COVID-19 first emerged in Wuhan, China in late December 2019. The disease majorly involves the lungs leading to various respiratory complications; however, neurological manifestations of the disease are also described in the literature. Here, we report a case of COVID-19-induced seronegative myasthenia gravis (MG). We discuss the cases of COVID-19 and MG already described in the literature in regard to their presentation and serological findings to better understand the association between the two disease processes. MG may be missed in patients after COVID-19 infections because of the comorbidities and anti-acetylcholine receptor and anti-muscle-specific tyrosine kinase antibodies being negative. Evidence from more studies will help analyze the pathological timeline of the disease process and the immunological characteristics of COVID-19-induced MG which can prove to have morbidity and mortality benefit in patients with COVID-19-induced MG.

We reported a case of secondary hemophagocytic lymphohistiocytosis (HLH), a rare and life-threatening condition, which was suspected to have been triggered by a severe case of coronavirus disease 2019 . A 50-year-old man with a past medical history of ulcerative colitis with recent pancolitis status post colectomy and ileostomy two weeks before presentation presented to the emergency department with one week of subjective fevers, weakness, watery diarrhea, and decreased oral intake. A CT scan showed fluid in the rectum and post-surgical changes from his recent colectomy along with diffuse reticulonodular opacities of the lungs. His COVID-19 reverse transcriptase-polymerase chain reaction (RT-PCR) test was positive. Over the subsequent days, the patient's condition worsened as he developed worsening acute hypoxic respiratory failure with diffuse lymphadenopathy, splenomegaly, worsening cytopenias, and increased ferritin of >100,000 ng/ml on hospital day six. Hematology oncology was consulted and he was started on empiric steroid therapy followed by etoposide. However, his condition continued to worsen, and eventually, the patient passed away on hospital day eight.

Coagulase-negative staphylococci (CoNS) can uncommonly cause native valve endocarditis. We present a case of left-sided infective endocarditis of native valves presenting with splenic, lung, and brain infarcts along with aortic and significant mitral valve involvement with mitral valve perforation. The patient was also found to be in atrial flutter and atrial fibrillation. Left-sided endocarditis is reported to cause brain and spleen infarcts but pulmonary embolisms are usually a complication of right-sided endocarditis. Atrial fibrillation is also known to increase mortality in patients with infective endocarditis.