Recurrent Liver Abscess in a Non-Toxic Patient

Introduction: Liver abscesses are caused by direct spread from peritonitis, biliary tract infection or via hematogenous seeding from a distant source. Most are polymicrobial, however Escherichia coli and Klebsiella pneumoniae are the most common offending pathogens. Patients usually present with pain, fever, and clinical signs of infection. We describe a case of spontaneous liver abscess in a non-toxic patient that recurred 10 years after a previous abscess. Case Description/Methods: A 73-year-old-man with a history of type 2 diabetes mellitus, hypertension, CAD status post CABG and PCI 3 years ago, and abdominal aortic aneurysm status post endovascular aneurysm repair presented with 2 weeks of dark urine. After receiving his COVID-19 booster and influenza vaccinations, he developed flu-like symptoms with a self-resolving fever of 101.8degreeF. He had dark amber urine without dysuria or hematuria. Later, he experienced generalized weakness and decreased oral intake. Outpatient labs showed elevated liver function tests, and he was told to present to the ED. On arrival, he was afebrile with stable vitals. Physical exam was unremarkable. Laboratory evaluation showed a hemoglobin of 11.7 g/dL, sodium of 133 mEq/L, creatinine of 1.4 mg/dL, aspartate aminotransferase of 117 U/L, alanine aminotransferase of 212 U/L, alkaline phosphatase of 825 U/L, total bilirubin of 4.1 mg/dL, and direct bilirubin of 2.1 mg/dL. Triple-phase CT showed a 2.8 cm mass in the right liver lobe with linear enhancement. Ultrasound showed mixed echogenicity measuring 3.6 x 2.9 x 3.3 cm in segment 8 of the liver. On further evaluation, patient had an E. coli abscess diagnosed 10 years prior, managed with antibiotics and drainage. At that time, the abscess was within the right inferior liver lobe, similar to his current abscess. LFTs downtrended. Abscess was aspirated, with culture growing oxidase negative, gramnegative rods, likely E. coli. Patient started on ceftriaxone and metronidazole, to undergo colonoscopy as an outpatient and rule out colonic bacterial translocation. Discussion(s): Pyogenic liver abscess can result in significant morbidity and mortality because of worsening infection and sepsis. Abscesses occur because of spread from adjacent infection or after recent surgeries. Recurrence is very rare. Here, we describe a very unusual case of a pyogenic liver abscess growing E. coli in a non-toxic patient, with the same location and causative organism as an abscess managed 10 years prior. (Figure Presented).

Scientific debrief: cirrhosis

Globally, hepatitis C (26%), alcohol (24%), and hepatitis B (23%) contribute almost equally to the global burden of cirrhosis. The contribution from nonalcoholic fatty liver disease (8%) is small but increasing. Patients with acutely decompensated cirrhosis have a dismal prognosis and frequently progress to acuteon-chronic liver failure, which is characterised by hepatic and extrahepatic organ failure, Cardiovascular alterations including portal hypertension trigger the formation of portocaval shunts and varices. Systemic under filling and arterial hypotension is compensated by vasoconstriction but might decline into a state of aggravated portal hypertension and cirrhotic cardiomyopathy, leading to a hyperdynamic state, microvascular dysfunction and reduced organ perfusion culminating in decompensation. The immune system is dysfunctional showing a contrary co-existence of immune paralysis and immune overstimulation leading to secondary infections and inflammatory response syndrome aggravating cardiovascular alterations but also initiating tissue injury and metabolic alteration. This transition from compensated to decompensated cirrhosis is characterised by the occurrence of ascites, variceal bleeding and/or hepatic encephalopathy or organ failures (in the case of ACLF. Precipitating events for ACLF vary between Western countries (bacterial infection, alcohol intake) and Eastern countries (flare of HBV, superimposed HAV or HEV). In the majority of patients, systemic inflammation is a major driver of progression from compensated to decompensated cirrhosis. Once the first episode of AD develops, systemic inflammation follows a chronic course, with transient periods of aggravation due to proinflammatory precipitants or bursts of bacterial translocation resulting in repeated episodes of AD. The multistate model describing the clinical outcomes of decompensated cirrhosis has been well validated. State 3 is defined by the occurrence of variceal bleeding alone, state 4 by any single non-bleeding event, state 5 by any 2 or more events and the late decompensate state by any event with organ failures either with or without ACLF. 5-year mortality across states from 3 to 5 is in the order of, respectively: 20%, 30%, 88%. With late decompensation mortality ranges between 60 and 80% at 1 year. Cirrhosis is increasingly common and morbid. Optimal utilisation of therapeutic strategies to prevent and control the complications of cirrhosis are central to improving clinical and patient-reported outcomes. Aetiology-focused therapies that can prevent cirrhosis and its complications. These include anti-viral therapies, psychopharmacological therapy for alcohol-use disorder, management of hepatic encephalopathy (HE), ascites, hepatorenal syndrome, non-pain symptoms of cirrhosis including pruritis, muscle cramps, sexual dysfunction and fatigue, and reduce the risk of hepatocellular carcinoma. New disease-modifying agents are expected to be identified in the next few years by systematic drug repurposing and the development of novel molecules currently undergoing pre-clinical or early clinical testing. COVID-19 continues to pose a significant healthcare challenge throughout the world. Comorbidities including diabetes and hypertension are associated with a significantly higher mortality risk. Cirrhosis is associated with an increased risk of all-cause mortality in COVID-19 infection compared to non-cirrhotic patients. Patients with cirrhosis should be considered for targeted public health interventions to prevent COVID-19 infection, such as shielding and prioritisation of vaccination.

