The rapid detection of pathogens in blood is critical for a favorable outcome of patients with suspected sepsis. Although blood culture (BC) is considered the criterion standard for diagnosis of bloodstream infection, it often takes several days to detect the causative organism. In this study, we compared BC with a commercially available multiplex real-time polymerase chain reaction (PCR) assay to detect bacteria and fungi in blood samples from 144 patients admitted to the emergency department with suspected sepsis. Of 144 blood samples examined, 91 (63%) were negative by both methods and 53 (37%) were positive by at least one of the two methods. In 30 among all positive cases (56.6%),both methods identified the same organisms, in 13 cases (24.5%), BC identified organisms not detected by real-time PCR,and in 10 cases (18.9%), SeptiFast PCR assay gave positive results, whereas the BC was negative. In this study, we wished to compare SeptiFast results obtained by standard procedures, but future clinical studies are necessary to define SeptiFast PCR as support for BC in the early diagnosis of severe bloodstream infections.
Sepsis is the result from a complex bacterial-host interaction, which is an often-fatal response when host protective molecular mechanisms designed to fight invading bacteria surpass the beneficial intensity to the point of causing injury to the host. Increasing evidences have implicated the bacterial translocation (BT) as the main source for the induction of sepsis, although the beneficial effect of BT process has been related to the development of the intestinal immune response by physiological interaction between bacteria and host. In this article, we examined evolving concepts concerning to BT and discussed about its potential role in the promotion of microcirculation injury, moreover, its possible participation in the sepsis induction. According to our data obtained from in-vivo BT animal-model, both bacterial overgrowth and bacterial pathogenic determinants seem to be major predisposing factors for the induction of BT. Besides, translocation of luminal bacteria through the lymphatic via elicits the activation of the GALT inflammatory response contributing to microcirculation injuries, and the haematological via of BT was responsible to the systemic bacterial spread. On other hand, the combination of BT process to the pre-existing host systemic infection played a crucial role in the worsening of the clinical outcome. In our understanding, studies concerning to intestinal immune response and the pathophysiology of bacterial-host interaction, under normal and disease conditions, seems to be the key elements to the development of therapeutic approaches towards sepsis.
Introduction: Marfan syndrome (OMIM #154700) was described for the first time in 1896 by Antoine Bernard-Jean Marfan. It is characterized by its autosomal dominant inheritance pattern, affects 1:5000 of those born alive, and involves the gene that codifies the structural protein fribrillin-1. Fibrillin-1 is critical for the formation of the elastic system backbone and for the negative regulation of the cytokine transforming growth factor beta 1 (TGF-β1). In the syndrome this fibrillar component causes the degeneration of the fibers of the elastic system, which no longer sequesters matrix TGF-β, causing disorganization of the collagen fibers and vascular smooth muscles. The disease affects mainly the cardiovascular system, cardiovascular problems being the main cause of death. This is because arteries have large amounts of elastic fibers that rupture in an adverse process, causing mainly dissections and aneurisms, which have been better clarified in experimental studies with mice. Objective: The objective of this study was to conduct an etiopathogenic and molecular review to describe the advances in the understanding of blood vessel dysmorphism in the syndrome, especially of the aorta. Materials and Methods: For this purpose the literature of the last 35 years was extensively reviewed. Conclusion:The origin of the aortic dysmorphism in the syndrome stems from a number of events that begin with the mutation of the gene fibrillin-1, causing fragmentation of the aortic elastic fibers. Excess cytokine TGF-β increases the amount of metalloproteinases and of vascular smooth muscle cell apoptosis, leading to matrix remodeling and increasing the susceptibility of the vessel to an aneurysm or dissecting process.
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