial) transmission through eggs which persist VIR/VHF/EC/8A.6 Page 3 between two rainy seasons. Although this mechanism may transmit the virus through the dry season only to a low percentage of the Fl generation, it may perpetuate the virus locally for two or three years if the virus circulation is enhanced each year by infection of non-immune monkeys which can be a source of virus to infect many more mosquitoes. R.M. Taylor stated in 1951 that "from the aspect of the time element and the reservoir of the virus, the mosquito qualities better as a host than does the vertebrate, for it is in the mosquito that the virus finds a more permanent abode" (1). In order to determine the risk for nearby villages, the enzootic or epizootic activity of the virus in the riverine forest can be monitored by capture of mosquitoes to find the presence of vector species and monkeys to find serological evidence of recent infection. At long intervals, the virus may progress further during the rainy season towards villages in the semi-arid zone where Aedes aegypti colonizes in domestic breeding sites, or in towns, where most of the human population no longer has any immunity since the last epidemic or vaccination campaign, and this may cause severe and extended epidemics of urban yellow fever. The virus may be transported from the jungle cycle to distant places by infected mosquitoes or patients. Incidence in the Population There is no ethnic difference in susceptibility to infections. Maternal immunity, if strong enough, may protect a child until about six months of age. It seems that repeated infections with certain other flaviviruses closely related antigenically to yellow fever virus such as Zika, Wesselsbron, Uganda S, might afford some degree of cross-protection by the age of 15 years. Experimentally, the viraemia after challenge with yellow fever virus is lower if the monkey has been immunized with dengue, Zika and Wesselsbron virus. However, whether dengue would result in cross-protection of man against yellow fever is not certain, knowing that yellow fever vaccination does not protect against dengue. During urban outbreaks of yellow fever in the past, it was observed that the epidemic "burned itself out" when about 60-80% of the population had been infected. These figures can be taken as targets for vaccination coverage. Epidemics which occurred in Africa during the period 1965-1983 are indicated in table 2. The numbers of notified cases are frequently under-estimated. By comparison with the regular pattern of yearly occurrence of yellow fever in the Americas it may be seen that outbreaks occur at less regular intervals in Africa. Sporadic cases of jungle yellow fever are rarely detected in Africa because of the scarcity of entomological surveys and lack of laboratory capabilities for virus isolation. Even outbreaks reaching some importance may also not be reported to health authorities. Situations have been documented where an important epizootic activity was going on in riverine forests and sero conversions occurred in the child population or nearby villages without any evidence of clinical outbreaks. This may be interpreted as a low virulence of the virus in the sylvatic cycle, whereas it can be enhanced after some man-to-man transmission cycles. VIR/VHF/EC/84.6 Page 4 2. CLINICAL FEATURES Classical severe torms of yellow fever can easily be recognized by their clinical features. The incubation period is 3-6 days after the bite of an infected mosquito. The onset is abrupt with lumbosacral and generalized muscular pains, intense headache, conjunctival infection, flushed face, nausea and vomiting. Faget's sign (slow pulse in relation to the fever) is typical. After a short remission of fever the toxic and haemorrhagic conditions develop; epistaxis, gum bleeding, black, spots (as flies) in vomiting which announce the massive black vomit of digested blood, the ascending albuminuria (a good sign but sometimes of late appearance and not constantly found), uremia, the deterioration of central nervous system functions, coma and terminal shock syndrome. Jaundice is in general moderate and may even not be visible before death. The case fatality ratio varies between 20-80^.