Toxin-producing Klebsiella oxytoca as a cause of antibiotic-associated colitis
Antibiotic-associated diarrhea remains an unresolved problem in current medicine. In the last decade, in addition to idiopathic antibiotic-associated diarrhea, diseases caused by cytotoxin-producing Klebsiella oxytoca strains are becoming increasingly detected. Clinical manifestations of this infection may vary from relatively mild diarrhea without signs of hemocolitis to severe antibiotic-associated hemorrhagic colitis with predominant involvement of the right hemicolon. High prevalence of resistance to ciprofloxacin, tetracycline, gentamicin, amikacyne, and trimethoprim/sulfamethoxazole is associated with the presence of all adhesion genes of K. oxytoca and its greater cytotoxicity. The genes encoding the K. oxytoca cytotoxin (tilivalline) are a part of the pathogenicity island (PAI) and are similar to the clusters responsible for the biosynthesis of pyrrolobenzodiazepine and found in gram-positive bacteria. The most important pathogenicity factor related to the development of K. oxytoca-associated hemorrhagic colitis is a cytotoxin kleboxymycin, which is a tilivalline metabolite. The treatment strategy in K. oxytoca-associated hemorrhagic colitis is to withdraw the trigger antimicrobial agent, to refrain from administration of new antimicrobials, to administer rehydration and rational pathogenetically based therapy. Studies on the development of therapeutic bacteriophages against K. oxytoca are of pilot nature.