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Evaluation of ultrastructural changes associated with encephalomyocarditis virus in the myocardium of experimentally infected piglets

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  • 1 Laboratory of Pathology, Faculty of Veterinary Medicine, Aristotle University, Thessaloniki, GR-54006, Greece.
  • | 2 Laboratory of Pathology, Faculty of Veterinary Medicine, Aristotle University, Thessaloniki, GR-54006, Greece.
  • | 3 Laboratory of Microbiology and Infectious Diseases, Faculty of Veterinary Medicine, Aristotle University, Thessaloniki, GR-54006, Greece.
  • | 4 Institute of Infectious and Parasitic Diseases, 80, 26th October St, Thessaloniki, GR-54624, Greece.
  • | 5 Laboratory of Pathology, Faculty of Veterinary Medicine, Aristotle University, Thessaloniki, GR-54006, Greece.
  • | 6 Laboratory of Microbiology and Infectious Diseases, Faculty of Veterinary Medicine, Aristotle University, Thessaloniki, GR-54006, Greece.
  • | 7 Laboratory of Pathology, Faculty of Veterinary Medicine, Aristotle University, Thessaloniki, GR-54006, Greece.
  • | 8 Laboratory of Pathology, Faculty of Veterinary Medicine, Aristotle University, Thessaloniki, GR-54006, Greece.

Abstract

Objective—To evaluate the ultrastructural changes and localization of encephalomyocarditis virus (EMCV) and viral pathogenesis in the myocardium of experimentally infected piglets.

Animals—Eight 20-day-old piglets.

Procedure—Six piglets were inoculated oronasally with 5 ml (106 median tissue culture infective dose/ml) of EMCV suspension, and 2 were used as uninfected controls. Piglets were euthanatized or died between postinoculation days 1 and 3. Samples of heart tissue from all piglets were evaluated histologically, by virus isolation, and by use of immunohistochemistry and electron microscopy.

Results—All infected piglets had gross or microscopic lesions of interstitial myocarditis. immunohistochemically, EMCV antigen was detected in the cytoplasm 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 cardiac muscle cells, Purkinje fibers, and endothelial cells of capillaries and intranuclearly in cardiac muscle cells. The cell membranes of the Purkinje fibers and endothelial cells had distinct protrusions that contained virus particles. In control piglets, no lesions were found, and no EMCV antigen was detected.

Conclusion and Clinical Relevance—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 vacuoles within the lumen of capillaries indicates that virus is released not only by disintegration of the host cell but also via exocytosis. (Am J Vet Res 2001;62:1653–1657)

Abstract

Objective—To evaluate the ultrastructural changes and localization of encephalomyocarditis virus (EMCV) and viral pathogenesis in the myocardium of experimentally infected piglets.

Animals—Eight 20-day-old piglets.

Procedure—Six piglets were inoculated oronasally with 5 ml (106 median tissue culture infective dose/ml) of EMCV suspension, and 2 were used as uninfected controls. Piglets were euthanatized or died between postinoculation days 1 and 3. Samples of heart tissue from all piglets were evaluated histologically, by virus isolation, and by use of immunohistochemistry and electron microscopy.

Results—All infected piglets had gross or microscopic lesions of interstitial myocarditis. immunohistochemically, EMCV antigen was detected in the cytoplasm 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 cardiac muscle cells, Purkinje fibers, and endothelial cells of capillaries and intranuclearly in cardiac muscle cells. The cell membranes of the Purkinje fibers and endothelial cells had distinct protrusions that contained virus particles. In control piglets, no lesions were found, and no EMCV antigen was detected.

Conclusion and Clinical Relevance—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 vacuoles within the lumen of capillaries indicates that virus is released not only by disintegration of the host cell but also via exocytosis. (Am J Vet Res 2001;62:1653–1657)