Lesions of Experimental Equine Morbillivirus Pneumonia in Horses

Abstract

Laboratory examinations of equine morbillivirus included experimental reproductions of the disease caused by the virus by transmission of mixed lung and spleen taken from two field equine cases into two horses and by inoculating tissue culture virus into a further two horses. The most distinctive gross lesions of the diseases that developed in three of the horses was that of pulmonary edema characterized by gelatinous distension of subpleural lymphatics. Histologically, the lesions in the lungs were those of serofibrinous alveolar edema, alveolar macrophages, hemorrhage, thrombosis of capillaries, and syncytial cells. Clearly defined vascular lesions in three horses that became clinically affected within 8 days of inoculation of virus included intramural hemorrhage, edema, and necrosis and syncytial cells in the endothelium of pulmonary vessels (approximately 40-70 microm in diameter). Vascular lesions accompanied by parenchymal degeneration were also seen in the heart, kidney, brain, spleen, lymph node, and stomach. A fourth horse, which survived for 12 days, had detectable lesions only in the lungs, which were more chronic than those in the other three horses, a greater degree of cellular infiltration, and fewer well-defined vascular lesions. Sections stained by an indirect immunocytochemical method showed equine morbillivirus antigen was present in the vascular lesions and along alveolar walls. When endothelial cells were examined by electron microscope, cytoplasmic virus inclusion bodies containing filamentous structures were seen that reacted to an immunogold test to equine morbillivirus antigen. The presence of the syncytia in the small blood vessels in the lungs and other organs was interpreted as an important characteristic of the disease and consistent with a reaction to a morbillivirus.

Reactivity of Anti-Nipah Virus Monoclonal Antibodies to Formalin-fixed, Paraffin-embedded Lung Tissues from Experimental Nipah and Hendra Virus Infections

“…The distribution of Hendra virus antigens in the equine lung was consistent with that in the previous report using polyclonal anti-Hendra virus antibody and experimentally Hendra virus-infected horses [4]. The present results suggest that the monoclonal antibodies (12A5, 12D7, 13C4, 18C4) raised against Nipah virus cross-react with the viral antigens in the cells in which Hendra virus replicates.…”

“…The tissue tropism of Nipah virus in humans and pigs has been examined by polyclonal anti-Nipah virus antibody [5,10,16] and anti-Hendra virus antibody [1,5,10,16]. Both Nipah and Hendra viruses induced syncytial cells in vascular tissues and they were primarily vasotropic and/or neurotropic, generating interstitial pneumonia or encephalitis [1,4,5,11,16]. Nipah virus in pigs was also epitheliotropic in respiratory epithelium [5,10].…”

“…Seven and 8 days after inoculation, each pig was killed by intravenous inoculation of pentobarbital sodium and the lung tissues were fixed with 10% neutral buffered formalin and embedded in paraffin. A 7-year-old horse was inoculated with 50,000 TCID 50 Hendra virus [4] subcutaneously. Necropsy was conducted after 7 days post-inoculation and the lung tissue was fixed with 10% neutral buffered formalin and embedded in paraffin.…”

Henipavirus: A Review of Laboratory Animal Pathology

“…17,36,53,63,84 Symptoms include increased respiratory rate, dyspnea, fever, increased heart rate, lethargy, neurological signs, muscle trembling, hemorrhagic nasal discharge, and swelling of the face, lips, neck, and supraorbital fossa. 36,53,63 Experimental work by Middleton indicates that infected horses have a potential to excrete virus through nasal secretions from 2 days following exposure to HeV. 2 The most significant gross lesions in horses are diffuse pulmonary edema and congestion, with marked dilation of the pulmonary lymphatics.…”

Fatal Nonneurological EHV-1 Infection in a Yearling Filly

“…6,13 There were also some similarities with acute equine respiratory syndrome due to Hendra virus infection, 9 African horse sickness, 19 purpura hemorrhagica, and shock. 11 Tissues from this filly did not contain EAV antigen.…”