Psittacara leucophthalmus (Aves: Psittacidae) como um novo hospedeiro de Paratanaisia bragai (Trematoda: Eucotylidae) no Brasil: achados clínicos e patológicos: relato de caso / Psittacara leucophthalmus as a new host of Paratanaisia bragai (Trematoda: Eucotylidae) in Brazil: clinical and pathological findings: case report

Paratanaisia bragai é um trematódeo que parasita rins e ureteres de aves domésticas e selvagens. Apesar de considerado pouco patogênico pode levar a complicações clínicas e morte em infecções severas. No presente estudo, um caso de parasitismo fatal em maritaca (Psittacara leucophthalmus) por P. bragai é relatado. A ave, oriunda da área urbana do município de Lavras, Minas Gerais, Brasil, teve manifestações clínicas de apatia, desidratação, dispneia e veio a óbito. Na necropsia foram observados rins aumentados de volume, pálidos, com superfície irregular e nodulações esbranquiçadas. Ao corte verificaram-se parasitos nos rins, que foram processados para montagem de lâminas permanentes e identificados segundo técnica de rotina como P. bragai. No exame histopatológico dos rins foram constatados infiltrado inflamatório linfoplasmocítico multifocal moderado, dilatação de túbulos e focos de regeneração tubular, associados a fibrose intersticial moderada no córtex renal. Na medula renal havia infiltrado de macrófagos, heterófilos, eosinófilos e células gigantes multinucleadas associado a parasitos em ductos coletores dilatados. O parasitismo de P. leucophthalmus por P. bragai é relatado pela primeira vez. A importância de se considerar este parasito entre as possibilidades diagnósticas em aves com insuficiência renal é brevemente discutida.(AU)

Paratanaisia bragai is a trematode parasite of the kidneys and ureters of poultry and wild birds. Despite its low pathogenicity, this parasite can lead to several clinical complications and death in heavy infections. In the present study, a fatal case of parasitism by P. bragai in a specimen of the White-eyed Parakeet, Psittacara leucophthalmus, is reported. The bird, coming from the urban area of the county of Lavras, Minas Gerais, Brazil, was clinically evaluated and revealed apathy, dehydration, dyspnea, and death. The gross findings were pale and enlarged kidneys, which also had irregular surface with whitish nodulations. Parasites were observed on cutting surface of the renal parenchyma. They were processed for assembly of permanent slides and identified as P. bragai according to routine technique. The histologic findings were mild multifocal lymphoplasmacytic infiltrate, tubular dilatation and foci of tubular regeneration related to mild interstitial fibrosis in the renal cortex, and infiltration of macrophages, heterophils, eosinophils and multinucleated giant cells associated with metazoan parasites in the collecting ducts in renal medulla. The parasitism of P. leucophthalmus by P. bragai is reported for the first time. The importance of considering this parasite among the diagnostic possibilities in birds with renal insufficiency is briefly discussed.(AU)

TNF-á and IL-6 immunohistochemistry in rat renal tissue experimentaly infected with Leptospira interrogans serovar Canicola

Leptospirosis is a public health problem worldwide and its etiology remains unclear. Its pathogenesis involves a complex interaction between host and infecting microorganism. The inflammatory reaction that controls the infection process also underscores many pathophysiological events occurring in leptospirosis. We investigated the presence of tumor necrosis factor-alfa (TNF-alfa) and interleukin-6 (IL-6) in renal tissues by immunohistochemical and histopathological examination in animals experimentally inoculated with Leptospira serovar Canicola. All the tests were carried out 2, 7, 14, 21 or 28 days after inoculation. Although TNF-alfa and IL-6 had been detected in tissues throughout the observation period, these cytokines appeared more intensely during the initial phase of infection. Therefore, both TNF-alfa and IL-6 were associated with the immunopathogenesis of leptospirosis. This profile suggests a high immunocellular response throughout the early infection stages followed by subsequent humoral response.

Response activity of alveolar macrophages in pulmonary dysfunction caused by Leptospira infection

Leptopspirosis is a syndrome with different clinical manifestations including the most severe and often fatal forms of pulmonary disease of unknown etiology. Pulmonary injury during the inflammatory process has been associated with the excessive number of alveolar macrophages (AMs) and polymorphonuclear leukocytes stimulated in the lungs and with the production of reactive oxygen and nitrogen intermediates and other inflammatory mediators. The aim of the present work was to evaluate the cellular immune response of AMs or inflammatory cells of hamsters during leptospirosis. The activity of AMs was determined by measuring nitric oxide (NO) and protein production as well as inflammatory cell infiltration in bronchoalveolar lavage (BAL) fluid. Pulmonary activity during infection was monitored by measuring pH, pressure of oxygen (PaO2), and pressure of carbon dioxide (PaCO2) in blood samples. Cellular immune response and its role in the genesis of leptospirosis have been incriminated as the main causes of tissue and pulmonary injuries, which consequently lead to the pulmonary dysfunction in severe cases of leptospirosis. The present results show a low production of NO in both supernatant of alveolar macrophage culture and BAL. In the latter, protein production was high and constant, especially during acute infection. Total and differential cell count values were 2.5X10(6) on day 4; 7.3X10(6) on day 21; and 2.3X10(6) on day 28 after infection, with lymphocytes (84.04 percent) predominating over neutrophils (11.88 percent) and monocytes (4.07 percent). Arterial blood gas analysis showed pulmonary compromising along with the infectious process, as observed in parameter values (mean±SD) evidenced in the infected versus control group: PaO2 (60.47mmHg±8.7 vs. 90.09mmHg±9.18), PaCO2 (57.01mmHg±7.87 vs. 47.39mmHg±4.5) and pH (7.39±0.03 vs. 6.8±1.3). Results indicated that Leptospira infection in hamsters is a good experimental model to study leptospirosis. However, some of the immune parameters showed variations which might be associated with the animal species.

