A 20-year-old Caucasian man with a history of psoriasis presented to the emergency department due to a 2-week history of severe polyarthralgia and a 3-week history of non-bloody diarrhoea. The initial workup 2 days prior in an urgent care clinic returned negative for all enteric pathogens including Clostridioides difficile nucleic acid amplification test. Investigations revealed colitis on CT and pseudomembranous colitis on colonoscopy. The aspirate returned positive for C. difficile toxin. Tissue biopsies of the ascending, transverse, sigmoid colon and rectum were negative for chronicity to suggest inflammatory bowel disease with extraintestinal manifestation as the aetiology of polyarthralgia, which had been the most likely differential diagnosis until that point. The biopsy confirmed the diagnosis of reactive arthritis in the setting of C. difficile colitis. The patient improved on treatment with naproxen and was referred to rheumatology where he was found to be HLA-B27 positive.

A 68-year-old man presented in late summer 2021 with fever, myalgias, generalized weakness, dizziness, and headache. Past medical history included rheumatoid arthritis treated with infliximab, congestive heart failure with preserved ejection fraction, and recent travel to Alaska. He was febrile, tachycardic, and tachypneic on admission. Physical exam and admission labs were overall unremarkable. On day 4, he complained of shortness of breath and central chest discomfort. Troponin was mildly elevated, electrocardiogram was unremarkable, and echocardiogram showed new global wall motion abnormalities and ejection fraction of 40%, which was 55% months prior. Serum West Nile IgM antibodies resulted positive near the end of hospitalization. Testing for SARS-CoV-2, influenza as well as multiple other viral, bacterial, and fungal organisms was negative. Overall, the patient recovered clinically including improvement in ejection fraction on echocardiogram with conservative management. West Nile virus (WNV) is associated with a myriad of symptoms and complications, most notably, neuroinvasive disease. However, cardiomyopathy secondary to WNV as illustrated in this case has been infrequently described. Clinicians should be aware of this potential rare complication in patients with WNV to improve rapid detection and treatment of myositis, associated cardiomyopathy, and related complications.

A 69-year-old female with a history of psoriatic arthritis was diagnosed with septic arthritis and started on broad-spectrum antibiotics. She underwent left hip excisional debridement of her prosthetic hip joint which grew group B Streptococcus ( S. agalactiae ). She was switched to IV ceftriaxone 2 g daily and her hemoglobin decreased to 5.4 g/dL on day 11. Peripheral blood smear showed normochromic normocytic anemia and thrombocytopenia without the presence of schistocytes. Increased lactate dehydrogenase (LDH), decreased haptoglobin and hemoglobin, and positive direct Coombs test (DCT) led to a presumptive diagnosis of drug-induced immune hemolytic anemia (DIIHA). As a result, she was switched from ceftriaxone to IV ertapenem 500 mg every 24 hours and oral prednisone 60 mg for four days during the initial phase. Her hemoglobin, LDH, and haptoglobin trended towards normal limits, further supporting the diagnosis of DIIHA secondary to ceftriaxone.

A 62-year-old woman with a history of end-stage renal disease on haemodialysis, essential hypertension and type 2 diabetes mellitus was diagnosed with sepsis and placed on 600 mg oral linezolid every 12 hours and 1 g intravenous ceftriaxone every 24 hours. Blood cultures grew Streptococcus dysgalactiae, and she was switched to intravenous ceftriaxone 2 g daily. Platelet counts slowly trended down after starting ceftriaxone reaching 5 K/μL on day 12 of treatment. Ceftriaxone was discontinued and heparin-induced thrombocytopaenia was ruled out. She was switched to vancomycin and her platelet count improved. Given the temporal relationship between changing platelet counts and starting and discontinuing ceftriaxone, a diagnosis of drug-induced thrombocytopaenia was made.