Equine Herpesvirus 1
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This article is still under construction. |
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Antigenicity
- Isolates vary in virulence based on tropism
- Note:
- Genital pustules are caused by EHV3
- EHV4 is serotypically identical to EHV1, but can be distinguished via monoclonal antibodies, PCR and RE (restriction enzyme) profiling
Pathogenesis
- Entry via aerosol
- Initial replication in the upper respiratory tract
- By 24hrs, coughing is induced once virus has reached bronchi and pulmonary lymph tissue
- Cell-associated viremia, with virus predominantly in the T cells
- Abortion can follow:
- Virus transfers from leukocytes to placental endothelium, causing thrombosis and ischemia
- 95% of abortions are in the last trimester, when chorionic placentomes have created an end-artery system vulnerable to ischemia
- Foals born will be weak and virus-positive
- Paresis is a rare clinical symptom caused by lesions in the CNS and resulting thrombosis
- Latency always follows infection, and the virus can be reactivated under stress
Epidemiology
- Aerosol infection occurs despite maternal antibody
- Over 60% of horses are latently infected and show antibody as yearlings
- Greatest threat or reinfection is to mares in late-term pregnancy
- Infected horses (coughing) can shed virus for up to 10 days
Diagnosis
- In the case of abortion:
- Whole fetus should be sent for testing
- Immunostaining of fetal tissues
- Nested PCR for envelope glycoproteins in nasal swab: more sensitive than virus isolation
- Paired serum samples to show increase in CFT titre
Control
- Isolation of pregnant mares in last trimester
- No movement for at least 1 month after last abortion
- Vaccination every 6 months
- Inactivated vaccine may reduce respiratory disease but cannot protect against abortion