Equine Infectious Anemia
Equine Infectious Anemia (EIA) is a Lentivirus from the
family Retroviridae. It has been known to infect equine
since the 1900s, 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 horses 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
|