Widely disseminated necrotizing infection and refractory septic shock with hypervirulent <i>Klebsiella pneumoniae</i> : A case report

Background: Emerging strains of hypervirulent Klebsiella pneumoniae are increasingly recognized to cause life-threatening, community-acquired infections in persons without significant immunocompromise. Beyond the association with pyogenic liver abscesses and bacteremia, additional sites of involvement include skin and soft tissue, bone, eyes, and the central nervous system. Individuals with diabetes mellitus and originating from the Asian Pacific Rim appear to be at higher risk for colonization and infection. Genetic testing for defining virulence factors was recently proposed as a standard for differentiating hypervirulent from classical K. pneumoniae strains. Method: Retrospective review of a K. pneumoniae infection in a middle-aged male. Results: The patient had untreated type 2 diabetes, hypertension, and obesity, and immigrated from a southeast Asian country to Canada over one decade prior. He presented with profound refractory septic shock leading to progressive multiorgan system failure. In totality, the infection involved necrotizing fasciitis of bilateral legs, bilateral emphysematous pyelonephritis, emphysematous cholecystitis, multifocal necrotizing pneumonia, and bacteremia notably without liver abscess. K. pneumoniae was later isolated from blood and sputum. Whole-genome sequencing identified K. pneumoniae sensu stricto with K1 capsule belonging to sequence type 23 and harbouring the characteristic virulence genes iucA , iroB , peg-344 , rmpA , and rmpA2 . Conclusion: This case demonstrates a remarkable extent of dissemination and expands the known clinical spectrum for hypervirulent K. pneumoniae infection. Genetic testing has the potential to proactively identify hypervirulent strains and inform clinical management. Heightened clinical vigilance, development of accessible rapid diagnostic tools, and further research into treatment strategies are needed for this emerging pathogen.