Equine Infectious Anemia (EIA / Coggins Disease)

Equine Infectious Anemia (EIA) is a chronic, persistent, and potentially fatal viral disease of equids caused by the equine infectious anemia virus (EIAV), a lentivirus belonging to the family Retroviridae. The disease is characterized by recurrent episodes of fever, anemia, thrombocytopenia, lethargy, and weight loss, with a variable clinical course ranging from acute fulminant disease to subclinical carrier states. EIA is a globally reportable disease (OIE-listed) and is of major economic and regulatory importance to the equine industry due to its impact on international movement, racing, breeding, and show events. The virus is transmitted primarily by mechanical transfer of contaminated blood via biting flies (e.g., Tabanus spp., Stomoxys calcitrans), but also through contaminated needles, surgical instruments, or blood products. The disease is also known as Coggins disease, named after Dr. Leroy Coggins who developed the agar gel immunodiffusion (AGID) test in the 1970s. EIA affects all equid species, including horses, donkeys, mules, and zebras, and has a worldwide distribution, with higher prevalence in tropical and subtropical regions. The clinical presentation can be acute, chronic, or inapparent, with the latter being the most common in endemic areas. The virus integrates into the host genome as a provirus, leading to lifelong infection and persistent antibody response, which is the basis for diagnostic testing. The disease is a significant concern for equine practitioners due to its zoonotic potential (none), but its high morbidity and mortality in acute cases, and the lack of effective treatment or vaccine, necessitate strict biosecurity and quarantine measures.

The causative agent of Equine Infectious Anemia is the equine infectious anemia virus (EIAV), a single-stranded RNA virus belonging to the genus Lentivirus within the family Retroviridae. EIAV is an enveloped virus with a diameter of approximately 80-100 nm, and its genome encodes for structural proteins (gag, pol, env) and regulatory proteins (tat, rev, S2). The virus exhibits a high degree of genetic and antigenic variability, particularly in the envelope glycoprotein (gp90), which allows it to evade the host immune response and establish persistent infection. EIAV infects cells of the monocyte/macrophage lineage, including tissue macrophages and circulating monocytes, and replicates actively during febrile episodes, leading to viremia and widespread dissemination. The virus is not directly cytopathic to erythrocytes; instead, anemia results from immune-mediated destruction of infected and uninfected red blood cells, as well as suppression of erythropoiesis. The primary mode of transmission is mechanical, through the interrupted feeding of blood-sucking insects, particularly horse flies (Tabanus spp.) and deer flies (Chrysops spp.), which can transmit the virus from an infected to a susceptible horse within minutes. Iatrogenic transmission can occur through the use of contaminated needles, syringes, or surgical instruments, as well as through blood transfusions or administration of contaminated biological products. Vertical transmission from mare to foal can occur in utero or via ingestion of infected colostrum or milk, although this is less common. The virus is relatively fragile in the environment and is inactivated by heat, detergents, and common disinfectants, but it can survive in blood samples for extended periods under appropriate conditions.

Equine Infectious Anemia occurs worldwide, with higher prevalence in regions where the insect vectors are abundant, such as the southeastern United States, parts of South America, Africa, Asia, and southern Europe. The disease affects all breeds of horses, but certain management practices and environmental conditions influence the risk. There is no breed or sex predilection, but age may play a role, with younger horses (under 3 years) more likely to develop acute disease, while older horses may become chronic carriers. The disease is more common in horses kept on pasture or in areas with high fly populations, as the primary mode of transmission is vector-borne. Stabled horses are at lower risk unless iatrogenic transmission occurs. The prevalence of EIA in the United States has been significantly reduced through mandatory testing and quarantine programs, but sporadic outbreaks still occur, particularly in the Gulf Coast states. The morbidity rate varies, but in an outbreak, up to 30-50% of exposed horses may become infected, with a case fatality rate of 10-30% in acute cases. Chronic carriers are the main reservoir of the virus and can transmit the disease to other horses for life, even in the absence of clinical signs. The economic impact of EIA is substantial due to the costs of testing, quarantine, euthanasia of positive animals, and restrictions on movement and trade. The disease is a major concern for the racing and performance horse industry, as a positive Coggins test results in lifelong quarantine or euthanasia, effectively ending the horse's athletic career. Seasonal variation is observed, with higher transmission rates during warm months when insect vectors are active. The incubation period ranges from 1 to 3 weeks after exposure, but can be longer in some cases.

