#SoMe the Money! Value, Strategy, and Implementation of Social Media Engagement for Infectious Diseases Trainees, Clinicians, and Divisions.

Social media platforms have revolutionized how we consume information, along with how to effectively present communication, education, and advocacy efforts. There is profound value in leveraging social media within these aspects for the field of infectious diseases, for divisions and individual clinicians. Herein, we provide the rationale to incorporate social media as a key competency for infectious diseases training and specific guidance on aspects of education and strategic development of new accounts critical for success.

Educational Impact of #IDJClub, a Twitter-Based Infectious Diseases Journal Club.

BACKGROUND: Journal clubs have been an enduring mainstay of medical education, and hosting these on social media platforms can expand accessibility and engagement. We describe the creation and impact of #IDJClub, an infectious diseases (ID) Twitter journal club. METHODS: We launched #IDJClub in October 2019. Using the account @IDJClub, an ID physician leads a 1-hour open-access Twitter discussion of a recent publication. All participants use the hashtag #IDJClub. Sessions started monthly, but increased due to demand during the coronavirus disease 2019 (COVID-19) pandemic. We used Symplur 's Healthcare Hashtag project to track engagement of #IDJClub per 60-minute discussion plus the following 30 minutes to capture ongoing conversations. We also conducted an online anonymous survey using Likert scales and open-ended questions to assess educational impact. RESULTS: In its first 20 months, 31 journal clubs were held, with medians of 42 (interquartile range [IQR], 28.5-60) participants and 312 (IQR, 205-427.5) tweets per session. 134 participants completed the survey, of whom 39% were ID physicians, 19% pharmacists, 13% ID fellows, and 10% medical residents. Most agreed or strongly agreed that #IDJClub provided clinically useful knowledge (95%), increased personal confidence in independent literature appraisal (72%), and was more educational than traditional journal clubs (72%). The format addressed several barriers to traditional journal club participation such as lack of access, subject experts, and time. CONCLUSIONS: #IDJClub is an effective virtual journal club, providing an engaging, open-access tool for critical literature appraisal that overcomes several barriers to traditional journal club participations while fostering connectedness within the global ID community.

A 26-Year-old Woman With Dysuria and Hematuria.

In this case, we present imaging findings characteristic of chronic genitourinary schistosomiasis. Schistosoma haematobium, a blood fluke endemic to Africa and the Middle East, is a prominent cause of hematuria and bladder cancer in regions lacking adequate water sanitation. Luminal calcifications of the genitourinary tract, that is, of the bladder and/or ureters, from deposition of fluke eggs are a classic sign of chronic S. haematobium infection and should raise suspicion for the disease even when urine or serological tests are negative. It is important to recognize these findings on CT or, in resource-limited settings, plain film to allow for prompt, effective treatment.

Chronic Osteomyelitis Caused by Haemophilus parainfluenzae: A Case Report.

CASE: A 14-year-old boy presented with a pathologic fracture of the distal aspect of the tibia and a remote history of a dog bite near the injury site. Imaging studies, biopsy, and presentation corroborated the diagnosis of chronic osteomyelitis. Multiple diagnostic methods were negative until an open biopsy identified Haemophilus parainfluenzae, a fastidious oropharyngeal bacterium, with polymerase chain reaction analysis. The patient underwent extensive debridement, placement of external fixation, and a year-long antibiotic therapy regimen. He subsequently required a tibial-fibular osteotomy at a second site with placement of an intramedullary nail for correction of a leg-length discrepancy. CONCLUSION: This case report illustrates the complex management of chronic osteomyelitis in pediatric patients, its sequelae, and the importance of considering treatment of atypical pathogens.

Multidrug Resistant Pseudomonas aeruginosa Causing Prosthetic Valve Endocarditis: A Genetic-Based Chronicle of Evolving Antibiotic Resistance.

Background. Successful treatment of infections caused by multidrug-resistant (MDR) Pseudomonas aeruginosa is thwarted by the emergence of antibiotic resistance and biofilm formation on prosthetic devices. Our aims were to decipher the molecular basis of resistance in a unique case of prosthetic valve endocarditis (PVE) caused by MDR P. aeruginosa. Methods. Five sequential MDR P. aeruginosa blood isolates collected during a 7-month period were recovered from a patient suffering from PVE previously exposed to ß-lactam antibiotics. Minimum inhibitory concentrations (MICs) of several classes of antibiotics were used to indicate clinical resistance characteristics; relatedness of the isolates was determined using multilocus sequence typing and repetitive sequence-based polymerase chain reaction. Amplification and sequencing of regulatory and resistance genes was performed. Results. All isolates belonged to ST 298, possessed blaPDC-16, and were resistant to fluoroquinolones and carbapenems. In the course of therapy, we observed a >2-fold increase in cephalosporin resistance (4 µg/mL to >16 µg/mL). Sequencing of the AmpC regulator, ampR, revealed a D135N point mutation in cephalosporin-resistant isolates. Common carbapenemase genes were not identified. All isolates demonstrated a premature stop codon at amino acid 79 of the outer membrane protein OprD and mutations in the quinolone resistance-determining regions of gyrA and parC. Point mutations in nalC, an efflux pump regulator, were also observed. Conclusions. In this analysis, we chart the molecular evolution of ß-lactam resistance in a case of PVE. We show that mutations in regulatory genes controlling efflux and cephalosporinase production contributed to the MDR phenotype.