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IMMUNOSUPPRESSION SECONDARY TO SEPSIS AND POSTACUTE CARE SYNDROME LEADING TO LATENT TUBERCULOSIS REACTIVATION
Journal of General Internal Medicine ; 37:S468, 2022.
Article in English | EMBASE | ID: covidwho-1995805
ABSTRACT
CASE A 59-year-old Mexican-American man with hypertension and type II diabetes (Hemoglobin A1c 11.5) was admitted for sepsis and Acute Respiratory Distress Syndrome secondary to COVID-19 pneumonia. He was ventilator- dependent for 66 days. His clinical course was complicated by acute renal failure requiring hemodialysis, pulmonary embolism, and recurrent ventilator-associated bacterial pneumonia. He was discharged to a long-term acute care center four months after his initial presentation, but was readmitted two weeks later for abdominal pain and fever. CT abdomen revealed diffuse mesenteric nodular stranding and pelvic ascites concerning for peritoneal carcinomatosis. Biopsy of an omental nodule, however, showed necrotizing granulomatous inflammation and no malignant cells. No cultures were sent from the initial biopsy, so repeat sampling was performed and culture was positive for Mycobacterium tuberculosis complex. Treatment for active tuberculosis was initiated with subsequent recovery. IMPACT/

DISCUSSION:

Initial infection by tuberculosis occurs in the lungs, where alveolar macrophages encounter and phagocytose the bacteria. The macrophages initiate a cytokine response and recruit lymphocytes to form a granuloma, which segregates the infection within the host. The granuloma is then perpetually maintained by an ongoing immune response that is driven by monocytes and CD-4 T cells. Reactivation of tuberculosis occurs when the ongoing immune response is disrupted. Sepsis has profound and complex effects on the immune system, including marked inhibition of lymphocyte proliferation that leads to reduced levels of B cells, CD-4 T cells, and follicular dendritic cells. Signaling pathways are disrupted without these lymphocytes, which then leads to the dysfunction of the remaining leukocytes. Further, critically ill patients often suffer from post-intensive care unit syndrome. This syndrome is marked by persistent inflammation, which prompts an immunosuppressive response that suppresses T-cell function and leads to T-cell apoptosis. Both sepsis and post-intensive care unit syndrome predispose patients to opportunistic infection by attenuation of the usual immune response. In this particular case, the specific loss of T-cell function in both syndromes allowed this patient's latent tuberculosis to reactivate several months after his initial presentation with sepsis from COVID-19 pneumonia. This case highlights the importance of maintaining a high index of suspicion for opportunistic infection after critical illness.

CONCLUSION:

Sepsis and post-intensive care unit syndrome disrupted this patient's ability to maintain the immune responses that prevent the progression of latent tuberculosis infection. The diagnosis was delayed due to a lack of awareness of the profound immunosuppression that accompanies and follows critical illness. Providers must recognize these syndromes and the impact they have on immunity in order to diagnose and treat opportunistic infections in a timely manner.
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Full text: Available Collection: Databases of international organizations Database: EMBASE Topics: Long Covid Language: English Journal: Journal of General Internal Medicine Year: 2022 Document Type: Article

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Full text: Available Collection: Databases of international organizations Database: EMBASE Topics: Long Covid Language: English Journal: Journal of General Internal Medicine Year: 2022 Document Type: Article