Abstract. Although the nephropathy of visceral leishmaniasis (VL) is known both in humans and dogs, histopathologic alterations have not been thoroughly studied. We examined renal alterations in 55 dogs with naturally acquired VL compared with five noninfected dogs from an endemic area in northeastern Brazil. Glomerulonephritis was found in 55 dogs, interstitial alterations in 53 dogs, and tubular changes in 43 dogs with VL. The glomerular alterations found were minor glomerular abnormalities (n ϭ 8, 14.5%), focal segmental glomerulosclerosis (n ϭ 10, 18.2%), mesangial proliferative glomerulonephritis (n ϭ 17, 32.7%), membranoproliferative glomerulonephritis ,(n ϭ 18, 30.9%), crescentic glomerulonephritis (n ϭ 1, 1.8%), and chronic glomerulonephritis (n ϭ 1, 1.8%). Morphometric and ultrastructural studies complemented the analysis. The five control animals exhibited no glomerular alterations. The glomerular lesions were related to functional alterations. Considering that the alterations of canine and human nephropathy in VL are very similar, the data obtained in this study constitute an important contribution to the understanding of canine and human VL nephropathy.Key words: Dogs; glomerulonephritis; morphometry; renal pathology; ultrastructure; visceral leishmaniasis.Canine visceral leishmaniasis (VL) is a highly prevalent infection encountered throughout the world. In Brazil, VL results from infection by the protozoan Leishmania (Leishmania) chagasi, which occurs in 18 of 27 Brazilian states. 20,22,26 VL is endemic to northeastern Brazil, and in Teresina, in the State of Piaui, some 1,600 dogs presenting naturally acquired VL were known when this study was initiated. At present, VL is also spreading to other urban areas in the southern and southeast regions, where the disease was not previously endemic. 31 In the infectious cycle of VL, the dog is the most important domestic reservoir and exhibits chronic evolution of the disease. 1,8,21 Leishmania is an obligatory intracellular parasite of mononuclear phagocytes. During infection, various host organs are affected including the kidney. Although VL-related nephropathy is known both in humans and dogs, the histopathologic patterns of the lesions present in VL have not been clearly established because most studies are based on very few cases and mainly because well-defined, lesion classification criteria were not used. 3,4,9,10,24,37,38 In human VL, glomerulosclerosis, mesangial cell proliferation, and interstitial nephritis have been reported. 3,9,10,16,18,38 Renal involvement in canine VL is also frequent, and the renal changes are similar to those seen in humans. 2,5,8,23,32 This similarity renders the study of canine VL nephropathy of interest with regard to human pathology. The renal lesion itself does not lead to renal insufficiency. However, when moderate or severe renal lesions are present, VL patients with systemic complications such as secondary infections, sepsis, and hypotension do develop renal insufficiency. 16 Furthermore, glomerular lesions appare...

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BackgroundImmune complex deposition is the accepted mechanism of pathogenesis of VL glomerulopathy however other immune elements may participate. Further in the present study, no difference was seen between immunoglobulin and C3b deposit intensity in glomeruli between infected and non-infected dogs thus T cells, adhesion molecules and parameters of proliferation and apoptosis were analysed in dogs with naturally acquired VL from an endemic area. The dog is the most important domestic reservoir of the protozoa Leishmania (L.) chagasi that causes visceral leishmaniasis (VL). The similarity of VL manifestation in humans and dogs renders the study of canine VL nephropathy of interest with regard to human pathology.MethodsFrom 55 dogs with VL and 8 control non-infected dogs from an endemic area, kidney samples were analyzed by immunohistochemistry for immunoglobulin and C3b deposits, staining for CD4+ and CD8+ T cells, ICAM-1, P-selectin and quantified using morphometry. Besides proliferation marker Ki-67, apoptosis markers M30 and TUNEL staining, and related cytokines TNF-α, IL-1α were searched and quantified.ResultsWe observed similar IgG, IgM and IgA and C3b deposit intensity in dogs with VL and non-infected control dogs. However we detected the Leishmania antigen in cells in glomeruli in 54, CD4+ T cells in the glomeruli of 44, and CD8+ T cells in 17 of a total of 55 dogs with VL. Leishmania antigen was absent and T cells were absent/scarse in eight non-infected control dogs. CD 4+ T cells predominate in proliferative patterns of glomerulonephritis, however the presence of CD4+ and CD8+ T cells were not different in intensity in different patterns of glomerulonephritis. The expression of ICAM-1 and P-selectin was significantly greater in the glomeruli of infected dogs than in control dogs. In all patterns of glomerulonephritis the expression of ICAM-1 ranged from minimum to moderately severe and P-selectin from absent to severe. In the control animals the expression of these molecules ranged from absent to medium intensity. It was not observed any correlation between severity of the disease and these markers. There was a correlation between the number of Leishmania antigen positive cells and CD4+ T cells, and between the number of CD4+ T cells and CD8+ T cells. In dogs presenting different histopathological patterns of glomerulonephritis, parameters of proliferation and apoptosis were studied. Ki-67, a proliferative marker, was not detected locally, but fewer apoptotic cells and lower TNF-α expression were seen in infected animals than in non-infected controls.ConclusionImmunopathogenic mechanisms of VL glomerulonephritis are complex and data in the present study suggest no clear participation of immunoglobulin and C3b deposits in these dogs but the possible migration of CD4+ T cells into the glomeruli, participation of adhesion molecules, and diminished apoptosis of cells contributing to determine the proliferative pattern of glomerulonephritis in VL.

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RESUMO Nos anos de 2001 e 2002, 46 cabritos (CAB) e 35 cordeiros (COR) de uma propriedade do agreste do Estado de Pernambuco foram acometidos por ataxia enzoótica (AE) de forma tardia. Houve aumento da incidência do 1 o ano (46,3% -CAB; 24,2% COR) para o ano subseqüente (100% -CAB e COR

In the present study, 256 7-wk-old Japanese quail were randomly distributed into four experimental groups (64 birds per group) and given rations containing 0 (controls), 25, 50, or 100 (g aflatoxin B, (AFB1)/kg feed for 168 d. Each treatment consisted of four replicates of 16 quail. Egg production and individual egg weight were checked daily. Feed consumption and feed use were determined weekly. Eggs laid in the last day of each 28-d laying period were collected and subjected to individual analysis for specific gravity, Haugh units, shell thickness and percentage eggshell. Results showed that average egg production, feed use, and body weights were not affected (P > 0.05) by AFB1. However, feed consumption was lower (P < 0.05) for groups fed 50 or 100 microg AFB1/kg. Egg weight was significantly lower (P < 0.05) only for groups exposed to 50 and 100 microg AFB1/kg. Average egg specific gravity, Haugh units, and shell thickness were not affected (P > 0.05) by AFB1. Percentage eggshell was higher (P < 0.05) in the group fed the ration containing 100 microg AFB1/kg. Treatment associated lesions were observed only in the liver. Hepatic cell vacuolation with fatty infiltration was observed in all liver samples of quail fed AFB1-contaminated rations. Bile duct proliferation and trabecular disorder were found only in livers of quail on the 100-microg AFB1/kg treatment. Results indicated that chronic exposure to AFB1 at levels above 50 microg/kg could adversely affect quail performance, emphasizing the importance of controlling aflatoxin contamination in quail rations.

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