Background The study aimed to describe the epidemiology and outcomes of hospital-acquired bloodstream infections (HABSIs) between COVID-19 and non-COVID-19 critically ill patients. Methods We used data from the Eurobact II study, a prospective observational multicontinental cohort study on HABSI treated in ICU. For the current analysis, we selected centers that included both COVID-19 and non-COVID-19 critically ill patients. We performed descriptive statistics between COVID-19 and non-COVID-19 in terms of patients’ characteristics, source of infection and microorganism distribution. We studied the association between COVID-19 status and mortality using multivariable fragility Cox models. Results A total of 53 centers from 19 countries over the 5 continents were eligible. Overall, 829 patients (median age 65 years [IQR 55; 74]; male, n = 538 [64.9%]) were treated for a HABSI. Included patients comprised 252 (30.4%) COVID-19 and 577 (69.6%) non-COVID-19 patients. The time interval between hospital admission and HABSI was similar between both groups. Respiratory sources (40.1 vs. 26.0%, p < 0.0001) and primary HABSI (25.4% vs. 17.2%, p = 0.006) were more frequent in COVID-19 patients. COVID-19 patients had more often enterococcal (20.5% vs. 9%) and Acinetobacter spp. (18.8% vs. 13.6%) HABSIs. Bacteremic COVID-19 patients had an increased mortality hazard ratio (HR) versus non-COVID-19 patients (HR 1.91, 95% CI 1.49–2.45). Conclusions We showed that the epidemiology of HABSI differed between COVID-19 and non-COVID-19 patients. Enterococcal HABSI predominated in COVID-19 patients. COVID-19 patients with HABSI had elevated risk of mortality. Trial registration ClinicalTrials.org number NCT03937245. Registered 3 May 2019.
This study provides molecular evidence associating co-infection of type 1 and 2 EBV with MS.
Sir: The role of Mycoplasma pneumoniae in the pathophysiology of Guillain-Barre syndrome (GBS) is unknown. Direct invasion of CSF by the micro-organism in GBS has been proved both by immuno¯uorescence [1] and culture [3] although an auto-immune mechanism is the most supported theory, with the key role of a demyelinating process.A 3-year-old boy was admitted to our hospital with a 6-day history of progressive weakness in his lower limbs, frequent falls and diculty in walking. Previously, he had mild respiratory tract symptoms. The most remarkable ®ndings were muscle weakness, absence of tendon re¯exes in the lower limbs and clumsy gait. Haemoglobin was 8.7 g/dl, haematocrit 25.8%, the ESR 25 mm/h and he had positive IgM anticardiolipin antibodies. Cold agglutinins were negative. CSF (lumbar puncture) revealed 1 leucocyte/ mm 3 , protein, 72 mg/dl, glucose, 54 mg/dl, IgG, 7.4 mg/dl (952 mg/dl in serum), and albumin, 44 mg/dl (3,920 mg/dl in serum). The CSF specimen was inadequate to culture for M. pneumoniae. Serological investigations for respiratory viruses (adenovirus, in¯uenza A, and B, para-in¯uenza 1, 2, and 3, cytomegalovirus, respiratory syncytial), and Epstein Barr viruses as well as stool culture for Campylobacter jejuni were negative. Based on conduction velocities in both right and left peroneal nerves of 24 and 17.9 m/s respectively, (normal range: 41±64 m/s), decreased amplitude of the compound muscle action potentials, and absence of sensory sural nerve responses, a diagnosis of GBS was made.Two serum specimens (days 5 and 21) revealed positive IgM and a four-fold increase in IgG antibodies (ELISA Virotech, Germany, and ELISA Bio Whittaker, Walkersville, USA, respectively) to M. pneumoniae. M. pneumoniae antigen was directly detected by a monoclonal antibody ELISA (Pneumofast Ag, International Microbio. Signes, France), in a throat swab and aspirated respiratory secretions.Intravenous immunoglobulins were administered (0.4 g/kg per day for 5 days) with no clinical improvement. A 10-day oral clarythromycin (15 mg/kg per day) course followed, with rapid improvement 2 days after initiating therapy. Tendon re¯exes became normal on day 21.
Primary biliary cholangitis (PBC), formerly known as primary biliary cirrhosis, is present worldwide. Autoantibodies, in particular anti-mitochondrial antibodies (AMA) detected by indirect immunofluorescence assays or newer solid phase immunoassays can detect most, but not all individuals with PBC. Detection of antibodies to the anti-nuclear antigens sp100 and gp210 can identify additional PBC patients, but some seronegative patients remain, often resulting in delayed diagnosis and treatment. Antibodies to kelch-like 12 (KLHL12) and hexokinase 1 (HK-1) were recently identified as new biomarkers for PBC and notably identify patients who are negative for conventional autoantibodies. To become globally adopted, it is important to validate these new biomarkers in different geographic areas. In the present study we evaluated the prevalence of anti-KLHL12 (measured by a KLHL12-derived peptide referred to as KL-p) and anti-HK-1 antibodies by ELISA at five sites within Europe and North America and demonstrated the presence of these antibodies in patients with PBC in all geographies.
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