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Am. J. Trop. Med. Hyg., 49(1), 1993, pp. 10-24
Copyright © 1993 by The American Society of Tropical Medicine and Hygiene

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Pathogenesis of Pichinde Virus Infection in Strain 13 Guinea Pigs: an Immunocytochemical, Virologic, and Clinical Chemistry Study

Brett M. Connolly, A. Bennett Jenson, C. J. Peters, Stanley J. Geyer, james F. Barth AND Richard A. McPherson
Department of Pathology, Georgetown University Medical Center, Washington, District of Columbia; Special Pathogens Branch, Centers for Disease Control and Prevention, Atlanta, Georgia; U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, Maryland; Scripps Immunology Reference Laboratory, The Scripps Research Institute, and Department of Pathology, Scripps Clinic and Research Foundation, La Jolla, California

Pichinde virus has been adapted to produce lethal infection of Strain 13 guinea pigs. Viral replication and presence of viral antigen in frozen tissues stained by immunofluorescence has been previously described. Further investigation into the pathogenesis of this disease has been hampered by the lack of a light microscopic method for correlating histologic lesions and the presence of Pichinde viral antigens. For this purpose, we developed a sensitive immunocytochemical technique for staining Pichinde viral antigens in formalin-fixed, paraffin-embedded tissue. Enhancement of the immunocytochemical staining with nickel chloride markedly improved detection of viral antigens. We examined frozen and formalin-fixed tissues from Strain 13 guinea pigs for viral antigens by light microscopy and immunocytochemistry at various intervals after infection with Pichinde virus. Progressive involvement of different tissues correlated with organ injury measured by serum biochemical abnormalities. Pichinde viral antigen was first detected in splenic macrophages five days after infection and their subsequent destruction facilitated persistent viremia. The inability to clear virus led to multiple organ infection and vascular involvement. Ensuing infections involved particularly the liver, spleen, adrenal glands, lungs, and intestines. Gastroenteritis developed, with extensive involvement of the muscularis mucosa throughout the gastrointestinal tract. Water and food intake decreased rapidly after day 8, leading to marked weight loss. Fatty changes of the liver suggested metabolic derangement that was further exacerbated terminally by adrenal infection and pulmonary impairment.




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Copyright © 1993 by the American Society of Tropical Medicine and Hygiene.