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Equine Infectious Anemia

  Equine Infectious Anemia (EIA) is a Lentivirus from the family Retroviridae.  It has been known to infect equine since the 1900’s, yet there is still no effective vaccination or treatment.  Infection is for life and many infected horses show no clinical signs.  EIA is related to the HIV in humans and this discovery has made new research into the disease available.

  Transmission is via hematophagous insects such as deerflies and horseflies.  Iatrogenic transmission via hypodermic needles and tattoo equipment can also occur.  Due to the pain involved with the feeding of these insects, they do not normally finish their blood meal on one host.  Transmission of the disease takes place when they are interrupted.  Since horses are housed very closely together, this allows for easy transmission.  The large mouth parts of these insects can hold up to 10 nL of blood.  The virus only lives for 30 minutes to 4 hours in the mouth.  The insects prefer to finish their blood meal rapidly, even though their flight range can be 4 miles.  If animals are separated by more than 200 yards, the fly will most likely try to finish the meal on the original animal.  Fly control is one of the major defenses against this disease.

  The disease can present with acute or chronic signs; the acute clinical signs include high fever, anemia, and thrombocytopenia.  Chronic disease presents with recurrent fever, weight loss, severe anemia, and ventral edema.  The strain and dose of virus in the horse’s system, along with immune response, are the determinant factors for disease.  The more virulent the strain, the higher the fever, which is usually 7-30 days post-infection.  The highest concentrations of virus at this time are found in the serum, liver, spleen, lymph nodes, bone marrow, lung and kidney.  The replication of the virus occurs within tissue macrophages, rather than circulating monocytes.  The majority of horses with EIA are chronically infected and overcome the initial infection.  They appear clinically normal for days to weeks, sometimes up to a year.  At this time, they may or may not develop recurring fever, thrombocytopenia, and depression.  Viremia occurs during the febrile period (viral particles are 1,000 – 10,000 times higher than when afebrile).  During the non-febrile period, the virus is cell-associated and not free in the plasma.  After approximately twelve months, most horses become inapparent carriers.  These horses go unnoticed and can serve as a reservoir for infection to others.  As carrier horses become immunocompromised, the virus re-appears in the blood stream.

  Reproductive ramifications include decreased fertility, abortion (if mare was infected on or before 203 days of gestation and occurs 21-64 days post-infection), transplacental transfer, colostral or milk transmission and , rarely, venereal transmission.

  Clinical diagnosis of EIA is via clinical signs, history and diagnostic testing.  Tests include agar gel immunodiffusion (AGID) or Coggins and competitive enzyme-linked immunosorbent assay (C-ELISA) on serum.  Different states recognize one or both of these tests.  These tests both detect antibody to p26 core protein of EIA.  The Coggins test was developed in the early 1970s and is highly sensitive and specific.  It has a 95% accuracy rate and is the most used test for EIA.  It is performed on a Petri dish in a layer of agar.  The C-ELISA has not been used as frequently as the Coggins, but is believed to have similar sensitivity and specificity.  Western immunoblot assay (this tests for virus specific antibodies) can be used for horses with questionable Coggins and C-ELISA results.  PCR can also be used on peripheral blood mononuclear cells and/or buffy coat cells.  This is another method of confirming the diagnosis.

  Gross necropsy lesions during febrile disease include generalized lymph node enlargement, an enlarged liver with a prominent lobular pattern, an enlarged meaty spleen, mucosal and visceral hemorrhages, ventral subcutaneous edema and vascular thrombosis.  Histopathology of these tissues usually reveals accumulations of lymphocytes and macrophages in sinusoids and portal areas of the liver, in medullary sinus of lymph nodes, adrenal glands, spleen,  meninges, and lung.  This lymphoproliferation may be due to an attempt to control the infection by the T- lymphocytes.  There is also marked extramedullary hematopoiesis.  Other liver lesions include fatty degeneration and hepatocellular necrosis.  Kupffer cells are swollen with hemosiderin accumulation.  In infected horses with no clinical signs, gross lesions  are generally unremarkable, although some may have glomerulitis, retinal depigmentation, and choroiditis.

  Although horses mount a strong humoral and cell-mediated immune response, they are unable to completely clear the virus and are infected for life.  Control is dependent on isolation, hygiene (needle usage), identification of positive animals, and fly control.  Interstate travel requires a negative EIA test.  A negative test is also required for most horse shows, as well as the sale of horses at public auction.  Action should be taken by owners, veterinarians, and regulatory officials to keep EIA under control.

 -by Angie Johnson, Class of 1999

 -by Melanie Greeley, DVM


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Phone: (812) 678-3401
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