Laboratory examinations of equine morbillivirus included experimental
reproductions of the disease caused by the virus by transmission of mi
xed 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 thre
e of the horses was that of pulmonary edema characterized by gelatinou
s distension of subpleural lymphatics. Histologically, the lesions in
the lungs were these of serofibrinous alveolar edema, alveolar macroph
ages, hemorrhage, thrombosis of capillaries, and syncytial cells. Clea
rly defined vascular lesions in three horses that became clinically af
fected within 8 days of inoculation of virus included intramural hemor
rhage, edema, and necrosis and syncytial cells in the endothelium of p
ulmonary vessels (similar to 40-70 mu m 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 degr
ee of cellular infiltration, and fewer well-defined vascular lesions.
Sections stained by an indirect immunocytochemical method showed equin
e morbillivirus antigen was present in the vascular lesions and along
alveolar walls. When endothelial cells were examined by electron micro
scope, cytoplasmic virus inclusion bodies containing filamentous struc
tures were seen that reacted to an immunogold test to equine morbilliv
irus antigen. The presence of the syncytia in the small blood vessels
in the lungs and other organs was interpreted as an important characte
ristic of the disease and consistent with a reaction to a morbilliviru
s.