Gut Microbiota and Infectious Complications in Advanced Chronic Liver Disease: Focus on Spontaneous Bacterial Peritonitis.

Liver cirrhosis is a chronic disease that can be complicated by episodes of decompensation such as variceal bleeding, hepatic encephalopathy, ascites, and jaundice, with subsequent increased mortality. Infections are also among the most common complications in cirrhotic patients, mostly due to a defect in immunosurveillance. Among them, one of the most frequent is spontaneous bacterial peritonitis (SBP), defined as the primary infection of ascitic fluid without other abdominal foci. SBP is mainly induced by Gram-negative bacteria living in the intestinal tract, and translocating through the intestinal barrier, which in cirrhotic patients is defective and more permeable. Moreover, in cirrhotic patients, the intestinal microbiota shows an altered composition, poor in beneficial elements and enriched in potentially pathogenic ones. This condition further promotes the development of leaky gut and increases the risk of SBP. The first-line treatment of SBP is antibiotic therapy; however, the antibiotics used have a broad spectrum of action and may adversely affect the composition of the gut microbiota, worsening dysbiosis. For this reason, the future goal is to use new therapeutic agents that act primarily on the gut microbiota, selectively modulating it, or on the intestinal barrier, reducing its permeability. In this review, we aim to describe the reciprocal relationship between gut microbiota and SBP, focusing on pathogenetic aspects but also on new future therapies.

Synbiotics: A Promising Approach For Improving Human Health

The present environmental condition and lifestyle are becoming the cause of an increase in health issues like diabetes, obesity, and intestinal disorders in a growing population. The demand for functional foods as nutritional and immunity-boosting supplements has increased due to people's increased health consciousness during the last few years, which has accelerated a number of clinical trials on the positive effects of combining probiotics and prebiotics as synbiotics on hosts. A healthy diet is extremely important in maintaining the health of an individual. There are multiple mechanisms that have proposed the effect of synbiotics in controlling various diseases. Hence present review focuses on the most recent finding regarding health benefits, formulation criteria, action mechanism, and future prospects of synbiotics with their positive effect on the host. Copyright © 2022 Wolters Kluwer Medknow Publications. All rights reserved.

