Abstract

TYPE: Case Report TOPIC: Lung Pathology INTRODUCTION: Without treatment, tuberculosis (TB) may lead to septic shock in immunocompetent individuals. Through the interaction of lipoarabinomannan (LAM) on the mycobacterium cell wall with antigen presenting cells, TB may be able to survive in host cells for long periods of time; causing widespread lung damage and systemic disease. We report a unique case of a 24-year-old woman with an untreated mycobacterial infection who developed bronchiectasis and TB-related septic shock. CASE PRESENTATION: A 24-year-old Guyanese woman with no past medical history presented to the hospital with shortness of breath, weight loss, and hemoptysis. She was hemodynamically unstable and severely cachectic with coarse lung sounds. Imaging demonstrated diffuse interstitial opacities and large cystic changes. Fluids were given, her sputum was positive for acid fast bacilli, and she was started on R.I.P.E. treatment for tuberculosis. The patient became severely hypoxic requiring intubation. She ultimately developed refractory hypotension despite 4 different vasopressors. She became pulseless and ACLS protocol was initated, though, she remained in asystole throughout the arrest. DISCUSSION: Lipoarabinomannan, a glycolipid on the mycobacterium cell wall with virulent properties, directly activates SHP-1 through phosphorylation. SHP-1, a signaling molecule which regulates many different cellular processes, may deactivate proinflammatory cytokines and inhibit INF-y release. This inability to activate macrophages promotes intracellular survival of TB in host cells. This mechanism may account for diffuse bronchiectasis and a systemic inflammatory response, as in our patient. CONCLUSIONS: This case highlights the possibility of tuberculosis-related septic shock in the critical care setting and draws attention to mechanisms of pathogenesis if left untreated. DISCLOSURE: Nothing to declare. KEYWORD: septic shock

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