The pathophysiology of Equine Infectious Anemia involves a complex interplay between viral replication, immune-mediated destruction of blood cells, and inflammatory responses. After transmission, EIAV infects tissue macrophages and circulating monocytes, where it replicates and produces new virions. The virus is released into the bloodstream, leading to a high-titer viremia that coincides with the onset of fever and clinical signs. The primary target cells are macrophages in the liver, spleen, lymph nodes, and bone marrow. The virus induces apoptosis of infected macrophages and activates the immune system, leading to the release of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6). These cytokines contribute to fever, lethargy, and anorexia. Anemia is a hallmark of EIA and results from multiple mechanisms: (1) immune-mediated hemolysis, where antibodies and complement bind to virus-infected erythrocytes (via immune complexes) and uninfected erythrocytes (via bystander hemolysis), leading to their destruction in the spleen and liver; (2) erythrophagocytosis by activated macrophages; (3) suppression of erythropoiesis in the bone marrow due to viral infection of erythroid progenitor cells and cytokine-mediated inhibition. Thrombocytopenia is also common and is caused by immune-mediated destruction of platelets and decreased platelet production. During acute episodes, there is a marked drop in packed cell volume (PCV) and platelet count, which can lead to clinical signs of anemia and bleeding tendencies. The virus undergoes antigenic variation, particularly in the envelope glycoprotein, allowing it to escape neutralizing antibodies and establish persistent infection. Between febrile episodes, the virus replicates at low levels in tissue macrophages, and the horse becomes a carrier with lifelong infection. Chronic carriers may develop glomerulonephritis due to immune complex deposition in the kidneys, leading to proteinuria and renal dysfunction. The severity of clinical signs is influenced by the virulence of the viral strain, the host's immune response, and the presence of concurrent infections or stressors.

Several factors increase the risk of EIA infection and the severity of clinical disease. Extrinsic factors include: (1) geographic location with high vector density, particularly in warm, humid climates; (2) seasonal exposure to biting flies, with peak transmission in summer and early fall; (3) management practices such as group housing on pasture, which increases contact with vectors; (4) iatrogenic transmission through contaminated needles, syringes, or surgical instruments, especially in veterinary practices that do not adhere to strict biosecurity; (5) blood transfusions or administration of contaminated biological products; (6) lack of routine testing and quarantine protocols for new horses entering a herd. Intrinsic factors include: (1) age, with younger horses (1-3 years) more susceptible to acute disease, while older horses may develop chronic infection; (2) immune status, as horses with compromised immunity (e.g., due to stress, malnutrition, or concurrent disease) may experience more severe clinical signs; (3) genetic susceptibility, as certain horse breeds or individuals may have a more robust immune response that limits viral replication; (4) pregnancy, as pregnant mares may experience recrudescence of latent infection due to hormonal changes and immunosuppression; (5) strenuous exercise or transportation stress, which can trigger clinical episodes in carrier horses. The presence of other infectious diseases, such as equine herpesvirus or strangles, may also exacerbate the clinical course of EIA.

The clinical signs of Equine Infectious Anemia vary depending on the stage of infection: acute, chronic, or subclinical. Acute EIA typically occurs 1-3 weeks after exposure and is characterized by a sudden onset of high fever (up to 106°F or 41°C), depression, lethargy, anorexia, and weakness. Affected horses may show signs of anemia, including pale mucous membranes, increased heart rate (tachycardia, >60 bpm), and increased respiratory rate (tachypnea). Petechial hemorrhages may be present on the mucous membranes, particularly the conjunctiva and oral mucosa, due to thrombocytopenia. Icterus (jaundice) may develop as a result of hemolysis. In severe cases, horses may develop edema of the ventral abdomen, limbs, and prepuce, and may show signs of colic due to gastrointestinal involvement. The acute episode may last for 3-5 days, after which the horse may recover or progress to chronic disease. Chronic EIA is characterized by recurrent episodes of fever, anemia, and weight loss, with periods of apparent clinical normality between episodes. The fever episodes are often associated with stress, exercise, or concurrent illness. Chronic carriers may show poor performance, exercise intolerance, and a rough hair coat. Subclinical carriers show no clinical signs but are persistently infected and serve as a source of infection for other horses. In some cases, acute EIA can be fatal, particularly in foals or immunocompromised animals. The clinical signs can be confused with other febrile diseases such as equine influenza, equine herpesvirus, or purpura hemorrhagica, so a thorough diagnostic workup is essential.

