Case Presentation: This is a 65-year-old man with cryptogenic cirrhosis who was transferred to a tertiary care hospital for liver transplant evaluation. His course prior to transfer was complicated by decompensated cirrhosis leading to ascites requiring large volume paracentesis (LVP), acute kidney injury, and upper gastrointestinal bleed due to severe esophagitis with non-bleeding esophageal varices. Records also indicated recent Clostridium difficile infection and culture-negative spontaneous bacterial peritonitis (SBP). On admission, abdominal discomfort was present due to recurring ascites. Physical examination was remarkable for BP 100/64, HR 91, mild jaundice, scleral icterus, abdominal distention, and peripheral edema.  He underwent laboratory evaluation (Table 1) and was continued on PO vancomycin and IV ceftriaxone.  LVP was performed and ascitic fluid analysis showed 707 WBCs/mm3 with 42% PMNs. Gram stain and ascitic fluid culture were negative. The peripheral WBC count then rose from 10.6 to 20.3/mm3 with 92% segmented neutrophils and 3% bands. The patient also experienced a syncopal episode due to orthostatic hypotension. Repeat LVP and ascitic fluid analysis showed 531 WBCs/mm3 with 55% PMNs and negative gram stain, but ascitic fluid cultures then grew pan-sensitive Listeria monocytogenes. Antibiotics were changed to IV ampicillin.

Discussion: Organisms commonly responsible for SBP include Escherichia coli, streptococci, and Klebsiella pneumoniae. Ascitic fluid cultures are positive in only 40% of cases. Empiric treatment of SBP consists of a third-generation cephalosporin, and a clinical response to therapy in 48-72 hours is expected. Continued signs of worsening infection despite empiric treatment (e.g., increasing peripheral leukocytosis and hypotension) indicate a resistant or atypical source.  Listeria infections are more common in newborns and immunocompromised adults. Cirrhosis leads to immune dysfunction, as 90% of reticuloendothelial cells are stored in the liver. Monocyte migration and bacterial phagocytosis are also diminished in cirrhotic patients. There have been >50 case reports of SBP due to Listeria, but most have occurred in Spain, while just >10 cases have been reported in the United States. Listeria is a rare cause of SBP but is occurring with greater frequency. It should be considered as a possible source in cases when clinical improvement is not seen after initiation of empiric antibiotics.

Conclusions: Patients with cirrhosis have immune dysfunction and are susceptible to infections caused by Listeria, including SBP. Although Listeria is a rare cause of SBP in the United States, it should be considered in patients who do not improve after 48-72 hours of empiric antibiotic therapy. Even in the setting of negative cultures, antibiotics should be broadened. Ampicillin with or without an aminoglycoside should be considered for Listeria coverage.