Klebsiella pneumoniae (KP), with production of abundant capsular
polysaccharide (CPS), is capable of causing invasive syndrome. Environmental
glucose stimuli may increase CPS biosynthesis. We aimed to investigate the relationship between
glycemic control and KP-mediated invasive syndrome in diabetic patients and the effect of
glucose on CPS biosynthesis. Diabetic patients with community-acquired KP
bacteremia were included to study the risk factors of invasive syndrome. KP-M1, a serotype-K1 KP clinical isolate, was used to examine the CPS biosynthesis and cps gene expression, and the effect of exogenous
glucose on bacterial phagocytosis and killing. We found that invasive syndrome was significantly more common in diabetic patients who were infected with strains expressing the K1 serotype (adjusted odds ratio [AOR], 8.32; 95% confidence interval [CI], 1.56-44.24; p=0.01), and had poor
glycemic control (HbA1c ≥9%; AOR, 5.66; 95% CI, 2.01-15.92; p<0.01). Pre-incubation of KP-M1 in media containing different gradient
glucose concentrations enhanced CPS biosynthesis and cps gene expression in high
glucose (0.5%) concentration, which leads to increasing bacterial resistance to phagocytosis and killing. High
glucose levels reflected by poor
glycemic control may stimulate CPS biosynthesis and cps gene expression of highly virulent KP, which increase resistance to phagocytosis and contribute to development of invasive syndrome.