To describe the microbiology and outcome of iliopsoas abscess (IPA) in a large case series, we analyzed 124 cases of IPA collected from 1990 through 2004 in 11 hospitals in Spain. Twenty-seven (21.8%) patients had primary and 97 (78.2%) had secondary IPA. The main sources of infection were bone (50.5%), gastrointestinal tract (24.7%), and urinary tract (17.5%). A definitive microbial diagnosis was achieved in 93 (75%) cases. Abscess culture was the most frequent procedure leading to microbial diagnosis, followed by blood cultures. Staphylococcus aureus, Escherichia coli, and Bacteroides species were the most frequent microbial causes: S. aureus was the most common organism in patients with primary abscesses (42.9%) and with abscesses of skeletal origin (35.2%), whereas E. coli was the leading organism in those with abscesses of urinary (61.5%) and gastrointestinal (42.1%) tracts. Mycobacterium tuberculosis was found in 15 patients, 4 of them associated with human immunodeficiency virus (HIV) infection. Twenty (21.5%) cases had polymicrobial infections; these were more common among patients with abscesses of gastrointestinal origin. Information on clinical outcome was available for 120 patients; 19 (15.8%) had a relapse and 6 (5%) died due to complications related to the IPA. Patients who died were older and more likely to have bacteremia and E. coli isolated from cultures. In conclusion, secondary IPA is more prevalent than primary IPA. Among those with secondary IPA, most abscesses are secondary to a skeletal source. A bacterial etiology can be identified in most cases. The overall prognosis of patients with this condition is good.

Objectives: Visceral leishmaniasis (VL) in HIV-positive patients is characterized by a chronic course with frequent relapse. The aim of this study was to evaluate the efficacy and safety of amphotericin B lipid complex (ABLC) in preventing VL relapses in HIV-infected patients. Methods: This was a multicentre, open-label (with blinded centralized randomization), parallel, no-treatment, controlled clinical trial. HIV-infected patients, with at least one previous treated episode of VL and with negative bone marrow aspirate for Leishmania parasites prior to the study, were randomized to receive either ABLC 3 mg/kg/day every 21 days (ABLC) or no treatment (NT). Patients were followed-up every 9 weeks for up to 12 months, and the efficacy was measured as the proportion of patients remaining free (non-relapse) of VL at 1 year of follow-up. The primary analysis was performed on an intention-to-treat basis. Results: One hundred and fifteen patients were screened, but only 17 were randomized: eight in the ABLC group and nine in the NT group. The intention-to-treat analysis of data showed 50% of patients remaining free of VL at 12 months of follow-up (95% CI = 15.7%, 84.3%) in the ABLC group, and 22.2% (95% CI = 2.8%, 60.0%) in the NT group. The non-relapse odds ratio was 3.5 (95% CI = 0.30%, 52.0%) favouring ABLC. ABLC was well tolerated: patients only presented infusion-related mild adverse events. No patients from either group discontinued treatment or died during follow-up. Conclusions: ABLC, administered every 21 days for 12 months, is useful as secondary prophylaxis in preventing VL relapse in HIV-infected patients, and is well tolerated.

Serum levels of potassium (K+) appear to be significantly lower in severe cases of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the clinical significance of this is unknown. The objective was to investigate whether hypokalemia acts as a biomarker of severity in coronavirus disease 2019 (COVID-19) pneumonia and is associated with major clinical outcomes. A retrospective cohort study of inpatients with COVID-19 pneumonia (March 3 to May 2, 2020) was performed. Patients were categorized according to nadir levels of K+ in the first 72 h of admission: hypokalemia (K+ ≤3.5 mmol/l) and normokalemia (K+ >3.5 mmol/l). The main outcomes were all-cause mortality and the need for invasive mechanical ventilation (IMV); these were analyzed by multiple logistic regression (odds ratio (OR), 95% confidence interval (CI)). Three hundred and six patients were enrolled. Ninety-four patients (30.7%) had hypokalemia and these patients showed significantly higher comorbidity (Charlson comorbidity index ≥3, 30.0% vs 16.3%; p = 0.02) and CURB65 scores (median (interquartile range): 1.5 (0.0–3.0) vs 1.0 (0.0–2.0); p = 0.04), as well as higher levels of some inflammatory parameters at baseline. After adjustment for confounders, hypokalemia was independently associated with requiring IMV during the admission (OR 8.98, 95% CI 2.54–31.74). Mortality was 15.0% (n = 46) and was not influenced by low K+. Hypokalemia was associated with longer hospital and ICU stays. Hypokalemia is prevalent in patients with COVID-19 pneumonia. Hypokalemia is an independent predictor of IMV requirement and seems to be a sensitive biomarker of severe progression of COVID-19.

