Elevated soluble endothelial protein C receptor levels at ICU admission are associated with sepsis development.

BACKGROUND: The endothelial protein C receptor (EPCR) is a protein that regulates the protein C anticoagulant and anti-inflammatory pathways. A soluble form of EPCR (sEPCR) circulates in plasma and inhibits activated protein C (APC) activities. The clinical impact of sEPCR and its involvement in the septic process is under investigation. In this study, we assessed the role of sEPCR levels as an early indicator of sepsis development. METHODS: Plasma sEPCR levels were measured in 59 critically-ill non-septic patients at the time of admission to the intensive care unit (ICU). Multiple logistic regression analysis was performed to identify potential risk factors for sepsis development and Cox-Regression models were fitted for variables to examine their relationship with time to sepsis development. RESULTS: Thirty patients subsequently developed sepsis and 29 did not. At ICU admission, sequential organ failure assessment (SOFA) scores were significantly higher in the subsequent sepsis group as compared to the non sepsis group (mean ± SD: 6.4±2.7 and 5±2.3, respectively, P=0.037). sEPCR levels were also higher in the patients who subsequently developed sepsis compared to the patients who did not (median and interquartile range: 173.4 [104.5-223.5] ng/mL vs. 98.3 [69.8-147.7] ng/mL, respectively; P=0.004). Cox regression analysis identified sEPCR as the only parameter related to sepsis development with time (relative risk: 1.078, 95% confidence interval: 1.016-1.144, by 10 units; P=0.013). CONCLUSION: Upon ICU admission, sEPCR levels in initially non-septic critically-ill patients appear elevated in the subjects who will subsequently become septic.

Secreted phosphoprotein-1 directly provokes vascular leakage to foster malignant pleural effusion.

Secreted phosphoprotein-1 (SPP1) promotes cancer cell survival and regulates tumor-associated angiogenesis and inflammation, both central to the pathogenesis of malignant pleural effusion (MPE). Here, we examined the impact of tumor- and host-derived SPP1 in MPE formation and explored the mechanisms by which the cytokine exerts its effects. We used a syngeneic murine model of lung adenocarcinoma-induced MPE. To dissect the effects of tumor- versus host-derived SPP1, we intrapleurally injected wild-type and SPP1-knockout C57/BL/6 mice with either wild-type or SPP1-deficient syngeneic lung cancer cells. We demonstrated that both tumor- and host-derived SPP1 promoted pleural fluid accumulation and tumor dissemination in a synergistic manner (P<0.001). SPP1 of host origin elicited macrophage recruitment into the cancer-affected pleural cavity and boosted tumor angiogenesis, whereas tumor-derived SPP1 curtailed cancer cell apoptosis in vivo. Moreover, the cytokine directly promoted vascular hyper-permeability independently of vascular endothelial growth factor. In addition, SPP1 of tumor and host origin differentially affected the expression of proinflammatory and angiogenic mediators in the tumor microenvironment. These results suggest that SPP1 of tumor and host origin impact distinct aspects of MPE pathobiology to synergistically promote pleural fluid formation and pleural tumor progression. SPP1 may present an attractive target of therapeutic interventions for patients with MPE.

Changing patterns of bacterial nosocomial infections: a nine-year study in a general hospital.

Surveillance data on 12,944 bacterial isolates derived from nosocomial infections, reported to the Department of Microbiology and Infectious Diseases of the Hellenic Air Force and VA General Hospital over a 9-year period (1986-1994), were analyzed by the use of a microbial infection control software system. Overall, the isolation rate of Escherichia coli decreased from 25.2% in 1986 to 18.2% in 1994 and Proteus spp. from 5.3 to 2.6%. Remarkably, Pseudomonas spp. increased from 7.2 to 11.3%, Enterobacter spp. from 1.6 to 5.1%, Klebsiella spp. from 5.9 to 7.8% and Enterococcus spp. from 3 to 7.4%. Interestingly, the above phenomenon was paralleled by a significant increase in resistance rate to various antibiotics. Specifically, Staphylococcus aureus and coagulase-negative staphylococci, though they did not display any significant variation in isolation rates, showed an alarming increase in resistance rate to oxacillin, from 11 and 21% in 1986 to 51 and 75% in 1994, respectively. Enterococcus spp. sensitivity to vancomycin remained unlatered at 90%. The above-mentioned serious shift towards more resistant bacteria should be a matter of consideration.

Streptococcus agalactiae: a vaginal pathogen?

The significance of Streptococcus agalactiae as an aetiological agent in vaginitis was evaluated. A total of 6226 samples from women who presented with vaginal symptoms was examined. The presence of >10 leucocytes/high-power field (h.p.f.) was taken to be the criterion of active infection. S. agalactiae was isolated from 10.1% of these samples. The isolation rates of other common pathogens such as Candida spp., Gardnerella vaginalis and Trichomonas spp. were 54.1%, 27.2% and 4.2%, respectively, in the same group of patients. In contrast, the isolation rates of these micro-organisms in the group of patients who had no infection (<10 leucocytes/h.p.f.) were 4.2%, 38.3%, 33% and 0.5%, respectively. In the majority of samples from which S. agalactiae was isolated, it was the sole pathogen isolated (83%) and its presence was associated with an inflammatory response in 80% of patients. Furthermore, the relative risk of vaginal infection with S. agalactiae (2.38) in patients with purulent vaginal discharge was greater than that of Candida spp. infection (1.41) and lower than that of Trichomonas spp. infection (8.32). These data suggest that S. agalactiae in symptomatic women with microscopic evidence of inflammation should be considered a causative agent of vaginitis.

Pseudomonas aeruginosa folliculitis due to non-O:11 serogroups: acquisition through use of contaminated synthetic sponges.

We describe the features of 13 cases of Pseudomonas aeruginosa folliculitis (eight of which occurred sporadically and five of which resulted from two family outbreaks) that developed subsequent to the use of commercial synthetic sponges for bathing. On the basis of O serogrouping and pyocin typing and subtyping, the strains recovered from the skin lesions were found to be identical to those isolated from household shower water and sponges. P. aeruginosa folliculitis is commonly caused by the serogroup O:11; The serogroups described in this study are rare causative agents of this type of skin infection. We believe that this is the first report of P. aeruginosa folliculitis due to serogroups O:3 and O:16.