The differential diagnoses for Equine Infectious Anemia include: (1) Equine Viral Arteritis (EVA) - caused by an arterivirus, presents with fever, edema (especially of the limbs and scrotum), conjunctivitis, and abortion in pregnant mares; EVA is also a reportable disease, and diagnosis is confirmed by virus isolation or serology. (2) Equine Herpesvirus-1 (EHV-1) - can cause respiratory disease, abortion, and neurologic signs; fever and viremia may be present, but anemia is less prominent; PCR testing of nasal swabs or blood is diagnostic. (3) Equine Influenza - acute febrile respiratory disease with cough, nasal discharge, and fever; anemia is not a typical feature; diagnosis via PCR or virus isolation. (4) Purpura Hemorrhagica - an immune-mediated vasculitis often secondary to Streptococcus equi infection; presents with edema, petechiae, and fever; diagnosis based on clinical signs and history of strangles. (5) Babesiosis (Piroplasmosis) - caused by Theileria equi or Babesia caballi, transmitted by ticks; presents with fever, anemia, icterus, and hemoglobinuria; diagnosis via blood smear or PCR. (6) Autoimmune Hemolytic Anemia - primary or secondary immune-mediated destruction of red blood cells; may be idiopathic or triggered by drugs or neoplasia; Coombs test is positive. (7) Leptospirosis - bacterial infection causing fever, icterus, and renal disease; may cause anemia; diagnosis via serology or PCR. (8) Salmonellosis - bacterial enteritis causing fever, diarrhea, and endotoxemia; may lead to anemia secondary to inflammation; fecal culture or PCR is diagnostic. (9) Equine Ehrlichiosis (Anaplasma phagocytophilum) - tick-borne disease causing fever, depression, and limb edema; may cause thrombocytopenia and anemia; diagnosis via PCR or serology. (10) Neonatal Isoerythrolysis - in foals, immune-mediated destruction of red blood cells due to maternal antibody ingestion; presents with anemia and icterus in the first days of life.

The diagnostic approach for Equine Infectious Anemia should be systematic and include the following steps: 1) History and physical examination: Assess for risk factors (exposure to vectors, recent introduction of new horses, history of blood transfusions) and clinical signs (fever, anemia, thrombocytopenia, edema). 2) Complete blood count (CBC): Look for anemia (decreased PCV, hemoglobin, and RBC count), thrombocytopenia, and possibly leukopenia or leukocytosis. 3) Serum biochemistry: Evaluate for hyperbilirubinemia (due to hemolysis), elevated liver enzymes (if hepatic involvement), and renal parameters (if glomerulonephritis). 4) Coggins test (Agar Gel Immunodiffusion, AGID): This is the official test for international movement and is highly specific; it detects antibodies against the p26 core protein of EIAV. A positive result indicates infection, but false positives are rare. 5) ELISA (Enzyme-Linked Immunosorbent Assay): More sensitive than AGID and can detect antibodies earlier; positive results should be confirmed with AGID or immunoblot. 6) PCR (Polymerase Chain Reaction): Detects viral RNA or proviral DNA and is useful in early infection before antibodies develop, or in cases of inconclusive serology. 7) Virus isolation: Not routinely performed due to cost and time, but can be used for research or confirmation. 8) Necropsy: In fatal cases, post-mortem findings include splenomegaly, hepatomegaly, lymphadenopathy, and petechial hemorrhages; histopathology shows macrophage infiltration and erythrophagocytosis. 9) Rule out other differentials: Perform tests for EVA, EHV-1, equine influenza, babesiosis, and leptospirosis as indicated. 10) Biosecurity: If EIA is suspected, immediately isolate the horse and implement strict biosecurity measures to prevent transmission to other horses. Report the case to the appropriate veterinary authorities.

