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Background Many patients with axial spondylarthritis (axSpA) experience lengthy diagnostic delays upwards of 14 years. (5–14 years). Screening tools for axSpA have been proposed for use in primary care settings, but whether this approach could be implemented into busy primary care settings remains unknown. Objective To solicit feedback from primary care physicians regarding questions from the Inflammatory Back Pain Assessment: the Assessment of Spondyloarthritis International Society (ASAS) Expert Criteria and gain insight about barriers and facilitators for implementing axSpA screening in primary care. Methods Guided by Consolidated Criteria for reporting Qualitative Research (COREQ-criteria), we recorded, transcribed, and analyzed in-depth interviews with eight family medicine physicians and ten internists (purposeful sampling) using immersion/crystallization techniques. Results Few physicians reported awareness of existing classification criteria for axSpA, and many reported a lack of confidence in their ability to distinguish between inflammatory and mechanical back pain. From three domains, 10 subthemes emerged: 1) typical work-up of axSpA patients in primary care, with subthemes including the clues involved in work-up and role of clinical examinations for axSpA; 2) feedback on questions from the Inflammatory Back Pain Assessment: ASAS Expert Criteria, with subthemes to evaluate contents/questions of a potential screening tool for axSpA; and 3) implementation of the screening tool in primary care settings, with subthemes of perceived barriers including awareness, time, other conditions to screen, rare disease, and lack of structured questionnaire for back pain and perceived facilitators including workflow issues and awareness. Conclusions Primary care physicians believed that an improved screening instrument and a strong evidence-base to support the need for screening for axSpA are required. The implementation of axSpA screening into a busy primary care practice requires integration into the practice workflow, with use of technology suggested as a possible way to improve efficiency.

Complicated parapneumonic effusions and empyema are a leading cause of morbidity in the United States with over 1 million admissions annually and a mortality rate that remains high in spite of recent advances in diagnosis and treatment. The identification of high risk patients is crucial for improved management and the provision of cost-effective care. The RAPID score is a scoring system comprised of the following variables: renal function, age, purulence, infection source, and dietary factors and has been shown to predict outcomes in patients with pleural space infections. In a single center retrospective study, we evaluated 98 patients with complicated parapneumonic effusions and empyema who had tube thoracostomy (with or without Intrapleural fibrinolytic therapy) and assessed treatment success rates, mortality, length of hospital stay, and direct hospitalization costs stratified by three RAPID score categories: low-risk (0–2), medium risk (3–4), and high-risk (5–7) groups. Treatment success rate was 71%, and the 90 day mortality rate was 12%. There was a positive-graded association between the low, medium and high RAPID score categories and mortality, (5.3%, 8.3% and 22.6%, respectively), length of hospital stay (10, 21, 19 days, respectively), and direct hospitalization costs ($19,909, $36,317 and $43,384, respectively). Our findings suggest that the RAPID score is a robust tool which could be used to identify patients with complicated parapneumonic effusions and empyema who may be at an increased risk of mortality, prolonged hospitalization, and who may incur a higher cost of treatment. Randomized controlled trials identifying the most effective initial treatment modality for medium- and high-risk patients are needed.

Viral myocarditis is a leading cause of death in the United States, contributing to numerous unexplained deaths in people ≤35 years old. Enteroviruses contribute to many cases of human myocarditis. Encephalomyocarditis virus (EMCV) infection causes viral myocarditis in rodent models, but its receptor requirements have not been fully identified. CRISPR-Cas9 screens can identify host dependency factors essential for EMCV infection and enhance our understanding of key events that follow viral infection, potentially leading to new strategies for preventing viral myocarditis. Using a CRISPR-Cas9 screen, we identified a disintegrin and metalloproteinase 9 domain (ADAM9) as a major factor required for the early stages of EMCV infection in both human and murine infection., Encephalomyocarditis virus (EMCV) is a picornavirus that produces lytic infections in murine and human cells. Employing a genome-wide CRISPR-Cas9 knockout screen to find host factors required for EMCV infection, we identified a role for ADAM9 in EMCV infection. CRISPR-mediated deletion of ADAM9 in multiple human cell lines rendered the cells highly resistant to EMCV infection and cell death. Primary fibroblasts from ADAM9 KO mice were also strongly resistant to EMCV infection and cell death. In contrast, ADAM9 KO and WT cells were equally susceptible to infection with other viruses, including the picornavirus Coxsackie virus B. ADAM9 KO cells failed to produce viral progeny when incubated with EMCV. However, bypassing EMCV entry into cells through delivery of viral RNA directly to the cytosol yielded infectious EMCV virions from ADAM9 KO cells, suggesting that ADAM9 is not required for EMCV replication post-entry. These findings establish that ADAM9 is required for the early stage of EMCV infection, likely for virus entry or viral genome delivery to the cytosol.

Encephalomyocarditis virus (EMCV) is a picornavirus that produces lytic infections in murine and human cells. Employing a genome-wide CRISPR-Cas9 knockout screen to find host factors required for EMCV infection, we identified a role for ADAM9 in EMCV infection. CRISPR-mediated deletion of ADAM9 in multiple human cell lines rendered the cells highly resistant to EMCV infection and cell death. Primary fibroblasts from ADAM9 KO mice were also strongly resistant to EMCV infection and cell death. In contrast, ADAM9 KO and WT cells were equally susceptible to infection with other viruses, including the picornavirus Coxsackie virus B. ADAM9 KO cells failed to produce viral progeny when incubated with EMCV. However, bypassing EMCV entry into cells through delivery of viral RNA directly to the cytosol yielded infectious EMCV virions from ADAM9 KO cells, suggesting that ADAM9 is not required for EMCV replication post-entry. These findings establish that ADAM9 is required for the early stage of EMCV infection, likely for virus entry or viral genome delivery to the cytosol.