Although the incidence of Clostridium difficile infection (CDI) is increasing, available CDI treatment options are limited in terms of sustained response after treatment. This phase 3 trial assessed the efficacy and safety of surotomycin, a novel bactericidal cyclic lipopeptide, versus oral vancomycin in subjects with CDI. In this randomized, double-blind, active-controlled, multicenter, international trial, subjects with CDI confirmed by a positive toxin result were randomized to receive surotomycin (250 mg twice daily) or vancomycin (125 mg 4 times daily) orally for 10 days. The primary endpoints were clinical response at end of treatment and evaluation of surotomycin safety. The key secondary endpoints were clinical response over time and sustained clinical response through a 30- to 40-day follow-up period. Clostridium difficile infection recurrence during follow-up and time to diarrhea resolution were also analyzed. In total, 570 subjects were randomized and had confirmed CDI; 290 subjects received surotomycin and 280 subjects received vancomycin. Surotomycin clinical cure rates at end of treatment (surotomycin/vancomycin: 79.0%/83.6%; difference of −4.6%; 95% confidence interval, −11.0 to 1.9]), clinical response over time (stratified log-rank test, P = .832), and sustained clinical response at end of trial (Day 40–50) (60.6%/61.4%; difference of −0.8%; 95% CI, −8.8 to 7.1) in the microbiological modified intent to treat population did not meet noninferiority or superiority criteria versus vancomycin. Both treatments were generally well tolerated. Surotomycin failed to meet the criteria for noninferiority versus vancomycin for the primary and key secondary endpoints in this trial.

Background: Decrease in HIV viral load (VL) is accompanied by decrease in microbial translocation (MT) and chronic inflammation, but the behavior of these markers in patients with HIV-VL <20 copies per milliliter is unknown. The aim of this study was to determine whether strict control of HIV-VL is associated with MT and chronic inflammation. Methods: Observational cross-sectional study. Inclusion criteria: HIV patients receiving antiretroviral therapy and HIV-VL <200 copies per milliliter for more than 6 months. Exclusion criteria: chronic liver disease, active infection, or antibiotic consumption. Recruitment: patients who consecutively visited the outpatient clinic in November 2011. Primary endpoint: molecular MT as determined by detection in plasma of 16S ribosomal DNA. Secondary variables: lipopolysaccharide, soluble CD14, tumor necrosis factor α, and interleukin 6. Primary explanatory variable: HIV-VL (COBAS AmpliPrep/COBAS TaqMan HIV-1 test, version 2.0) with a detection limit of 20 copies per milliliter. Results: Fifty-two patients were included: 65% men, median age 45 years, HIV acquired predominantly through sex (75%), 40% Centers for Disease Control and Prevention stage C, and median CD4 lymphocyte count 552 cells per cubic millimeter (range, 126–1640 cells/mm³). Molecular MT was observed in 46% and 18% of patients with low-level (20–200 copies/mL) and negative (<20 copies/mL) HIV-VL, respectively (P < 0.05). Plasma levels of inflammatory markers (tumor necrosis factor α and interleukin 6) were higher in patients with molecular MT (P < 0.01) and were not influenced for HIV-VL. Conclusions: Patients with HIV infection receiving treatment and negative HIV-VL (<20 copies/mL) present less frequently MT than patients with low-level HIV viremias (20–200 copies/mL). MT is associated with higher levels of inflammation markers, independent of HIV-VL.