Equine Viral Arteritis Study Guide

Overview and Clinical Importance

Equine viral arteritis (EVA) is an economically important, contagious viral disease of equids caused by equine arteritis virus (EAV). The virus was first isolated in 1953 following an outbreak of respiratory disease and abortion on a Standardbred breeding farm in Bucyrus, Ohio. The disease derives its name from the characteristic panvasculitis affecting small arteries and venules throughout the body.

EVA is of significant veterinary and economic importance because it can cause: abortion in pregnant mares with rates as high as 60% in naive populations, fatal interstitial pneumonia in neonatal foals, and establishment of a long-term carrier state in stallions. The carrier stallion is the critical natural reservoir of EAV, as venereal transmission frequently occurs during breeding.

Etiology

Virus Classification and Structure

EAV is classified as a member of the family Arteriviridae, genus Alphaarterivirus, order Nidovirales. The virus has been officially renamed Alphaarterivirus equid. It is the prototype virus of the Arteriviridae family, which also includes porcine reproductive and respiratory syndrome virus (PRRSV), simian hemorrhagic fever virus (SHFV), and lactate dehydrogenase-elevating virus (LDV) of mice.

Viral Characteristics

Epidemiology

Distribution and Prevalence

EAV is present in equine populations in many countries worldwide, with notable exceptions including Japan, Iceland, and New Zealand, which have successfully eradicated the disease. The prevalence of infection varies widely between countries and among breeds in the same country. Seroprevalence is frequently highest in Standardbreds and Warmbloods. Despite clinical disease being uncommon in Standardbreds, subclinical infection is very common in this breed.

Transmission Routes

Pathogenesis

Mechanism of Infection

Following respiratory exposure, EAV invades the upper and lower respiratory tract and multiplies in nasopharyngeal epithelium, tonsillar tissue, and bronchial and alveolar macrophages. Infected CD14+ monocytes and a subpopulation of CD3+ T lymphocytes transport EAV to regional lymph nodes (bronchial lymph node), where further replication occurs before release into the bloodstream.

Timeline of EAV Infection

Mechanism of Vascular Damage

The hallmark pathological feature of EVA is a panvasculitis affecting small arterioles and venules throughout the body. Vascular lesions include endothelial swelling and degeneration, neutrophilic infiltration, and fibrinoid necrosis of the tunica media. These lesions lead to edema and hemorrhage, believed to result from activation of proinflammatory cytokines including IL-1 beta, IL-6, IL-8, and TNF-alpha.

The Carrier State in Stallions

Following natural EAV infection, 30-70% of stallions become persistently infected. The virus persists in the ampulla of the vas deferens and other accessory sex glands. The carrier state is testosterone-dependent, which is why mares, geldings, prepubertal colts, and sexually immature colts cannot become carriers. Carrier stallions shed virus constantly in the sperm-rich fraction of their semen but not in any other secretions or excretions.

Clinical Signs

The majority of naturally acquired EAV infections are subclinical or inapparent. Clinical signs, when present, develop 2-14 days post-exposure (6-8 days if venereal transmission) and persist for 2-9 days. The severity depends on virus strain virulence, challenge dose, age, physical condition of the horse, and environmental factors.

Clinical Signs by Category

Clinical Presentation by Age Group

Adult Horses

Pyrexia and leukopenia are the most consistently observed clinical features. Most adult horses recover completely within 2-3 weeks without adverse sequelae. The case-fatality rate is very low in healthy adults; mortality from naturally occurring strains is essentially nil.

Pregnant Mares - Abortion

Abortion occurs 1-4 weeks after infection, typically during the acute or early convalescent phase. Abortion can occur at any gestational age from 2-10+ months. Importantly, mares bred with EAV-infective semen do NOT abort later in gestation - abortion only occurs in mares already pregnant at the time of respiratory exposure. Fetuses are usually partly autolyzed at expulsion.

Neonatal Foals

Congenitally infected or very young foals develop severe interstitial pneumonia and/or pneumoenteritis. These foals have high viral loads, shed large amounts of virus, and have an extremely poor prognosis. Euthanasia is typically recommended to prevent further viral spread, especially to pregnant mares.

Pathology

Gross Lesions

The gross lesions reflect the extensive vascular damage caused by the virus. The most significant findings include edema, congestion, and hemorrhage, especially in the subcutis of limbs and abdomen; excess peritoneal, pleural, and pericardial fluid; and edema and hemorrhage of intra-abdominal and thoracic lymph nodes.

Histopathology

The characteristic and pathognomonic microscopic lesion is necrotizing panvasculitis involving endothelial and medial cells of small arteries and venules. Histologic changes include vascular and perivascular edema, lymphocytic infiltration, endothelial cell hypertrophy progressing to fibrinoid necrosis of the tunica media, extensive lymphocytic infiltration, necrosis and loss of endothelium, and thrombus formation in severe cases.

Diagnosis

EVA cannot be diagnosed on clinical signs alone because the presentation can mimic many other equine diseases. Laboratory confirmation is required.

Differential Diagnosis

• Equine herpesvirus 1 and 4 (EHV-1/4)
• Equine influenza virus
• Equine rhinitis A and B viruses
• Equine infectious anemia
• Purpura hemorrhagica
• Allergy-induced urticaria
• Hoary alyssum (Berteroa incana) toxicosis
• African horse sickness (foreign animal disease)

Diagnostic Methods

Diagnosis of Carrier Stallions

Identification of carrier stallions follows a two-step process:

• Serologic screening: Test serum using virus neutralization test
• If seropositive (titer 1:4 or greater): Test sperm-rich fraction of semen by virus isolation and/or RT-PCR

Treatment

There is no specific antiviral treatment for EVA. Treatment is supportive and symptomatic. Virtually all naturally infected adult horses make complete clinical recoveries.

Prevention and Control

Vaccination

Two commercial vaccines are available:

Vaccination Protocols

• Stallions: Vaccinate at least 3 weeks before breeding season; annual boosters; test serum and confirm negative before first vaccination
• Colts (6-12 months): Vaccinate before puberty to prevent future carrier state; especially important in Standardbreds and Warmbloods
• Mares to be bred to carrier stallions: Vaccinate at least 21 days before insemination; isolate for 21 days post-vaccination
• Pregnant mares: MLV vaccine NOT recommended in last 2 months of gestation due to risk of fetal infection

Management Strategies

• Identify and manage carrier stallions: Screen all breeding stallions; breed only to seropositive or vaccinated mares
• Test transported semen: Screen all shipped semen; virus remains viable in fresh, cooled, or frozen semen
• Isolate newly bred mares: Mares bred to carrier stallions should be isolated for 3 weeks to prevent respiratory spread
• Outbreak response: Suspend breeding; isolate clinical cases; sanitize equipment; consider emergency vaccination; movement restrictions for 3 weeks after last case

Prognosis