Equine infectious anemia virus (EIAV) is an RNA virus in the Retroviridae family, genus Lentivirus. It shares structural and genomic features with other lentiviruses, including human immunodeficiency virus (HIV).
Veterinarian using microscope to help identify cause of disease.
High-risk regions for equine infectious anemia virus include Texas and Louisiana, while areas like New England and Alaska are considered low risk, but sporadic outbreaks can occur anywhere.
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Like HIV, EIAV uses reverse transcriptase to convert its RNA genome nto DNA, which is then integrated into the host genome via the virally encoded enzyme, integrase. Once integrated, EIAV establishes a lifelong nfection by hijacking the host cell’s machinery to replicate and produce new virions.
The virus causes equine infectious anemia (EIA), a disease first recognized in 1843 and identified as viral in origin in 1904. Identification of EIAV-Positive Equids EIA is a federally regulated disease in the United States. The U.S. Department of Agriculture oversees nationwide serosurveillance through mandated testing protocols.
In 2023, 1,364,247 tests were conducted, identifying 61 seropositive horses across 45 sites, up from 29 seropositive horses in 2020.
The Coggins test, developed in 1970, remains a USDA-approved diagnostic tool. Additionally, licensed ELISA tests detect antibodies to viral antigens such as gp45 and p26.
Equids must test seronegative before crossing state lines or participating in events. However, many infected horses are inapparent carriers, displaying no clinical signs yet capable of transmitting the virus—either via blood transfer or mechanicaltransmission by biting flies like tabanids. These inapparent carriers pose a serious risk, especially to naïve horses, for whom the infection can be fatal.
Clinical Disease
EIA progresses through three stages: acute, chronic and inapparent. The acute phase is marked by high fever, thrombocytopenia (lower than normal number of platlets in the blood) – which may cause hemorrhaging, and malaise.
Clinical signs may include petechiae (tiny dots on the skin, caused by the leakage of blood from tiny capillaries under the skin) and ecchymoses (bruising). In the chronic phase, clinical signs recur intermittently with decreasing intensity. The inapparent phase is asymptomatic, though the horse remains infected and capable of transmitting the virus.
Regardless, fever accompanied by recurrent or unexplained thrombocytopenia should prompt suspicion for EIA.
Stress or immunosuppressive treatments such as corticosteroids can trigger disease recrudescence, or reoccurance. Other potential clinical signs include edema, weight loss, anemia, and—less commonly— leukoencephalitis (inflammation of the white matter of the brain) or enterocolitis (inflammation of the intestines).
The expression of disease varies based on factors such as viral dose, strain, virulence, host immune competence and environmental stressors. Notably, high-titered viremia during the acute phase significantly increases transmission risk.
Like other lentiviruses, EIAV mutates rapidly due to error-prone reverse transcription. These genetic changes in the viral genome (genetic variation) result in antigenic variation and escape from acquired immune responses. Antigenic variation complicates vaccine development and contributes to recurring clinical episodes in chronic infections.
Pathogenesis
EIAV infects monocytes, macrophages, dendritic cells and endothelial cells. Infection of the endothelium is implicated in vascular damage, which may trigger disseminated intravascular coagulation (DIC), promote platelet aggregation and contribute to tissue edema
Pathology and Clinical Pathology
Common necropsy findings in EIA cases include splenomegaly, lymphadenopathy, hepatomegaly, mucosal and visceral hemorrhages, subcutaneous edema and thrombi. Histopathologic examination often reveals mononuclear cell infiltration and hemosiderophages within lymphoid tissues.
Immune complex-mediated glomerulonephritis is also frequently observed. Thrombocytopenia typically coincides with febrile episodes and may be compounded by platelet dysfunction, further exacerbating hemorrhagic risk and contributing to DIC.
Anemia arises from both hemolysis and reduced erythropoiesis. In inapparent carriers, mild anemia, hyperglobulinemia and hypoalbuminemia are common. Persistent polyclonal B cell activation reflects ongoing immune stimulation.
Prevention, Control and Regulations
EIA risk varies geographically. High-risk regions include Texas and Louisiana, while areas like New England and Alaska are considered low risk. Nevertheless, sporadic outbreaks can occur anywhere, underscoring the need for continued vigilance.
Veterinarians should promote annual EIAV testing, particularly for newarrivals, and advocate for robust tabanid fly control measures. Organizers of equine events should require documented proof of EIAV seronegativity.
When a horse tests positive, all potentially exposed horses must be quarantined and retested until two negative results, taken 30 to 60 days apart, are confirmed. EIAV-positive horses must either be euthanized or permanently isolated at least 200 yards from other equids—sufficient distance to prevent mechanical transmission by insect vectors. Positive horses must also be permanently identified with a USDA-issued brand or tattoo.
With no nationwide eradication program in place, reservoirs of EIAV persist. Of the estimated 6.65 million horses in the U.S., fewer than 20%are tested annually, allowing inapparent carriers to remain undetected. Identifying and managing these carriers is essential for effective disease control.
Veterinarians play a critical role in educating owners about the economic, emotional and epidemiologic consequences of EIA and the importance of proactive prevention.
Iatrogenic and Emerging Modes of Transmission
Veterinarians, horse owners and farm and venue managers must recognize that EIAV transmission remains a serious threat to the equine population, especially via iatrogenic routes—a frequent, yet preventable, mode of spread. Iatrogenic transmission occurs through mechanical transfer of EIAV via contaminated needles, surgical instruments, blood products
or contamination of multi-dose vials. It should be a constant concern in veterinary biosafety protocols.
Other transmission routes—such as via infected secretions or mechanical vectors like biting flies—can be mitigated through careful management practices.
Recently, a cluster of EIAV cases originating at a Texas equine clinic was linked to iatrogenic transmission via catheter flushes using multi-dose vials of heparinized saline. As of the end of May 2025, the USDA Animal and Plant Health Inspection Service (USDA-APHIS) has confirmed 21 seropositive horses across four states: Texas, California, Colorado and
Oklahoma. According to USDA-APHIS epidemiologist Angela Pelzel-
McCluskey, DVM, additional cases are anticipated.
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In clinical medicine, previously unrecognized transmission routes may initially seem unlikely until they are fully understood. For example, during a 2006 outbreak in Ireland involving two clusters in County Meath and County Kildare, the possibility of aerosol transmission was raised. It was speculated that aerosolization occurred during cleanup of infectious bloody secretions—suggesting a previously unidentified transmission mode in a clinical setting (Equine Veterinary Journal, 2008, 40(7):709–711).
Together with the recent Texas outbreak, these events underscore theevolving landscape of infectious disease transmission and biosecurity, and highlight the need for ongoing research, vigilance and adaptation of veterinary protocols.
Press release by Equine Disease Quarterly - Article by Brett Sponseller, DVM, PhD, DACVIM - Professor and Chair, Department of Veterinary Science Gluck Equine Research Center