Two day old, male Thoroughbred, Equus caballus, equine.The colt presented at 9 hours of age with a history of premature placental separation at birth. Severe respiratory disease developed whilst the colt was hospitalized and worsened despite mechanical ventilation
The lungs are heavy and edematous, and mottled red purple.Â The most cranioventral portions have numerous air filled pockets under the pleura.Â Scattered on the pleural surface and also on cut section are multiple white, less than 3mm diameter, foci (figure 1).Â The pericardium is expanded by edema.Â The capsular surface and parenchyma of the liver contain randomly disseminated pinpoint to less that 3mm diameter white-gray foci (figure 1).Â The cortex of the adrenal glands contains scattered hemorrhagic foci.Â
Within the lung, there is extensive necrosis of the respiratory epithelium, predominantly affecting bronchioles but also bronchi and terminal airways.Â Sloughed cells admixed with necrotic debris and inflammatory cells accumulate within the lumens.Â Both necrotic cells and viable epithelium contain eosinophilic nuclear inclusion bodies that peripheralize the chromatin (Cowdry type A), and there is formation of epithelial syncytia.Â Extending into alveoli (which are often necrotic) are accumulations of fibrin, neutrophils and macrophages.Â Type II pneumocytes are hyperplastic.Â Interlobular septa are edematous and contain an infiltrate of macrophages and neutrophils.Â
Scattered randomly within the adrenal cortex are areas of congestion, hemorrhage and necrosis.Â Immediately adjacent to the cytoclastic debris are cells that contain eosinophilic nuclear inclusion bodies that peripheralize the chromatin.
Equine herpesvirus 1 (EHV-1) antigen was detected by immunohistochemisty within the nucleus and cytoplasm of several epithelial cells and leukocytes in the lung (figure 2) and adrenal gland (figure 3).Â Appropriate positive and negative controls were used and examined and worked accordingly.
Lung: bronchointerstitial pneumonia, necrotizing, acute, diffuse, severe with eosinophilic nuclear inclusion bodies and epithelial syncytia.
Adrenal gland: adrenalitis, necrotizing, acute, multifocal, moderate with eosinophilic nuclear inclusion bodies.
Virus isolation performed on lung, liver, kidney, spleen and thymus was positive for EHV-1 and negative for EVA.Â FA performed for EHV-1 antigens on lung and liver was also positive, and EVA FA was negative.Â Aerobic culture of the lung produced no growth.Â Leptospira was not detected in the lung, liver, spleen and kidney by FA.Â
Equine herpes virus 1 is an alphaherpes virus, responsible for causing abortion, perinatal foal mortality, respiratory disease and neurologic disease in horses7.Â Due to its direct effect on breeding and performance, and also through interference with horse movement, EHV-1 is of major economic and welfare importance in horse related industries throughout the world3.Â Pregnant mares exposed to infection abort three weeks to four months after exposure to infection.Â Abortion occurs anytime after five months gestation, but more commonly from nine months to term.Â Foals may be born alive, as in this case, but death occurs within a few days4,11.Â
The pathogenesis of EHV-1 abortion is not fully elucidated11.Â Virus is translocated from the maternal circulation to the uterus and placenta.Â Uterine lesions consist of vasculitis in the small arterioles of the endometrium11.Â In some cases, abortion can occur without fetal lesions or virus spread to the fetus, presumably from widespread virus-related thrombosis and infarction leading to premature placental separation and expulsion of the fetus14.Â Placental lesions in these cases consist of chorionic necrosis and fibrinoid vascular necrosis of chorionic blood vessels with fibrin thrombi13,14.Â EHV-1 has been detected in endometrial and chorionic endothelial cells in experimental and spontaneous cases of abortion by ISH and immunohistochemistry12,13,15.
More commonly virus spreads to the fetus.Â In addition to placental endothelial cells, DNA ISH also has identified EHV-1 in necrotic debris associated within infarcted microcotyledons, debris within endometrial glands and also trophoblasts, suggesting trophoblast infection results from diffusion of virus from sites of endometrial infarction and also from emptying of debris from infected glands directly onto the surface of trophoblasts12.Â
EHV-1 infection of the fetus results in well described and documented lesions.Â Grossly, the aborted fetus is usually fresh with subcutaneous edema and petechiae of the mucous membranes.Â The lungs are edematous and the trachea may contain a fibrinous cast.Â The liver contains miliary white foci of necrosis.Â The spleen may contain prominent lymphoid follicles2,9.Â Histologic lesions consist of necrosis and eosinophilic intranuclear inclusion bodies in parenchymal organs, especially the liver and adrenal glands, with minimal inflammatory cell infiltrate, lymphocytolysis in the thymus and bronchointerstitial pneumonia2,6.Â Syncytia formation in EHV-1 infection, as seen in this case, is rarely described.Â Previous reports include syncytia in the lungs of aborted fetuses6 and in experimental neurologic disease3.Â
1.Â Lung: Pneumonia, bronchointerstitial, necrotizing, acute, multifocal, moderate, with fibrin, edema, syncytia, and eosinophilic intranuclear inclusion bodies, Thoroughbred (Equus caballus).
2.Â Adrenal gland, cortex: Necrosis, multifocal, with rare eosinophilic intranuclear inclusion bodies.
The contributor includes an excellent review of EHV-1
associated abortions.Â EHV-1 is transmitted primarily through the respiratory system.
Following an initial replication in the upper respiratory mucosal epithelium, the virus is
transmitted throughout the body via mononuclear cells, primarily T-lymphocytes.
Horses are latently infected for life.
There are three types of Equine Alphaherpes viruses:
- EHV-1: Equine viral abortion, myeloencephalopathy, respiratory disease
- EHV-3: Equine coital exanthema
- EHV-4: Rhinopneumonitis virus
EHV-1 and EHV-4 both can cause abortion, although it occurs more often with EHV-1. EHV-1 and EHV-4 both can cause respiratory disease, although it is more common with EHV-4.
Slide variation includes some slides with syncytia in the adrenal cortex.
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