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T De Brito

Publications and source records attributed to T De Brito.

12 recordsLinked to original sources
PubMed1992

Human fatal yellow fever. Immunohistochemical detection of viral antigens in the liver, kidney and heart.

An immunohistochemical method to detect yellow fever antigen was developed using immune sera from rabbits and hamsters and hyperimmune ascitic fluid from mice. A search for the antigen was carried out in liver, kidney and heart in three fatal cases of yellow fever. In the liver it was present in the cytoplasm of hepatocytes, Councilman bodies and Kupffer cells. Yellow fever antigen was also detected in renal tubular epithelium and in groups of myocardial fibers. These findings suggest that viral replication occurs at sites other than the liver. Since yellow fever shares many features with other haemorrhagic fevers the use of immunohistochemistry can impart a significant improvement in the accuracy of its histopathological diagnosis.

Adult↗
PubMed1992

Leptospiral antigens in the liver of experimentally infected guinea pig and their relation to the morphogenesis of liver damage.

In order to investigate the morphogenes of experimental leptospirosis by morphologic and immunohistologic methods, 24 guinea-pigs were inoculated intraperitoneally with L. interrogans serogroup Icterohaemorrhagiae. They were divided in 6 groups, sacrificed from the 1st to the 6th day of infection. Semiquantitative analyses of histopathological liver lesions were performed in 1 micron sections of tissue embedded in glycol-methacrylate. The distribution of leptospiral antigen (L. Ag) and its glycolipoprotein (GLP) was demonstrated by peroxidase-antiperoxidase on paraffin embedded tissue. Significant lesions appeared at the 4th day of infection, progressing to a peak on the 6th day. Inflammation was associated with injury of the portal triad. Liver cells showed either swelling or acidophilic degeneration and necrosis, together with loss of cell cohesion, leading to disarray of liver cell plates. Mitochondria were found progressively enlarged and irregularly distributed. L. Ag expression was parallel to the morphological changes. Portal distribution was significant at the 4th day and on later stages centrilobular localization became predominant. Spiral forms suggestive of intact leptospires were initially found but, chiefly at the 6th day, L. Ag was seen in granules, probably resulting from phagocytosis. GLP staining was similar to granular L. Ag in morphology, and distribution. Cytokeratin condensation was seen in liver cells with acidophilic necrosis and was marked in areas of disorganization of cell plates. Our findings lead us to hypothesize a direct leptospiral cytotoxic effect on endothelial and on liver-cell membranes. At first, leptospires themselves would induce subcellular changes acting mainly on membrane permeability. Afterwards, their granular forms, including GLP, would act as adjuvant factors. These findings demonstrate that the disarray of liver cell plates at the late phase of the disease is genuine.

Animals↗
PubMed1992

Detection of leptospiral antigen (L. interrogans serovar copenhageni serogroup Icterohaemorrhagiae) by immunoelectron microscopy in the liver and kidney of experimentally infected guinea-pigs.

Guinea-pigs were experimentally infected with L. interrogans serovar copenhageni serogroup Icterohaemorrhagiae and their liver and kidney were studied by immunoelectron microscopy using the post embedding indirect immunogold labelling technique. Primary antibody was a purified rabbit anti-serum produced against the same leptospiral strain used in the inoculum. Gold-labelled leptospiral antigen (LAg) was found close to cell membranes of hepatocytes, kidney tubular cells and endothelial cells of the interstitial capillaries of the kidney. Afterwards it was internalized by hepatic and tubular cells, and eventually found in lysosomes. Phagolysosomes of Kupffer cells were also found to contain remnants of degraded leptospires and gold-labelled LAg. Gold-labelled intact leptospires were detected at the enlarged intercellular spaces between hepatocytes at the areas of hepatic cell plate disarray, showing the potential for leptospiral migration during the septicaemic phase of the disease potentially contributing to the pathogenesis of the lesions. The affinity of leptospiral antigenic material for cell membranes suggests an initial interaction with cell surface proteins followed by its internalization and cell damage. The nature of antigenic material detected, however, remains undefined; it may be a toxin, an enzyme or any other factor/s involved in leptospiral virulence.

Animals↗
PubMed1992

Antigens involved in the human antibody response to natural infections with Leptospira interrogans serovar copenhageni.

