Incubation Period
 
History
 
 
Physical Exam
 
Attitude
 
Temperature
 
 
Respiratory
 
Clinical Pathology
 
Blood Work
 
Neurologic signs
 
 
 
 
 
 
 
 
Reproductive Effects
 
 
 
 
 
 
Pathology
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Complications
 
 
 
 
Diagnosis
 
Differentials
 
 
 
 
 
Abortion
 
 
 
 
 
Neurologic Form
 
 
 
 
 
 
2-10 Days
 
 
inappetence, fever, cough, abortion
 
 
 
 
Malaise
 
febrile; 102-107°F (38.9-41.7°C), often a diphasic fever in EHV-1 with cell-associated viremia coincident with second fever peak.
 
cough, serous nasal discharge (see also complications), pharyngitis
 
 
 
 
neutropenia and lymphopenia
 
the result of specific strains of EHV-1. Mild signs are slight incoordination and hind end paresis whereas a severe case may progress to posterior paralysis and recumbence with loss of tail and bladder function. There will also be loss of cutaneous sensation in the inguinal and perineal areas. In rare cases signs may be as severe as quadriplegia and death. Prognosis of the neurological form unsurprisingly depends upon severity and extend of time spent in recumbency. Incidence of this form is thought to be greater in mares following abortion storms but it has also been seen in both sexes and all ages following an outbreak of the respiratory form of EHV-1
 
Abortion is a common and important manifestation of the virus and occurs 2-12 weeks (usually between 7 and 11 months of gestation) after infection although mares that do abort seldom display associated signs beforehand.  Placental expulsion is normal. There is no damage to the mare reproductive tract and thus fertility is unimpaired. Mares infected late in gestation may not abort but give birth to live foals that have rampant viral pneumonitis. Such foals usually die within a few days due to secondary bacterial infections
 
Pathogenesis: significant differences between EHV-1 and EHV-4. In the latter form, infection is restricted to respiratory tract epithelium and associated lymph nodes; EHV-1 strains have a predilection for vascular endothelium, especially the nasal mucosa, lungs, adrenal, thyroid, and CNS. EHV-1 gains access to peripheral tissues via cell-associated viremia, which may manifest as abortion or neurologic disease.  
 
Fetal necropsy: Aborted fetuses that are fresh will be minimally autolyzed.  
Lungs will show interlobular edema and pleural fluid.  
Liver shows multifocal random areas of necrotic foci.
Heart: petechiation of the myocardium (also of the adrenal gland and spleen)
Thymus: necrosis
 
Gross pathology: lesions of viral rhinopneumonitis are hyperemia and ulceration of the respiratory epithelium, and multiple, tiny, plum-colored foci in the lungs. The neurologic form of EHV-1 may show minimal gross lesions and any evidence will be mild hemorrhage in the meninges, brain and spinal cord.
 
Histology: there is evidence of inflammation, necrosis, and intranuclear inclusions in the respiratory epithelium and germinal centers of the associated lymph nodes. Lung lesions are characterized by neutrophilic infiltration of the terminal bronchioles, peribronchiolar and perivascular mononuclear cell infiltration, and serofibrinous exudate in the alveoli. Intranuclear inclusions are found in lung, liver, adrenal, and lymphoreticular tissues.  For the neurologic form, discrete areas of vasculitis, endothelial cell damage, perivascular cuffing, thrombus formation and hemorrhage, progressing to malacia in advanced cases. Lesions may occur at any level of the brain or spinal cord.
 
 
Secondary bacterial infections are common. Signs include mucopurulent nasal exudates and pulmonary disease.
Signs may not be apparent in horses immunologically sensitized to the virus such that control of spread is complicated by this fact.  
 
 
 
Viral rhinopneumonitis cannot be differentiated from influenza, equine viral arteritis or other equine respiratory infections on clinical signs alone. Therefore, virus isolation from nasopharyngeal swabs, citrated blood samples and isolation of the buffy coat are necessary in the early part of the infection and serology may be performed on both acute and convalescent sera.
 
Fetus and placenta should be submitted for necropsy and examined grossly and histologically for characteristic lesions. Also samples should be taken to isolate the virus and viral antigens in fetal tissue. Specific tissues to sample include: lung, liver, adrenal and lymphoreticular tissues.  Serology of mares post-abortion is of little diagnostic value.
 
Characteristic vascular lesions are sought in the diagnosis of myeloencephalopathy due to herpes virus at necropsy. Other diagnostic avenues are based on clinical signs and CSF analysis with a positive result being: xanthochromia and albuminocytologic dissociation.