Using sterile nylon flocked swabs, we sampled the nasopharynx and pustules from each arm and also collected pustular roof tissue and serum, which were sent to the Public Health Ontario Laboratory. Roof tissue and pustule swabs were positive
Key points• Monkeypox is classically a zoonotic infection; its recent spread by person-to-person contact led to the declaration of a new monkeypox pandemic in June 2022.
Patients with cancer, especially those receiving anticancer therapy, are at risk amidst the coronavirus disease 2019 (COVID-19) pandemic. 1-3 Given the frequency of asymptomatic COVID-19, 2,4,5 and presymptomatic transmission, 5 symptombased screening may inadequately triage patients to safely resume anticancer therapy. 2,6 We thus implemented a pilot microbiologic screening program in Al Zahra Hospital in the United Arab Emirates (UAE), identifying presymptomatic COVID-19 in nearly 1 in 10 patients with cancer. 2 We have since expanded this program across serial anticancer therapy cycles.
BACKGROUND: Treatment of infective endocarditis secondary to Pseudomonas aeruginosa can be challenging because of this organism’s ability to acquire antimicrobial resistance over time. METHODS: We describe a patient with native aortic valve infective endocarditis due to P. aeruginosa who developed progressive multi-drug resistance while on therapy. The resistance mechanisms were characterized using whole-genome sequencing. RESULTS: We identified two mutations in subsequent isolates ( dacB and OprD) that conferred resistance to anti-pseudomonal penicillins, cephalosporins, and carbapenems. The patient was treated with combination high-dose continuous infusion meropenem and ciprofloxacin therapy, in addition to bioprosthetic aortic valve replacement and repair of ventricular septal wall defect. Antibiotics were continued for 6 weeks post–cardiac surgery and the patient remains infection free 18 months post-completion of antibiotic therapy. CONCLUSION: Clinicians should be aware of the ability of P. aeruginosa to acquire resistance mechanisms in response to selective antibiotic pressures in high-inoculum infections such as infective endocarditis. The mutations identified in this case report correlated well with the evolving antimicrobial resistance profile observed.
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