BASICS
Panvasculitis leading to edema, hemorrhage, and abortion in mares; respiratory disease and edema in other adults; severe illness or death in the neonate.
- Small, enveloped, positive-stranded RNA virus, resistant to freezing, drying, and long storage at – 70°C. Reliably destroyed by a 1:32 dilution of commercially available sodium hypochlorite solution
- 1 serotype—Bucyrus. Evidence of antigenic variation among different isolates and variation in the degree of clinical signs produced
- Incidence, determined seroconversion, varies considerably by population and geographic location
- Highly contagious. Spread by direct contact with infected horses and their bodily secretions, including urine and milk, nasal droplet spray among racehorses, and venereal route at breeding farms. Isolated from the urine for up to 3 weeks post infection
- High morbidity and low mortality in adults—high mortality in neonates
- Carrier stallions harbor the virus in their accessory sex glands and shed virus in their semen. Carrier state is testosterone dependent. Virus may be present in frozen or cooled semen from carrier stallions. Seronegative mares bred to either short- or long-term carrier stallions are primary source of virus spread
- Seropositive mares bred to a carrier stallion may shed virus for a short period. Abortion due to infection secondary to myometrial necrosis and edema, resulting in failure of the uteroplacental unit
- Foals born to seropositive dams acquire passive immunity through the colostrum and become seronegative after passive immunity wanes. Foals may also acquire the virus through colostrum and milk; at least 2 foals are thought to have acquired a fatal form of the disease in this manner
- Nasal challenge—virus first replicates within alveolar macrophages and then appears in the bronchial lymph nodes; virus spreads throughout the body via the circulation. Vascular lesions develop associated with virus present in the tunica media of myocytes and within the endothelium. Arterial damage may persist for weeks after infection. The kidney is a site of virus localization, as is the placenta, bronchiolar epithelium, thymic tissue, and enterocytes in foals
- Whole body, except central nervous system
- Predominant systems affected—respiratory system in young horses, foals; urogenital system in pregnant broodmares and intact males
- Any age or breed. Standardbreds have the highest seroconversion rates in the USA
- Immediate perinatal period foals; young racehorses, and broodmares at farms with a carrier stallion have the highest rates of incidence
From clinically silent and recognizable only by seroconversion to acute-onset severe disease resulting in abortion and neonatal death.
- Abortion and neonatal death—possible exposure by residing on a farm where a carrier stallion is present
- Seronegative mare returning to the farm after being bred by a carrier stallion
- Young horses in training—association with an outbreak of respiratory disease ranging from mild to severe
- Neonates born to seronegative mares or that have failure of passive transfer of maternal antibody when born to seropositive mares
- Young adults and broodmares that develop clinical signs typically are febrile for 5–9 days
- Distal limb (often hindlimbs), conjunctival, periorbital, scrotal, and preputial edema
- Epiphora and nasal discharge associated with rhinitis and conjunctivitis
- Urticarial skin rash
- Cough, lethargy, anorexia, lameness, and exercise intolerance
- Abortion and stillbirth
- Rare sudden death in adults with particularly virulent isolates
- Foals—born normal or weak, edema, lethargy; sudden death or period similar to hypoxic–ischemic asphyxia syndrome before progressing to respiratory failure and death; can survive for more than 2 weeks prior to death
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS