[Trypanosoma cruzi infection in hamsters].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to E Chapadeiro.
Explore the source record for details and available documents.
We did mast cell and eosinophil granulocyte counts in the myocardium of forty chronic chagasic Wistar albino rats. We used 10 controls rats and 30 animals with late-stage (8th month) infection of São Felipe, Y and Colombian Trypanosoma cruzi strains, with variable degree of chronic myocarditis. We found chronic fibrosing myocarditis (fibrosis) in 40% of the infected animals. It was detected increased mast cell count in the chagasic rats associated with infection and not related with myocardial fibrosis. There was no increase in the eosinophil counts.
An analysis of the intracardiac autonomic nervous system (ICANS) has been made in 150 histological sections obtained from atrial fragments of a 74 year-old man who died of cardiac failure, as a consequence of acute Chagas' disease (ACD), probably acquired via digestive tract. Small quantities of mononuclear infiltrate around ganglia and/or nerve branches without significant morphologic alterations of the neurons were found in 10 slides; another slide showed ganglionitis and periganglionitis of moderate intensity associated to neuronal alterations. Focal epicarditis, usually of slight degree, was observed in all slides. The findings suggest: a) that the inflammation of ganglia and fibers of the ICANS in the ACD occurs at least in part by expansion from adjacent epicarditis; b) that even in the fatal cases of the trypanosomiasis cruzi the pathologic lesions of the ICANS may be slight.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Myocardial exsudate CD4+ and CD8+ lymphocytes were counted in transmural left ventricular free wall frozen sections taken from 10 necropsied chronic cardiac chagasic patients. The cells were labeled with monoclonal antibodies using a streptavidin-biotin technique. We counted: 1) lymphocytes in the total exsudate (LTE) and, separately, 2) the lymphocytes touching or very near to myocells (LTVNM). Lymphocytes were considered very near whenever their own nuclear shortest nuclear diameter was larger than their distance from myocells. CD8+ lymphocytes were more numerous than CD4+ lymphocytes, especially among the LTVNM. The LTE CD4/CD8 ratio was 0.37 +/- 0.20, but the LTVNM CD4/CD8 ratio was smaller (0.23 +/- 0.11). Among the LTE, 34 +/- 11% of CD8+ (against 24 +/- 12% of CD4+) were LTVNM. All these differences were statistically significant. Both subtypes of T-lymphocytes were found to have an intimate relationship with both ruptured and unruptured myocells, and parasites were not seen. These findings are in accordance with the idea that the myocardial cell lesions in the cardiac form of human Chagas' disease are mediated mainly by T-cytotoxic lymphocytes.
This research characterizes the acute and chronic phases of Chagas' disease in hamster through parasitological and histopathological studies. The acute phase was achieved with 44 young hamsters injected intraperitoneally with 100,000 blood trypomastigotes of Benedito and Y strains of T. cruzi. The chronic phase was induced in 46 hamsters injected intraperitoneally with 35,000 trypomastigotes of Vicentia, Benedito and Y strains. Animals were sacrificed at regular intervals of 24 hours of acute phase and from the 3rd to the 10th month of infection of chronic phase. In the acute phase, parasites were easily recovered from all animals and there was an inflammatory reaction characterized by mononuclear and polymorphous leukocyte infiltration of variable degree in the majority of tissues and organs, specially in the connective loose and fatty tissues, smooth muscle myocardium and skeletal muscle. In the chronic phase the lesions occurred in the same tissues and organs, but the inflammatory response was less severe and characterized by mononuclear infiltration mainly with focal or zonal fibrosis in the myocardium. In 50% of infected animals parasites were found in myocardium and recovered from pericardic, peritoneal and ascitic fluids in some animals. Signs of heart failure, sudden death and enlargement of bowel were observed regularly. We concluded that the hamster is an useful model for Chagas' disease studies.
Surgical liver biopsies of patients of both sexes, between 18 and 72 years old, with the compensated hepatoesplenic form of schistosomiasis mansoni, previously treated with oxaminique (Mansil) were studied by histological and immunohistochemical methods. Although the search for parasites and/or granulomas was negative in all specimen studied, the portal fibrosis remained.
