Clinical Presentation


Clinical Signs
    1) Acute
    2) Chronic
   
3) Innaparent carrier

Equids infected with EIA will show different manifestations.

Many never show obvious clinical signs. Those that develop disease can progress through three stages: acute, chronic, and inapparent carrier.

 

1) Acute

When a horse is exposed to EIAV, clinical symptoms will arise within 1 to 4 weeks of infection. This stage is the hardest to diagnose due to the rapid onset of signs, and often only an elevated body temperature is noted. Most horses will survive this stage, recover for a brief period ( 5 to 30 days) where virus levels will decrease substantially and clinical signs resolve.

 

Clinical signs:

 

High fever (107° F,41.6° C),

Thrombocytopenia; If severe, horses may develop mucosal petechiations, epistaxis and ventral pitting edema that may be fatal.

Depression,

Inappetence

Splenomegaly

Abdominal/Splenic lymph node enlargement

 

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    2) Chronic

 

The chronic stage is characterized by recurring and intermittent cycles of the clinical signs below which typically decrease in severity over the course of 1 year.

Antigenic variations allow the virus to escape the immune system, increase its replication, and are responsible for the recurring nature of the disease.

Horses may survive this stage moving to inapparent carrier stage, die during a recurrent disease episode, or progress to a debilitating form of the disease characterized by ill-thrift, anemia, ventral pitting edema, progressive weight loss, and ultimately death.

 

Clinical signs:

 

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    3) Innaparent carrier

 

The majority of horses with EIA can be found in this stage of the disease. The level of virus replication is decreased owing to a temporary development of a strong humoral and cell-mediated immune response. However, the virus is not able to be cleared and is still in high enough concentration for transmission to a susceptible horse. Stress, hard work and administration of immunosuppressive drugs such as corticosteroids may induce increased viral replication leading to clinical disease in innapparent carriers.

 

 



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