BackgroundTrichosporon species may colonize the skin, respiratory tract and gastrointestinal tract of human beings. The yeast is recognized as etiological agent of white piedra, a superficial mycosis. Nevertheless, immunocompromised hosts may develop invasive Trichosporonosis. Central nervous system trichosporonosis is a very rare clinical manifestation. In fact, only a few cases have been published in the literature and none of them was caused by Trichosporon inkin.Case presentationHere we report the first clinical case of meningoencephalitis due to this species in a female previously healthy patient under corticosteroids and antibiotics therapy for several months. She was submitted to an invasive procedure to remove a left sided acoustic neuroma and further developed a cerebrospinal fistula. After some days of the procedure, she presented a predominantly and intensive occipital holocranial headache, followed by vomiting, hyporexia, weight loss, asthenia, irritability, difficulty to concentrate and rotator vertigo. The patient further developed a cerebrospinal fistula in the occipital region and was submitted to a surgical correction. After several months of clinical interventions, she was diagnosed with CNS Trichosporonosis, after Magnetic Resonance Imaging and positive microbiological cultures obtained within two different occasions (2 weeks apart). Despite the antifungal therapy with Amphotericin B and Voriconazole, the patient did not survive.ConclusionsDespite CNS Fungal infections are mostly due to Cryptococcus spp., other emergent yeasts, such as T. inkin may be considered as a likely etiological agent. This is the first case report of CNS Trichosporonosis, where species identification was performed with rDNA sequencing.
Cryptosporidiosis is a very prominent disease in the fi eld of public health, and usually causes diarrhea. We describe two immunocompetent patients who presented with chronic diarrhea that was ultimately found to be caused by continuous exposure to well water contaminated with the microbial cysts (oocysts) of the Cryptosporidium spp parasite. We describe the patients' histories and possible explanations for their prolonged symptoms.
Background/objetive: The liver ischemia and reperfusion is important for procedures occurring in liver and intestinal trauma injuries that require intestinal resection and anastomosis. The aim of this study was to evaluate the influence of hepatic ischemia/reperfusion in vivo in the healing of duodenal anastomoses. Methods: Wistar rats were randomly selected and allocated into two groups of six animals each: liver ischemia/reperfusion + duodenal anastomosis group and duodenal anastomoses group. Hepatic ischemia was induced for 30 minutes by occlusion of the vessels that supply the median and lateral lobes of the liver, using a microvascular clip. In all rats the duodenum was sectioned and an end-to-end anastomosis was performed. After liver reperfusion, animals were observed for 6 days; the maximum bursting pressure of anastomoses was determined and duodenum samples were taken for histopathological examination. Results: As a result, the maximum bursting pressure of anastomosis in ischemia/reperfusion + duodenal anastomosis group (64.5±5.5mmHg) was significantly lower (p<0.001) than in duodenal anastomosis group rats (89.7±3.4mmHg). The inflammatory tissue response in ischemia/reperfusion + duodenal anastomosis group had scores higher than in duodenal anastomosis group rats (p=0.004). Conclusion: In conclusion, the hepatic ischemia-reperfusion negatively affected the healing process of duodenal anastomoses.
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