LIVER ABSCESS DEVELOPMENT IN THE POSTACUTE COVID-19 PHASE

SESSION TITLE: Post-COVID-19 Infection Complications SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: COVID-19 is a systemic infectious and inflammatory disease, with multifactorial immunosuppression during the recovery phase which predisposes to serious infections. Although the gastrointestinal (GI) system is often affected in post-acute COVID-19 patients, liver abscess formation is rare. Here, we present a case of septic shock caused by a bacterial liver abscess in a survivor of severe COVID-19. CASE PRESENTATION: 78-year-old man with no past medical or surgical history was admitted to an outside hospital (OSH) with severe COVID-19 pneumonia and discharged after 14 days. He required high flow nasal cannula and was treated with Remdesevir, Dexamethasone, and Baricitinib. D-dimer was elevated without evidence of acute venous thromboembolism. Four weeks later he returned to the OSH due to dyspnea and was found to be hypotensive and hypoxemic. Laboratories showed leukocytosis, hyperlactatemia, and mild elevation of total bilirubin and transaminases. Whole-body CT scan revealed a small RUL pulmonary embolus and a 7cm multifocal loculated complex fluid collection indicative of a left hepatic lobe abscess. He was managed with supplemental oxygen, anticoagulation, broad-spectrum antibiotics, IV fluids, and vasopressors and transferred to our hospital for abscess drainage. The liver abscess was aspirated after an abdominal MR confirmed the findings and the septic shock subsequently resolved. Body fluid and blood cultures grew pan-sensitive Klebsiella pneumoniae. Antibiotics were narrowed to levofloxacin. He remained hemodynamically stable and was discharged home. DISCUSSION: In our patient, the underlying cause of bacterial inoculation of the liver and abscess formation remains unclear and is not fully explained by drug-induced immunosuppression given the frequency with which these medications are used. Hepatic abscesses often develop after liver injury and, in COVID-19, multiple mechanisms of liver injury have been proposed which may predispose to abscess formation. Specifically, in our case, it is likely that hypoxic hepatitis and arterial/venous thrombosis from hypercoagulability played a role in abscess formation given the need for supplemental oxygen and the presence of a pulmonary embolism. Additionally, in COVID-19, increased hepatobiliary expression of ACE2 may contribute to direct viral cytotoxicity of the liver and substantial dysbiosis may lead to cholestasis and bacterial translocation. CONCLUSIONS: Our case is unique and underlines the importance of having a high index of suspicion and monitoring for "occult infections,” such as liver abscesses in the COVID-19 recovery phase, even in those without prior GI medical history and with non-specific signs and symptoms. Further elucidation of the cause of liver injury and abscess formation are warranted;however, early identification and treatment can reduce morbidity and mortality. Reference #1: Nalbandian, A., et al, 2021. Post-acute COVID-19 syndrome. Nat Med, 27(4): 601–615. Reference #2: Liemarto, A.K., et al, 2021. Liver abscess with necrosis in post COVID-19: A case report. Ann Med Surg (Lond), 72: 103107. Reference #3: Alhaddad O., et al, 2022. A case report of COVID-19 evoked cholangitic liver abscess. Egypt Liver J, 12(1):5. DISCLOSURES: No relevant relationships by Christian Ascoli No relevant relationships by Anna Duchnowska No relevant relationships by Tirsa Ferrer Marrero No relevant relationships by Manasa Reddy

SARS CoV-2-Induced Viral Sepsis: The Role of Gut Barrier Dysfunction.

A considerable proportion of patients with severe COVID-19 meet Sepsis-3 criteria and share common pathophysiological mechanisms of multiorgan injury with bacterial sepsis, in absence of secondary bacterial infections, a process characterized as "viral sepsis". The intestinal barrier exerts a central role in the pathophysiological sequence of events that lead from SARS-CoV-2 infection to severe systemic complications. Accumulating evidence suggests that SARS-CoV-2 disrupts the integrity of the biological, mechanical and immunological gut barrier. Specifically, microbiota diversity and beneficial bacteria population are reduced, concurrently with overgrowth of pathogenic bacteria (dysbiosis). Enterocytes' tight junctions (TJs) are disrupted, and the apoptotic death of intestinal epithelial cells is increased leading to increased gut permeability. In addition, mucosal CD4(+) and CD8(+) T cells, Th17 cells, neutrophils, dendritic cells and macrophages are activated, and T-regulatory cells are decreased, thus promoting an overactivated immune response, which further injures the intestinal epithelium. This dysfunctional gut barrier in SARS-CoV-2 infection permits the escape of luminal bacteria, fungi and endotoxin to normally sterile extraintestinal sites and the systemic circulation. Pre-existing gut barrier dysfunction and endotoxemia in patients with comorbidities including cardiovascular disease, obesity, diabetes and immunosuppression predisposes to aggravated endotoxemia. Bacterial and endotoxin translocation promote the systemic inflammation and immune activation, which characterize the SARS-CoV-2 induced "viral sepsis" syndrome associated with multisystemic complications of severe COVID-19.