Twenty-two HIV+ patients with encephalitis were studied. Of these, 7 had meningoencephalitis due to Toxoplasma gondii (MT) and 15 due to Trypanosoma cruzi (MC). Pathologic and computerized axial tomography (CAT) changes were compared. We found that focal necrotizing encephalitis due to Toxoplasma involved the cerebral cortex and the basal ganglia, whereas lesions due to Trypanosoma cruzi were centered in the white matter, sometimes extending into the cortex. Hemorrhages, myelin lesions and organisms were more pronounced in chagasic than in toxoplasmic encephalitis. These findings are consistent with the literature reviewed.
Biopsy specimens of the skin and oral mucosa from twenty-five patients bearing the disseminated form of histoplasmosis (H. capsulatum) associated with AIDS (acquired immunodeficiency syndrome) were studied by histologic and immunohistochemistry techniques. Histologically, the skin lesions showed four different patterns: diffuse macrophage, granulomatous, vasculitic with leukocytoclastic and scarce inflammatory reaction. The cell markers for macrophages, lymphocytes B and T and H. capsulatum revealed CD68, UCHL-1 and L26 associated with variable amounts of fungi.
The aim of this study was to obtain an experimental animal model of destruction of cardiac neurons in order to investigate the behavior of the cardiac nervous system of hamsters chronically infected with Trypanosoma cruzi. We counted the neuronal cells of the cardiac autonomic nervous plexus in hamsters inoculated with 35,000 blood forms of three different T. cruzi strains and killed 5, 8 and 10 months after infection. We showed for the first time severe neuronal destruction in an experimental animal model with characteristics similar to those observed in human Chagas'disease.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In order to investigate the value of the rabbit as an experimental model for Chagas' disease, seventy one animals were inoculated with different Trypanosoma cruzi strains and routes. The rabbits were submitted to necropsy in acute (earlier than three months of infection), recent chronic (three to six months) and late chronic (later than six months) phases. Myocarditis, generally focal and endomysial, occurred in 94.1%, 66.7% and 70.8% of the infected rabbits respectively in the acute, recent chronic and late chronic phases. The myocardial inflammatory exudate was composed by mononuclear cells, and also polymorphonuclear cells in the acute phase. In most cases of the late chronic phase, the myocarditis was similar to that described in the indeterminate form of human chagasic patients. Initial fibrosis occurred in the three phases but was more severe and frequent in the early chronic. Advanced fibrosis occurred only in the late chronic phase. Tissue parasites occurred only in the acute phase. The digestive tract and skeletal muscles showed mild and occasional lesions. Our data indicate that experimentally infected chagasic rabbits repeat some lesions similar to that of humans chagasic patients, specially that of the indeterminate form. So, it may be a useful, however not an ideal, model.
Explore the source record for details and available documents.
Systematized study was made in 56 esophagi of chronic chagasics (17 with and 39 without megas) aiming to: 1) to evaluate the esophageal caliber and thickness ranges; 2) analyse qualitative and quantitatively, the myenteric plexuses, trying to evaluate the relation of their lesions and the development of megaesophagus (ME); 3) study the lesions of the muscularis propria to verify if they contribute or not to the beginning of the process; 4) search for T. cruzi and its eventual relationship with the inflammation; 5) identify the principal mucosal alterations. It was confirmed that the severest lesions were found in the muscularis propria and in the plexures of Auerbach ganglia. In the former, the main alterations were myositis and fibrosis. The myentric plexuses showed inflammation and neuronal depopulation when compared with non-mega chagasic esophagi and even more when compared with the controls. On the other hand, there were normal caliber esophagi with severe denervation. It is possible that several factors may lead to the esophagopathy, especially to the ME. The search for T. cruzi was found positive in four out of eight esophagi with mega and in none of eight chagasic esophagi without mega. Mucosal and submucosal lesions were unremarkable and do not seem to be involved with the development of the process.
This is a review of 4.690 necropsies and 24.209 surgical pathology specimens describing the association between megacolon chagasic and malignant tumors of the large bowel. The prevalence of malignant tumors of the large bowel was not higher in megacolon.
Explore the source record for details and available documents.