Infection with African horse sickness virus

Horse sickness fever: fever and mild malaise for a day or two, rarely fatal. Cardiac form: fever, then swelling of the supraorbital fossae and eyelids spreading to the face, tongue, neck and chest, with petechiae under the tongue and in the conjunctivae and colic before death from heart failure. Pulmonary form: fever, then sudden severe dyspnoea, spasmodic coughing, sweating and frothy nasal discharge, often fatal within hours. The mixed form is the most common. Necropsy shows lung oedema, hydropericardium and pleural effusion, or yellow gelatinous oedema of head and neck with epicardial haemorrhages.

African horse sickness is caused by African horse sickness virus, an orbivirus of the family Reoviridae with nine serotypes; recovery from one gives good immunity to it but only partial protection against the others. After an infected Culicoides bite the virus first replicates in regional lymph nodes. A primary viraemia, with virus associated with red cells and monocytes, carries it to endothelial cells of the lungs, spleen and other lymphoid tissue. Replication there is modest, but endothelial injury raises vascular permeability, so fluid leaks into the lungs, chest cavity, pericardial sac and the subcutis of the head and neck, impairing respiration and circulation.

Equids are the natural hosts. Horses are most susceptible, then mules; donkeys are more resistant and zebras, thought to be the reservoir, are infected subclinically with viraemia up to 40 days. Dogs can die after eating infected horsemeat but do not maintain spread. Culicoides imicola is the principal field vector, with C. bolitinos; the disease is not contagious and peaks in late summer and autumn. It is endemic in sub-Saharan Africa but has repeatedly spread: to Egypt, Syria, Jordan, Lebanon and Palestine in 1943-44, killing over 300,000 equids across the Middle East and South-West Asia in 1959-60, and into Morocco, Algeria and Tunisia from 1965. It is not zoonotic.

WOAH lists anthrax, equine infectious anaemia, equine viral arteritis, trypanosomosis, equine encephalosis, piroplasmosis, purpura haemorrhagica and Hendra virus infection. Confirmation relies on group-specific real-time RT-PCR or virus isolation, followed by serotyping, which also guides the choice of a matched vaccine.

Vascular endothelium, lungs, pleura, heart and pericardium, subcutaneous tissue of head and neck, supraorbital fossae, lymph nodes, spleen, kidneys, gastrointestinal tract

Serotype-matched live attenuated vaccines, annually where endemic (teratogenic in pregnant mares, may reassort); insect-proof stabling from dusk to dawn, repellents, insecticides; quarantine, movement control and testing of imported equids.

No specific treatment. Pulmonary form nearly always fatal (over 95%), cardiac form about 50% or more, mixed form 70-80%. Mortality in horses 50-95%, mules about 50%, European and Asian donkeys 5-10%. Survivors are immune to the infecting serotype.