Serum samples from patients with leptospirosis were screened by the microscopic agglutination test (MAT), ELISA and by immunoblotting. The latter two tests were performed with L. interrogans serovar copenhageni isolated from human blood culture. Immunoblotting with patients' sera revealed antibodies recognizing several leptospiral components in the molecular weight range 14.5-105 kDa of both IgM and IgG response. All patients' serum samples presented IgM antibodies reacting with a diffuse band of mol. wt of 14.8-22 kDa proteinase-K resistant and most reacted with bands of 26.5-28.7, 38-39 and 43-43.5 kDa. The IgG response appeared to be at variance. Examination of sequential serum samples obtained over a 4-8-month period revealed little change in the profile of antigen recognized after the 40th day of infection. Sera from healthy individuals presented IgM antibodies reacting with several leptospiral antigens, but lacked response against those of diffuse band of 14.8-22 kDa.

Agglutination Tests↗
PubMed1991

Leptospiral antigens (L. interrogans serogroup ictero-haemorrhagiae) in the kidney of experimentally infected guinea pigs and their relation to the pathogenesis of the renal injury.

The search for leptospiral antigens (L. interrogans serogroup icterohaemorrhagiae) was carried out in 24 guinea pigs experimentally inoculated with 1 ml of culture containing 10(7)-10(8) leprospires and sequentially sacrificed from the first until the 6th day of infection. Semiquantitative analysis of histopathological variables comprising kidney interstitium, tubules and glomeruli was done in 1 micron sections of tissue embedded in glycolmetacrylate. Leptospiral antigen (LAg) and its glycolipoprotein (GLP) expression were detected through PAP in paraffin embedded tissue. The mild interstitial involvement of the kidney, manifested chiefly by oedema and focal interstitial nephritis seen at the 4th day, progressed to tubular damage at the 6th day, characterized by either swelling or cytoplasmic acidophilia of epithelial cells with loss of cell cohesion and sloughing of cells into the tubular lumina. Brush border alterations and mitochondrial changes were observed. Endothelial cell injury was noted in the interstitial vessels. LAg expression was parallel to the kidney changes: small deposits of elongated forms of LAg were detected at the 4th day either within the vascular lumen or free in the interstitium. A rise in the antigen expression was observed at the 5th day when it was seen either around tubules or in their walls. LAg was detected inside the tubular lumina at the 6th day of infection when granular LAg and GLP were abundant. This sequence reproduces the pathway of leptospires in the kidney and the crescent amounts of antigens detected toward the end of the experiment, with antigen concentration in cases of major tissue damage suggesting a direct action of the microorganisms and/or their products in the pathogesis of the lesions.

Animals↗
PubMed1991

Indeterminate leprosy: histopathologic and histochemical predictive parameters involved in its possible change to paucibacillary or multibacillary leprosy.

In an attempt to find clinical, bacteriological, histopathological, and immunohistochemical parameters to predict the progress of indeterminate leprosy patients to either paucibacillary (PB) or multibacillary (MB) leprosy, skin biopsies from 51 patients with indeterminate leprosy were retrieved from the files of the São Paulo Health Institute (Brazil). All of these patients had progressed to either PB or MB leprosy over a period of time which varied from 2 months to 24 years. Clinical records were examined, and new sections were cut from the paraffin blocks and stained by hematoxylin-eosin and Fite-Faraco stains; the avidin-biotin peroxidase technique was used with primary antibodies to detect bacillary antigens (anti-BCG serum) and nerve branches (anti-S-100 protein anti-serum). A moderate (++) or strongly positive ( ) Mitsuda skin test was observed in some patients progressing to PB leprosy. Noteworthy is that even patients initially Mitsuda negative may evolve to PB leprosy. a) A 2+ bacterial index and/or the presence of bacilli, even though few in number, in various dermal structures; b) multiple positive antigen sites as detected by anti-BCG anti-serum; and c) dermal nerve involvement, when evaluated as single parameters, correlated with a progression indeterminate to MB leprosy. An index resulting from the summation of the above three parameters identified 13 (72%) of 18 of these cases which progressed to MB leprosy.

Adolescent↗
PubMed1986

Experimental leptospirosis (L. interrogans serovar icterohaemorrhagiae) of the guinea pig: leptospiral antigen, gamma globulin and complement C3 detection in the kidney.

