Infectivity of hepatic strain Klebsiella pneumoniae in diabetic mice.
Besides urinary tract infection (UTI) and pneumonia, increased severe liver abscesses caused by Klebsiella pneumoniae (KP), especially in diabetic patients, have been observed in infections acquired in hospitals. This indicates that different KP strains with higher virulence have emerged in recent years. Our goal was to investigate the infectivity of KP isolates in mice from liver abscess or UTI patients. Mice were injected with streptozotocin to induce diabetes. Male ICR mice were infected with KpU1 (UTI strain CG3 for survival experiment only) and KpL1 (liver abscess strain CG5) by tail-vein injection of 5 x 10(4) colony-forming units (CFU) bacterial suspension. The mice survival rates, cytokine level by enzyme-linked immunosorbent assay (ELISA), and bacterial presence in liver tissue by Giemsa stain were examined. The survival rates for the KpL1-infected animals were 28% and 0% in normal and diabetic groups, respectively, whereas, for the KpU1-infected mice, the rates were 100% and 75% during a 30-day observation. Nonsurviving KpL1-infected mice showed > 10(5) bacteria/ml blood and the bacteria appeared in the liver sinus area and inside liver cells. The KpL1-infected mice showed a tendency to increase the blood interleukin 1beta (IL-1beta) level in both nondiabetic and diabetic groups, whereas the tumor necrosis factor-alpha (TNF-alpha) level was significantly decreased in the KpL1-infected diabetic mice (P = 0.002). In conclusion, the KP strain from liver abscess showed a greater virulence in mice than the KP from UTI and was more virulent in diabetic than in nondiabetic mice. The infection with KP from liver abscess significantly decreased the blood TNF-alpha level in diabetes mellitus (DM) mice and the blood IL-1beta level tended to increase in both infected nondiabetic and diabetic groups. High blood bacterial count and appearance of bacteria in liver sinus and cells usually contribute to death of the animals.
Wu
June Hsieh
JH
Department of Microbiology and Immunology, College of Medicine, Chang Gung University, 259 Wen Hua 1 Road, Kwei San, Tao Yuan 333 Taiwan. jhwu@mail.cgu.edu.tw
Tsai
Cheng Gie
CG
D000038:Abscess / Q000150:complications / Q000378:metabolism / Q000382:microbiology; D000818:Animals; D001399:Azure Stains; D015169:Colony Count, Microbial; D003921:Diabetes Mellitus, Experimental / Q000150:complications*; D004797:Enzyme-Linked Immunosorbent Assay; D007375:Interleukin-1 / Q000032:analysis / Q000378:metabolism; D007710:Klebsiella Infections / Q000276:immunology* / Q000517:prevention & control; D007711:Klebsiella pneumoniae; D008099:Liver / Q000276:immunology*; D051379:Mice; D013194:Staining and Labeling; D015996:Survival Rate; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000378:metabolism
D001399:Azure Stains; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha