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African horse sickness virus
Transcript of African horse sickness virus
African horse sickness virus
District surgeon at Graaff-Reinet
History of AHS
“If the animal is rode during the Sickness, or urged by driving or otherwise to any degree of speed, he falls at once, literally suffocated by the quantity of frothy matter which fills his trachea and issues in abundance from his nostrils”.
Epidemics every 20-30 years
Warm phase of the El Niño/Southern Oscillation phenomenon
65 000 horses, 40% of the entire horse population of the Cape of Good Hope
Horses that survived - "salted", worth 6-10X more
“When a horse takes the sickness, or at least shows indications of it, thirty-six hours will terminate the matter one way or the other; if the unfortunate animal is alive after that, experienced persons would pronounce an opinion, or express a hope, that the creature was going to salt”.
Breed in damp soil rich in organic matter
Associated with rain
Active at night
Tend to not enter buildings
Virogenesis in the midge - 8 days
Netting on windows and door impregnated with insecticide
topical insecticide/repellents on the horse
Initial mutiplication - regional lymph node
Target organs - lung, heart, spleen
Replication - microvascular endothelial cells, monocyte-macrophages
vasculitis - oedema
up to 21 days in horses
up to 40 days in zebras
Virus isolation - heparin blood
RT-PCR - EDTA
Serology - serum
Organs - lung, spleen on ice for isolation/PCR, or formalin for IHC
Unvaccinated horses, foals, dogs
Very rapid onset of severe dyspnoea
Sometimes frothy discharge from nostrils
Rapid deaths (< 24 h)
Less than 5% recover
Lung oedema, hydrothorax
“At day-break, one of our horses exhibited symptoms of a fatal disease, called in this Colony, The Sickness. His eyelids were swollen and the blood vessels of his mouth and tongue were in a state of congestion. He appeared to be in perfect health last night when tied to the wagon wheel to secure him from Hyenas which are numerous here. The disease usually comes on suddenly and runs its course quickly. On being loosed, he began to browse, but had difficulty in swallowing: he was bled without delay and dosed with Calomel and Tartarized Antimony. After this, he neighed cheerfully to his companion, went to him on an adjacent hill, where he lay down; he soon rose again, and began to eat, but quickly lay down, and then struggled and died. His death took place about an hour after the symptoms of “The Sickness” were first noticed; before night, his carcase was nearly consumed by Vultures and by the dogs of the Hottentots. Thus quickly is a horse finished in Africa!
T.B. Bayley, 1856
Avoid low lying areas
AHS “could be traced, almost without exception, to the deleterious influence of the night air”.
“The distemper was everywhere most destructive in the low grounds and along the watershed of each district; the fatal miasma seeming to be held in suspension during the day, and to descend again at night with the heavy dews”.
before 1900: dew, grass, cobwebs
McFadyean: transmitted the disease with a bacterial-free filtrate of blood
Confirmed by Theiler and Nocard
Conclusion: cause was a virus
Horses protected in mosquito proof enclosures
Winged night insects
1905: 1st vaccine developed by Arnold Theiler
Simultaneous inoculation of virus and hyperimmune serum from salted horses
Used till 1933
Attenuation of AHSV through passage of virus in mouse brains
Propagation of virus in chicken embryos
Theiler - 1st to suggest that there was a plurality of “immunologically distinct strains” of AHSV
Alexander and McIntosh - 7 serotypes (1955)
Howell - 9 serotypes (1962)
Propagation of AHSV in tissue culture
large plaques avirulent
10 segments of dsRNA
300 000 deaths!
Heavy rains followed by warm, dry spells
not a carrier!
Breed in cattle, buffalo, wildebeest dung
Not dependent on rainfall
horsesickness fever form
oedema of fat in coronary groove
congestion of glandular part of the stomach
both "pulmonary" and "cardiac" forms present
mortality rate - 70%
subcutaneous oedema of head and neck
mortality rate - 50%
swollen supra-orbital fossae
oedema of the conjunctiva
Subcutaneous and intermuscular oedema
vaccinated horses, donkeys, zebra
Fever only clinical signs
Oedema - purpura haemorrhagica and equine viral arteritis, swelling in AHS does not extend to legs
No specific treatment
Vaccination - bottle 1 and 3 weeks later bottle 2, repeat annually late winter, early spring
Bottle 1 - serotypes 1, 3, 4
Bottle 2 - serotypes 2, 6, 7, 8
Cross reaction between 1 and 2, 3 and 7, 5 and 8, 6 and 9
Which samples should be submitted for AHS diagnosis?
What is a CT value and does a positive PCR assay confirm that my horse has AHS?
My horse has been vaccinated every year with the AHS vaccine yet still got AHS.
Can my horse be worked after vaccination?
Neighbours have moved zebras onto their properties and now my horses have AHS.
A horse in the yard has AHS and I’m worried that it will infect the other horses
I want to move my horse into the AHS controlled area – what do I need to do?