African horse sickness: transmission and epidemiology Ps Mellor To cite this version: Ps Mellor. African horse sickness: transmission and epidemiology. Veterinary Research, BioMed Central, 1993, 24 (2), pp.199-212. hal-00902118 HAL Id: hal-00902118 https://hal.archives-ouvertes.fr/hal-00902118 Submitted on 1 Jan 1993 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Review article African horse sickness: transmission and epidemiology PS Mellor Institute for Animal Health, Pirbright Laboratory, Ash Road, Pirbright, Woking, Surrey, UK (Received 29 June 1992; accepted 27 August 1992) Summary ― African horse sickness (AHS) virus causes a non-contagious, infectious, arthropod- borne disease of equines and occasionally of dogs. The virus is widely distributed across sub- Saharan African where it is transmitted between susceptible vertebrate hosts by the vectors. These are usually considered to be species of Culicoides biting midges but mosquitoes and/or ticks may also be involved to a greater or lesser extent. Periodically the virus makes excursions beyond its sub-Saharan enzootic zones but until recently does not appear to have been able to maintain itself outside these areas for more than 2-3 consecutive years at most. This is probably due to a number of factors including the apparent absence of a long term vertebrate reservoir, the prevalence and seasonal incidence of the vectors and the efficiency of control measures (vaccination and vector abatement). The recent AHS epizootics in Iberia and N Africa spanning as they do, 5 or more yr, seem to have established a new pattern in AHS virus persistence. This is probably linked to the con- tinuous presence of adult C imicola in the area. Culicoides imicola is basically an Afro-Asiatic insect and prefers warm climates. Therefore its continuous adult presence in parts of Iberia and N Africa may be due to some recent moderations of the climate in these areas. African horse sickness / transmission / epidemiology Résumé ― La peste équine : transmission et épidémiologie. Le virus de la peste équine provo- que chez les équins et occasionnellement chez le chien, une maladie infectieuse non contagieuse, transmise par des arthropodes. Ce virus est largement réparti au Sud du Sahara où il est transmis aux hôtes vertébrés sensibles par des vecteurs. On a l’habitude de considérer que ceux-ci sont des moucherons piqueurs (Culicoides) mais des moustiques et/ou des tiques peuvent être également impliqués dans une plus ou moins grande mesure. Périodiquement, le virus fait des apparitions au- delà des zones enzootiques sub-sahariennes mais pendant longtemps il n’a pas réussi à se mainte- nir en dehors de ces zones pendant plus de 2-3 ans consécutifs. Ce fait est probablement dû à de nombreux facteurs mais en particulier à l’absence apparente d’un réservoir de vertébrés de longue durée chez les vertébrés, à la prévalence et à l’incidence saisonnière des vecteurs et à l’efficacité des mesures de contrôles (vaccination et réduction des vecteurs). Les épizooties récentes de peste équine dans la péninsule ibérique et en Afrique du Nord, qui se sont étendues sur 5 ans ou plus, semblent avoir établi un nouveau modèle de persistence du virus. Ceci est probablement dû à la présence permanente d’adultes de C imicola dans cette zone. C imicola est un insecte localisé es- sentiellement en Afrique et en Asie et qui préfère les climats chauds. La présence permanente d’adultes dans certaines parties de la péninsule ibérique et en Afrique du Nord pourrait s’expliquer par une modification récente du climat dans ces régions. peste équine / transmission / épidémiologie INTRODUCTION which occurred in 1327 (Mouie. 1896). However despite this early record the virus group appears to have originated in Africa African horse sickness (AHS) virus is a and was first as a distinct dis- double stranded RNA virus which causes recognised ease entity there subsequent to the intro- a non-contagious, infectious, arthropod- duction of breeds of borne disease of equines. The disease is highly susceptible characterised by clinical signs which de- equine during the exploration of Central Af- rica. The earliest account comes from East velop as a result of the impaired function In of the circulatory and respiratory systems Central Africa in 1569 (Theal, 1899). southern Africa the disease has been rec- giving rise to serous effusions and hae- since the of the morrhage in various organs and tissues ognised occupation Cape (Howell, 1963). The extent and severity of of Good Hope by the Dutch East India at the of the l8th cen- the clinical signs caused by AHS virus are Company beginning frequently used to classify the disease into tury when large numbers of deaths oc- curred in horses 4 distinct forms. In increasing order of se- imported (Henning, 1956). verity these