RARE CASE OF SERRATIA PNEUMONIA CAUSING TRANSIENT APLASTIC ANEMIA

Abstract

SESSION TITLE: Critical Care 1 SESSION TYPE: Med Student/Res Case Report PRESENTED ON: 10/09/2018 03:45 PM - 04:45 PM INTRODUCTION: Aplastic anemia (AA) is defined as two or three cell line cytopenias due to hematopoietic stem cell (HSC) dysfunction. Incidence is 2 cases/million people. Symptoms include fatigue, dyspnea, cardiac symptoms, bruising, mucosal bleeding and increased infection risk. The most common causes include PNH, drugs, toxins and viruses (parvovirus B19, EBV, CMV, hepatitis, HSV6 and dengue). Overall prognosis for AA is poor. CASE PRESENTATION: 71 year-old female with past medical history of hypertension and hypothyroidism presented with weakness and word slurring. Five days prior, she awoke with dizziness and difficulty swallowing, then developed vomiting and diarrhea. Travel in the past 3 months included Morocco, France and Chile. Patient denied sick contacts, chills, night sweats or weight loss; endorsed hematuria one month ago, which resolved after nitrofurantoin course. Initial vitals: BP 84/50, HR 127, RR 32, T 101.8F, SpO2 89% on 3LPM O2. She appeared toxic with bronchial breath sounds and abdominal tenderness. Initial labs: WBC 0.2K/uL, Hb 9.9g/dL, plt 4K/uL, reticulocytes 0.6%, ESR 124, INR 1.5, D-dimer 2.35 mg/L, lactic acid 1.5 mmol/L, troponin undetectable, and BNP 287 pg/mL. CXR showed right lower lobe hazy opacity with a small right pleural effusion. CT abdomen/pelvis showed ascites and hepatomegaly. CTA chest was negative for PE. The patient was intubated and given IV fluids, broad spectrum antibiotics and 2U platelets. Respiratory cultures grew Serratia (not speciated) and antibiotic treatment was narrowed to meropenem and vancomycin. Thrombocyto- and leukocytopenia persisted, requiring multiple transfusions. Serum rheumatology, infectious, vasculitis, SIFE/SPEP, G6PD deficiency, hepatitis and labs PNH studies were negative. Positive findings included high IgE, parvovirus/EBV IgG and ferritin 5544 ng/mL. Bone marrow (BM) biopsy showed hypocellular BM (0-15%) with rare megakaryocytes, scanty myeloid and erythroid precursors, and slight plasmacytosis. The patient was started on anti-thymocyte globulin and cyclosporine, and then switched to a thrombopoietin nonpeptide agonist, for severe AA. After 14 days of antibiotics and 10 days of AA treatment, the patient’s WBC and platelets increased then stabilized. DISCUSSION: The above case of Serratia as the cause of transient AA suggests that the infectious mechanism leading to BM failure was likely T-cell mediated. Most viruses, like parvovirus B19, directly destroy HSCs while other pathogens, like bacteria, cause AA secondary to excessive immune activation via T-cells. Thus, the transient nature of bacterial-induced AA likely occurs after treating the inciting pathogen, like in this case. CONCLUSIONS: Bacterial causes of transient AA are rare and the specific mechanisms of bacterial-induced, T-cell-mediated HSC injury are largely unknown. This case highlights Serratia as a likely cause of HSC dysfunction causing transient AA. Reference #1: Espinoza, J. L., Kotecha, R., & Nakao, S. (2017). Microbe-induced inflammatory signals triggering acquired bone marrow failure syndromes. Frontiers in Immunology, 8, 186. 10.3389/fimmu.2017.00186 [doi] Reference #2: Keisu, M., Heit, W., Lambertenghi-Deliliers, G., Parcells-Kelly, J., Polliack, A., & Heimpel, H. (1990). Transient pancytopenia. A report from the international agranulocytosis and aplastic study. Blut, 61(4), 240-244. Reference #3: Young, N. S. (2002). Acquired aplastic anemia. Annals of Internal Medicine, 136(7), 534-546. 200204020-00011 [pii] DISCLOSURES: No relevant relationships by Eric Bondarsky, source=Web Response No relevant relationships by Lindsay Hammons, source=Web Response