Histological changes caused by experimental Riedeliella graciliflora (Leg. Papilionoideae) poisoning in cattle and laboratory animals Alterações histológicas na intoxicação experimental por Riedeliella graciliflora (Leg. Papilionoideae) em bovinos e animais de laboratório

Tissues from cattle, mice, rats and guinea pigs experimentally intoxicated by Riedeliella graciliflora were studied histologically. Cattle lymph nodes, spleen, Peyer patches and peribronchial lymphoid tissues had diffuse necrosis of lymphocytes, mainly in the germinal centers of the follicles. This lesion was less severe in laboratory animals. All species had severe enteritis with infiltration of the lamina propria by mononuclear cells. Some cells in this infiltrate were necrotic. Degeneration and necrosis of the epithelial cells, mainly in the tip of the villi, and detachment of the epithelial lining from the lamina propria were also observed. In the liver the trabecular structure was disrupted and the hepatocytes had some degree of individual necrosis and degeneration. A tubular nephrosis was observed in the kidneys. Liver, lung, kidney, intestine and lymph nodes had different degrees of congestion. Those lesions are similar than those caused by Polygala klotzschii, a plant that contains 5-metoxi-podophyllotoxin.Foi realizado um estudo histológico de bovinos, camundongos, ratos e coelhos intoxicados experimentalmente por Riedeliella graciliflora. Em bovinos os gânglios linfáticos, baço, placas de Peyer e tecido peribronquial apresentavam necrose do tecido linfático, afetando, principalmente, os centros germinativos dos folículos. Esta lesão foi menos severa em animais de laboratório. Em todas as espécies havia severa enterite e infiltração da lâmina propria do intestino por células mononucleares. Algumas destas células estavam necróticas. Degeneração e necrose do epitélio, principalmente na superfície das vilosidades, e descamação das células epiteliais foram, também, observadas. No fígado havia desorganização da estrutura trabecular e alguns hepatócitos apresentavam-se degenerados ou necróticos. Os rins apresentavam nefrose tubular. Diferentes graus de congestão foram observados no fígado, pulmão, rins, intestinos e linfonodos. As lesões observadas são similares às causadas por Polygala klotzschii, uma planta que contém 5-metoxi-podofilotoxina

Pathology Affects Different Organs in Two Mouse Strains Chronically Infected by a Trypanosoma cruzi Clone: a Model for Genetic Studies of Chagas’ Disease

Chagas’ disease is a chronic infection caused by Trypanosoma cruzi and represents an important public health burden in Latin America. Frequently the disease evolves undetectable for decades, while in a significant fraction of the affected individuals it culminates in death by heart failure. Here, we describe a novel murine model of the chronic infection with T. cruzi using a stable clone isolated from a human patient (Sylvio X10/4). The infection in the C3H/HePAS mouse strain progresses chronically and is mainly characterized by intense cardiac inflammatory lesions that recapitulate the chronic cardiac pathology observed in the human disease. Moderate striated muscle lesions are also present in C3H/HePAS mice. Viable parasites are detected and recovered from the chronic heart lesions of C3H/HePAS mice, supporting the current notion that development of heart pathology in Chagas’ disease is related to parasite persistence in the inflamed tissue. By contrast, in infected A/J mice, chronic inflammatory lesions are targeted to the liver and the skeletal muscle, while pathology and parasites are undetectable in the heart. The phenotypic analysis of F(1) (A/J × C3H/HePAS) and F(2) (A/J × C3H/HePAS) mice suggests that the genetic predisposition to develop the inflammatory lesions caused by T. cruzi (Sylvio X10/4 clone) is heterogeneous because the heart and liver pathology segregate in the F(2) generation. These findings raise the hypothesis that the pathology heterogeneity observed in humans with Chagas’ disease (absence and presence of cardiac or digestive chronic lesions) may be attributable to host genetic factors