Effect of pentoxifylline on lung inflammation and gas exchange in a sepsis-induced acute lung injury model

Experimental models of sepsis-induced pulmonary alterations are important for the study of pathogenesis and for potential intervention therapies. The objective of the present study was to characterize lung dysfunction (low PaO2 and high PaCO2, and increased cellular infiltration, protein extravasation, and malondialdehyde (MDA) production assessed in bronchoalveolar lavage) in a sepsis model consisting of intraperitoneal (ip) injection of Escherichia coli and the protective effects of pentoxifylline (PTX). Male Wistar rats (weighing between 270 and 350 g) were injected ip with 10(7) or 10(9) CFU/100 g body weight or saline and samples were collected 2, 6, 12, and 24 h later (N = 5 each group). PaO2, PaCO2 and pH were measured in blood, and cellular influx, protein extravasation and MDA concentration were measured in bronchoalveolar lavage. In a second set of experiments either PTX or saline was administered 1 h prior to E. coli ip injection (N = 5 each group) and the animals were observed for 6 h. Injection of 10(7) or 10(9) CFU/100 g body weight of E. coli induced acidosis, hypoxemia, and hypercapnia. An increased (P < 0.05) cell influx was observed in bronchoalveolar lavage, with a predominance of neutrophils. Total protein and MDA concentrations were also higher (P < 0.05) in the septic groups compared to control. A higher tumor necrosis factor-alpha (P < 0.05) concentration was also found in these animals. Changes in all parameters were more pronounced with the higher bacterial inoculum. PTX administered prior to sepsis reduced (P < 0.05) most functional alterations. These data show that an E. coli ip inoculum is a good model for the induction of lung dysfunction in sepsis, and suitable for studies of therapeutic interventions.

Pentoxifylline decreases tumor necrosis factor and interleukin-1 during high tidal volume

Tumor necrosis factor-alpha (TNF-alpha) is one of the most important proinflammatory cytokines which plays a central role in host defense and in the acute inflammatory response related to tissue injury. The major source of TNF-alpha are immune cells such as neutrophils and macrophages. We tested the hypothesis that pentoxifylline, a methylxanthine derivative, down-regulates proinflammatory cytokine expression during acute lung injury in rats. Male Wistar rats weighing 250 to 450 g were anesthetized ip with 50 mg/kg sodium thiopental and randomly divided into three groups: group 1 (N = 7): tidal volume (V T) = 7 ml/kg, respiratory rate (RR) = 50 breaths/min and normal saline infusion; group 2 (N = 7): V T = 42 ml/kg, RR = 9 breaths/min and normal saline infusion; group 3 (N = 7): V T = 42 ml/kg, RR = 9 breaths/min and pentoxifylline infusion. The animals were ventilated with an inspired oxygen fraction of 1.0, a positive end-expiratory pressure of 3 cmH2O, and normal saline or pentoxifylline injected into the left femoral vein. The mRNA of TNF-alpha rapidly increased in the lung tissue within 180 min of ventilation with a higher V T with normal saline infusion. The concentrations of inflammatory mediators were decreased in plasma and bronchoalveolar lavage (BAL) in the presence of higher V T with pentoxifylline infusion (TNF-alpha: plasma, 102.2 ± 90.9 and BAL, 118.2 ± 82.1; IL-1ß: plasma, 45.2 ± 42.7 and BAL, 50.2 ± 34.9, P < 0.05). We conclude that TNF-alpha produced by neutrophil influx may function as an alert signal in host defense to induce production of other inflammatory mediators

Ventilation with high tidal volume induces inflammatory lung injury

Mechanical ventilation with high tidal volumes (V T) has been shown to induce lung injury. We examined the hypothesis that this procedure induces lung injury with inflammatory features. Anesthetized male Wistar rats were randomized into three groups: group 1 (N = 12): V T = 7 ml/kg, respiratory rate (RR) = 50 breaths/min; group 2 (N = 10): V T = 21 ml/kg, RR = 16 breaths/min; group 3 (N = 11): V T = 42 ml/kg, RR = 8 breaths/min. The animals were ventilated with fraction of inspired oxygen of 1 and positive end-expiratory pressure of 2 cmH2O. After 4 h of ventilation, group 3, compared to groups 1 and 2, had lower PaO2 [280 (range 73-458) vs 517 (range 307-596), and 547 mmHg (range 330-662), respectively, P<0.05], higher wet lung weight [3.62 ± 0.91 vs 1.69 ± 0.48 and 1.44 ± 0.20 g, respectively, P<0.05], and higher wet lung weight/dry lung weight ratio [18.14 (range 11.55-26.31) vs 7.80 (range 4.79-12.18), and 6.34 (range 5.92-7.04), respectively, P<0.05]. Total cell and neutrophil counts were higher in group 3 compared to groups 1 and 2 (P<0.05), as were baseline TNF-alpha concentrations [134 (range <10-386) vs 16 (range <10-24), and 17 pg/ml (range <10-23), respectively, P<0.05]. Serum TNF-alpha concentrations reached a higher level in group 3, but without statistical significance. These results suggest that mechanical ventilation with high V T induces lung injury with inflammatory characteristics. This ventilatory strategy can affect the release of TNF-alpha in the lungs and can reach the systemic circulation, a finding that may have relevance for the development of a systemic inflammatory response