Abstract
Pulmonary Vasculotropic EHV-1 Infection in Equids
Equine herpesvirus 1 (EHV-1) is a very important pathogen for the equine industry. Three forms have been described: abortigenic, respiratory, and neurologic. The abortigenic form is characterized by late abortion, stillbirth, or the birth of highly infected and weak foals that die shortly after parturition. The respiratory form is generally considered nonfatal, may involve any age group, and is characterized by rhinitis, tracheitis, and bronchiolitis. The neurologic form is characterized by ischemic myeloencephalopathy secondary to EHV-1–associated endothelium and myocyte necrosis and thrombosis. We would like to make our colleagues aware of a new sporadic form of EHV-1 infection in young adult horses in which the major target of the virus appears to be the pulmonary endothelium.
Historically, affected horses have been treated for fever for a period of time before death. Severely affected horses die in respiratory distress or are found dead. Other horses on the premises may be mildly affected. Gross lesions in confirmed cases include extensive pulmonary edema characterized by prominent septa. Histologically, there is vasculitis, hemorrhage, and edema with fibrin in the lungs. Intranuclear inclusion bodies are rare. The perivascular and vascular inflammatory infiltrates are comprised mainly of T lymphocytes and a few macrophages. EHV-1 is detectable within the nucleus and cytoplasm of endothelial cells and intravascular monocytes but also may be detected in other less involved cell types, including dendritic cells of the pharyngeal lymphoid follicles, pharyngeal glandular epithelium, and crypt enterocytes. Virus isolation may be negative because of the paucity of virus in some lung areas. Herpesvirus particles can be identified within endothelial cells by transmission electron microscopy. Polymerase chain reaction techniques amplifying 369- and 188–base pair fragments specific for EHV-1 may also help in the identification, especially following immunohistochemical screening of the infected tissues. Seroconversion may be absent or weak and nondiagnostic. The scarcity of pathognomonic viral inclusions and lesions may make this condition difficult to recognize, particularly in situations when ancillary laboratory procedures are limited. It may be mistaken for equine viral arteritis, African horse sickness, Hendra disease, anaphylactic shock, and purpura hemorrhagica.
We believe we have identified at least four cases that represent this new clinical and pathologic entity. The first was described in a 2-year-old horse, 3 and the second was described in a zebra. 1 The third and forth cases were observed at the University of Pennsylvania, New Bolton Center: one was recognized in 1999 in a yearling filly, 2 and this year another case in a 2-year-old filly was diagnosed. We propose this new presentation of EHV-1 be added to the abortigenic, respiratory, and neurologic forms as another diagnostic category with the name pulmonary vasculotropic form. This acute nonneurologic pulmonary vasculotropic EHV-1 infection affects young adults where, with the exception of the central nervous system, multisystemic endothelial distribution of the virus occurs, but the major lesions involve the pulmonary blood vessels. We invite discussion of these cases and would appreciate information regarding similar findings by others.