equine infectious anaemia=lecture
TRANSCRIPT
EIA
MP Gupta
EIA
Swamp fever, Equine Malaria
• Equine infectious anemia is viral
disease limited to horse donkeys and
mules and is characterized by
recurrent episodes of fever hemolytic
anemia, icterus depression edema and
chronic weight loss.
• This disease is more likely occurs in the
low-lying areas where water and
marshy condition are conducive to
insect multiplication.
Etiology
• It is caused by Lentivirus of the family
Retroviridae.
• Virus can survive boiling for 15
minutes and is killed by sunlight.
• Virus persists for several months in
dried blood and excretions.
Etiology
• A feature of lentiviruses is their ability
to hijack macrophages.
• ( Reoviridae is NE whereas REtroviridae
is E- Maedi visna, commonly called
ovine progressive pneumonia, Avian
Leukosis, HIV, EIA, Simian
Immunodeficiency virus belong to
Retroviridae)
Epidemiology
• All breeds and age groups of Equidae
are susceptible.
• Use of unsterilized syringes in the
treatment or control of other disease
can transmit the disease.
Geographic Distribution
•
• Equine infectious anemia has been
found nearly worldwide. This disease
appears to be absent from a few
countries including Iceland and Japan.
• Biting flies particularly Tabanidae
(Tabanus) Stable flies (Stomoxys
calcitrans) and mosquitoes can
transmit the infection.
• Intrauterine infection may occur but it
is uncommon.
• Virus is present in all tissue secretions
and excretions and may present in the
body for upto 18 years preventing re-
infection but providing a source of
infection for most of the animal’s life.
These clinically normal carriers are
usual means by which the disease is
introduced into clean areas.
Pathogenesis
After entry the virus is present in the blood and all tissues and discharges (liver, kidney, spleen and lymph nodes)
Viral titres in the blood are particularly high during febrile episodes and it is at these times that the potential for transmission to unaffected horses is highest.
Virus persists in the WBC of all infected horses and is quite stable in serum. The intima of the small blood vessels and erythrocytes are damaged.
Damage to the intima of the blood vessels and reticuloendothelial involvement is followed by inflammatory changes in the parenchymatousorgans particularly the liver.
Changes occur in the nervous tissue and result in the ataxia and encephalomyelitis.
The hemolysis, which is both intravascular and extravascular, is characterized by shorter lifespan of erythrocytes
Virus can pass the placental barrier and infect the fetal foal.
It is generally assumed that the anemia and glomerulonephritisresults from the deposition of complexes composed of viral antigen and antibody.
Clinical Signs
• Initial depression, weakness and
anemia and in-cordination.
• Intermittent fever,105oF which may
vary 1oF with in 1 hour.
• Jaundice, edema of the ventral
abdomen, the prepuce and legs and
petechial hemorrhage in the mucosa
under the tongue (alos in AHS) and in
the conjunctiva.
• In chronic stages, the appetite is
usually good although alllotrophagia
may be observed. Some affected
animal appears to make a complete
recovery although they may remain
infected and suffer relapse in later
years.
• Alimentary involvement is not
commonly recorded in the EIA but a
fetid watery diarrhea has been
observed.
• Death occurs after a course of 10 – 14
days of illness.
• Morbidity rate is 100% and mortality
rate is 70 % in some herds.
Dx• 1.By hematological examination
• Marked reduction of RBC
• PCV decreased (14 to 20%)
• Increased monocytosis
• Increased ESR about 50% in 15 minute
• Slight Leukopenia (down to 2000/ml) with a
marked neutropenia and a lymphopenia
• Total serum protein is reduced and albumin:
globulin ratio is below normal.
• 2. By serological tests
• Immunodiffusion test
• cELISA
• 3. Reverse-transcriptase polymerase
chain reaction (RT-PCR)
Samples to collect
• Serum should be collected for
serology. Blood samples are taken for
RT-PCR, virus isolation or inoculation
into a test animal.
• 3.PM findings
• S/c edema, jaundice and petechial and
ecchymotic hemorrhage
• Enlargement of liver, spleen and local lymph
nodes
• Intravascular clotting(DIC)
• Emaciation and pallor tissues
• Extensive proliferation of reticuloendothelial
system, perivascular round cell infiltration,
especially in the liver, hemosiderosis and a
• Horse, heart. Pale
cardiac muscle,
focal white areas of
myocardial
degeneration, and
reddened
hemorrhagic areas
(possible hypoxia
during death).
Differential Dx
• a) Leptospirosis
• Milder and spontaneous recovery
• Hemoglobinuria is present
• Caused by Leptospira sp.
• b) Babesiosis
• Caused by Babesia sp.
• Hemoglobinuria? and hemoglobinemia
is present
• Transmitted by [email protected]
• c) Ehrlichiosis
• Limb edema and ataxia in the infected
horses
• Leukopenia, thrombocytopenia and
hyperbilinemia.
• equine viral arteritis,
• purpura hemorrhagica,
• severe strongyliasis or fascioliasis,
• phenothiazine toxicity,
• autoimmune hemolytic anemia
• and other diseases that cause fever,
edema and/or anemia.
Control
• Quarantine management: 6 month
quarantine
• Destruction of all infected animals
after confirmation of the infection
(Test and slaughter policy)
• Drainage of marshy land and insect
control use of sterilized syringe and
needles
• No satisfactory vaccine has been
developed [email protected]
Disease Prevention
• Equine Infectious
Anemia
– Coggins Test
• A vaccine is available, called "Chinese
Live Attenuated EIA vaccine",
developed in China and widely used
there since 1983. Another attenuated
live virus vaccine is in development in
the United States
• Reuse of syringes and needles is a risk factor
for transfer of the disease.
• Options for the horse include sending the
horse to a recognized research facility,
branding the horse and quarantining it at
least 200 yards from other horses for the
rest of its life, and euthanizing the horse.
• EIA-positive horses are infected for life.
Public Health
• There is no evidence that equine
infectious anemia is a threat to
humans.