November 2014



Signalment (AFIP #627741):  A six-month old colt


HISTORY:  This colt’s mother was immune to African horse sickness.  This animal had been vaccinated once against African horse sickness at three months of age.


HISTOPATHOLOGIC DESCRIPTION:  Lung:  Over 90% of alveoli contain moderate to abundant amounts of fibrin and edema admixed with low numbers of macrophages, lymphocytes, and small amounts of hemorrhage.  Diffusely, alveolar and interlobular septa, perivascular and peribronchial adventitia, and the pleura are expanded by edema, fibrin, few lymphocytes, plasma cells and macrophages.  Endothelial cells within venules are swollen with vacuolated, reticular cytoplasm and large reactive nuclei. Multifocally, the bronchi and bronchioles contain moderate amounts of hemorrhage, fibrin, and edema. There is mild BALT hyperplasia.  In less affected lobules, there is mild emphysema characterized by large confluent alveolar lumina and shortened alveolar septa with blunt, clubbed ends. 


MORPHOLOGIC DIAGNOSIS:  Lung: Edema, intralveolar and intrabronchiolar, acute, diffuse, severe, with reactive endothelium and mild interstitial pneumonia, breed not specified, equine.


ETIOLOGIC DIAGNOSIS:  Orbiviral pneumonia


CAUSE:  African Horse Sickness virus (AHSV)


CONDITION:  African Horse Sickness



·         African horse sickness (AHS) is an infectious, non-contagious, arthropod-borne, peracute to subacute, often fatal disease of Equidae characterized by respiratory distress or cardiovascular failure

·         Horses are most susceptible; mortality rates reach 95% in horses, 50% in mules, and 5-10% in donkeys

·         AHSV is a member of the genus Orbivirus in the family Reoviridae; nine serotypes are recognized and determine the organs that are most severely affected

·         Endemic in Africa; occasional epizootics occur in the Mediterranean, Spain, India, and Middle East; not found in the US (OIE List A infectious disease)

·         Cases commonly occur seasonally in low-lying areas, particularly in horses not stabled at night



·         Zebras are the natural host and reservoir; transmission is via biting arthropods and midges (Culicoides sp.) are the most important vector

·         Infection results in damage to the circulatory and respiratory systems resulting in serous effusion and hemorrhage in various organs and tissues

·         Horse is bitten by an infected midge > initial viral replication in regional lymph nodes > primary viremia > infection of target organs (endothelial cells and mononuclear cells of the lung, spleen, and lymphoid tissue) > secondary viremia > virally induced endothelial cell damage and activation of infected macrophages with subsequent cytokine production (IL-1, IL-6, TNFa, IFN beta) > increased vascular permeability > edema

·         Distinct serotypes demonstrate individual tropisms for pulmonary and cardiac endothelial cells and account for the four frequently overlapping clinical forms of AHS:  Pulmonary (peracute) form, cardiac (subacute) form, cardiopulmonary (mixed) form, horse sickness fever (mild form)

·         The mild form occurs in immune animals or in resistant species (mules, donkeys, zebras)



·         Pulmonary (peracute) form:

·         “Dunkop” = thin head

·         Dyspnea, tachypnea, fever, coughing

·         Frothy nasal exudate, widely spread forelegs and extended neck

·         Three to five day incubation; death within minutes to hours

·         Cardiac (subacute) form:

·         “Dikkop” = thick head 

·         Fever, depression, signs of colic, inability to swallow

·         Supraorbital and palpebral edema, subcutaneous edema of the neck and chest, absence of edema in the lower limbs

·         Seven to fourteen day incubation; death within four to eight days

·         Cardiopulmonary (mixed) form: 

·         Mixture of the cardiac and pulmonary form

·         Commonly a subclinical cardiac form is followed by marked dyspnea

·         Five to seven day incubation; death within three to six days

·         Horse sickness fever (mild form):  Fever; minimal clinical signs

·         Clinical pathology:  leukopenia (lymphopenia, neutropenia with a  left shift), thrombocytopenia, polycythemia, metabolic acidosis; increased FDPs and prolonged APTT, PT, and TT (DIC)



·         Pulmonary: 

·         Copious amounts of fluid and froth in the airways

·         Peritracheal, periaortic, and pulmonary edema

·         Hydrothorax, edematous lymph nodes

·         Hyperemia and petechia of intestinal serosa and mucosa

·         Cardiac:

·         Palpebral and supraorbital edema

·         Prominent gelatinous, yellow edema of subcutaneous, sub-fascia (nuchal ligament), and intramuscular tissue and lymph nodes

·         Hydropericardium; epicardial and endocardial petechia and ecchymoses

·         Edema of the gastrointestinal tract

·         Mixed:  Any combination of the above lesions

·         Mild:  No significant gross lesions




·         Lung: 

·         Alveolar exudate composed of fibrin, protein rich fluid, and few mixed inflammatory cells

