[Factors associated with mortality in Acinetobacter baumannii infected intensive care unit patients]. / Yogun Bakim Hastalarinda Gelisen Acinetobacter baumannii Enfeksiyonunda Mortaliteyi Etkileyen Faktörler.

Acinetobacter baumannii can survive for prolonged periods in unsuitable environmental conditions and easily spread to patients in the hospital settings leading to healthcare-associated infections. Major risk factors for A.baumannii infections are mechanical ventilation, invasive procedures such as central venous catheter or urinary catheter and the use of broad-spectrum antibiotics. The mortality rates of nosocomial A.baumannii infections have been reported between 50-60%, changing due to several factors. The aim of this study was to investigate the factors associated with mortality in intensive care unit (ICU) patients diagnosed as nosocomial A.baumannii infections. The demographical, clinical and microbiological data of the patients who were followed in ICUs between September 2008 to March 2010 were evaluated retrospectively, and analyzed regarding the factors related to mortality. Blood, urine and tracheal aspirate samples were collected from suspected patients and cultivated on conventional agar media. The identification of the isolates and antibiotic susceptibilities were performed by using VITEK-2 (bioMerieux, USA) automated system. The patients with A.baumannii infections were grouped as "died" and "survived" cases, and the groups were compared according to following factors: age, gender, isolation day of bacteria in intensive care unit, type of clinical sample, implementation day of the central venous catheter, implementation of tracheotomy and/or intubation, operation, presence of diabetes mellitus, antibiotic use, day of hospitalization, day of mechanical ventilation and APACHE (Acute Physiology and Chronic Health Evaluation)-II score. A.baumannii infection was identified in 56 patients (29 female, 27 male; mean age: 63 years) in the intensive care units during the study period, and the total mortality rate was estimated as 77% (43/56). The implementation of intubation, mechanical ventilation, high APACHE II score and recovery of bacteria from respiratory tract were found statistically significant for A.baumannii infections related mortality (p< 0.05 for each parameter). Our data showed that Acinetobacter infection in the respiratory tract, implementation of intubation, mechanical ventilation and high APACHE II scores were the major risk factors related to mortality.

The dithiol glutaredoxins of african trypanosomes have distinct roles and are closely linked to the unique trypanothione metabolism.

Trypanosoma brucei, the causative agent of African sleeping sickness, possesses two dithiol glutaredoxins (Grx1 and Grx2). Grx1 occurs in the cytosol and catalyzes protein deglutathionylations with k(cat)/K(m)-values of up to 2 × 10(5) M(-1) S(-1). It accelerates the reduction of ribonucleotide reductase by trypanothione although less efficiently than the parasite tryparedoxin and has low insulin disulfide reductase activity. Despite its classical CPYC active site, Grx1 forms dimeric iron-sulfur complexes with GSH, glutathionylspermidine, or trypanothione as non-protein ligands. Thus, contrary to the generally accepted assumption, replacement of the Pro is not a prerequisite for cluster formation. T. brucei Grx2 shows an unusual CQFC active site, and orthologues occur exclusively in trypanosomatids. Grx2 is enriched in mitoplasts, and fractionated digitonin lysis resulted in a co-elution with cytochrome c, suggesting localization in the mitochondrial intermembrane space. Grx2 catalyzes the reduction of insulin disulfide but not of ribonucleotide reductase and exerts deglutathionylation activity 10-fold lower than that of Grx1. RNA interference against Grx2 caused a growth retardation of procyclic cells consistent with an essential role. Grx1 and Grx2 are constitutively expressed with cellular concentrations of about 2 µM and 200 nM, respectively, in both the mammalian bloodstream and insect procyclic forms. Trypanothione reduces the disulfide form of both proteins with apparent rate constants that are 3 orders of magnitude higher than those with glutathione. Grx1 and, less efficiently, also Grx2 catalyze the reduction of GSSG by trypanothione. Thus, the Grxs play exclusive roles in the trypanothione-based thiol redox metabolism of African trypanosomes.