S5124 Aspergillus niger Peritonitis in Decompensated Cirrhosis Successfully Managed With Voriconazole

Introduction: Fungal peritonitis (FP) causes 3%–6% of peritonitis episodes and 20–30% mortality. Risk rises with prolonged broad-spectrum antibiotics that foster gut fungal overgrowth and with weakened peritoneal defenses in cirrhosis or peritoneal dialysis. Candida predominates, but molds such as Aspergillus can produce fulminant disease. Voriconazole reaches high peritoneal levels without renal toxicity, suiting mold infections. We report Aspergillus niger FP in a cirrhotic patient, underscoring diagnostic and therapeutic challenges. Case Description/Methods: A 58-year-old woman with atrial fibrillation, hypertrophic cardiomyopathy, alcoholic cirrhosis with portal hypertension, and chronic hypotension collapsed from syncope. She was hypotensive and bradycardic; the abdomen was distended with a fluid wave. Labs: creatinine 2.4 mg/dL (baseline 0.8), bilirubin 4.1 mg/dL, international normalized ratio (INR) 2.1, hemoglobin 8.1 g/dL. Computed tomography (CT) showed cirrhosis, moderate ascites, and a 3 cm loculated collection by the distal esophagus. Paracentesis yielded cloudy fluid; analysis 1780 cells/µL (85% neutrophils), serum–ascites albumin gradient 1.6 g/dL. Ascitic cultures grew Aspergillus niger at 48 h. Broad-spectrum antibiotics were stopped and intravenous (IV) micafungin 100 mg/d begun. Persistent fever, leukocytosis, and positive cultures prompted escalation to IV voriconazole (6 mg/kg q12 h × 2, then 4 mg/kg q12 h). She deteriorated, required intubation and norepinephrine, and died after pulseless electrical-activity arrest. Discussion: Aspergillus FP is rare outside peritoneal dialysis and highly lethal in cirrhosis, where immune dysfunction and portal-hypertensive translocation facilitate invasion. Early pathogen identification is vital because first-line fluconazole lacks mold activity. Amphotericin B is active but nephrotoxic—problematic in hepatorenal physiology. Voriconazole offers superior Aspergillus coverage, excellent bioavailability, and dialysate-to-plasma ratios ≈ 0.7, indicating good peritoneal penetration with renal safety. Despite timely voriconazole, mortality rises once multiorgan failure occurs, as in this case. Earlier combined drainage of loculated ascites or expedited liver-transplant evaluation may improve outcomes. Prompt paracentesis with fungal culture, rapid mold-active therapy, and coordinated care among hepatology, infectious-disease, and critical-care teams remain essential to optimize survival.

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001147956.62173.95
Primary Topic
Antifungal resistance and susceptibility
Type
article
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article

S5124 Aspergillus niger Peritonitis in Decompensated Cirrhosis Successfully Managed With Voriconazole

The American Journal of Gastroenterology
Antifungal resistance and susceptibility
article

S5124 Aspergillus niger Peritonitis in Decompensated Cirrhosis Successfully Managed With Voriconazole

article en

Abstract

Introduction: Fungal peritonitis (FP) causes 3%–6% of peritonitis episodes and 20–30% mortality. Risk rises with prolonged broad-spectrum antibiotics that foster gut fungal overgrowth and with weakened peritoneal defenses in cirrhosis or peritoneal dialysis. Candida predominates, but molds such as Aspergillus can produce fulminant disease. Voriconazole reaches high peritoneal levels without renal toxicity, suiting mold infections. We report Aspergillus niger FP in a cirrhotic patient, underscoring diagnostic and therapeutic challenges. Case Description/Methods: A 58-year-old woman with atrial fibrillation, hypertrophic cardiomyopathy, alcoholic cirrhosis with portal hypertension, and chronic hypotension collapsed from syncope. She was hypotensive and bradycardic; the abdomen was distended with a fluid wave. Labs: creatinine 2.4 mg/dL (baseline 0.8), bilirubin 4.1 mg/dL, international normalized ratio (INR) 2.1, hemoglobin 8.1 g/dL. Computed tomography (CT) showed cirrhosis, moderate ascites, and a 3 cm loculated collection by the distal esophagus. Paracentesis yielded cloudy fluid; analysis 1780 cells/µL (85% neutrophils), serum–ascites albumin gradient 1.6 g/dL. Ascitic cultures grew Aspergillus niger at 48 h. Broad-spectrum antibiotics were stopped and intravenous (IV) micafungin 100 mg/d begun. Persistent fever, leukocytosis, and positive cultures prompted escalation to IV voriconazole (6 mg/kg q12 h × 2, then 4 mg/kg q12 h). She deteriorated, required intubation and norepinephrine, and died after pulseless electrical-activity arrest. Discussion: Aspergillus FP is rare outside peritoneal dialysis and highly lethal in cirrhosis, where immune dysfunction and portal-hypertensive translocation facilitate invasion. Early pathogen identification is vital because first-line fluconazole lacks mold activity. Amphotericin B is active but nephrotoxic—problematic in hepatorenal physiology. Voriconazole offers superior Aspergillus coverage, excellent bioavailability, and dialysate-to-plasma ratios ≈ 0.7, indicating good peritoneal penetration with renal safety. Despite timely voriconazole, mortality rises once multiorgan failure occurs, as in this case. Earlier combined drainage of loculated ascites or expedited liver-transplant evaluation may improve outcomes. Prompt paracentesis with fungal culture, rapid mold-active therapy, and coordinated care among hepatology, infectious-disease, and critical-care teams remain essential to optimize survival.

The American Journal of GastroenterologyVol. 120(10S2)
Good health and well-being
Openalex Percentile: Top 33%
Antifungal resistance and susceptibility
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