- Definition
- Pathophysiology
- Systems Affected
- Genetics
- Geographic Distribution
- Signalment
- Signs
- Causes
- Risk Factors
BASICS
- An infectious disease caused by the EIAV, a lentivirus of the family Retroviridae
- EIAV is closely related to HIV-1, the cause of AIDS in humans
- EIAV is transmitted primarily by blood-feeding insects, especially tabanids (i.e. horseflies and deerflies); iatrogenic transmission can occur via contaminated needles, syringes, and surgical instruments as well as through contaminated semen and transfusion of contaminated blood or plasma
- Once infected, a horse remains so for life
- EIAV infects cells of the monocyte/macrophage lineage and can be detected in the cytoplasm of this cell type in the liver, spleen, lymph nodes, lung, bone marrow, and circulation
- EIAV also replicates in endothelial cells, which may serve as a viral reservoir; viral replication in endothelial cells may cause vasculitis
- EIAV can be characterized by 3 clinical syndromes—acute, chronic, and inapparent carrier; not all horses progress through all 3 syndromes
- Acute disease—usually occurs 1–4 weeks after infection; is associated with high levels of viremia; can be characterized by fever, anorexia, lethargy, ventral edema, thrombocytopenia, anemia, and, occasionally, epistaxis and death; and is usually <1 week in duration and sometimes mild enough to go completely unnoticed
- Chronic disease—associated with recurrent episodes of viral replication, causing repeated bouts of clinical signs; classic signs of anemia, ventral edema, and weight loss occur during this phase
- With time, episodes of clinical disease decrease in duration and severity, and most horses control the infection within 1 year, becoming inapparent carriers
- Inapparent carriers show no clinical signs, are seropositive, and are reservoirs of infection, capable of transmitting the virus to uninfected horses
- Hemic/lymphatic/immune—anemia caused by immune-mediated intravascular and extravascular hemolysis as well as bone marrow suppression. Likewise, thrombocytopenia is caused by both bone marrow suppression and enhanced platelet destruction; severe thrombocytopenia can lead to mucous membrane petechiae and epistaxis
- Cardiovascular—immune-mediated vasculitis leads to hemorrhage, thrombosis, and edema
- Hepatobiliary—accumulations of lymphocytes and macrophages in the liver can result in hepatomegaly, fatty degeneration, and hepatic cell necrosis
- Renal/urologic—immune complex deposition can result in glomerulonephritis
- Neurologic—vasculitis and lymphocyte accumulation in meninges occasionally result in ataxia
In the USA, since less than 25% of the total United States horse population is tested, the true prevalence is unknown and a reservoir of infected horses remains undetected. Prevalence varies by state, and ranges from 0% to 0.14% of horses tested. The prevalence is usually higher in the Gulf Coast states, because the climate is favorable for vectors and virus transmission.
- Horses, ponies, mules, and donkeys are susceptible; however, donkeys and mules appear to be less severely affected
- No breed, age, or sex predilections
- Clinical signs—vary, depending on the stage of disease
- Inapparent carriers—clinically normal
- Chronic stage—affected animals may show no signs between clinical episodes
- Signs can go unnoticed
- May be a history of inappetence, lethargy, and fever
- Severely affected horses may have a history of high fever (40.5–41.5°C; 105–106°F), depression, ventral edema, weight loss, ataxia, and epistaxis
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS