“…This pathogen produces a wide range of infections including, pneumonia, bacteremia, urinary tract infection, meningitis, intraabdominal infections, and communityacquired pyogenic liver abscess (PLA). [1][2][3][4][5] Several virulence factors have been characterized clearly demonstrating their contribution to K. pneumoniae pathogenesis. The major virulence factors so far described are: a) the capsular polysaccharide (CPS), which confers the bacteria the ability to evade phagocytosis by immune cells and impedes bacterial killing by bactericidal complement serum; 6 b) the LPS O-antigen, prevents complement protein deposition and complement-associated serum lytic activity; 7 c) several pili or fimbrial adherence factors required for epithelial cell attachment and host colonization such as type 1 and type 3 pili, K. pneumoniae fimbriae 28 (KPF-28), the non-fimbrial adhesin CF29K, and the E. coli common pilus (ECP) have been described; 2,8 d) enterobactin and aerobactin siderophores, are required for a pathogen to establish infection when entering the hosts and enhance iron uptake by K. pneumoniae, 9 e) mucosity, a phenotype associated with a muco-polysaccharide network associated outside the capsule can facilitate mucosal colonization by K. pneumoniae and protects it from the interaction with anticapsule-specific antibodies to evade phagocytosis.…”