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African Horse Sickness

African Horse Sickness

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Published by kinokina1
Review of sub-Saharn virus.
Review of sub-Saharn virus.

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Categories:Types, Research
Published by: kinokina1 on Apr 25, 2013
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445Vet. Res. 35 (2004) 445–466© INRA, EDP Sciences, 2004DOI: 10.1051/vetres:2004021
Review article
African horse sickness
Philip Scott M
ELLOR
*, Christopher H
AMBLIN
Institute for Animal Health, Department of Arbovirology, Pirbright Laboratory, Ash Rd., Pirbright,Woking, Surrey, GU24 0NF, United Kingdom(Received 30 December 2003; accepted 1 March 2004)
Abstract
– African horse sickness virus (AHSV) causes a non-contagious, infectious insect-bornedisease of equids and is endemic in many areas of sub-Saharan Africa and possibly Yemen in theArabian Peninsula. However, periodically the virus makes excursions beyond its endemic areas andhas at times extended as far as India and Pakistan in the east and Spain and Portugal in the west. Thevectors are certain species of 
Culicoides
biting midge the most important of which is the Afro-Asiatic species
C. imicola
. This paper describes the effects that AHSV has on its equid hosts, aspectsof its epidemiology, and present and future prospects for control. The distribution of AHSV seemsto be governed by a number of factors including the efficiency of control measures, the presence orabsence of a long term vertebrate reservoir and, most importantly, the prevalence and seasonalincidence of the major vector which is controlled by climate. However, with the advent of climate-change the major vector,
C.
 
imicola,
has now significantly extended its range northwards to includemuch of Portugal, Spain, Italy and Greece and has even been recorded from southern Switzerland.Furthermore, in many of these new locations the insect is present and active throughout the entireyear. With the related bluetongue virus, which utilises the same vector species of 
Culicoides
thishas, since 1998, precipitated the worst outbreaks of bluetongue disease ever recorded with the virusextending further north in Europe than ever before and apparently becoming endemic in thatcontinent. The prospects for similar changes in the epidemiology and distribution of AHSV arediscussed.
Culicoides / 
vectors / epidemiology / climate / disease prediction
Table of contents
1.Introduction......................................................................................................................................4462.History.............................................................................................................................................4463.Aetiology.........................................................................................................................................4474.Host range........................................................................................................................................4475.Pathogenesis.....................................................................................................................................4485.1.Clinical signs...........................................................................................................................4485.2.Pathology.................................................................................................................................4495.2.1.Macrolesions................................................................................................................4495.2.2.Microlesions.................................................................................................................4496.Epidemiology...................................................................................................................................4506.1.Distribution.............................................................................................................................450* Corresponding author: philip.mellor@bbsrc.ac.uk
 
446P.S. Mellor, C. Hamblin
6.1.1.AHSV in South Africa..................................................................................................4506.1.2.AHSV outside sub-Saharan Africa...............................................................................4506.2.Vectors, transmission and climate...........................................................................................4516.2.1.
Culicoides imicola
........................................................................................................4516.2.2.Prediction of AHS risk by modelling the distribution of the major vector..................4526.2.3.Other potential
Culicoides
vectors of AHSV...............................................................4526.2.4.Temperature and AHSV infection of vector
Culicoides
..............................................4536.2.5.AHS and the El Niño/Southern Oscillation..................................................................4547.Diagnosis..........................................................................................................................................4547.1.Antigen identification..............................................................................................................4557.2.Antibody identification............................................................................................................4558.Differential diagnosis.......................................................................................................................4569.Prevention and control......................................................................................................................4569.1.Husbandry modification..........................................................................................................4569.2.Vector control..........................................................................................................................4569.2.1.Habitat alteration..........................................................................................................4569.2.2.Adulticiding..................................................................................................................4579.2.3.Larviciding...................................................................................................................4579.2.4.Repellents.....................................................................................................................4579.3.Vaccination..............................................................................................................................4579.3.1.Attenuated vaccines......................................................................................................4579.3.2.Inactivated vaccines......................................................................................................4599.3.3.Sub-unit vaccines..........................................................................................................45910.Conclusion........................................................................................................................................460
1.INTRODUCTION
African horse sickness (AHS) is a non-contagious, infectious, insect-borne diseaseof equids caused by a virus of the samename (AHSV). Although zebra and donkeysrarely exhibit clinical signs, the effects of the disease, particularly in susceptible pop-ulations of horses can be devastating andmortality rates for this species may exceed90%. As a consequence of its severity andbecause it is able to expand rapidly and with-out apparent warning out of its endemicareas AHS has been allocated OIE (OfficeInternational des Epizooties) List A status.In horses, AHS is characterised by clin-ical signs, which develop as a result of dam-age to the circulatory and respiratory sys-tems giving rise to serous effusion andhaemorrhage in various organs and tissues.The extent and severity of the clinico-path-ological findings have been used to classifythe disease into four forms. In ascendingorder of severity these are horse sicknessfever (which usually affects only mules,donkeys and partially immune horses), thesubacute or cardiac form, the cardio-pul-monary or mixed form and the peracute orpulmonary form. All forms of disease canoccur in any one outbreak but in susceptiblepopulations of horses the mixed and pulmo-nary forms tend to predominate so mortalityrates in these animals will be very high. Theclinical signs occurring in naturally andexperimentally infected horses have beendescribed in detail by various workers [7,25, 70, 73, 98, 122].
2.HISTORY
AHS is an ancient disease and the firstreference to it concerns an epidemic thatapparently occurred in 1327 in the Yemen[97]. However, the virus almost certainlyoriginated in Africa and was first recog-nised there subsequent to the introductionof horses during the exploration of centraland east Africa, the first observations being
 
