Equine Infectious Anemia - contd.
EIA is caused by the equine infectious anemia virus, or EIAV, a lentivirus of the family Retroviridae. Lentiviruses are those that generally cause a permanent, chronic infection. EIAV is closely related to the human immunodeficiency virus, or HIV-1, the cause of AIDS. Blood-feeding insects, especially horseflies and deerflies, primarily transmit EIAV. Iatrogenic transmission can also occur via contaminated needles, syringes, and surgical instruments, as well as through transfusion of contaminated blood. Once infected, a horse remains infected for life. EIAV infects monocytes and macrophages, and can be detected inside these white blood cells in the liver, spleen, lymph nodes, lung, bone marrow, and circulation of infected animals.
EIA virus particles replicate inside the monocytes and macrophages and are subsequently released in large numbers. The affected horse's immune system reacts to this viremia, or presence of virus particles in the bloodstream. This causes immune-mediated intravascular and extravascular hemolysis, or red blood cell breakdown, as well as bone marrow suppression. Anemia, which is an abnormally low red blood cell count, is the result. Likewise, thrombocytopenia, or low platelet count, is caused by both bone marrow suppression and immune-mediated destruction of platelets. Severe thrombocytopenia can lead to mucous membrane petechiae, or pinpoint hemorrhage, as well as epistaxis, or nose bleed.
The immune reaction to EIAV may also affect blood vessels and vital organs. Hemorrhage, thrombosis, or blockage of blood vessels, and edema can occur, and are secondary to immune-mediated vasculitis, or inflammation of the vessels. Vasculitis and lymphocyte accumulation in the meninges, or lining tissues of the brain and spinal cord, occasionally result in ataxia, or incoordination of movement. Accumulations of lymphocytes and macrophages in the liver can result in hepatomegaly, or liver enlargement, fatty degeneration, and hepatic cell death, while immune complex deposition can result in glomerulitis, or inflammation of specialized structures in the kidney.
There are essentially three stages of EIAV-associated disease. These are the acute stage, the chronic stage, and the inapparent stage. Generally, the disease's clinical signs correlate with the stage of the disease. Acute disease usually occurs one to four weeks after infection and is associated with high levels of viremia. The acute phase is usually less than one week in duration, and is sometimes mild enough to go completely unnoticed. Affected horses not previously infected will experience the acute phase.
Chronic disease is associated with recurrent episodes of viral replication and clinical signs. With time, clinical disease episodes decrease in duration and severity. Most horses develop sufficient immunity to control the infection within one year, and become inapparent carriers of EIAV. These horses show no clinical signs. A few horses may develop very severe disease in either the acute or chronic stages and will die from organ system complications or other sequela of equine infectious anemia.