·         Endothelial cells within venules are swollen with vacuolated, reticular cytoplasm and large reactive nuclei(from virus infecting them)

·         Interstitial, alveolar, subpleural, and perivascular edema

·         Fibrinous microthrombi; capillary congestion

·         Heart: 

·         Epicardial and endocardial hemorrhage

·         Multifocal myocardial necrosis, hemorrhage of great vessels

·         Subcutaneous and intramuscular tissue:  Edema

·         Lymph nodes; gastrointestinal tract:  Edema



·         Icosahedral; dsRNA; approximately 60-80nm in diameter; paracrystalline arrays

·         Vascular endothelial cell changes: hypertrophy, alterations in intercellular junctions, subendothelial deposition of cellular debris/fibrin, loss of endothelium



·         Viral isolation, PCR, in-situ hybridization, immunohistochemistry

·         Recent article found antigen present in heart, lung, liver, spleen, but NOT kidney



·         Hendra virus (Paramyxoviridae)

·         Microscopic changes:  Alveolar edema, vasculitis, endothelial syncytial cells

·         Gross findings:  Pulmonary and visceral edema

·         Equine viral arteritis (Arterivirus): 

·         Microscopic changes:  Fibrinoid vasculitis, interstitial pneumonia

·         Clinical findings:  Ventral and lower limb edema, serous nasal discharge

·         Gross findings:  Widespread hemorrhage, pulmonary edema, hydrothorax and hydroperitoneum

·         Equine infectious anemia (Lentivirus): 

·         Anemia; immune mediated (C3 complement) hemolysis

·         Gross findings:  Edema, petechia, hepatosplenomegaly, erythroid hyperplasia

·         Clinical findings:  Fever, anemia, thrombocytopenia

·         Purpura hemorrhagica:  Post streptococcal leukocytoclastic vasculitis; severe and widespread hemorrhage and edema (face and limbs)

·         Babesia caballi or equi (Piroplasmosis):  Fever, anemia, supraorbital edema; intraerythrocytic protozoa evident during acute phase



·         Dogs:  Disease follows ingestion of infected horseflesh and resembles the pulmonary form in horses with high mortality.

·         Zebras are the natural host and reservoir and rarely exhibit clinical signs.

·         AHS has been reported in elephants, camels, and other wildlife in sub-Saharan Africa



·         Equine: 

·         African Horse sickness virus

·         Equine encephalosis virus-  Facial swelling;  Central nervous signs particularly loss of control or co-ordination of the hindquarters

·         Ruminants, deer: ovine Orbivirus (Bluetongue)

·         Coronitis, hemorrhage and ulceration of the mucosal lining of the oral cavity and forestomachs, hemorrhage in the wall of the pulmonary artery, and focally extensive necrosis of skeletal muscle, especially of the neck

·         Cattle:  Ibaraki virus

·         In Japan, similar clinically to bluetongue in sheep

·         Deer:  Epizootic hemorrhagic disease virus

·         Severe, rapid edema of the head; swelling of the tongue, conjunctiva; rapid death

·         Hemorrhage in skin, heart, GIT



1.  Caswell JL, Williams KJ. Respiratory system. In:  Maxie M, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. 5th ed. Vol 2.  Philadelphia, PA: Elsevier; 2007:546-548.

2.  Clift SJ, Penrith ML. Tissue and Cell Tropism of African Horse Sickness Virus Demonstrated by Immunoperoxidase Labeling in Natural and Experimental Infection in Horses in South Africa.  Vet Pathol. 2010;47: 690.

3.  Coetzer JAW, Guthrie AJ. African horse sickness. In: Coetzer JAW, Tustin RC, eds. Infectious Diseases of Livestock. 2nd ed. Oxford, OX:Oxford University Press;2004:1231-1246.

4.  Erasmus BJ. African horse sickness. In: United States Animal Health Association. Foreign Animal Diseases. Richmond, VA: Carter printing Co and Cummings Corporation;1992: 54-65.

5.  Lopez A. Respiratory system. In:  McGavin M, Zachary J, eds. Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, MO: Mosby; 2012:505.

6.  Maclachlan NJ, Crafford JE, Vernau W, Gardner IA, Goddard A, Guthrie AJ, Venter EH.

Experimental Reproduction of Severe Bluetongue in Sheep.  Vet Pathol.2008; 45: 310.

7.  MacLachlan J, Guthrie A. Re-emergence of bluetongue, African horse sickness, and other Orbivirus diseases. Vet Res. 2010;41(6):35.

8.  Robinson W, Maxie M. Cardiovascular system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol. 3. 5th ed. St. Louis, MO: Elsevier Limited; 2007:74-76.

9.  Wilson A, Mellor PS, Szmaragd C, Clement Mertens PP. Adaptive strategies of African horse sickness virus to facilitate vector transmission. Vet Res. 2009;40(2):16. 

10.  Zachary JF. Mechanisms of Microbial Disease. In:  McGavin M, Zachary J, eds. Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, MO: Mosby; 2012:220-221.












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