Pathogenesis of Trypanosoma brucei Infection in Deer Mice (Peromyscus maniculatus).

Abstract

Abstract. Trypanosoma brucei EATRO 110 infection of the deer mice (Peromyscus maniculatus) produced moderate to marked lesions in the spleen, liver, heart, and kidney seven to ten weeks after infection. Splenic lesions consisted of marked splenomegaly, with infected spleens weighing 25.9 times control spleens. Transmission electron microscopy of the sinuses and Billroth's cords of the splenic red pulp demonstrated an increased cellularity with greater contact between cells due partly to proliferation of macrophages, transformed lymphocytes and plasma cells and partly to accelerated erythropoiesis with increases in the numbers of rubricytes and reticulocytes. Erythrocytes also were present in large numbers, and erythroclasis was accelerated.Hepatic lesions consisted of necrosis of few hepatocytes, proliferation and hypertrophy of Kupffer's cells which exhibited increased phagocytosis-particularly of erythrocytes, as well as penvascular cuffs consisting of lymphocytes, plasma cells and macrophages. Myocarditis was marked and was characterized by degeneration of myocardial fibers with decreases in mitochondria1 size and myofibril contents and fragmentation of some degenerating fibers, and was accompanied by accumulation of inflammatory cells including lymphocytes, transformed lymphocytes, plasma cells, and macrophages between the myocardial fibers. Renal lesions consisted of severe glomerulonephritis characterized by deposition of electron dense material along the basement membrane and in the mesangium of the glomerular tufts, and less frequently beneath the basement membrane and visceral epithelium of the Bowman's capsule and within the peritubular vessels. Neutrophils with fewer macrophages and lymphocytes invaded the glomeruli. The glomerular capillaries and Bowman's space were obliterated partially by these changes. Inflammatory cells similar to those observed in the heart accumulated in the peritubular vascular channels and extravascularly between the tubules and glomeruli.

Comparative bone marrow responses of albino rats experimentally infected with single and mixed species of <i>Trypanosoma congolense</i> and <i>Trypanosoma brucei</i> and ability to control anaemia

“…This was characterized by marked erythroid hyperplasia and increase in numbers of mitotic figures which were dominantly of erythroid origin and severe fall in the M:E ratio. This supports earlier observations in T. brucei infected deer mice (13) and horses (14) in which marked erythroid hyperplasia also resulted in very high reticulocyte responses in the infected animals. Similar responses were observed in vervet monkeys infected with the human infective T. brucei gambiense (15).…”

Trypanosoma vivax nos tecidos testicular e epididimário de ovinos experimentalmente infectados

“…Outro achado relatado pelos autores foi a presença de depósitos de cálcio nos ductos seminíferos e epididimários. T. brucei (Anosa & Kaneko 1984) e T. congolense (Sekoni et al 1990(Sekoni et al , 2004 também foram descritos como causadores de lesões no sistema genital masculino de animais.…”

Surtos de tripanossomíase por Trypanosoma evansi em eqüinos no Rio Grande do Sul: aspectos epidemiológicos, clínicos, hematológicos e patológicos

“…A patogênese da anemia em animais infectados por T. evansi não é completamente esclarecida (Silva et al 1995a, Marques et al 2000, mas é sugerido um processo hemolítico (Anosa & Kaneko 1983, Jenkins & Facer 1985 provavelmente relacionado à destruição dos eritrócitos pelo sistema imune (Jenkins & Facer 1985). Anemias hemolíticas imunomediadas podem ocorrer como uma doença primária ou como um processo secundário à ingestão de medicamentos, contato com substâncias químicas ou infecção por microorganismos (Day 2000).…”