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Candida species are a common cause of invasive infection in neonates and children. The aim of our study was to evaluate the epidemiology and microbiology of invasive candidiasis (IC) in the largest tertiary Greek pediatric hospital during a 10-year period. A retrospective cohort study was performed from January 2008 to December 2017. Identification of species and antifungal susceptibility testing was performed according to the Clinical and Laboratory Standards Institute (CLSI) methodology. During the study period, 178 cases of IC were recorded. The tissue distribution included blood (87.1%), cerebrospinal (7.9%), peritoneal (3.9%) and pleural fluids (1.1%). Candida albicans and Candida parapsilosis (sensu lato) were the most frequently isolated species (47.8% and 28.7% respectively). From period 2008&ndash, 2012 to period 2013&ndash, 2017, a significant decrease in IC rates was detected (0.21 cases/1000 hospitalization days VS 0.11 cases/1000 hospitalization days, P = 0.040), while median minimum inhibitory concentrations (MICs) of amphotericin B were significantly increased for both C. albicans and C. parapsilosis (sl) (P = 0.037 and P = 0.004 respectively). The decrease in IC rates may reflect the increased awareness as well as the effective infection control initiatives and antifungal interventions. However, the significant increase in the MICs for amphotericin B and echinocandins such as caspofungin, raises concerns about their common use as first-line treatment. Epidemiologic monitoring is, therefore, critically important in order to evaluate and optimize therapeutic protocols for IC in pediatric populations.

Purpose. To investigate the clinical, phenotypic and genotypic characteristics of Staphylococcus aureus strains causing osteoarticular infections in a large paediatric series. Methodology. Medical records of children who were hospitalized with the diagnosis of community-associated S. aureus (CA-SA) osteomyelitis and/or septic arthritis in the two major tertiary paediatric hospitals of Athens during an 8-year period (2007–2015) were reviewed, and S. aureus isolates were analysed regarding antimicrobial resistance, detection of pathogenicity genes and genotyping using SCCmec, agr typing, PFGE and MLST. Results. During the study period, 123 children with CA-SA osteoarticular infections were identified, and methicillin-resistant S. aureus (MRSA) accounted for 44 of these (35.8 %). Children with MRSA infection had a significantly higher admission rate to the ICU (5.7 vs 0 %, P=0.04) and longer duration of hospitalization (21.6 vs 16.7 days, P=0.04). Sixty-eight isolates [42 (methicillin-sensitive S. aureus) MSSA and 26 MRSA] were available for molecular analysis. All MRSA strains were mecA-positive and most carried the SCCmec IV cassette (23/26, 88 %) and belonged to the PFGE type C (24/26, 92.3 %), agr type 3 (24/26, 92.3 %) and the MLST ST80 clone (24/26, 92.3 %). In contrast, MSSA strains showed polyclonality by PFGE and agr typing. Regarding pathogenicity genes, MRSA vs MSSA isolates showed higher detection rates of PVL (96.2 vs 4.8 %, P

Background A previous randomized study showed that clarithromycin decreases the risk of death due to ventilator-associated pneumonia and shortens the time until infection resolution. The efficacy of clarithromycin was tested in a larger population with sepsis. Methods Six hundred patients with systemic inflammatory response syndrome due to acute pyelonephritis, acute intra-abdominal infections or primary Gram-negative bacteraemia were enrolled in a double-blind, randomized, multicentre trial. Clarithromycin (1 g) was administered intravenously once daily for 4 days consecutively in 302 patients; another 298 patients were treated with placebo. Mortality was the primary outcome; resolution of infection and hospitalization costs were the secondary outcomes. Results The groups were well matched for demographics, disease severity, microbiology and appropriateness of the administered antimicrobials. Overall 28 day mortality was 17.1% (51 deaths) in the placebo arm and 18.5% (56 deaths) in the clarithromycin arm (P = 0.671). Nineteen out of 26 placebo-treated patients with septic shock and multiple organ dysfunctions died (73.1%) compared with 15 out of 28 clarithromycin-treated patients (53.6%, P = 0.020). The median time until resolution of infection was 5 days in both arms. In the subgroup with severe sepsis/shock, this was 10 days in the placebo arm and 6 days in the clarithromycin arm (P = 0.037). The cost of hospitalization was lower after treatment with clarithromycin (P = 0.044). Serious adverse events were observed in 1.3% and 0.7% of placebo- and clarithromycin-treated patients, respectively (P = 0.502). Conclusions Intravenous clarithromycin did not affect overall mortality; however, administration shortened the time to resolution of infection and decreased the hospitalization costs.

