AIM: To identify and critically appraise existing clinical prediction models of extended-spectrum β-lactamase-producing Enterobacteriaceae (ESBL-EKP) infection or colonization.
METHODS: Electronic databases, reference lists, and citations were searched from inception to April 2018. Papers were included in any language describing the development or validation, or both, of models and scores to predict the risk of ESBL-EKP infection or colonization.
FINDINGS: In all, 1795 references were screened, of which four articles were included in the review. The included studies were carried out in different geographical locations with differing study designs, and inclusion and exclusion criteria. Most if not all studies lacked external validation and blinding of reviewers during the evaluation of the predictor variables and outcome. All studies excluded missing data and most studies did not report the number of patients excluded due to missing data. Fifteen predictors of infection or colonization with ESBL-EKP were identified. Commonly included predictors were previous antibiotic use, previous hospitalization, transfer from another healthcare facility, and previous procedures (urinary catheterization and invasive procedures).
CONCLUSION: Due to limitations and variations in the study design, clinicians would have to take these differences into consideration when deciding on how to use these models in clinical practice. Due to lack of external validation, the generalizability of these models remains a question. Therefore, further external validation in local settings is needed to confirm the usefulness of these models in supporting decision-making.
METHOD: An electrical cell-substrate impedance-sensing tool was utilized to study the real-time cell-cell barrier or morphological changes in response to the virus infection.
RESULTS: Herpes simplex virus, regardless of type (i.e., 1 or 2), reduced the cell-cell barrier resistance almost immediately after virus addition to endothelial cells, with negligible involvement of cell-matrix adhesion changes. There is no exclusivity in the infection ability of endothelial cells. From 30 h after HSV infection, there was an increase in cell membrane capacitance with a subsequent loss of cell-matrix adhesion capability, indicating a viability loss of the infected endothelial cells.
CONCLUSION: This study shows for the first time that destruction of human brain micro-vascular endothelial cells as an in vitro model of the blood-brain barrier could be an alternative invasion mechanism during herpes simplex virus infection.
CASE PRESENTATION: A 14-year-old Chinese Malaysian boy presented with a history of recurrent pneumonia, poor growth and steatorrhoea since childhood, and was diagnosed with CF. B. pseudomallei was cultured from his sputum during three different admissions between 2013 and 2016. However, the patient succumbed to end stage of respiratory failure in 2017 despite antibiotics treatment against B.pseudomallei. The isolates were compared using multilocus-sequence typing and repetitive-element polymerase chain reaction (PCR), and confirmed that two of the isolates were of same sequence type, which may indicate relapse.
CONCLUSIONS: CF patients should be aware of melioidosis in endemic regions, as it is an emerging infectious disease, especially when persistent or recurrent respiratory symptoms and signs of infection occur. The high prevalence rates of melioidosis in Malaysia warrants better management options to improve quality of life, and life expectancy in patients with CF. Travel activities to endemic regions should also be given more consideration, as this would be crucial to identify and initiate appropriate empiric treatment.