Laboratory findings in Equine Infectious Anemia are characteristic and include: 1) Complete Blood Count (CBC): Anemia is a consistent finding, with a decrease in packed cell volume (PCV) to as low as 10-15% (reference range 32-52%). The anemia is typically normocytic, normochromic, and regenerative in acute cases, but may become non-regenerative in chronic cases. Thrombocytopenia is common, with platelet counts often below 50,000/µL (reference range 100,000-300,000/µL). Leukocyte counts may be normal or decreased during febrile episodes, with lymphopenia and neutropenia. 2) Serum Biochemistry: Hyperbilirubinemia (elevated total and indirect bilirubin) due to hemolysis; elevated liver enzymes (AST, GGT) may be seen if there is hepatic involvement; blood urea nitrogen (BUN) and creatinine may be elevated if renal disease is present. 3) Acute Phase Proteins: Serum amyloid A (SAA) and fibrinogen may be elevated during acute episodes, indicating inflammation. 4) Coagulation Profile: Prolonged bleeding times and decreased platelet function may be observed due to thrombocytopenia. 5) Urinalysis: Proteinuria and hemoglobinuria may be present due to glomerulonephritis and hemolysis. 6) Serology: The Coggins test (AGID) is the gold standard and detects antibodies to the p26 protein; a positive result confirms infection. ELISA is more sensitive and can detect antibodies earlier; positive ELISA results should be confirmed with AGID or immunoblot. 7) PCR: Detection of EIAV RNA or proviral DNA in blood is highly sensitive and specific, and can be positive before seroconversion. 8) Bone Marrow Aspiration: May show erythroid hyperplasia in regenerative anemia, but is not routinely performed. 9) Cerebrospinal Fluid Analysis: Not typically indicated unless neurologic signs are present, but may show elevated protein and cell counts in cases of encephalitis.

Imaging modalities are not typically used for the diagnosis of Equine Infectious Anemia, as the disease is primarily diagnosed through laboratory testing. However, imaging may be useful to evaluate for complications or concurrent conditions. 1) Abdominal Ultrasonography: May be performed to assess for splenomegaly, hepatomegaly, or ascites in chronic cases. The spleen may appear enlarged with a mottled echotexture due to macrophage infiltration. 2) Thoracic Radiography: May be indicated if respiratory signs are present, but is not specific for EIA. 3) Echocardiography: May be performed to evaluate cardiac function in horses with severe anemia, as tachycardia and murmurs may be present. 4) Endoscopy: Not directly useful for EIA diagnosis, but may be used to evaluate the upper respiratory tract if concurrent infections are suspected. 5) Magnetic Resonance Imaging (MRI) or Computed Tomography (CT): Not indicated for EIA, but may be used to evaluate neurologic signs if EIA is considered a differential. 6) Scintigraphy: Not used in EIA diagnosis. Overall, imaging plays a limited role in the diagnosis of EIA, and the primary diagnostic tools are serology and PCR.

Cytological and histopathological findings in Equine Infectious Anemia are characteristic but not pathognomonic. 1) Peripheral Blood Smear: May show anisocytosis, polychromasia, and nucleated red blood cells (reticulocytosis) in regenerative anemia. Platelet counts are decreased, and large platelets may be seen. 2) Bone Marrow Aspiration: In acute cases, the bone marrow may show erythroid hyperplasia, while in chronic cases, there may be suppression of erythropoiesis. Macrophages may contain phagocytosed erythrocytes (erythrophagocytosis). 3) Lymph Node Aspiration: May show reactive hyperplasia with increased numbers of macrophages and plasma cells. 4) Liver Biopsy: Histopathology may reveal periportal infiltration of mononuclear cells, Kupffer cell hyperplasia, and erythrophagocytosis. In chronic cases, there may be evidence of glomerulonephritis. 5) Spleen: Splenomegaly with lymphoid hyperplasia and macrophage infiltration. 6) Kidney: Glomerulonephritis with immune complex deposition, which can be detected by immunofluorescence. 7) Brain: In cases with neurologic signs, perivascular cuffing and gliosis may be observed. 8) Immunohistochemistry: Can be used to detect EIAV antigens in tissues, particularly in macrophages. 9) Electron Microscopy: May show viral particles in macrophages, but is not routinely performed. These findings are supportive of EIA but are not definitive; confirmation requires serology or PCR.

