Case Presentation: A 61-year-old man with decompensated non-alcoholic steatohepatitis cirrhosis and end-stage renal disease (ESRD) presented with sudden-onset hypotension. He described 3 days of fatigue, lethargy, and loss of appetite with a history of breeding chickens. He was afebrile, blood pressure was 70/40, and abdomen was distended without tenderness to palpation. Initial diagnostic paracentesis showed 13,000 white blood cells with neutrophilic predominance. Culture of peritoneal fluid revealed pan-sensitive salmonella and negative blood cultures. He was diagnosed with spontaneous bacterial peritonitis (SBP) secondary to salmonella and treated with a 7 day course of ceftriaxone with subsequent transition to oral levofloxacin. Despite completing a course of ceftriaxone, repeat paracentesis revealed increased WBC count to 26,000 and ascitic cultures remained persistently positive for salmonella. CT of his abdomen demonstrated no abscesses, bowel leak, or other intra-abdominal infections. He was restarted on a 4 day course of ceftriaxone after which peritoneal fluid showed improved WBC count without bacterial growth. Given his refractory SBP and inability to tolerate hemodialysis due to hypotension, he was transitioned to home hospice.
Discussion: SBP is a frequently encountered condition in patients with advanced liver cirrhosis. Pathogens commonly associated with SBP include E. coli, streptococcal species, and Klebsiella pneumoniae. Non-typhoidal salmonella is a rare cause of SBP with previous case reports citing immunocompromised states such as AIDS and extrahepatic malignancies as risk factors. However, in this case, occupational exposure to poultry placed this patient at a higher risk and ESRD may have contributed to an immunocompromised state. Patients with salmonella SBP are frequently asymptomatic, lacking overt peritoneal signs as in this patient reporting only lethargy and decreased appetite. Previous reports of salmonella SBP responded well to a one-week course of ceftriaxone, after which patients typically show decreased neutrophils on ascitic fluid and clinical improvement. However, in our patient, repeat paracentesis revealed an increased neutrophil count consistent with persistent peritonitis despite appropriate therapy. Our patient demonstrated that a prolonged antibiotic course may be necessary in these cases, especially given his immunocompromised state. Furthermore, initial failure to respond to treatment required additional investigation for a possible surgical source of infection such as an abscess or other intra-abdominal infection. No definite source of bacterial translocation was identified since no abscess or perforation was noted on imaging. It is important to recognize persistent SBP as it can occur in end-stage liver failure and portend a poor prognosis suggestive of hepatocellular carcinoma or gut bacteria translocating into the peritoneal space.
Conclusions: In summary, this case is a reminder to consider salmonella SBP in patients with occupational exposures without conspicuous immunosuppression. Heightened clinical vigilance and patient centered communication about a guarded prognosis is necessary given the higher mortality rates associated with persistent SBP despite patients feeling asymptomatic. Hospitalists should be aware that salmonella SBP may require a prolonged course of antibiotics and investigation for possible sources of gut translocation if ascitic fluid cultures do not demonstrate improvement with treatment.