Browsing by Keyword "Enfermedades infecciosas"
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Item INFECCION DE PROTESIS DE CADERA: APROXIMACION DIAGNOSTICA Y TRATAMIENTO DE 27 EPISODIOS(1994) Salavert Lleti, M.; Martinez, J.; Sanchez, C.; Matamala, A.; Pons, M.; Angles, F.; Cuchi, E.; Lite, J.; Ferrer, H.; Garau, J.; ADAPTACIÓN AL CAMBIO CLIMÁTICOBackground: Preoperative diagnosis of hip prosthesis infection (HPI) is difficult. There is no therapeutic option which is completely effective and without risk. The aim of this study was to evaluate a diagnostic approach and therapeutic strategy in a group of patients with HPI. Patients and Methods: A retrospective study of 27 episodes of HPI diagnosed by anatomopathologic and/or microbiologic examination of surgical samples was performed. Results: Twenty-three patients with 27 episodes of HPI out of a total of 24 hip prosthesis (HP) were treated. The infection was early in 15 episodes. The etiologic agents were plasmocoagulase negative staphylococcus (NSP) in 11 cases, P. aeruginosa in 8, S. aureus in 5, Enterococcus sp. in 2 and miscellaneous in the remaining cases. In 2 cases the infection was polymycrobial. Following a mean follow period of 22.6 ± 15.2 months, 13 out of the 14 patients in whom the prosthesis was withdrawn were cured (in 4 a second prosthesis was implanted), one out of 6 in those in whom the prosthesis remained in situ following debridement, and 2 out of 3 episodes in whom reimplantation was performed over time. The withdrawal of the prosthesis was significantly greater than debridement in the treatment of early infection (p < 0.001). The total mean length of postoperative antibiotherapy was 48.2 ± 17 days. No differences were observed in the oral versus parenteral treatment (p = 0.22), and nor was prognosis worse in those treated for less than 42 days. Conclusions: The authors' experience suggests that attempts to save a hip prosthesis in early infection usually fail. In addition to prosthesis withdrawal or implantation of another prosthesis, six weeks of postoperative antibiotic therapy, which may be oral route, appear to be sufficient.Item ¿Qué hace que Aspergillus fumigatus sea un patógeno de éxito? Genes y moléculas involucrados en la aspergilosis invasora(2010-10) Abad, Ana; Victoria Fernández-Molina, Jimena; Bikandi, Joseba; Ramírez, Andoni; Margareto, Javier; Sendino, Javier; Luis Hernando, Fernando; Pontón, Jose; Garaizar, Javier; Rementeria, Aitor; GenéticaAspergillus fumigatus is an opportunistic pathogen that causes 90% of invasive aspergillosis (IA) due to Aspergillus genus, with a 50-95% mortality rate. It has been postulated that certain virulence factors are characteristic of A. fumigatus, but the "non-classical" virulence factors seem to be highly variable. Overall, published studies have demonstrated that the virulence of this fungus is multifactorial, associated with its structure, its capacity for growth and adaptation to stress conditions, its mechanisms for evading the immune system and its ability to cause damage to the host. In this review we intend to give a general overview of the genes and molecules involved in the development of IA. The thermotolerance section focuses on five genes related with the capacity of the fungus to grow at temperatures above 30°C (thtA, cgrA, afpmt1, kre2/afmnt1, and hsp1/asp f 12). The following sections discuss molecules and genes related to interaction with the host and with the immune responses. These sections include Β-glucan, α-glucan, chitin, galactomannan, galactomannoproteins (afmp1/asp f 17 and afmp2), hydrophobins (rodA/hyp1 and rodB), DHN-melanin, their respective synthases (fks1, rho1-4, ags1-3, chsA-G, och1-4, mnn9, van1, anp1, glfA, pksP/alb1, arp1, arp2, abr1, abr2, and ayg1), and modifying enzymes (gel1-7, bgt1, eng1, ecm33, afpigA, afpmt1-2, afpmt4, kre2/afmnt1, afmnt2-3, afcwh41 and pmi); several enzymes related to oxidative stress protection such as catalases (catA, cat1/catB, cat2/katG, catC, and catE), superoxide dismutases (sod1, sod2, sod3/asp f 6, and sod4), fatty acid oxygenases (ppoA-C), glutathione tranferases (gstA-E), and others (afyap1, skn7, and pes1); and efflux transporters (mdr1-4, atrF, abcA-E, and msfA-E). In addition, this review considers toxins and related genes, such as a diffusible toxic substance from conidia, gliotoxin (gliP and gliZ), mitogillin (res/mitF/asp f 1), hemolysin (aspHS), festuclavine and fumigaclavine A-C, fumitremorgin A-C, verruculogen, fumagillin, helvolic acid, aflatoxin B1 and G1, and laeA. Two sections cover genes and molecules related with nutrient uptake, signaling and metabolic regulations involved in virulence, including enzymes, such as serine proteases (alp/asp f 13, alp2, and asp f 18), metalloproteases (mep/asp f 5, mepB, and mep20), aspartic proteases (pep/asp f 10, pep2, and ctsD), dipeptidylpeptidases (dppIV and dppV), and phospholipases (plb1-3 and phospholipase C); siderophores and iron acquisition (sidA-G, sreA, ftrA, fetC, mirB-C, and amcA); zinc acquisition (zrfA-H, zafA, and pacC); amino acid biosynthesis, nitrogen uptake, and cross-pathways control (areA, rhbA, mcsA, lysF, cpcA/gcn4p, and cpcC/gcn2p); general biosynthetic pathway (pyrG, hcsA, and pabaA), trehalose biosynthesis (tpsA and tpsB), and other regulation pathways such as those of the MAP kinases (sakA/hogA, mpkA-C, ste7, pbs2, mkk2, steC/ste11, bck1, ssk2, and sho1), G-proteins (gpaA, sfaD, and cpgA), cAMP-PKA signaling (acyA, gpaB, pkaC1, and pkaR), His kinases (fos1 and tcsB), Ca2+ signaling (calA/cnaA, crzA, gprC and gprD), and Ras family (rasA, rasB, and rhbA), and others (ace2, medA, and srbA). Finally, we also comment on the effect of A. fumigatus allergens (Asp f 1-Asp f 34) on IA. The data gathered generate a complex puzzle, the pieces representing virulence factors or the different activities of the fungus, and these need to be arranged to obtain a comprehensive vision of the virulence of A. fumigatus. The most recent gene expression studies using DNA-microarrays may be help us to understand this complex virulence, and to detect targets to develop rapid diagnostic methods and new antifungal agents.