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Background: The incidence of Enterococcus faecalis infective endocarditis is increasing over time. Data on the impact of minimum inhibitory concentration (MIC) of amoxicillin on treatment outcomes are scarce. The objective of this study was to describe the epidemiology of E. faecalis infective endocarditis and to evaluate whether the MIC of amoxicillin might influence mortality., Materials: We retrospectively included all consecutive patients diagnosed with definite E. faecalis infective endocarditis between 2013 and 2020 in 11 French hospitals. We extracted data from the local diagnosis-related group (DRG) database and matched these data with microbiological results. Amoxicillin MIC was determined by Etest strip. The primary endpoints were endocarditis-related mortality and risk factors for endocarditis-related mortality including amoxicillin MIC., Results: A total of 403 patients with definite E. faecalis infective endocarditis were included. Patients were predominantly male (76.4%) with a median age of 74 years (67-82). Embolic complications occurred in 170 (42.1%) patients. Cardiac surgery was performed in 158 (61.5%) patients. The endocarditis-related mortality rate was 28.3% and the median delay between mortality and onset of hospitalization was 24 (9; 41) days. E. faecalis MIC of amoxicillin was available for 246 (61%) patients. The median MIC was 0.5 mg/L (0.4-0.7). Amoxicillin MIC was not found to be associated with in-hospital mortality. None of the variables included in the multivariate model were identified as a risk factor for mortality and there was no correlation between mortality and the duration of treatment for 4 weeks versus 6 weeks., Conclusions: Higher amoxicillin MIC was not a risk factor leading to endocarditis-related mortality in definite E. faecalis infective endocarditis. However, further studies are needed to assess the effect of amoxicillin MIC on relapse., (© The Author(s) 2024. Published by Oxford University Press on behalf of British Society for Antimicrobial Chemotherapy.)

Staphylococcus aureus is the main bacterial pathogen encountered in mediastinitis after cardiac surgical procedures; it remains a devastating complication with a high mortality rate. As neutrophils have a primordial role in the defense against staphylococcus infection and cardiopulmonary bypass (CPB) is known to induce immunosuppression, the aim of this study was to investigate CPB impact on neutrophil functions. Patients without known immunosuppression scheduled for cardiac surgery with CPB were included. Bone marrow and blood samples were harvested before, during, and after surgery. Neutrophil phenotypic maturation and functions (migration, adhesion, neutrophil extracellular trap [NET] release, reactive oxygen species (ROS) production, phagocytosis, and bacteria killing) were investigated. Two types of Staphylococcus aureus strains (one from asymptomatic nasal carriage and another from mediastinitis infected tissues) were used to assess in vitro bacterial direct impact on neutrophils. We found that CPB induced a systemic inflammation with an increase in circulating mature neutrophils after surgery. Bone marrow sample analysis did not reveal any modification of neutrophil maturation during CPB. Neutrophil lifespan was significantly increased and functions such as NET release and ROS production were enhanced after CPB whereas bacteria killing and phagocytosis were not impacted. Results were similar with the two different isolates of Staphylococcus aureus. These data suggest that CPB induces a recruitment of mature neutrophils via a demargination process rather than impacting their maturation in the bone marrow. In addition, neutrophils are fully efficient after CPB and do not contribute to postoperative immunosuppression., (©2021 Society for Leukocyte Biology.)

Sepsis is accompanied by the initial activation of proinflammatory pathways and long-lasting immunosuppression that appears to contribute to late-occurring mortality. Although high-mobility group box 1 (HMGB1) is involved in many aspects of inflammation, its role in sepsis-induced immune suppression remains unclear. In this study, we examined HMGB1's contribution to neutrophil NADPH oxidase activity dysfunction and associated neutrophil-dependent bacterial clearance in mice subjected to sepsis and in patients who survive septic shock. Using a murine model of polymicrobial septic peritonitis, we demonstrated that treatment with anti-HMGB1 Ab significantly diminished sepsis-induced dysfunction of neutrophil NADPH oxidase activity. In a subsequent set of experiments, we found that blocking HMGB1 preserved the ability of neutrophils from patients recovering from septic shock to activate NADPH oxidase. Taken together, our data suggest that HMGB1 accumulation in the late phase of sepsis plays a specific role in the development of postsepsis immunosuppression and specifically affects neutrophil-dependent antibacterial defense mechanisms. Thus, blocking HMGB1 may be a promising therapeutic intervention to diminish the adverse effects of sepsis-induced immunosuppression., (© Society for Leukocyte Biology.)

Leptospirosis is one of the most common pathogens responsible for life-threatening tropical disease in travelers. We report a case of massive intra-alveolar hemorrhage caused by Leptospira serovar Djasiman in a 38-year-old man returning from Laos, who was cured with antibiotics and salvage treatment with extra-corporeal membrane oxygenation., (© 2015 International Society of Travel Medicine.)