▪ widespread throughout the world

▪ causes respiratory, neurologic, and

generalized neonatal disease, as well
as abortion.
▪ a cause of intrauterine death of
nearterm equine fetuses worldwide.
➢Family herpesviridae
➢Subfamily alphaherpesviridae
➢ Genus varicellovirus.
❖ The virus is transported in leukocytes
through the bloodstream to the
placenta and hence the fetus.
❖ Death of the fetus does not occur until
the onset of the usually prompt and
uncomplicated abortion.
❖ The dam shows no signs and the fetus is
aborted in a fresh state.
❖ The disease affects the fetus during the
eighth to eleventh months of pregnancy
❖ the majority of abortions occur in the
ninth and tenth months.
❖ The fetus is expelled from the uterus
promptly after death or, in some cases,
before the heart beat stops
❖ usually with no more difficulty than is
experienced in normal parturition.
❖ Complications, such as retained placenta,
delayed involution, and postparturient
metritis, are seldom encountered.
❖ The mare usually recovers, showing little
more than a slight transitory fever.
❖ A storm of abortions may occur, 90% of the
pregnant mares in a band being affected, or
the disease may be limited to only a small
fraction of the susceptible mares.
❖ Neonatal infection may lead to fatal
generalized disease.
In the aborted fetus
✓the lesions are typically found in the lungs,
liver, and lymph nodes
✓although some icteric discoloration,
interlobular pulmonary edema, and excess
peritoneal fluid are significant gross findings.
✓The most consistent gross lesion is severe
pulmonary edema (interlobular edema and
excessive pleural fluid) . The lungs are heavy
and rubbery, show the impressions of the ribs,
and exhibit a pitting response to pressure.
✓The liver, is congested, with tiny gray
subcapsular foci, usually from 2 to 5 mm in
diameter, scattered throughout the lobules.
liver
➢ Hepatic foci consist of sharply demarcated
aggregations of necrotic liver cells.
➢Liver cells surrounding the foci of necrosis often
contain small eosinophilic intranuclear
inclusions.
➢Enlargement of the nucleus or margination of
the chromatin is seldom associated with these
inclusions, which usually are quite small,
although large enough to replace most of the
internal structure of the nucleus.
lung
➢in the lung consist of cellular debris in the
lumen of the bronchi and bronchioles, and
partial or complete erosion of adjacent
epithelium.
➢In epithelial cells near the eroded areas, the
nuclei contain eosinophilic inclusions similar to
those in liver cells.
spleen and lymph nodes
➢Similar intranuclear inclusions and foci of
necrosis are found in the spleen and lymph
nodes spleen and lymph nodes m many cases.
Equine viral rhinopneumonitis
(EVR)
❖ a mild respiratory disease in weanling
foals and young racehorses. .
❖ The portal of entry for the respiratory
form is typically aerogenous and the disease
is generally transient
❖ the primary viral-induced lesions in the
nasal mucosa and lungs are rarely seen at
necropsy unless complicated by secondary
bacterial infection.
Equine viral rhinopneumonitis
(EVR)
❖ The virus persists latently in the
trigeminal ganglia for long periods of time.
❖ Reactivation because of stress or
immunosuppression and subsequent
shedding of the virus are the typical source of
infection for susceptible animals on the farm.
❖ Complications with secondary bacterial
infections cause a fatal bronchopneumonia
(Streptococrus equi, Streptococrus
zooepidemirus, Staphylococrus aureus).
 Equine viral rhinopneumonitis
(EVR)
❖ Uncomplicated lesions in EVR are seen only
in aborted fetuses or in foals that die within the
first few days of life. They consist of focal areas
of necrosis 0.5 to 2 mm) in various organs,
including liver, adrenal glands, and lungs.
❖ In some cases intranuclear inclusion bodies
are microscopically observed in these organs.
❖ Clinically, horses affected with the
respiratory form of EVR exhibit fever, anorexia,
conjunctivitis, cough, and nasal discharge.
 Equine viral rhinopneumonitis
(EVR)
❖ EHV-1 may cause systemic disease in live-
born neonates. Lesions are similar to those in
aborted foals.
❖ These lesions include bronchointerstitial
pneumonia, multifocal necrosis in liver, spleen,
adrenal, and other tissues, and prominent
intranuclear inclusion bodies.
❖ EHV-1 occasionally causes systemic disease in
yearling or adult horses.
❖ Lesions include pulmonary or systemic
necrotizing vasculitis, pulmonary edema and
hemorrhage, lymphoid necrosis, and
encephalomyelitis with vasculitis.
 Equine herpesviral
myeloencepholopothy
❖ an important neurological disease
characterized clinically by ataxia, paresis, and
paralysis, and caused mainly by EHV-1
❖ EHV-1 replicates first in upper respiratory
tract epithelium and local lymph nodes, and
then induces T-cell and monocyte-associated
viremia that ends with invasion of endothelial
cells of the CNS and pregnant uterus.
❖ This leukocyte-associated viremia protects
the virus from humoral immunity.
 Equine herpesviral
myeloencepholopothy
❖ The replication of virus in endothelial cells of
the CNS leads to initiation of the inflammatory
cascade that ends in thrombo-occlusive necrotizing
vasculitis.
❖ The resultant myeloencephalopathy is due to
destruction of CNS tissue secondary to vasculitis.
❖ The vasculitis is either due to direct viral
cytotoxic effect or due to an immune-mediated
(Arthus-type reaction) mechanism.
❖ A similar mechanism is responsible for EHV-1-
induced abortion and pulmonary vasculotropic
disease.
 Equine herpesviral
myeloencepholopothy
❖ The incubation period is 6-10 days and usually
occurs in association with abortion and/or
respiratory disease but can occur without
preceding signs.
❖ All ages are susceptible, but pregnant mares and
mares nursing foals are over-represented.
❖ there is sudden onset of unilateral or
bilateral foreleg and/of hind leg lameness.
causing ataxia.
❖ This may rapidly progress to fore or hind leg
paralysis or complete quadriplegia and
recumbency, often causing death.
❖ The nature of die meningeoecphaloumyelilis
is not comparable to that caused by other
alphaherpesviiuses.
❖ Inclusion bodies are absent, and it is difficult
to recover virus.
❖ The characteristic histologic lesions are
nonsuppurative necrotizing vasculitis and
thrombosis, with greater prevalence in the
meningeal and parenchymal blood vessels of
the brain stem and spinal cord.
❖ Perivascular edema, hemorrhage, focal areas
of malacia, and infarction are present
adjacent to the affected blood vessels.
❖ The principle lesions, which may present in the
brain, spinal cord, meninges, and ganglia, consist of
arteriolitis characterized by mononuclear cuffing
and infiltration, medial necrosis, endothelial
hyperplasia and necrosis and thrombosis.
❖ Multinucleated giant cells may be present in the
Virchow-Robin space, but the cells lack the inclusion
bodies usually seen in alphaherpesvirus-induccd
polykaryocytes.
❖ Focal poliomalacia and leukomalacia are present
and arc thought to be secondary to vascular damage.
❖ There is no evidence of primary viral neurotropism.