Topic:African Horse Sickness
African Horse Sickness (AHS) is a viral disease affecting equines, caused by the African Horse Sickness Virus (AHSV), which is an orbivirus transmitted primarily by Culicoides midges. The disease is characterized by clinical signs such as fever, respiratory distress, and edema, with varying degrees of severity depending on the form of the disease. AHS is endemic to sub-Saharan Africa but poses a risk of outbreaks in other regions due to the movement of infected animals and vectors. The disease has significant implications for equine health and management due to its high mortality rate in susceptible populations. This page compiles peer-reviewed research studies and scholarly articles that explore the epidemiology, pathogenesis, clinical presentation, and control measures of African Horse Sickness in horses.
Isolation and identification of African horsesickness virus from naturally infected dogs in Upper Egypt. African horsesickness virus was isolated from blood samples of street dogs in Aswan Province in Arab Republic of Egypt. Of six isolated "dog strain" African horsesickness viruses, three viruses designated D2, D6 and D10 have been identified as type 9 African horsesickness virus. Methods of isolation, tissue culture adaptation, serological indentification and typing are described. Horses experimentally infected with dog viruses showed febrile reaction and characteristic clinical and pathological signs of African horsesickness. Reisolation of African horsesickness virus type 9 was achieved from ...
The reaction of imported British Shire horses to African Horse Sickness: A case report. Summary Twelve (12) heavy horses of the Shire breed imported into Nigeria in 1974 died within two months after importation. This was because of inclement weather and non-availability of AHS vaccine.
The reaction of imported British Shire horses to African Horse Sickness: A case report. Summary Twelve (12) heavy horses of the Shire breed imported into Nigeria in 1974 died within two months after importation. This was because of inclement weather and non-availability of AHS vaccine.
Rates of infection in, and transmission of, African horse-sickness virus by Aedes aegypti mosquitoes. Very low infection rates (less than 3%) were obtained when Aedes aegypti mosquitoes ingested blood contained 5.8--6.5 log10 MLD50/0.02 ml African horse sickness virus (AHSV). When A. aegypti mosquitoes were inoculated intrathoracically with virus, however, high infection rates were achieved. Mosquitoes infected by inoculum failed to transmit virus to embryonated hens eggs by bite, and virus could not be detected in membrane or blood when inoculated mosquitoes were allowed to engorge on uninfected blood through a chick skin membrane. It was concluded that the mosquito A. aegypti is unlikely to ...
The growth of African horse-sickness virus in embryonated hen eggs and the transmission of virus by Culicoides variipennis Coquillett (Diptera, Ceratopogonidae). Seven-day-old embryonated hen eggs were infected with African Horse Sickness virus by the yolk sac and intravenous routes. Virus reached a high titre in the blood of infected embryos. Culicoides variipennis midges which took a blood meal from infected eggs became infected with virus, and after 7 days at 26 degrees - 27 degrees C transmitted African Horse Sickness virus to uninfected eggs. C. variipennis may therefore be considered a biological vector of African Horse Sickness virus in the laboratory.
Detection of African horsesickness viral antigens in tissues by immunofluorescence. The fluorescent antibody reaction was studied in tissues of ponies infected with African horsesickness virus (AHSV). Lung, spleen, lymph node, liver, skeletal muscle, intestine, stomach, nerve ganglion and kidney were sectioned and stained by the direct fluorescent antibody technique (FA). Fluorescence was demonstrated only in the spleen and could be inhibited by using unconjugated antiserum.
African horse-sickness killed-virus tissue culture vaccine. Formalized African horse-sickness (AHS) type 9 virus cultivated in monkey kidney stable (MS) cell cultures was experimentally used for immunizing horses. Inactivated vaccines prepared either from viscerotropic or neurotropic type 9 AHS virus produced antibodies in vaccinated horses. Immunity developed in all horses vaccinated with various amounts of the vaccine, and protected them from infection, when challenged 5 weeks after vaccination.