African Horse Sickness(AHS)

 Definition
 African horse sickness (AHS) is an acute or
subacute, highly fatal viscerotropic arthropod-
borne virus disease of Equidae, characterized by
impaired respiratory and circulatory functions. 
 Etiology
 The causative organism of AHS is a pantropic
arbo-virus of the Genus Orbivirus of the Family
Reoviridae.
 Susceptibility

 Manifestations of AHS is most pronounced

in horses, less in mules, and lowest in
donkeys and zebras.
 Angora goats may succumb to AHS,
however, cattle and sheep are not known
to develop clinical signs.
 Specific antibodies to AHS virus were
identified in equine, dogs, sheep, cattle,
goats, buffaloes, camels and elephants
 Transmission

 The disease is transmitted primarily by nocturnal

biting Culicoides (midgies, gnats, punkies, no
seeums). Zebras and elephants are considered as
possible reservoirs.
 Other modes of transmission include:
 1. The use of unsterilized intravenous needles
between animals.
 2. Several species of ticks have been incriminated
as mechanical transmitters of AHS
 3. Aedes aegypti, Anopheles sephensi, and Culex
pipiens mosquitoes have been shown to transmit
the AHS virus. 
 Pathophysiology

 Circulating virus and possibly toxic factors

increase the permeability of the
endothelial lining of the capillaries.
 This results in transudation of plasma into
tissues and body cavities.
 Virus clones affect the endothelial linings
in different organs, resulting in the various
forms of the disease.
 Leukopenia develops and the rate of
disappearance is often a good sign of the
severity of the disease. 
 Classical Manifestations

 Following natural infection, the incubation

period varies from 3 days to 3 weeks.
 The acute or pulmonary form usually has
an incubation period of 3 to 5 days.
 The incubation period for the subacute or
cardiac form is longer and ranges
between 5 to 9 days.
 The Acute or Pulmonary Form
(Dunkop)

 There is a febrile reaction for 1 to 2 days with

temperatures as high as 104-105°F.
 dyspnea and coughing.
 Moribund animals are unable to stand and frothy
exudate may flow from their mouths and nostrils
several hours before death occurs. T
 here may be profuse sweating and sudden death
frequently occurs within a few hours following the
onset of pulmonary edema.
 Recovery from this form is rare.
 The Subacute or Cardiac Form
(Dikkop)

 fever
 Edema of the supraorbital fossa and
conjunctivitis
 In severe cases there is edema of the
brisket, thorax and ventral abdomen.
 In animals that recover the edema
subsides in 3 to 8 days
 Necropsy Finding

 1. Pulmonary form - marked edema with

edematous separation of interlobular septa
and hydrothorax are characteristic lesions.
Froth in the trachea is a reflection of
pulmonary edema.
 2. Cardiac form - hydropericardium ,Subtle
subcutaneous and interfascial edema of the
neck, often most prominent around the
ligamentum nuchae is seen.
 Microscopic examination
 Pulmonary edema chracterize by
seperation of interalveolar tissue from
alveoli
 Infiltration of MNC in interalveolar space
 Subendocardial haemorrhage
 Necrosis of liver
 Diagnosis
 In the field history (including introduction of animals from
countries where AHS has occurred or is endemic),
season, and gross lesions are suggestive of the disease.
 There are no pathognomonic lesions in AHS. Serological
tests for detection of antibody to the group antigen of AHS
include:
 a. ELISA
 b. Complement fixation
 c. Indirect fluorescent antibody
 d. Agar gel immunodiffusion test
 e. Serum neutralization test
 Isolation of virus is possible from washed erythrocytes
collected from experimentally inoculated animals at one to
eight days post inoculation. 
 Differential Diagnosis

 1. Viral arteritis 5. Equine encephalomyelitis

 2. Equine rhinopneumonitis 6. Purpura
hemorrhagica
 3. Equine infectious anemia 7. Equine
influenza
 4. Equine piroplasmosis 8. Equine monocytic
ehrlichiosis