Malakoplakia after renal transplantation in the current era of immunosuppressive therapy: case report and literature review.

Malakoplakia is a rare chronic granulomatous disease of unknown cause. It is thought to be caused by an acquired bactericidal defect of macrophages. Malakoplakia is associated with chronic infections and immunosuppression. Although it occurs mainly in the urinary tract, it has already been reported in almost every organ system. The isolation of bacteria, especially Escherichia coli, is common in malakoplakia patients. Here, we present a case of primary cutaneous malakoplakia in a kidney transplant recipient who had been taking prednisone, tacrolimus, and mycophenolate. Culture of a lesion grew Burkholderia cepacia complex. Treatment with high doses of trimethoprim-sulfamethoxazole was successful. We also present a systematic review of the literature, identifying 4 previously reported cases of malakoplakia after renal transplantation under similar immunosuppressive therapy, most occurring in the urinary tract or perineum and following benign courses to cure. Data in the literature suggest that malakoplakia has become even rarer since changes were made in the immunosuppressive therapy employed after kidney transplantation.

Cdc42p controls yeast-cell shape and virulence of Paracoccidioides brasiliensis.

Paracoccidioides brasiliensis is characterized by a multiple budding phenotype and a polymorphic cell growth, leading to the formation of cells with extreme variations in shape and size. Since Cdc42 is a pivotal molecule in establishing and maintaining polarized growth for diverse cell types, as well as during pathogenesis of certain fungi, we evaluated its role during cell growth and virulence of the yeast-form of P. brasiliensis. We used antisense technology to knock-down PbCDC42's expression in P. brasiliensis yeast cells, promoting a decrease in cell size and more homogenous cell growth, altering the typical polymorphism of wild-type cells. Reduced expression levels also lead to increased phagocytosis and decreased virulence in a mouse model of infection. We provide genetic evidences underlying Pbcdc42p as an important protein during host-pathogen interaction and the relevance of the polymorphic nature and cell size in the pathogenesis of P. brasiliensis.

Vascular permeability, neutrophil migration and edematogenic effects induced by the latex of Cryptostegia grandiflora.

Inflammatory responses have been described as occurring after exposure to some latex materials. In this study pro-inflammatory activity in the latex of Cryptostegia grandiflora was investigated. The soluble proteins of the latex (CgLP) were isolated from the whole latex and evaluated by in vivo assays. CgLP induced strong inflammatory activity mediated by neutrophil migration, enlarging vascular permeability and increasing myeloperoxidase activity locally in rats. CgLP-induced inflammation was observed in peritonitis, paw edema and air push models. In addition, CgLP caused hyperemia in a healing model. The peritonitis effect was lost when CgLP was previously boiled suggesting the involvement of pro-inflammatory proteins. Thioglycollate increased the neutrophil migration induced by CgLP, but not by fMLP. Mast cell depletion provoked by 40/80 compound did not modify the course of inflammation triggered by CgLP, being similar to fMLP, which suggested that neutrophil migration was induced by direct mechanism mediated by macrophages. Neutrophil migration stimulated by CgLP was strongly inhibited by Dexamethasone and to a lesser extent by Thalidomide, indicating the involvement of cytokines in mediating neutrophil infiltration. Celecoxib and Indomethacin were inhibitory suggesting the involvement of prostaglandins. Cimetidine was effective only in the initial phase of edema. PCA 4248 was ineffective. It is concluded that the latex of C. grandiflora is a potent inflammatory fluid, and also that laticifer proteins may be implicated in this process.

Tratamento das infecções em pacientes com pancitopenia secundária e tratamento citorredutor / Treatment of infections in patients with pancytopenia resulting from cytoreductive treatment

Febre de etiologia desconhecida é a causa mais freqüente de internação hospitalar de pacientes neutropênicos em quimioterapia. O paciente é, em geral, oligossintomático, e a avaliação inicial deve incluir história e exames físicos completos e minuciosos, além de exames laboratoriais, procurando identificar a etiologia da febre e complicações decorrentes da quimioterapia. O tratamento com antibióticos de largo espectro deve ser iniciado prontamente, e o esquema terapêutico reavaliado 72 h, depois, com base nos estudos microbiológicos. No texto, discorremos sobre o diagnóstico da neutropenia febril, suas particularidades e o manejo do paciente

Isolation and characterization of Kluyveromyces marxianus mutants deficient in malate transport.

In malic acid-grown cells of the strains ATCC 10022 and KMS3 of Kluyveromyces marxianus the transport of malic acid occurred by a malate-proton symport, which accepted L-malic, D-malic, succinic and fumaric acids, but not tartaric, malonic or maleic acids. The system was inducible and subjected to glucose repression. Mutants of the strain KMS3, unable to grow in a medium with malic acid, were isolated and checked for their capacity to utilize several carbon sources and to transport dicarboxylic acids by the malate-proton symport. Two distinct clones affected on malate transport were obtained. Both were able to grow on a medium with glycerol or ethanol but not with DL-malic, succinic, oxoglutaric and oxaloacetic acids as the sole carbon and energy sources. However, while one of the mutants (Mal7) displayed activity levels for the enzymes malate dehydrogenase, isocitrate lyase, and phosphoenolpyruvate carboxykinase similar to those of the wild strain, in the other mutant type (Mal6) the activities for the same enzymes were significantly reduced. Plasma membranes from derepressed cells of the wild strain and of the mutants Mal6 and Mal7 were isolated and the protein analysed by SDS-PAGE. The electrophoretic patterns of these preparations differed in a polypeptide with an apparent molecular mass of about 28 kDa, which was absent only in the mutant Mal7. The results indicated that Mal7 can be affected in a gene that encodes a malate carrier in K. marxianus.

Renal effect of gentamicin in diabetic rats

To evaluate the protective effect of diabetes mellitus (DM) on renal function of rats treated with gentamicin (GM), male Wistar-EPM rats (250-350 g) were treated with streptozotocin (SZ; 45 mg/kg) and starting 10 days after induction of diabetes, GM was given for ten consecutive days at a daily dose of 40 mg/kg. In the GM-treated group (G), a significant fall in inulin and sodium-p-aminohippurate clearance was obtained (3.57 + or - 0.16 and 12.59 + or - 0.61 ml min-1kg-1 vs 6.43 + or - 0.21 and 17.98 + or - 0.47 ml min-1 kg-1 in control rats (C), respectively) while in the animals previously injected with SZ (diabetic + gentamicin, DG group) these changes injected with SZ (diabetic + gentamicin, DG group) these changes were not observed. The diabetic (D), g and DG group showed a significant rise in urinary flow compared to C (0.165 + or - 0.009, 0.145 + or - 0.007 and 0.173 + or - 0.009 ml min-1kg-1 vs 0.109 + or - 0.003 ml min-1kg-1, respectively); however, only in G was the U/P inulin ration significantly decreased when compared to C. The fractional excretion (FE) of sodium and postassium was significantly augmented in G when compared to C, D and DG. Thus, diabetes protected against gentamicin nephrotoxicity at both the glomerular and tubular level, although it did not promote a reduction in urinary flow