Bacteraemia due to Comamonas Kerstersii of Unknown Origin in a Patient with Decompensated Liver Cirrhosis and Type 2 Diabetes Mellitus.

Background: Comamonas kerstersii is a Gram-negative, non-fermenting bacterium previously considered non-pathogenic. Recent reports demonstrate its pathogenicity in humans, particularly in intra-abdominal infections and bacteraemia among at-risk populations. Case description: A 44-year-old male with decompensated liver cirrhosis due to alcohol abuse and type 2 diabetes mellitus presented with fever, altered consciousness and jaundice. Blood cultures grew C. kerstersii, confirmed by matrix-assisted laser desorption/ionisation-time of flight mass spectrometry. The ascitic fluid culture was negative and transudative, excluding intra-abdominal infection as the source of bacteraemia. The patient was treated with ceftazidime and made a full recovery. Conclusion: This case highlights the emerging pathogenic potential of C. kerstersii in immunocompromised patients, particularly those with liver cirrhosis and diabetes mellitus. Unlike previously reported cases, which were mainly associated with intra-abdominal infections, our case represents bacteraemia of unknown origin, suggesting bacterial translocation across the intestinal barrier and causing a systemic infection. Accurate identification of C. kerstersii by matrix-assisted laser desorption/ionisation-time of flight mass spectrometry is crucial for appropriate antibiotic therapy. LEARNING POINTS: Comamonas kerstersii is an emerging opportunistic pathogen in immunocompromised patients, particularly those with liver cirrhosis or diabetes, who present with bacteraemia of unknown origin after the exclusion of common pathogens.Matrix-assisted laser desorption/ionisation-time of flight mass spectrometry enables precise identification of C. kerstersii. Conventional automated systems may misidentify it as C. testosteroni, potentially leading to inappropriate therapy and missed diagnoses.In decompensated liver cirrhosis, C. kerstersii bacteraemia may result from bacterial translocation across the impaired intestinal barrier, rather than typical intra-abdominal sources, highlighting a novel pathogenic mechanism.