Inpatients with culture-positive diabetic foot infections are at elevated risk for subsequent invasive infection with the same causative organism. In outpatients with index diabetic foot ulcers, we found that wound culture positivity was independently associated with increased odds of 1-year admission for systemic infection when compared with culture-negative wounds.

OBJECTIVE: Rapid and reliable exclusion of invasive fungal infections (IFI) by markers able to avoid unnecessary empirical antifungal treatment is still a critical unmet clinical need. We investigated the diagnostic performance of a newly available β-d-Glucan (BDG) quantification assay, focusing on the optimisation of the BDG cut-off values for IFI exclusion.
METHODS: BDG results by Wako β-glucan assay (lower limit of detection [LLOD] = 2.16 pg/mL, positivity ≥ 11 pg/mL) on two consecutive serum samples were retrospectively analysed in 170 patients, admitted to haematological wards (N = 42), intensive care units (ICUs; N = 80), or other wards (N = 48), exhibiting clinical signs and/or symptoms suspected for IFI. Only patients with proven IFI (EORTC/MSG criteria) were considered as true positives in the assessment of BDG sensitivity, specificity and predictive values.
RESULTS: Patients were diagnosed with no IFI (69.4%), proven IFI (25.3%) or probable IFI (5.3%). Two consecutive BDG values < LLOD performed within a median of 1 (interquartile range: 1-3) day were able to exclude a proven IFI with 100% sensitivity and negative predictive value (primary study goal). Test\'s specificity improved by using two distinct positivity and negativity cut-offs (7.7 pg/mL and LLOD, respectively), but remained suboptimal in ICU patients (50%), as compared to haematological or other patients (93% and 90%, respectively).
CONCLUSIONS: The classification of Wako\'s results as negative when < LLOD, and positive when > 7.7 pg/mL, could be a promising diagnostic approach to confidently rule out an IFI in both ICU and non-ICU patients. The poor specificity in the ICU setting remains a concern, due to the difficulty to interpret positive results in this fragile population.

To determine if ending the practice of administering prophylactic antibiotics prior to the placement of totally implantable venous access devices (TIVADs) is correlated with an increase in 30-day bloodstream infection-related TIVADs removals.
The practice of administering prophylactic antibiotics prior to the placement of TIVADs ended in July 2013 at our institution. We compiled a list of patients who had TIVADs placed between July 2010 and July 2016 and cross-referenced this list to a list of patients who had TIVADs removed between July 2010 and August 2016 to evaluate the 30-day bloodstream infection-related TIVAD removals. Retrospective chart review of all patients was performed to collect demographic information, indication for placement, and type of antibiotic administered, if applicable.
Over the study period of 6 years, a total of 1,513 TIVADs were placed, of which 28 cases were excluded because of death within 30 days unrelated to TIVAD placement. Of the remaining 1,485 cases, 733 TIVADs were placed in 709 unique patients with prophylactic antibiotic treatment and 752 TIVADs were placed in 709 unique patients without treatment. A total of 8 patients were identified to have TIVADs removed within 30 days owing to infection, of which 4 patients were treated with prophylactic antibiotics. The odds of infection-related removals without prophylactic treatment compared with prophylactic treatment was 0.97 (95% confidence interval, 0.24-3.91; P = .97).
Ending the practice of administrating systemic antibiotic prophylaxis prior to the placement of TIVADs had no effect on the 30-day bloodstream infection-related TIVAD removals rate at our institution. We do not recommend the use of prophylactic antibiotics for the placement of TIVAD.

From flies to humans, many components of the innate immune system have been conserved during metazoan evolution. This foundational observation has allowed us to develop Drosophila melanogaster, the fruit fly, into a powerful model to study innate immunity in animals. Thanks to an ever-growing arsenal of genetic tools, an easily manipulated genome, and its winning disposition, Drosophila is now employed to study not only basic molecular mechanisms of pathogen recognition and immune signaling, but also the nature of physiological responses activated in the host by microbial challenge and how dysregulation of these processes contributes to disease. Here, we present a collection of methods and protocols to challenge the fly with an assortment of microbes, both systemically and orally, and assess its humoral, cellular, and epithelial response to infection. Our review covers techniques for measuring the reaction to microbial infection both qualitatively and quantitatively. Specifically, we describe survival, bacterial load, BLUD (a measure of disease tolerance), phagocytosis, melanization, clotting, and ROS production assays, as well as efficient protocols to collect hemolymph and measure immune gene expression. We also offer an updated catalog of online resources and a collection of popular reporter lines and mutants to facilitate research efforts. This article is categorized under: Technologies > Analysis of Cell, Tissue, and Animal Phenotypes.

Malassezia pachydermatis is a yeast that is commonly found in the skin of most animals. Changes in the physical, chemical or immunological processes of the skin may render the host more susceptible to the yeast, which then may cause otitis, dermatitis or, less often, systemic infection. We tested the pathogenicity of M. pachydermatis in wild-type (WT) and Toll-deficient Drosophila melanogaster. Flies were inoculated in the thorax with a needle previously dipped in inoculum concentrations ranging from 103 and 107 yeast cells/mL. After infection, flies were housed at 29 °C and mortality was evaluated daily until day seven. WT flies were resistant to the infection, whereas Toll-deficient flies showed inoculum-dependent mortality rates. Fungal burden, assessed by histopathological analysis and by counting the number of colony-forming units of dead flies, corroborated the results. The D. melanogaster model is a promising minihost model for future large-scale studies of virulence mechanisms and antifungal drug activity in malasseziosis.