An uncommon culprit of neutropenic fever: a case of Sweet syndrome following induction therapy for acute myeloid leukemia.

Sweet syndrome (SS) is a rare inflammatory disorder characterized by the rapid onset of a characteristically tender rash, fever, and other systemic symptoms. These manifestations are often mistaken for an infection that is not responding to antimicrobials, especially in immunocompromised hosts. We present the case of a 44-year-old woman who developed SS following induction chemotherapy for newly diagnosed acute myeloid leukemia (AML). She exhibited a painful rash on the anterior chest, which spread centrifugally, along with neutropenic fever unresponsive to broad-spectrum antimicrobials. Biopsy of the rash revealed a dense neutrophilic infiltrate within the dermis, confirming the diagnosis of SS. The patient was subsequently treated with systemic steroids with prompt resolution of fevers and improvement of her rash. This case highlights that SS can manifest with a robust neutrophilic infiltrate, even in the context of neutropenia stemming from chemotherapy. SS serves as a crucial consideration in hematologic malignancies, particularly AML, when patients present with fever and cutaneous eruptions. Prompt recognition followed by systemic steroid therapy often leads to symptom resolution.

Catching the diagnosis: A peculiar presentation of Chiari malformation type I.

Chiari I malformation is a congenital anatomic anomaly of the cerebellar tonsils resulting in their downward displacement through the foramen magnum. While often incidentally discovered on imaging with no attributable symptoms, the most common symptomatic presentation is non-specific headache. Herein, we describe a case of symptomatic Chiari I malformation in a woman with psychiatric comorbidities manifesting as a sensation of brain catching. While a peculiar description easily misconstrued by her mental health history, clinicians should consider this diagnosis in those describing symptoms compatible with headaches or occiput pain related to meningeal irritation.

Rifaximin as a rare cause of rhabdomyolysis in cirrhosis.

Rifaximin has only been rarely reported to cause rhabdomyolysis. When physical and nonphysical etiologies have been excluded, thorough review of the patient's medication list is necessary. In cirrhotics, the potential harm of rifaximin in treatment or prophylaxis of hepatic encephalopathy should be recognized.

Facile Discovery of a Diverse Panel of Anti-Ebola Virus Antibodies by Immune Repertoire Mining.

The ongoing evolution of Ebolaviruses poses significant challenges to the development of immunodiagnostics for detecting emergent viral variants. There is a critical need for the discovery of monoclonal antibodies with distinct affinities and specificities for different Ebolaviruses. We developed an efficient technology for the rapid discovery of a plethora of antigen-specific monoclonal antibodies from immunized animals by mining the VH:VL paired antibody repertoire encoded by highly expanded B cells in the draining popliteal lymph node (PLN). This approach requires neither screening nor selection for antigen-binding. Specifically we show that mouse immunization with Ebola VLPs gives rise to a highly polarized antibody repertoire in CD138(+) antibody-secreting cells within the PLN. All highly expanded antibody clones (7/7 distinct clones/animal) were expressed recombinantly, and shown to recognize the VLPs used for immunization. Using this approach we obtained diverse panels of antibodies including: (i) antibodies with high affinity towards GP; (ii) antibodies which bound Ebola VLP Kissidougou-C15, the strain circulating in the recent West African outbreak; (iii) non-GP binding antibodies that recognize wild type Sudan or Bundibugyo viruses that have 39% and 37% sequence divergence from Ebola virus, respectively and (iv) antibodies to the Reston virus GP for which no antibodies have been reported.