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African Horse Sickness (AHS)

African Horse Sickness (AHS) is an acute or sub acute, febrile, arthropod borne viral disease of equids, characterized by clinical signs and lesions associated with respiratory and circulatory impairment.

Etiology

African Horse Sickness (AHS) disease is caused by orbivirus belonging to the family Reoviridae, which is a double stranded RNA virus.
There are 9 immunologically distinct serotypes are recognized.
On the other hand only a single antigenic type involved in the Asian outbreak in 1961.
The virus is inactivated at pH< 6.0 or > 12 or by formalin and ß- Propiolactone.

Epidemiology

The disease is endemic in Africa, and has been recorded in Afghanistan, West Pakistan, Turkey and Iraq.
Mortality: In virulent form it is as high as 90% in horses and lower in mules. In milder outbreaks mortality is 25%.
It is a seasonal disease, common in late summer in warm, humid, low lying marshy districts.
Horses of all breeds are highly susceptible to natural infection.
Mules and zebras are less Affected and donkeys are generally resistant.
Transmitted by blood sucking mosquitoes (culicoides) midges and stomoxys.

Pathogenesis

Clinical manifestation

Incubation period is 5-7 days.
Four different clinical form of illness were described.

Acute or pulmonary form (DUNKOP)

Most common in epizootic area.
This form is more severe than cardiac form.
Fever followed by labored breathing, severe paroxysms of coughing (spasmodic coughing).
Yellowish profuse nasal discharge with froth.
Animal stands with leg apart and head extended.
Profuse sweating, profound weakness and staggering gait progress to recumbency.
Total course of the disease is 4-5 days.
Animal die of anoxia.

Sub acute form cardiac form (DIKKOP)

Most common in enzootic area.
Edema in the head, particularly temporal fossa, eyelids and lips.
Edema develops in the chest, after one week of febrile period.
Oral mucosa is bluish in color and petechiae may develop under the tongue.
Auscultation of heart reveals hydrocaridium, endocarditis and pulmonary edema.
Restless, mild abdominal pain, paralysis of oesophagus.
Regurgitation of food and water through nostrils.
Animal stands leg apart and extension of head.
Animal die of congestive heart failure.
Recovery is prolonged.

Mixed form

Combination of both acute or pulmonary form and sub acute form or cardiac form.
The mixed form is not common in field outbreak.

Mild form or horse sickness fever

Common in enzootic area.
Temperature rises to 40.5^oC over a period of 1-3 days.
Poor appetite, conjunctivitis and moderate respiratory distress.

Necropsy Finding

Pharynx, trachea and bronchi are filled with yellowish frothy serous fluid.
Severe hydrothorax, hydropericardium, pulmonary edema and moderate ascites.
Endocardial haemorrhage and myocardial degeneration.

Sample collection

Live animals: Blood from affected animal should be collected during early febrile phase.
Dead animals : Spleen, lung and lymph node.

Diagnosis

Based on clinical signs and lesions.
Hematology and biochemical parameters- lymphopenia, neutropenia with left shift and thrombocytopenia, increased level of creatine kinase (CK), alkaline phosphatise (ALP), Lactate dehydrogenase (LDH), creatinine and bilirubin concentration.
Isolation of virus in baby hamster kidney-21 (BHK-21), monkey stable (MS) or African green monkey kidney (Vero), intravenously in embryonated eggs, and intracerebrally in newborn mice.
Detection of viral antigen by ELISA and RT-PCR.
Detection of antibody in serum by AGID, IFAT, CFT VNT and ELISA.

Treatment

There is no specific treatment.

Control

Live attenuated cell culture polyvalent vaccine (contain 9 serotype) provide good protection, although annual revaccination is recommended.
Foals are vaccinated at 3-4 months of age.
Now, Inactivated and subunit vaccine is under development.
Restricting importation of horse from country known to have disease.
Quarantine of affected horse.
Stabling of horse indoors in insect proof stable.
Use fly repellent when risk is high.
Vector control.