V. Psychas et al., Evaluation of ultrastructural changes associated with encephalomyocarditisvirus in the myocardium of experimentally infected piglets, AM J VET RE, 62(10), 2001, pp. 1653-1657
Objective-To evaluate the ultrastructural changes and localization of encep
halomyocarditis virus (EMCV) and viral pathogenesis in the myocardium of ex
perimentally infected piglets.
Animals-Eight 20-day-old piglets,
Procedure-Six piglets were inoculated oronasally with 5 ml (10(6) median ti
ssue culture infective dose/ml) of EMCV suspension, and 2 were used as unin
fected controls, Piglets were euthanatized or died between postinoculation
days 1 and 3. Samples of heart tissue from all piglets were evaluated histo
logically, by virus isolation, and by use of immunohistochemistry and elect
ron microscopy.
Results-All Infected piglets had gross or microscopic lesions of interstiti
al myocarditis. immunohistochemically, EMCV antigen was detected in the cyt
oplasm of cardiac muscle cells, Purkinje fibers, and endothelial cells and
in the nucleus of cardiac muscle cells and Purkinje fibers. Ultrastructural
lesions were characterized by degeneration and necrosis of cardiac muscle
cells and Purkinje fibers. Virus was present intracytoplasmically In cardia
c muscle cells, Purkinje fibers, and endothelial cells of capillaries and i
ntranuclearly in cardiac muscle cells. The cell membranes of the Purkinje f
ibers and endothelial cells had distinct protrusions that contained virus p
articles. In control piglets, no lesions were found, and no EMCV antigen wa
s detected.
Conclusions-Localization of EMCV intracytoplasmically or intranuclearly In
various myocardial cells may well reflect the sites of viral proliferation.
The presence of virus particles In cell membrane protrusions and in vacuol
es within the lumen of capillaries indicates that virus is released not onl
y by disintegration of the host cell but also via exocytosis.