are horse sickness fever, the However, it was not until 1900 that subacute or cardiac form, the cardio- M’Fadyean using samples of infected pulmonary or mixed form and the peracute horse blood showed that the agent of or pulmonary form. Comprehensive ac- horse sickness fever was able to pass counts of the clinical signs, pathogenesis through bacterial filters and concluded that and pathology caused in equines by AHS it was an &dquo;ultravisible&dquo; virus. Theiler in a se- virus have been published by Rafyi (1961), ries of experiments covering several years Howell (1963), Erasmus (1973), Mircham- (1908, 1915 and 1921) then recognised sy and Hazrati (1973) and Lubroth (1988). that AHS virus existed as a number of anti- AHS virus exists as a number of distinct genically distinct strains but not until 1962 serotypes and to date 9 have been inter- were the 2 most recent internationally ac- nationally recognised. Animals recovering cepted serotypes (8 and 9) identified and from an infection with any one of these characterised (Howell, 1962). The isolation serotypes develop a solid immunity to it of an additional strain of AHS virus in Ken- but may continue to be susceptible to het- ya (G-75), that apparently is not neutral- erologous serotypes (Anonymous, 1978). ised by antisera to any of the 9 recognised Since under natural conditions AHS vi- serotypes, suggests that a further serotype rus is transmitted between its vertebrate should now be added to the internationally hosts virtually exclusively by the bites of recognised list (Davies and Lund, 1974; various species of haematophagous ar- Davies, 1976). thropods its distribution is limited to those geographical areas where competent vec- tors are present and to those times of the GEOGRAPHICAL DISTRIBUTION year when conditions are favourable for AND OCCURRENCE vector activity. AHS virus is widely distributed across sub- Saharan Africa and is enzootic in a band HISTORY stretching from Senegal and Gambia in the west to Ethiopia and Somalia in the east Probably the first historical reference to (Howell, 1963). It also occurs as far south AHS concerns an epizootic in the Yemen as S Africa and may extend at times to Egypt in the north. The Sahara desert, Africa and appeared in southern Morocco, however, provides an effective geographi- rapidly extending into Algeria and Tunisia cal barrier which usually, though not invari- and eventualy crossing the Straits of Gi- ably, prevents incursions into North and braltar into southern Spain in October NW Africa from the infected areas further 1966 (Rabah, 1966; Diaz Montilla and south. Panos Marti, 1967, 1968; Mornet et al, Until relatively recently AHS virus was 1967; Sers, 1967; Laaberki, 1969). The ep- believed to be confined to Africa with the izootic once more was caused by AHS vi- rus 9 Montilla and Panos exception of occasional excursions across serotype (Diaz the Red Sea into SW Arabia (Rafyi, 1961; Marti, 1968). Pilo-Moron et al (1969) re- Mirchamsy and Hazrati, 1973). However, garded the appearance of AHS in N Africa in the summer of 1959 the situation as being due to the movement of nomads changed. Horse sickness fever appeared and their animals, particularly donkeys first in Saudi Arabia and the southern re- across the Sahara from Central Africa gions of Iran, and then spread northwards, where AHS virus serotype 9 was apparently eastwards and westwards to involve Af- enzootic (Maurice and Provost, 1967). The ghanistan and Pakistan by the autumn of 1965-1966 epizootic succeeded in &dquo;over- 1959. During the spring and summer of the wintering&dquo; once in N Africa but the northern following year the disease continued to extension into southern Spain was eliminat- spread, particularly along the courses of ed within 3 wk apparently through a vigor- the great rivers which formed the major ous vaccination and slaughter policy (Diaz trade routes, its progress being facilitated Montilla and Panos Marti, 1968). by the movements of nomadic tribesmen Subsequent to 1966 AHS virus appar- and their animals (Howell, 1960). Syria, ently remained quiescent in sub-Saharan Lebanon, Jordon, Iraq, Turkey, Cyprus and Africa for over 20 yrs. However, in 1987 an extensive tracts of India were rapidly in- outbreak of AHS due to serotype 4 was volved all within the next 6 months (How- confirmed in the provinces of Madrid, Tole- ell, 1960, 1965; Rafyi, 1961; Gorhe et al, do and Avila in Central Spain (Lubroth, 1965; Mirchamsy and Hazrati, 1973). How- 1988). The origin of the outbreak is be- ever, by the end of 1961 in the face of a lieved to have been the importation of 10 massive vaccination campaign and the zebra from Namibia, 5 of which were taken deaths of over 300 000 equines the dis- to a Safari Park (El Rincon) 50 km SW of ease in Asia apparently came to a halt (An- Madrid.