We present a case of disseminated Nocardia otitidiscaviarum infection in a 72-year-old male with a history of renal transplantation on chronic immunosuppressive therapy with prednisone, cyclosporine, and mycophenolate mofetil. He presented with pneumonia and was initially treated with ceftriaxone and azithromycin. Bronchoalveolar lavage (BAL) and cultures from a biopsied thigh lesion both grew N. otitidiscaviarum. His hospital course was complicated by visual hallucinations, and brain magnetic resonance imaging (MRI) revealed multiple intracranial abscesses. He initially received meropenem, trimethoprim-sulfamethoxazole (TMP-SMX), and linezolid. His antimicrobial regimen was subsequently modified during the treatment course. Linezolid was discontinued after hematologic abnormalities developed, TMP-SMX was temporarily held because of worsening renal function and later reintroduced, and meropenem was also discontinued. He was discharged on TMP-SMX and minocycline and completed an initial six-week antimicrobial treatment course from the time of diagnosis. He was subsequently maintained on minocycline and moxifloxacin; moxifloxacin was later discontinued because of QT-interval prolongation, while minocycline was continued for slightly longer than one year, with clinical and radiologic resolution.

A 54 year old male was seen for abdominal discomfort and was subsequently diagnosed with a Grade 3 primary liver neuroendocrine tumor replacing the left lobe.

Purpureocillium lilacinum (formerly Paecilomyces lilacinus) is an environmental saprophytic mold and an increasingly recognized opportunistic pathogen in immunocompromised hosts, most often causing cutaneous, ocular, or sinopulmonary disease; bloodstream infection (fungemia) is rare. The initial microscopic morphology on Gram stain of a positive blood culture can simulate yeast, delaying correct identification and appropriate antifungal therapy. We describe a 67-year-old man with relapsed multiple myeloma and therapy-related mixed-phenotype acute leukemia, further complicated by a prior Mycobacterium abscessus vertebral epidural abscess, who was admitted with neutropenic fever, hypoxic Burkholderia cenocepacia pneumonia, and multiorgan dysfunction. Blood culture demonstrated a yeast-like organism that could not be identified as any common Candida species by rapid multiplex polymerase chain reaction (PCR). The patient was later found to have port-associated Paecilomyces/Purpureocillium fungemia, with only one day of documented fungemia. The port was removed, and repeat blood cultures were negative. The isolate was submitted to a reference mycology laboratory and was identified as P. lilacinum approximately two weeks after the index blood culture. Susceptibility testing reported resistance to amphotericin B and a high minimum inhibitory concentration (MIC) to itraconazole, with lower MICs to posaconazole and voriconazole. He received posaconazole and liposomal amphotericin B briefly, followed by voriconazole, with clinical improvement and no recurrent fungemia. This case illustrates a clinically important diagnostic pitfall: rare filamentous molds such as P. lilacinum can mimic yeast morphologically and evade rapid yeast-identification panels, leading to delayed diagnosis in critically ill, heavily immunosuppressed patients. Early involvement of a reference mycology laboratory with molecular sequencing capabilities, when phenotypic identification is inconclusive, is warranted. The possibility of an amphotericin B-resistant mold simulating “yeast” fungemia should be considered in high-risk hematology-oncology patients.

Direct oral anticoagulants (DOACs) are the standard first treatment for patients with venous thromboembolism. Unfortunately, some patients develop recurrent thromboembolism despite adherence to anticoagulation. This remains a significant clinical challenge with no randomized data to guide therapy. This review summarizes the available evidence for the management of recurrent venous thromboembolism (VTE) and DOAC failure, and we propose our group consensus and management algorithm.

Purulent pericarditis due to Escherichia coli is rare, typically occurring in immunocompromised hosts. We report a patient with acute myeloid leukemia presenting with recurrent E. coli bacteremia complicated by purulent pericarditis, with concurrent pericardial myeloid sarcoma and ecthyma gangrenosum-like cutaneous lesion. Microbiologic concordance of E. coli isolates from blood, pericardial fluid, and the skin lesion suggested hematogenous dissemination from a single source. The patient underwent surgical pericardial drainage and received intravenous antimicrobial therapy, resulting in microbiologic clearance and initial clinical improvement. However, the patient died five days after discharge in the setting of persistent profound neutropenia. This case illustrates that in patients with refractory hematologic malignancy and prolonged neutropenia, infection may persist or recur despite adequate source control and antimicrobial therapy, as durable control ultimately depends on recovery of host immune function. The case also highlights diagnostic challenges in pericardial disease, including discordance between cytologic analysis of pericardial fluid and histopathologic findings, and emphasizes the necessity of tissue biopsy in patients with acute myeloid leukemia presenting with pericardial effusion.