Equine encephalosis

Equine encephalosis

Synonyms: Perde enkefalose (Afrik.)


Current Authors:
P COETZEE, PhD, Researcher, Onderstepoort Biological Products SOC Ltd, Private Bag X07, Onderstepoort, 0110, South Africa
P G HOWELL (deceased)
A J GUTHRIE, BVSc, PhD, Director, Equine Research Centre, Faculty of Veterinary Science, University of Pretoria, South Africa
J A W COETZER, BVSc, MMedVet(Path), Emeritus Professor, Faculty of Veterinary Science, University of Pretoria, South Africa


Equine encephalosis (EE) is the name assigned to a mild or subclinical orbivirus infection of equids. The virus is transmitted by species of Culicoides, and as a result the epidemiology has much in common with African horse sickness (AHS). The designated name of the infection is unfortunately a misnomer since, by definition, neither lesions nor dysfunctions of the brain are characteristic features of the disease.

The first isolate of equine encephalosis virus (EEV) was recovered in March 1967 in South Africa from the blood and tissues of a 13-year-old Thoroughbred mare that was euthanased after showing a peracute nervous derangement. It was reported that two other mares on the same stud farm became ill during the following few days. One died, while the second recovered after a convalescence of 14 days. Although it was recorded that virus was also recovered from blood samples taken from horses that had exhibited no clinical signs of disease except for a fever, virus was also recovered from the organs of horses that had died in other parts of South Africa.7   


Equine encephalosis virus is classified as an Orbivirus in the family Reoviridae (subfamily Sedoreovirinae) and shares many morphological, physiochemical and genomic characteristics with other orbiviruses (see Bluetongue, and African horse sickness.)

Field samples of blood and tissues from infected horses have provided seven valid serotypes (Table 1), which on cross-neutralization tests have shown insignificant cross-reactivity between heterologous antigens and antisera.8, 9, 14  Antisera produced in sheep have given unequivocal specificity in the routine identification and classification of all field isolates recovered to date.

In a transmission electron microscopic study undertaken on infected BHK21/C13 cells, it was found that the negatively stained virus particles closely resemble those of AHS and bluetongue (BT).15 Examination of thin sections of infected cells revealed a replication cycle in the cytoplasm in the perinuclear area, with progeny particles visible after 28 hours. Irregularly shaped, granular inclusion bodies without a membrane in which maturing virus particles embedded in the matrix were observed became evident in the perinuclear region. The aggregations of virus particles in the cytoplasmic matrix resemble large crystals in which sectioned particles have a diameter of 73 nm. It was concluded that the observations suggested that the capsid is composed of 32 morphological subunits, as described for bluetongue virus (BTV),6 and represent subviral particles, while the larger ill-defined particles in the crystalline bodies are the complete virion with an outer diffuse polypeptide layer.

Table 1 Classification, identification, source and origin of currently recognized serotypes of equine encephalosis virus

1 Bryanston, M8/76 Foetal liver/spleen Colesberg, Western Cape (1976) 5
2 Cascara Organ suspension Kimberley, Northern Cape (1967) 4
3 Gamil, M9/71 Blood Naboomspruit, Limpopo Province (1971) 5
4 Kaalplaas, 7088 (7 –2) Blood Onderstepoort, Gauteng (1974) 5
5 Kyalami, 7084 (12 –3) Blood Johannesburg, Gauteng (1974) 11
6 Potchefstroom, Else EP8/91 Blood Potchefstroom, North West Province (1991) 6
7 E21/20 Blood St. Lucia –KwaZulu-Natal (2000) 8
7 Northrand ? Johannesburg, Gauteng Province (2008) *, 1, 16, 25

*  The EEV-7 Northrand isolate is given as the reference isolate in several publications, in the absence of a full genome sequence from isolate E21/20 - see GenBank accession numbers HQ630949-HQ630958 for the complete genome.

Equine encephalosis virus replicates in BHK21/C13 monolayers and produces a distinctive cytopathology when the monolayers are viewed under low-power light microscopy. Affected monolayers show a fine-textured cytopathic effect in contrast to the development of more focal refractile cells which rapidly become detached when such monolayers are infected with AHSV. Lines of Vero (ATCC CCL81) cells vary in their susceptibility to EEV. Plaque assay may be undertaken in susceptible lines: plaques become visible after five to six days’ incubation. Serotype 1 of EEV produces high yields with no cytopathic effect in C6/36 (Aedes albopictus) cell cultures.

The replication of EEV is unaffected by exposure to 5-bromodeoxyuridine at a concentration of 30 µg/ml, whereas actinomycin D at a concentration of 0,01 µg/ml reduces the yield of virus a hundred-fold. Exposure to a pH of 3 for one hour at 37 °C produces a considerable drop in the infectivity titre, whereas chloroform at a final concentration of 5 per cent has no effect on viral infectivity.7         

The early molecular characterization of EEV and an attempt to develop genetic probes to distinguish between EEV and AHSV has been reported.32

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