Morphofunctional and immunofluorescent studies were done in guinea pigs experimentally infected with Leptospira interrogans serovar icterohaemorrhagiae to determine the role of leptospiral antigen, gamma-globulin, and complement C3 deposits in the pathogenesis of the renal lesions. A sharp increase in leptospiral antigen deposits was observed in the late phase of the experimental infection. Immunoglobulin and complement C3 were small compared with the heavy leptospiral antigen deposits. Moreover, leptospiral antigen was observed mainly in the interstitium whereas immunoglobulin and complement C3 deposits were seen in glomeruli and small blood vessel walls. In our experimental model bacterial migration and local liberation of factors causing virulence seems more likely to determine the renal damage.

Animals↗
PubMed1979

Vascular damage in acute experimental leptospirosis of the guinea-pig.

The pathogenesis of the haemorrhagic diathesis in experimental leptospirosis of the guinea-pig was investigated in the lung, diaphragm and kidney. The vascular damage was found to be focal and mainly capillary. Swollen endothelium with dilated endoplasmic reticulum, enlarged mitochondriae and open junctions seemed to be the initial lesions and endothelial necrosis the final picture in all tissues. The lung capillaries showed endothelial and epithelial blebs and desquamation with many myelin figures. Capillary thrombosis was observed in the pulmonary microcirculation, probably acting as an aggravating factor and being partly responsible for the particularly impressive lung haemorrhages. The peritubular renal capillaries as well as open junctions and gaps due to necrosis also had enlarged fenestrae which were permeable to colloidal carbon particles. The paucity of micro-organisms in the vicinity of the lesions is in accordance with the toxic genesis postulated for the vascular damage in leptospirosis. It is suggested that the vascular lesions induced by leptospirosis begin with increased permeability prior to endothelial necrosis.

Acute Disease↗
PubMed1978

Morphological patterns of the liver in South American blastomycosis.

Histological features were semi-quantitatively analysed in 60 livers, obtained by necropsy, from patients who died of South American blastomycosis. These findings were classified and correlated with duration of the disease and treatment. Bile-duct lesions were prominent and a particular pattern was found in which segments of bile ducts were "disrupted" and replaced by inflammatory reaction. A classification of the lesions is proposed: Class o--near normal livers; Class I--predominance of necrosis and suppuration; Class II--predominance of tuberculoid granulomas; Class III--portal fibrosis and non-specific infiltrate. There has been no evidence that treatment could induce bile-duct proliferation, fatty change of liver cells, or cholestasis. On the other hand, less fibrosis was found in treated patients. Pathogenesis of the bile-duct lesions is discussed.

Adolescent↗
PubMed1977

Human chronic Mansonian schistosomiasis-cell proliferation and fibre formation in the hepatic sinusoidal wall: a morphometric, light and electron-microscopy study.

A morphometric, light and electron-microscopy study of the sinusoids in human Mansonian schistosomiasis with and without portal hypertension showed a sequence of events beginning with an increased number of cell nuclei, particularly evident at the centrolobular region. This is followed by deposition of reticulin fibres along the perisinusoidal space. Later, increased numbers of cells and reticulin fibres are seen throughout the lobule. Other findings, such as reduplication of the sinusoidal lining and the focal appearance beneath the cell layer of the thin discontinuous membrane, were also reported. This perisinusoidal fibrosis probably adds an element of heightened intrasinusoidal pressure to the perisinusoidal hypertension already described in this disease. Its pathogenic mechanism is obscure. The hepatic sinusoids in Mansonian schistosomiasis receive mainly arterial blood. High intraluminal pressure could be one explanation of the perisinusoidal fibrosis in these cases. However, as possibly occurs in primary sinusoidal portal hypertension, chronic immunological stimulation leading to proliferation of Küpffer cells and lipocytes could be an alternative mechanism.

Cell Division↗
PubMed1976

Human schistosomiasis: Schistosoma mansoni antigen detection in renal glomeruli.

Twelve kidney, five biopsy and seven necropsy specimens, all from schistosomiasis mansoni patients were studied by light and immunoflurescent microscopy in an attempt to detect antigen in the glomerular walls. Deposits of IgM, IgG,I gA, IgE, complement C3 and fibrinogen were observered in most cases. Antigen was successfully detected in two cases(one biopsy and one necropsy specimen), both exhibiting proliferative glomerulonephritis. The only clinical manifestation was a slight proteinuria. IgG antibodies eluted from the sutopsy kidney homogenates showed specific binding mostly to Schistosoma mansoni gut, thus spggesting that the fixed antibodies (eluates) are, at least partially, consituted by antibodies similar to the anti-circulating antigen. These data reinfroce the hypothesis that renal injury in schistosomiasis is mediated through an immune complex disease.

Adolescent↗