While traditionally an infection of the endocardial surface of heart valves, infective endocarditis (IE), can atypically present as infection of cardiac implantable electronic devices (CIED), including permanent pacemakers (PPM) or automatic implantable cardioverter-defibrillators (AICD). CIED endocarditis, similar to valvular IE, is generally caused by Gram-positive organisms such as Staphylococcus spp., most frequently S. Auerus, but is rarely caused by gram-negative bacteria, both HACEK and non-HACEK species. We present the case of Enterobacter cloacae CIED endocarditis. We also present a scoping study of previous case reports and case series highlighting the risk factors, surgical interventions, and mortality outcomes associated with E. Cloacae endocarditis. We also discuss the current guidelines and recommendations on antibiotic therapies for non-HACEK Gram-negative endocarditis and surgical management of infected CIED extraction and replacement.

Cytopenias in systemic lupus erythematosus (SLE) require clinical and laboratory workup and bone marrow (BM) examination to determine the cause and for appropriate patient management. Common causes include an increase in SLE activity, immunemediated hemolysis, iron deficiency, antiphospholipid antibody syndrome, infection, or the effect of medications. We retrospectively evaluated the clinical and laboratory findings of patients with SLE and cytopenias who had undergone BM studies to determine the indicators of malignancy.We retrospectively reviewed medical records of patients with SLE who presented with cytopenias for their disease course, medications, laboratory parameters and documented the spectrum of morphological changes in BM including CD34 expression.Twenty patients with SLE had undergone BM biopsy for evaluation of cytopenias. 14/20 (70%) of the patients had reactive BM, and the rest had hematologic malignancies involving the BM. Of these 14 patients, 8 had hypocellular marrow with loss of precursor cells (low CD34), 4 had left shift in myeloid lineage, 3 had serous atrophy, and 1had multilineage dysplasia. The 6 patients with hematologic malignancies included 2 with diffuse large B cell lymphoma, and one each of natural killer/T cell lymphoma, post-transplant lymphoproliferative disorder, Hodgkin lymphoma, and myelodysplastic syndrome evolving to acute myelogenous leukemia. The presence of autoantibodies, SLE activity, and lupus nephritis were comparable in patients with and without neoplasia. However, the duration of the use of multiple immunosuppressants, years since renal transplant (22 vs 10), multiple transplants, and the presence of other autoimmune diseases were greater in those with neoplasia. Two of the 14 patients with non-neoplastic BM and 1 with the neoplastic BM had nonhematological malignancy.Clinical and laboratory findings, the number of transplants, and the use of immunosuppressive agents can guide physicians to identify patients with a higher risk of developing hematologic malignancy. BM findings of cytopenia in SLE are often due to increased disease activity causing global cell death and dysmaturation. SLE patients presenting with cytopenias, with a history of long-term exposure to immunosuppressive drugs, should be regularly screened for hematologic and nonhematologic malignancies.Abbreviations: anti-dsDNA = anti-double stranded DNA, aPL = anti-phospholipid antibodies, AZA = azathioprine, BM = bone marrow, Hgb = hemoglobin, MDS = myelodysplastic syndrome, MTX = methotrexate, NHL = non-Hodgkin lymphoma, SLE = systemic lupus erythematosus.

Vitamin B12 deficiency is a cause of reversible dementia that must be ruled out in the evaluation of neurocognitive decline. We present a case of neurocognitive decline secondary to B12 deficiency where the workup was obscured by multiple competing diagnoses and treatment with empiric B12 supplementation reversed symptoms. Although the pretest probability was low, the morbidity from undiagnosed B12 deficiency is high, warranting a trial of B12 supplementation that resolved the patient’s symptoms.