There is no specific antiviral treatment for Equine Infectious Anemia, and the disease is considered incurable. Management focuses on supportive care and prevention of transmission. 1) Supportive Care: Affected horses should be provided with a quiet, comfortable environment, and adequate nutrition. Fluid therapy may be necessary to maintain hydration, especially if the horse is anorexic or has diarrhea. 2) Anti-inflammatory Drugs: Non-steroidal anti-inflammatory drugs (NSAIDs) such as flunixin meglumine (1.1 mg/kg IV or PO q12h) or phenylbutazone (2.2-4.4 mg/kg PO q12h) may be used to reduce fever and inflammation. However, caution is advised in horses with renal or hepatic impairment. 3) Blood Transfusion: In severe anemia (PCV < 15%) with clinical signs of weakness or respiratory distress, a blood transfusion may be life-saving. Whole blood or packed red blood cells can be administered, but careful cross-matching is required to avoid transfusion reactions. 4) Immunomodulatory Therapy: Some studies have investigated the use of immunomodulators such as interferon or corticosteroids, but evidence is limited and not recommended. 5) Antibiotics: Not indicated unless there is a secondary bacterial infection. 6) Management of Chronic Carriers: Asymptomatic carriers do not require treatment but must be permanently isolated or euthanized according to regulatory requirements. 7) Prevention: There is no vaccine available for EIA. Prevention relies on strict biosecurity, including testing new horses before introduction, using sterile needles and equipment, controlling insect vectors, and following quarantine protocols for positive horses. 8) Euthanasia: In many countries, euthanasia is recommended for positive horses to prevent further transmission, as there is no cure and the horse remains a lifelong carrier. 9) Experimental Therapies: Research is ongoing into antiviral drugs such as reverse transcriptase inhibitors, but none are approved for use in horses.

The prognosis for Equine Infectious Anemia is generally poor, as the disease is lifelong and there is no cure. The prognosis depends on the stage of infection and the severity of clinical signs. 1) Acute EIA: The mortality rate can be high, especially in foals and immunocompromised horses. Some horses may survive the acute episode and become chronic carriers. 2) Chronic EIA: Horses with chronic EIA may have recurrent episodes of fever and anemia, leading to progressive weight loss and debilitation. The prognosis for long-term survival is guarded, and many horses are eventually euthanized due to poor quality of life or regulatory requirements. 3) Subclinical Carriers: These horses may live a normal lifespan but remain infected and can transmit the disease to other horses. They are often euthanized or permanently quarantined due to movement restrictions. 4) Athletic Career: A positive Coggins test effectively ends a horse's athletic career, as most equine events and racing jurisdictions require a negative test for entry. 5) Negative Prognostic Indicators: Severe anemia (PCV < 15%), thrombocytopenia (< 20,000/µL), and the presence of neurologic signs are associated with a poorer prognosis. 6) Positive Prognostic Indicators: Horses that survive the initial acute episode and have a strong immune response may have longer intervals between clinical episodes. 7) Overall, the prognosis is grave, and the focus is on preventing transmission to other horses.

Follow-up for Equine Infectious Anemia is primarily focused on biosecurity and monitoring of affected horses. 1) Quarantine: Positive horses must be permanently isolated from other equids to prevent transmission. In some jurisdictions, euthanasia is required. 2) Testing of In-Contact Horses: All horses that have been in contact with a positive horse should be tested for EIA immediately and again after 30-60 days to account for the incubation period. 3) Vector Control: Implement measures to reduce fly populations, such as regular manure removal, use of insecticides, and stabling during peak fly hours. 4) Monitoring of Chronic Carriers: If a horse is kept alive, regular monitoring of PCV, platelet count, and clinical signs is recommended. 5) Biosecurity Protocols: Strict adherence to using sterile needles and equipment, and avoiding blood transfusions from untested donors. 6) Regulatory Reporting: EIA is a reportable disease, and cases must be reported to the appropriate veterinary authorities. 7) Education: Educate horse owners about the disease, its transmission, and prevention strategies. 8) Long-term Management: For horses that are euthanized, proper disposal of carcasses is important to prevent scavenging and potential transmission. 9) Re-testing: Horses that have recovered from acute EIA may remain seropositive for life, so re-testing is not necessary for diagnosis but may be required for regulatory purposes.