Obstructive Sleep Apnea as a Risk Factor for COVID-19 Severity-The Gut Microbiome as a Common Player Mediating Systemic Inflammation via Gut Barrier Dysfunction.

The novel corona virus that is now known as (SARS-CoV-2) has killed more than six million people worldwide. The disease presentation varies from mild respiratory symptoms to acute respiratory distress syndrome and ultimately death. Several risk factors have been shown to worsen the severity of COVID-19 outcomes (such as age, hypertension, diabetes mellitus, and obesity). Since many of these risk factors are known to be influenced by obstructive sleep apnea, this raises the possibility that OSA might be an independent risk factor for COVID-19 severity. A shift in the gut microbiota has been proposed to contribute to outcomes in both COVID-19 and OSA. To further evaluate the potential triangular interrelationships between these three elements, we conducted a thorough literature review attempting to elucidate these interactions. From this review, it is concluded that OSA may be a risk factor for worse COVID-19 clinical outcomes, and the shifts in gut microbiota associated with both COVID-19 and OSA may mediate processes leading to bacterial translocation via a defective gut barrier which can then foster systemic inflammation. Thus, targeting biomarkers of intestinal tight junction dysfunction in conjunction with restoring gut dysbiosis may provide novel avenues for both risk detection and adjuvant therapy.

Obstructive Sleep Apnea as a Risk Factor for COVID-19 Severity—The Gut Microbiome as a Common Player Mediating Systemic Inflammation via Gut Barrier Dysfunction

The novel corona virus that is now known as (SARS-CoV-2) has killed more than six million people worldwide. The disease presentation varies from mild respiratory symptoms to acute respiratory distress syndrome and ultimately death. Several risk factors have been shown to worsen the severity of COVID-19 outcomes (such as age, hypertension, diabetes mellitus, and obesity). Since many of these risk factors are known to be influenced by obstructive sleep apnea, this raises the possibility that OSA might be an independent risk factor for COVID-19 severity. A shift in the gut microbiota has been proposed to contribute to outcomes in both COVID-19 and OSA. To further evaluate the potential triangular interrelationships between these three elements, we conducted a thorough literature review attempting to elucidate these interactions. From this review, it is concluded that OSA may be a risk factor for worse COVID-19 clinical outcomes, and the shifts in gut microbiota associated with both COVID-19 and OSA may mediate processes leading to bacterial translocation via a defective gut barrier which can then foster systemic inflammation. Thus, targeting biomarkers of intestinal tight junction dysfunction in conjunction with restoring gut dysbiosis may provide novel avenues for both risk detection and adjuvant therapy.

Intestinal Barrier Biomarker ZO1 and Endotoxin Are Increased in Blood of Patients With COVID-19-associated Pneumonia.

BACKGROUND/AIM: The present study was undertaken to investigate (i) whether hospitalized patients with COVID-19 pneumonia present intestinal barrier dysfunction with consequent translocation of endotoxin into the systemic circulation and (ii) whether intestinal barrier biomarkers have any prognostic role in terms of progression to severe respiratory failure. PATIENTS AND METHODS: In this prospective study, 22 patients with COVID-19-associated pneumonia and 19 patients with non-COVID-19-related community-acquired pneumonia (CAP group) were studied while 12 healthy persons comprised the control group. Blood samples were collected on admission and analysed for serum levels of endotoxin and zonula occludens-1 (ZO1). Clinical courses regarding progression to severe respiratory failure (SRF) requiring mechanical ventilation were recorded. RESULTS: Patients with COVID-19-associated pneumonia and patients with CAP presented significantly higher serum endotoxin and ZO1 concentrations on admission as compared to healthy controls. There was no difference in endotoxin levels between patients with COVID-19-related pneumonia and patients with CAP. In patients with COVID-19-related pneumonia, serum endotoxin concentrations were positively correlated with C-reactive protein and ferritin values. There were no significant differences in serum endotoxin and ZO1 concentrations between patients with severe and not severe COVID-19-related pneumonia, nor between patients who developed SRF and those who did not Conclusion: Patients with COVID-19-related pneumonia present intestinal barrier dysfunction leading to systemic endotoxemia. Admission values of endotoxin and ZO1 do not have any prognostic role for progression to SRF.