African horse sickness447
made by a certain Father Monclaro in 1569[121]. In southern Africa the virus has prob-ably been present from distant times but dis-ease was not recognised until some 60 yearsafter the first introduction of horses in 1657,the first major outbreak occurring in 1719when over 1700 animals died [50]. Subse-quently and over the next 217 years at least10 major and several lesser outbreaks of AHS have been recorded in southern Africathe largest being in South Africa in 1854–1855 when over 70000 horses died [9, 25].The frequency, extent and severity of out-breaks in southern Africa has declined sig-nificantly over the last century, coincidingwith major decrease in the horse and zebrapopulations and the introduction of AHSvaccines.
3.AETIOLOGY
African horse sickness virus (AHSV) isa member of the genus
Orbivirus
in the fam-ily Reoviridae and as such is morphologi-cally similar to other orbiviruses such asbluetongue virus (BTV) of ruminants andequine encephalosis virus [117, 119, 129].The virion is an unenveloped particle about70 nm in diameter and is made up of a two-layered icosahedral capsid, which is com-posed of 32 capsomeres [25]. The genomecomprises 10 double stranded RNA seg-ments, each of which encodes at least onepolypeptide [43]. The genome is enclosedwithin the core particle, which comprisestwo major proteins, VP3 and 7 which arehighly conserved among the nine AHSVserotypes, and three minor proteins, VP 1,4 and 6 [20, 100, 108]. Together they makeup the group specific epitopes [42, 52, 105].The core particle is surrounded by the outercapsid composed of two proteins VP2 and 5.VP2 is the protein that has most responsi-bility for antigenic variation [21, 72, 130].At least three non-structural proteins havebeen identified in infected cells (NS1, 2 and3/3a) [28, 60, 69].To date, nine antigenically distinct sero-types have been identified the last being in1960 [58]. There is considered to be somecross relatedness between the serotypes,typically between AHSV types 1 and 2; 3and 7; 5 and 8; and 6 and 9, although thereis no evidence from the field that there isany intratypic variation [25]. Of the nineserotypes, types 1 to 8 are typically foundonly in restricted areas of sub-SaharanAfrica while type 9 is more widespread andhas been responsible for virtually all epi-demics outside Africa, the only exceptionbeing the 1987–1990 Spanish-Portugueseoutbreaks which were due to AHSV-4.The physio-chemical characteristics of AHSV are fairly typical for the genus
Orbi-virus
. The virus is acid sensitive, beingreadily inactivated at pH values below 6.0but remains relatively stable at more alka-line pH values (7.0–8.5). It is resistant tolipid solvents and relatively heat resistant.Infectivity is remarkably stable at 4 °C, par-ticularly in the presence of stabilisers suchas serum and OCG (sodium oxalate, car-bolic acid and glycerine). Minimal loss of titre occurs with viruses that have beenlyophilised or frozen at –70 °C with ParkerDavis Medium but the viruses are fairlylabile between –20
 
°C and –30 °C [25, 91].
4.HOST RANGE
Zebra have long been considered the nat-ural vertebrate host and reservoir of AHSV,and are believed to play a vital role in thepersistence of the virus in Africa. This spe-cies rarely exhibits clinical signs of infec-tion. All other equid species and crossbreedsare also susceptible to infection but becauseof the high mortality rate frequently recordedin horses and occasionally mules these shouldbe regarded as accidental or indicator hosts.Indeed, the failure of AHSV to become estab-lished outside tropical and sub-tropicalregions of Africa, where zebra principallyreside, indicates that horses, mules and don-keys generally speaking are not long-termreservoirs of AHSV and are not involved inthe permanent persistence of the virus. The

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