INTRODUCTION: Myocarditis is an inflammation of the myocardium, which may be caused by a variety of infectious or noninfectious conditions. The most common etiology is due to a viral infection secondary to coxsackie B virus, adenovirus, hepatitis C, cytomegalovirus (CMV), or influenza virus. The presentation of myocarditis is highly variable, ranging from heart failure, acute coronary syndrome and even sudden cardiac death.

Cardiac tamponade constitutes a medical emergency, which requires prompt recognition, diagnosis and treatment that is geared towards preventing cardiovascular collapse and cardiac arrest.

INTRODUCTION: Hypereosinophilic Syndrome (HES) is a rare condition characterized by sustained eosinophil counts greater than 1.5x103/uL with pathologic confirmation of tissue hypereosinophilia (HE). It usually affects multiple organs in the absence of clonal or other secondary causes of eosinophilia. The most common organs affected are the lungs, skin, heart, gastrointestinal tract, and brain.CASE PRESENTATION: This is an 81-year-old male patient with history of alcohol abuse, hypertension, and atrial fibrillation, who presented with diffuse skin itching and burning sensation for three days after working with polyvinyl chloride (PVC) tubing material. He referred having associated generalized weakness, anorexia, and dry cough. Labs were remarkable for having eosinophilia of 17x10^3/uL, mild transaminitis (SGPT:54 U/L, SGOT:45 U/L), elevated high sensitive troponins of 41-43 without delta and worsening renal function with serum creatinine increasing from 0.9 to 1.9 mg/dL. Immunoglobulin E was found to be elevated in 774.8, however Strongyloides IgG antibody and Schistosoma antibody were negative, ruling out endemic parasite involvement. Chest CT scan without contrast revealed moderate centrilobular emphysema, mild areas of ground glass opacities and tree-in-bud opacities bilaterally, for which it was decided to undergo bronchoscopy examination to exclude other etiologies, including malignancy or pneumoconiosis. This procedure revealed no lesions or masses, with bronchoalveolar lavage reporting no malignant cells, as well as negative acid-fast bacilli or fungal organisms. To rule out myelodysplastic syndrome a bone marrow biopsy was performed revealing hypercellular marrow with 48 percent of eosinophils, however flow cytometry showed no clonal cells or blasts, as well as negative BCL/ABL and PDGFR alpha. These findings were consistent with Idiopathic Hypereosinophilic Syndrome, for which he was started on prednisone 40 mg PO daily.DISCUSSION: HE can be confirmed by bone marrow biopsy of more than 20 percent of eosinophils. Most of these patients tolerate and respond well to glucocorticoid therapy, however in refractory cases the tyrosine kinase inhibitor imatinib has shown to improve the patient's outcome. CONCLUSIONS:It is essential to rule out secondary causes of hypereosinophilia, which may be seen in parasitic infections, pneumoconiosis, or malignancy, to prevent delay in diagnosis and prompt adequate therapy.

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INTRODUCTION: Myelodysplastic syndrome (MDS) refers to an heterogenous group of clonal hematopoietic disorders, characterized by peripheral blood cytopenia. This disorder may present with clinical manifestations of anemia, thrombocytopenia or neutropenia, including symptomatic anemia, progression to acute myeloid leukemia or infections. Patients with MDS and severe neutropenia are at high risk for bacterial infections, however infections may rarely occur secondary to fungal invasion.CASE PRESENTATION: This is a 71-year-old female with history of hypertension, hyperlipidemia, coronary artery disease and MDS with positive RAEB2 and p53, treated with decitabine. She was initially admitted with diagnosis of symptomatic anemia, after developing general malaise, with associated shortness of breath and lightheadedness 2 days prior. Denied fever, cough, chest pain, abdominal pain, hematemesis, hematochezia, melena, insect bites or recent travel. Vital signs showed temperature of 37 C, heart rate in 109 bpm and blood pressure of 115/70 mmHg. Initial physical exam was remarkable for conjunctival pallor. Laboratories revealed leukocytopenia of 0.7 x10^3/uL, anemia of 6.1 g/dL, thrombocytopenia in 95 x10^3/ uL and absolute neutrophil count in 0 cells/uL. Chest x-ray revealed no acute cardiopulmonary pathologies. She underwent transfusion of 2 units of PRBCs, after which hemoglobin levels reached 8.2 g/dL. Nevertheless, on the third day, she developed fever of 39.4C and nonproductive cough, for which ongoing diagnosis of neutropenic fever was considered. Cultures were taken and was started on cefepime. Upon examination, she had decreased breath sounds and developed 1.5cm circular violaceous lesion on the left cheek, circular violaceous lesion on the hard palate, as well as, multiple 0.5cm circular violaceous lesions on the left lower extremity and abdomen. Chest CT scan exhibited bilateral upper consolidations, raising concern for possible disseminated Fusarium fungal infection, for which amphotericin B was started. Biopsies of the lower extremity's lesion, revealed cutaneous hemorrhage, however biopsy of the hard palate's lesion revealed aspergillus spp. These findings were consistent with invasive aspergillosis.DISCUSSION: Invasive aspergillosis refers to illness caused by pulmonary or extrapulmonary dissemination of Aspergillus spp. This condition is uncommon and occurs primarily in immunocompromised patients associated with therapy for hematologic malignancies, hematopoietic cell transplant or solid organ transplantation. Management should focus on prevention, prompt diagnosis, as well as early initiation of antifungal therapy. Surgery is reserved for severe cases.CONCLUSIONS: Tissue invasion is an unusual presentation of invasive aspergillosis, however its appearance in an immunocompromised individual should raise suspicion of fungal dissemination and further evaluation should be pursued.