Investigations have been carried out to elucidate the possible role of
the donkey in the epidemiology of African horse sickness (AHS). These
studies have shown that despite the absence of pyrexia or other obser
vable clinical signs, donkeys become infected with virulent AHS virus
serotype 4 (AHSV 4) and that they develop a viraemia which can persist
for at least 12 days, albeit at a comparatively lower titre than that
recorded for similarly infected ponies. AHSV fl, showed a similar tis
sue tropism in the pony and donkey but the virus appeared to replicate
less efficiently in donkey tissues. The only gross pathological chang
es observed in the donkeys post mortem were increased fluid accumulati
on in the serosal lined compartments, particularly the peritoneal cavi
ty, and petechial and ecchymotic haemorrhages on the left hepatic liga
ment. The absence of infectious virus or viral antigens in any of the
tissues collected at 14 and 19 days post inoculation (dpi) from 6 expe
rimental donkeys suggest that, though susceptible to infection, the do
nkey is unlikely to be a long term reservoir for AHSV. Although AHSV 4
was detected in all 6 donkeys following the primary inoculation, no v
irus could be isolated from blood collected from two donkeys subsequen
tly challenged with a second virulent virus, AHSV 5. Data generated fr
om virus neutralisation tests showed a second primary antibody respons
e, against AHSV 5, in these donkeys at 12 dpi. In contrast, the boost
in antibody levels detected from 5 dpi, as measured by ELISA, was prob
ably due to an anamnestic response against the AHSV group-specific vir
al proteins. Homogenised spleen tissue, collected post mortem from a d
onkey 7 dpi with AHSV 4, caused a lethal, cardiac form of AHS when ino
culated into a susceptible pony.