A 73-year-old male with a history of alcoholic cirrhosis on ciprofloxacin for spontaneous bacterial peritonitis (SBP) prophylaxis presented to the emergency department with one week of abdominal pain and nausea. On admission he had a leukocytosis, stable liver function tests, and acute kidney injury. Paracentesis revealed 2,434 neutrophils in the peritoneal fluid. He was started on vancomycin and ertapenem but continued to worsen clinically over the next several days despite treatment. On day four of hospitalization he was tachycardic and hypotensive with a worsening leukocytosis. Repeat paracentesis suggested worsening SBP. Computer tomography of the abdomen did not reveal an abscess or perforation of hollow viscus. Peritoneal fluid cultures returned positive for Lactobacillus paracasei as the sole pathogen isolated from both aerobic and anaerobic plates, resistant to meropenem and vancomycin. He was switched to high dose penicillin. Despite a rapid improvement in his peripheral leukocytosis and hemodynamic parameters, the patient’s creatinine continued to rise rapidly to a peak of 3.7mg/dL. He ultimately developed type 1 hepatorenal syndrome and died six days later.
Discussion:
Lactobacillus species are facultatively anaerobic gram-positive bacilli that are part of normal human gastrointestinal flora and are seldom pathogenic. Although there is ongoing debate about the clinical relevance of Lactobacillus isolated from clinical material, most cases of Lactobacillus-associated serious infections occur in immunocompromised patients and have an estimated 30% mortality. The recent interest in Lactobacillus as an adjunctive therapy in hepatic encephalopathy demands increased awareness of the risks in critically ill patients. We describe a case of SBP in which the sole pathogen isolated from peritoneal fluid cultures was L. paracasei. While most Lactobacillus associated intra-abdominal infections occur following hollow organ perforation, there have been rare reports of Lactobacillus peritonitis in the setting of decompensated cirrhosis. In such cases, seeding of ascites fluid most likely occurs via transmural migration across the impaired intestinal wall. Microbiologic identification of Lactobacilli is made more challenging by their slow and minimal growth on common media. Early recognition of the potential pathogenicity of lactobacilli is essential, however, because they are intrinsically resistant to vancomycin and commonly resistant to cephalosporins. As a result, patients are unlikely to respond to empiric antibiotic selections for SBP. In the rare case that Lactobacillus requires treatment, recommended therapy is high-dose penicillin at 25 million units/day.
Conclusions:
Clinicians should be aware of the potential pathogenic role of Lactobacillus, particularly given their unusual antibiotic resistance pattern and recent interest in probiotics for the prevention of hepatic encephalopathy in end-stage cirrhosis