African Horse Sickness

• It is acute, sub-acute, insect borne viral disease of Equidae characterized by clinical signs and lesion associated with respiratory and circulatory impairment.
• It is highly fatal disease of horse, mules and donkeys.

Etiology:

• Orbivirus of Reoviridae family
• RNA virus
• There are 9 distinct serotypes of AHS virus identified by virus neutralization test
• Virus is relatively heat stable, virus can be inactivated at 72°C for 120 minutes.
• Virus can be destroyed at pH <6 or pH ≥ 12. It can be inactivated by formalin for 48 hours.

Epidemiology:

• Disease has both seasonal and epizootic cyclical incidence, with disease associated with drought followed by heavy rain.
• Mortality rate in horses is 70-95%, mules around 50%, and donkeys around 10%.
• AHSV is endemic in tropical and subtropical areas of Africa, south of the Sahara, from Senegal in the west to Ethiopia and Somalia in the east and extending as far south as South Africa.
• The virus repeatedly spread out of its African basin during the last century and caused severe outbreaks in the newly infected territories.
• In 1943–1944 in Egypt, Syria, Jordan, Lebanon and Palestine, and in 1959–1960 outbreaks which caused the death of over 300,000 equids occurred in the Middle East and South West Asia (Cyprus, Turkey, Lebanon, Iran, Iraq, Syria, Jordan, Palestine, Pakistan and India).
• In 1965, AHS was first reported in Morocco before reaching Algeria and Tunisia and crossing the Strait of Gibraltar into Spain in 1966. These latter outbreaks were all caused by serotype 9 viruses.
• Europe faced a second AHS epizootic, this time due to serotype 4 virus, in 1987.

Transmission:

• Culicoides sps are the principal vector of transmission. C. imicola appears to be the principal vector.
• Disease is not transmitted through direct contact.
• Occasional mode of transmission: mosquitoes – Culex, Anopheles and Aedes spp.; ticks – Hyalomma, Rhipicephalus; and possibly biting flies – Stomoxys and Tabanus.
• Viscera and blood of infected horses, Semen, urine and nearly all secretions during viremia are sources of virus, but transmission has not been documented.

Pathogenesis:

• Infected arthropod vector bites horses and releases virus into host.
• After entry, virus localizes in regional lymph node, spleen, lungs where primary replication occurs.
• Transient primary viremia
• Virus travels to endothelial cells in blood vessels
• Secondary replication occurs in endothelial cells resulting secondary viremia
• Destruction of vascular endothelium results increased vascular permeability, edema, hemorrhage, intravascular coagulation.

Clinical Signs:

• Incubation period in equids is approximately 3 days to 2 weeks; typically, less than 9 days
• There are four principal manifestation of disease

1. Sub-clinical form (Horse sickness fever):

• Fever 40-40.5°C
• Mild form; general malaise for 1-2 days
• Very rarely results in death

2. Sub-acute or cardiac form (Dinkop or peripheral):

• Fever (39-41°C)
• Edema appears involving supraorbital fossa and eyelids
• Congestion and hemorrhages in conjunctiva
• Edema extends to tongue, lips, intermandibular space and laryngeal region
• Mortality is usually 50% or higher; death occurs within 1 week.

3. Peracute or respiratory or pulmonary form (Dunkop):

• It is characterized by severe and progressive respiratory distress and death
• Fever after 3-5 days of IP
• Increased respiratory rate
• Affected animals stand with forelegs apart, head extended, nostril dilated.
• Spasmodic coughing accompanied by profuse sweating and discharge of frothy fluid from nostril.
• Nearly always fatal, death occurs due to anoxia within 1 week

4. Mixed form (cardiac and pulmonary):

• Fever
• Edema of head and subcutis
• Mortality is about 70-80% or greater.

PM Findings:

• Striking pulmonary edema is characteristics of infection.
• Hydropericardium, pleural effusion
• Oedema of thoracic lymph nodes
• Frothy fluid fills trachea, bronchi and bronchioles
• Pericardial hemorrhages with pleural and pericardial effusion
• Congestion of gastric fundus
• Sub capsular hemorrhages in the spleen, congestion in the renal cortex, edematous infiltration around the aorta and trachea, and petechial hemorrhages on various serosal and pleural surfaces.
• Epicardial and endocardial ecchymosis; myocarditis; hydropericardium is common.
• Ascites can also be seen.
• Subcutaneous and intramuscular yellow gelatinous oedema on the fascia of the head, neck and shoulders, and occasionally the brisket, ventral abdomen and rump.

Diagnosis:

• On the basis of clinical findings, PM findings
• Isolation and identification of virus
• Serological test: CFT, ELISA, VNT, HA test
• Real-time reverse-transcription polymerase chain reaction (RT-PCR)
• VN test has been the method of choice for typing as well as the ‘gold’ standard test for identifying AHSV’s isolated from the field using type specific antisera.

Differential Diagnosis:

1. Anthrax:

• Sudden death of animals with unclotted dark blood from natural orifices.

2. Equine infectious anemia:

• Recurrent fever, anemia
• Weight loss
• History of blood-feeding flies

3. Equine viral arteritis:

• There is history of abortion
• Edema, mild respiratory signs
• Serous to mucopurulent nasal discharge
• Conjunctivitis

4. Trypanosomiasis:

• Demonstration of parasite via blood smear
• Neurological signs
• Intermittent fever, anemia
• Emaciation

5. Piroplasmosis:

• Tick-borne; intravascular hemolysis
• No head edema or pulmonary edema like AHS

Treatment and Control Measures:

• There is no specific curative treatment for animals with AHS except for supportive treatment aimed at cardiac and pulmonary support, rest, and good, general husbandry.
• To reduce pain and inflammation, flunixin meglumine @1.1 mg/kg, IV
• Diuretics; Furosemide @ 0.5-1 mg/kg, b.wt. IV/IM.
• IV fluids such as Ringer’s lactate, 0.9% saline to correct dehydration and support perfusion
• Broad-spectrum antibiotics such as penicillin, oxytetracyclines to counter pneumonia.
• Affected horse should be isolated to prevent vector exposure and further spread.
• Horses should be kept in clean, insect-proof stable.
• Soft bedding should be provided and stress should be minimized.
• Molasses water should be provided for energy and stimulate drinking.