Observations on the Pathogenesis of Canine Encephalitozoonosis
The in vivo infection of neonatal dogs by the microsporidian, Encephalitozoon cuniculi and the in vitro lymphocyte-monocyte interactions in the phagocytosis and killing of E. cuniculi were studied. Microscopic examination of tissues from infected animals showed granulomatous nephritis, meningoencephalitis, hepatitis, and pneumonitis. A large component of the inflammatory infiltrate consisted of plasma cells and lymphocytes. In addition, hyperplasia of B-lymphocyte dependent regions of lymph nodes and erythrophagocytosis were consistently seen in infected dogs. Infected dogs developed a lymphocytosis, a hypergammaglobulinemia, an anti-Encephalitzoon antibody titer, and an antigen-specific blastogenic response to E. cuniculi spores. Lymphocyte blastogenic responses to the lectin PHA were depressed compared to controls. The antibody response to T-lymphocyte dependent antigens, sheep erythrocytes, and keyhole-limpet hemocyanin were slightly slower than controls or not significantly different. Lymphocytes from adult dogs infected with E. cuniculi produced lymphokines when cultured with E. cuniculi spores. Lymphocytes from both noninfected and infected adult dogs cultured with concanavillin A produced lymphokines. Lymphokines, either antigen-specific (E. cuniculi) or nonspecific (Con-A), activated monocytes to significantly kill E. cuniculi spores compared to serum treatment of the organisms. Pretreatment of E. cuniculi spores with normal dog serum or infected dog serum enhanced the killing of the parasite (normal dog serum < infected dog serum) over that of unstimulated canine monocytes. The results of these experiments suggest complex interactions between monocytes/macrophages and T-lymphocytes in the pathogenesis of canine encephalitozoonosis.
University of Illinois - Urbana-Champaign
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University of Illinois at Urbana-Champaign