Pica (Allotriophagy): An Underestimated Risk Factor for Severe Leptospirosis (Weil’s Diseases)? Report of a Leptospira Septic Shock Successfully Managed with ECMO

Leptospirosis is a zoonosis caused by infection with pathogenic strains of the bacterium Leptospira. The disease can be complicated by pulmonary hemorrhages and acute respiratory distress syndrome, with the mortality rate increasing to 51–100%. We report the case of a 37-year-old man who was admitted to the emergency department with a 6-day history of fever, weakness, vomiting and diarrhea, followed by jaundice. On admission, he presented leukocytosis, thrombocytopenia and acute liver and kidney injuries. His clinical course was critical, as it was immediately complicated by sepsis and severe respiratory failure, requiring haemodialysis, mechanical ventilation and broad-spectrum antibiotic therapy. In the following days, a veno-venous extracorporeal membrane oxygenation (VV-ECMO) was started due to a dramatic deterioration in respiratory function; 20 h later, it was switched to veno-arterial ECMO because of refractory cardiogenic shock. Hantavirus or Leptospira infection etiology was suspected, so penicillin G and methylprednisolone were initiated as an empirical therapy and subsequently confirmed after a laboratory diagnosis of leptospirosis. Although the clinical course was further complicated by hemorrhagic pneumonia, a gradual, full recovery occurred, and the patient was discharged from the hospital. After excluding other sources of contact with Leptospira-infected material, an unsuspected abnormal eating behavior was identified as the most probable cause of the patient’s Leptospira infection.

2432 The relationship between cognitive functioning and abnormal eating behavior in behavioral variant frontotemporal dementia

OBJECTIVES/SPECIFIC AIMS: Abnormal eating behavior is a core and distinguishing diagnostic feature of behavioral variant frontotemporal dementia (bvFTD) that differentiates it from other neurodegenerative disorders and late-life psychiatric conditions. Though it has been proposed that hyperphagia in bvFTD results from cognitive dysfunction, the observation of altered sweet preferences and food foraging indicate that bvFTD is accompanied by fundamental dietary changes associated with hypothalamic and insular atrophy. In the current study, we examined how cognitive dysfunction contributes to abnormal feeding behavior in bvFTD. METHODS/STUDY POPULATION: We analyzed first-visit eating and neuropsychological data from the National Alzheimer’s Coordinating Center database (7 centers; September 2017 data freeze) in a subset of bvFTD patients with clinician-rated characterization of disturbed feeding severity. Group differences in cognitive domains of attention, processing speed, language, memory, and executive functioning were examined between patients with abnormal eating behavior (n=59) and a demographically-matched sample of patients with normal feeding behavior (n=60). Group differences in informant-reported empathy, behavioral inhibition, and depressive symptoms were also examined. RESULTS/ANTICIPATED RESULTS: Cognitive profiles in bvFTD patients did not vary as a function of disturbed feeding behavior. In a subset of cases pathologically-confirmed at autopsy, processing speed was better in cases with abnormal feeding behavior. No significant group differences were found for behavioral indices. DISCUSSION/SIGNIFICANCE OF IMPACT: These findings suggest that cognitive dysfunction is not the sole driver of abnormal eating behavior in bvFTD. Future studies with comprehensive characterization of feeding behavior, cognition and physiological/neuroimaging indices are warranted.