Clinical Pearls: 1) Always consider EIA in any horse with fever, anemia, and thrombocytopenia, especially if there is a history of insect exposure or recent introduction to a herd. 2) The Coggins test is the gold standard for international movement, but ELISA is more sensitive for early detection. 3) A positive Coggins test is a death sentence for the horse in many countries, so confirm with a second test (e.g., immunoblot) before making a final diagnosis. 4) EIA is a reportable disease, so follow local regulations and report cases promptly. 5) Use sterile needles and syringes for every horse to prevent iatrogenic transmission. 6) Control insect vectors to reduce the risk of transmission. 7) In acute cases, provide aggressive supportive care, including blood transfusion if PCV is critically low. 8) Educate owners about the importance of testing new horses before introducing them to the herd. 9) Remember that EIA is not zoonotic, so there is no risk to humans. 10) In endemic areas, consider EIA in the differential diagnosis of any febrile illness in horses. Pitfalls: 1) Failing to consider EIA in a horse with anemia and fever, leading to misdiagnosis and potential spread. 2) Relying solely on clinical signs, as many other diseases can mimic EIA. 3) Using contaminated needles or equipment, which can transmit the virus. 4) Not isolating a positive horse immediately, leading to an outbreak. 5) Misinterpreting a positive Coggins test without confirmatory testing, leading to unnecessary euthanasia. 6) Failing to report the disease to authorities, which is a legal requirement. 7) Not implementing vector control measures, allowing continued transmission. 8) Assuming that a horse with a negative Coggins test is not infected, as the test may be negative during the early incubation period. 9) Not considering EIA in a horse with chronic weight loss and poor performance. 10) Failing to educate owners about the lifelong carrier state and the need for permanent isolation or euthanasia.

There is no specific antiviral therapy for Equine Infectious Anemia, and treatment is supportive. The following drug protocols may be used based on clinical signs and veterinary judgment: 1) Flunixin meglumine: 1.1 mg/kg IV or PO every 12 hours for up to 3-5 days to control fever and inflammation. 2) Phenylbutazone: 2.2-4.4 mg/kg PO every 12 hours, but use with caution due to potential renal and gastrointestinal side effects. 3) Dexamethasone: 0.05-0.1 mg/kg IV or IM every 24 hours for 1-3 days may be used in severe immune-mediated hemolysis, but is controversial and may cause immunosuppression. 4) Blood transfusion: Administer 4-8 liters of whole blood or packed red blood cells IV slowly, after cross-matching, if PCV is below 15% and clinical signs of anemia are severe. 5) Fluid therapy: Balanced polyionic fluids (e.g., lactated Ringer's solution) at a rate of 50-80 mL/kg/day IV to maintain hydration and support renal function. 6) Antibiotics: Not indicated unless there is a secondary bacterial infection; if needed, use broad-spectrum antibiotics such as penicillin G (22,000 IU/kg IV or IM q6h) and gentamicin (6.6 mg/kg IV q24h). 7) Gastroprotectants: If NSAIDs are used, consider omeprazole (2-4 mg/kg PO q24h) or sucralfate (20 mg/kg PO q8h) to prevent gastric ulcers. 8) Immunomodulators: Some practitioners use interferon-alpha or levamisole, but evidence is lacking and not recommended. 9) Vitamin and mineral supplementation: May be beneficial to support overall health, but no specific protocol is established. 10) Euthanasia: In many cases, euthanasia is the most humane and practical option to prevent suffering and transmission. Always consult with a veterinary specialist and adhere to local regulations.

Equine Infectious Anemia has been extensively studied, and the literature provides a strong evidence base for understanding the disease. Key studies include: 1) Coggins et al. (1972) developed the AGID test, which remains the gold standard for diagnosis. 2) Issel and Coggins (1979) provided a comprehensive review of the epidemiology and control of EIA. 3) Leroux et al. (2004) reviewed the molecular biology of EIAV, highlighting the mechanisms of antigenic variation and persistence. 4) Cook et al. (2001) studied the immune response to EIAV, demonstrating the role of cytotoxic T lymphocytes in controlling viremia. 5) Sponseller et al. (2007) investigated the use of a live-attenuated vaccine in ponies, showing partial protection but not sterilizing immunity. 6) Craigo et al. (2007) studied the envelope glycoprotein diversity and its implications for vaccine development. 7) Oaks et al. (2004) evaluated the use of PCR for early detection of EIAV infection, showing high sensitivity. 8) The OIE Terrestrial Manual provides standardized diagnostic protocols and guidelines for international trade. 9) The American Association of Equine Practitioners (AAEP) has published guidelines for EIA control, emphasizing testing and biosecurity. 10) Recent studies have explored the use of antiviral drugs, such as tenofovir, in experimental models, but none are approved for clinical use. Overall, the literature supports the current approach of testing, quarantine, and euthanasia for positive horses, as there is no effective treatment or vaccine.