Porcine iucA+ but rmpA- Klebsiella pneumoniae strains proliferate in blood of young piglets but are killed by IgM and complement dependent opsonophagocytosis when these piglets get older

•Veterinary K. pneumoniae isolates show great diversity in siderophore profiles.•iucA+ rmpA- K. pneumoniae proliferate in blood of young piglets.•Supernatants of iucA+ strains boost bacterial growth in serum.•Opsonophagocytosis is crucial for bactericidal immunity of growing piglets. Klebsiella (K.) pneumoniae causes different diseases in humans and animals including the life-threatening liver abscess syndrome and septicemia, respectively. However, host-pathogen interactions of K. pneumoniae in porcine blood have not been studied. We investigated the working hypothesis that only distinct K. pneumoniae strains have the capacity to survive in porcine blood and that this feature is associated with specific molecular markers such as sequence type, profile of siderophore genes and the regulator of the mucoid phenotype (rmp). Furthermore, we characterize the immune response in growing piglets leading to killing of an invasive K. pneumoniae strain. The veterinary isolates showed great diversity in sequence types and profile of siderophore genes. Porcine isolates were mainly positive for the aerobactin gene iucA but did not carry rmpA and this genotype was associated with proliferation in blood of 4-week-old piglets. Supernatants of an iucA+ but not an iucA- strain boosted growth in porcine serum. Between four and eight weeks of age, piglets showed a prominent increase of IgM binding to K. pneumoniae. Immunglobulin M and complement were crucial for killing of a serum-resistant iucA+ porcine K. pneumoniae strain at eight weeks of age. Flow cytometry analysis confirmed induction of phagocytosis and oxidative burst mediated by serum samples of 8-week-old piglets. Based on our in vitro findings we propose that many porcine iucA+ rmpA- K. pneumoniae strains have the ability to cause bacteremia in young piglets in association with aerobactin-mediated iron acquisition and that this phenotype is lost as specific IgM increases after weaning.