Vascular graft infection (VGI) remains a severe disease with high mortality and relapse rates. We performed a retrospective single-center cohort study to highlight factors associated with long-term all-cause mortality in patients with vascular graft infection. All patients hospitalized in our facility over 10 years for VGI were included. VGI was defined by the presence of a vascular graft or an aortic stent graft (stent or fabric), associated with 2 criteria among clinical, biological, imaging, or microbiological elements in favor of VGI. The primary outcome was all-cause mortality. Empirical antibiotic therapy was considered as appropriate when all involved pathogens were susceptible in vitro to the antibiotics used. The surgical strategy was defined as nonoptimal when the graft was not removed in a late-onset surgery (>3 months) or no surgery was performed. One hundred forty-six patients were included. Empirical antibiotic therapy was administered in 98 (67%) patients and considered appropriate in 55 (56%) patients. Surgery was performed in 136 patients (96%) and considered as optimal in 106 (73%) patients. In multivariable analysis, appropriate empirical antibiotic therapy was associated with a lower probability of mortality (hazard ratio, 0.47 [95% confidence interval, .30–.79]; P = .002). Long-term survival did not differ according to whether the surgical strategy was considered optimal or not (log-rank = 0.66). Appropriate empirical antibiotic therapy is a cornerstone of the management of VGI. Whenever possible, antibiotics must be associated with optimal surgical management. However, surgery could potentially be avoided in comorbid patients who are treated with appropriate antibiotics.

Background: Switching to oral therapy has become an option for treating infective endocarditis (IE) in well-selected patients. This study aimed to assess its effectiveness in real-life settings, including patients who would not have been eligible under current guidelines based on the POET trial results. Methods: All adults treated for IE in two French tertiary centers from January 2016 to December 2023 were included in a retrospective cohort. For each participant, clinical, microbiological, and therapeutic data were collected retrospectively. Patients who received at least 10 days of effective antibiotic therapy were included and categorized based on the route of administration (exclusively intravenous or with a switch to oral therapy). POET-ineligible patients were those who were not eligible in the POET trial. Treatment failure (death, recurrence, or need for suppressive therapy, within 3 months following completion of the initial antibiotic course) was assessed using propensity score (PS) analysis, with oral switch as a time-dependent variable. Results: Three hundred and thirty-three participants were included (233 in the intravenous group and 100 patients in the oral group). No significant difference in treatment failure was observed between groups after adjustment using a PS (HR = 0.55 in favor of oral switch, 95% CI = .27–1.17). The results were similar in the POET-ineligible subgroup, which accounted for 44.7% of participants. Days alive outside the hospital were significantly higher in the oral group (59 vs 47 days, P = .001). Conclusions: Oral switch is a suitable option beyond “classical” frontiers in the management of IE, with potential direct and indirect benefits.

Nocardiosis, a bacterial opportunistic infection caused by Nocardia spp, has recently been reported in patients with anti–granulocyte-macrophage colony-stimulating factor (GM-CSF) autoantibodies, but insufficient data are available about disease presentation, outcomes, and occurrence of autoimmune pulmonary alveolar proteinosis (aPAP) in this population. We performed a prospective, multicenter, nationwide study in France and included patients with a Nocardia infection who had anti-GM-CSF autoantibodies. We describe their clinical, microbiological, and radiological characteristics, and their outcome at 1 year of follow-up. Twenty patients (18 [90%] male) were included, with a median age of 69 (interquartile range, 44–75) years. The organs most frequently involved were the brain (14/20 [70%]) and the lung (12/20 [60%]). Half of the infections were disseminated (10/20 [50%]). Nocardia identification was predominantly made in abscess fluid (17/20 [85%]), among which 10 (59%) were brain abscesses. The 1-year all-cause mortality was 5% (1/20), and only 1 case of aPAP (1/20 [5%]) occurred during the follow-up period. Nocardiosis with anti-GM-CSF autoantibodies is associated with a low mortality rate despite a high incidence of brain involvement. Although the occurrence of aPAP was infrequent during the 1-year follow-up period, long-term clinical data are needed to fully understand the potential relationship between nocardiosis, anti-GM-CSF autoantibodies, and aPAP.

Objective: To assess the clinical relevance of concurrent measurement of anti-chromatin antibodies and anti-double-stranded DNA (anti-dsDNA) antibodies using a multiplex immunoassay in systemic lupus erythematosus (SLE), focusing on their association with organ-specific manifestations and disease activity. Methods: Adult patients diagnosed with SLE based on the 2012 Systemic Lupus International Collaborating Clinics or 2019 European Alliance of Associations for Rheumatology/American College of Rheumatology criteria and followed in our university hospital between 2015 and 2019 were retrospectively included if they had at least one positive detection of anti-dsDNA and/or anti-chromatin result by a multiplex immunoassay, with clinical data available within the 30 days before or after testing. Clinical manifestations, treatments, laboratory parameters and disease activity (SLE Disease Activity Index 2000 (SLEDAI-2K)) were compared using mixed models and correlation coefficients. Results: 98 patients (88% women; median age 42 (IQR: 35–50)) had 677 antibody evaluations. Levels of anti-dsDNA and anti-chromatin antibodies were correlated (r=0.39, 95% CI 0.21 to 0.55). Results were discordant in 59 patients (60%), representing 215 assessments (32%), with anti-chromatin antibodies being detected without anti-dsDNA in 111/677 samples (16%). Rise in anti-dsDNA antibody titre was associated with cutaneous (OR 2.29, 95% CI 1.43 to 3.68) and musculoskeletal involvement (OR 1.29, 95% CI 1.02 to 1.64), while anti-chromatin antibody increase was linked to neuropsychiatric manifestations (OR 1.54, 95% CI 1.03 to 2.29). The increase of either antibody titre was independently associated with proteinuria >0.5 g/24 hours (anti-dsDNA antibody: OR 1.17, 95% CI 1.11 to 2.74; anti-chromatin antibody: OR 1.71, 95% CI 1.02 to 2.87). Correlation with SLEDAI-2K was moderate for anti-dsDNA (r=0.55; 95% CI 0.39 to 0.67), and weaker for anti-chromatin (r=0.32; 95% CI 0.16 to 0.51]). Conclusions: Concomitant measurement of anti-dsDNA and anti-chromatin antibodies using a multiplex immunoassay system brings complementary information for diagnosis and monitoring of SLE. Both antibodies are associated with disease activity and renal involvement, while anti-chromatin antibodies are associated with neuropsychiatric flares. Anti-chromatin antibodies provide additional diagnostic value, particularly in the absence of anti-dsDNA positivity that was observed in 16% of our cohort.