Page 124 - VHSA - Onderstepoort 100 Years - Part 3
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ONDERSTEPOORT 100
and at different points in time. Phylogenetic trees revealed
try. The clinical signs of the disease were so typical that a provisional diagnosis of EI could be made. Within 3 days of receiving the first samples, Erasmus, with the capable assistance of Pieterse and Boshoff isolated the virus in
embryonated eggs and identified it as the equi-2 (H3N8) subtype of EI.
Once a diagnosis was made vaccine was imported from abroad but prices were inflated and many horse owners could not afford it. It was then decided to develop a local vaccine, containing the standard Miami 63 strain as well as the Johannesburg 86 isolate. The vaccine was made commercially available within 3 months of the diagnosis, mainly as a result of the excellent team work of everyone concerned. The vaccine performed well in the field and probably made a major contribution to the eradication of EI from South Africa by 1989.
The biggest advantage of the local vaccine was undoubtedly the fact that it contained the subtype responsible for the outbreak. In 1994 the vaccine was further improved by the inclusion of the Newmarket 94 isolate.
considerable genetic variation and the existence of several clusters among isolates of especially the ‘viverrid’ type whereas the ‘canid’ type is more homogeneous. Both types are transmissible to other animals and man
but the latter is more important in terms of human cases, especially in the rural areas where feral dogs abound. Attempts were therefore also made to develop an oral bait vaccine for dogs. In 1997 the responsibility for the Rabies Programme, which included the OIE Rabies Reference Laboratory, was taken over by J. (John) Bingham and when he resigned at the beginning of the new millennium by C.T. Sabeta.
• Equine influenza
In 1963 equine influenza (EI) broke out in horses in a quarantine station in Miami. The virus proved to be a new serotype (H3N8) and rapidly spread to horses in the vicinity of the quarantine station and eventually throughout the USA and Canada. In 1965 the infection spread to England and in 1966 to the rest of Europe. With the increase in transportation of horses from Europe to South Africa by air it was just a matter of time before EI would spread to South Africa.
“The vaccine against equine influenza performed well in the field and probably made a major contribution to the eradication of EI from South Africa by 1989. The biggest advantage
of the local vaccine was undoubtedly the fact that it contained the subtype responsible for the outbreak. In 1994 the vaccine was further improved by the inclusion of the Newmarket 94 isolate.”
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Erasmus had been invited to attend the First International Conference of Equine Infectious Diseases to be held in Stresa, Italy in July 1966. He applied for funds from the Department of Agriculture and the SA Jockey Club to visit laboratories across Europe in order to study all aspects of EI. He returned with valuable experience as well as with the necessary diagnostic reagents. This enabled him to prove that South Africa was free from EI despite frequent clinical diagnoses of ‘flu’ during winter months.
In December 1985 five horses arrived at the quarantine station at the Johannesburg Airport (presently O.R. Tambo International Airport) suffering from a serious respiratory disease. They originated from Lexington, Kentucky, travelled by road to Canada from where they were flown to Johannesburg via Paris. They were supposed to have been vaccinated against EI but acute phase sera collected upon arrival proved that they were seronegative.
Unfortunately the infection spread from the quarantine station to horses at the Newmarket Race Course in Alberton and in a short period of time throughout most of the coun-
• Equine encephalosis virus and serologically related orbiviruses
In March 1967 a new virus called equine encephalosis virus (EEV) was isolated by Erasmus from several horses that were ill or died peracutely after having shown violent behaviour. The prototype virus (Cascara) was a typical orbivirus but was not serologically related to other known members of the genus. In subsequent years a number of virus isolates were made by Erasmus that shared group-specific antigens with EEV (Cascara) but were distinct on neutralization tests. The Gamil isolate originated from a case diagnosed as atypical AHS.
The Bryanston virus was isolated from horses that died peracutely from cardiac fibrosis. Many isolates of the Kyalami virus were made from horses showing mild icterus, probably indicative of hepatitis. Gerdes isolated the Potchefstroom virus in 1991. Despite their serological relatedness these viruses produce a variety of clinical syndromes. The vast majority of infections in horses appear to be mild or even subclinical but occasionally they produce extremely serious clinical signs and even peracute mortality.
PART 3
History of Individual Disciplines
1908-2008
Years


































































































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