We aimed to investigate if angiopoietin-2 (Ang-2) participates in the septic process and what may be the role of monocytes as a site of release of Ang-2 in sepsis. Concentrations of Ang-2 were estimated in sera and in supernatants of monocytes derived form one already described cohort of 90 patients with septic syndrome due to ventilator-associated pneumonia (VAP). Mononuclear cells of 17 healthy volunteers were stimulated by serum of patients in the presence or absence of various intracellular pathway inhibitors. Ang-2 gene expression after stimulation was also tested. Ang-2 was higher in patients with septic shock compared to patients with sepsis, severe sepsis and controls. Ang-2 was significantly increased in non-survivors compared with survivors. Serum levels greater than 9700 pg/ml were accompanied by a 3.254 odds ratio for death (p: 0.033). Ang-2 release from monocytes of septic patients was slightly decreased after stimulation with lipopolysaccharide (LPS) of Escherichia coli O55:B5. Release of Ang-2 from healthy mononuclear cells was stimulated by serum of patients with shock but not by serum of non-shocked patients (p: 0.016). Release was decreased by LPS; increased in the presence of a TLR4 antagonist; and decreased by anti-TNF antibody. RNA transcripts of PBMCs after stimulation with serum of patients with septic shock were higher than those after LPS stimulation. It is concluded that Ang-2 is increased in serum in the event of septic shock and that its increase is related to unfavorable outcome. It seems that a circulating factor may exist in the serum of patients with septic shock that stimulates gene expression and subsequent release of Ang-2 from monocytes. TLR4 and TNFalpha modulate release of Ang-2.

AIM: To investigate the role of gastric mucosa at the secretion of sTREM-1 in peptic ulcer. METHODS: Seventy two patients were enrolled; 35 with duodenal, 21 with gastric ulcer and 16 with chronic gastritis. Patients were endoscoped and gastric juice was aspirated. Patients with duodenal and gastric ulcer underwent a second endoscopy post-treatment. Biopsies were incubated in the absence/presence of endotoxins or gastric juice. Supernatants were collected and sTREM-1 and TNFα were measured by enzyme immunoabsorbent assays. Scoring of gastritis was performed before and after treatment according to updated Sydney score. RESULTS: Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis. sTREM-1 was higher in supernatants of tissue samples of H pylori-positive than of H pylori-negative patients with gastric ulcer. Median (± SE) sTREM-1 was found increased in supernatants of patients with gastric ulcer before treatment (203.21 ± 88.91 pg/1000 cells) compared to supernatants either from the same patients post-treatment (8.23 ± 5.79 pg/1000 cells) or from patients with chronic gastritis (6.21 ± 0.71 pg/1000 cells) (P < 0.001 and < 0.001, respectively). Similar differences for sTREM-1 were recorded among LPS-stimulated tissue samples of patients (P = 0.001). Similar differences were not found for TNFα. Positive correlations were found between sTREM-1 of supernatants from patients with both duodenal and gastric ulcer before treatment and the degree of infiltration of neutrophils and monocytes. CONCLUSION: sTREM-1 secreted by the gastric mucosa is an independent mechanism connected to the pathogenesis of peptic ulcer. sTREM-1 was released at the presence of H pylori from the inflamed gastric mucosa in the field of gastric ulcer.