在台灣的肝膿瘍通常是由克雷伯氏肺炎桿菌引起，而糖尿病被認為是容易感染克雷伯氏肺炎桿菌(Klebsiella pneumoniae, KP)的危險因子，另一方面，KP是腸道中的正常菌叢，因此，為了解KP是如何在腸道中建立起繁殖並造成感染，首先利用正常鼠及以streptozotocin(STZ)誘發成糖尿病小鼠，將轉型成為帶有GFP的高黏性及低黏性兩株KP，以口灌食模式感染小鼠；首先我們在不同時間點犧牲後，取下器官均質及血液做細菌培養，發現在糖尿病及正常小鼠上，KP於24到32小時就能進入血液中造成感染，另外在器官的培養發現，肝臟及脾臟都是KP容易侵犯的器官。更進一步以H & E 染色觀察在感染小鼠腸道的病理變化，發現隨著時間增加，腸上皮損傷情形越嚴重，為了解糖尿病以及使用抗生素Metronidazole(MTZ)清除腸道厭氧菌，是否可以造成高黏性或低黏性KP，在正常及糖尿病小鼠的腸道菌落聚集與感染，於是利用腹腔注射MTZ先清除腸道中的厭氧菌，之後再以口灌食模式給予105 CFU的KP，比較小鼠的糞便培養KP菌量的改變，發現給予低黏性KP 1084，在糞便中培養出的菌數量都少於高黏性的KP 1112，並且不論有無給予MTZ，KP都可在腸道中存活兩天，於第4-7天被清除；經過一星期後的血液及器官培養中發現，105 CFU的KP並不會引起糖尿病鼠的感染。雖然腸道中有培養出KP，但同時間也在肝及腸繫膜淋巴節培養出來，顯示KP已經形成感染。因此，能由糞便中持續培養出的KP，也能在器官中培養出來，顯示出糖尿病及腸道中的厭氧菌，並不是影響KP在腸道中形成菌落聚集的主要因素，並且我們也無法在小鼠腸道中建立起KP的菌落聚集模式。
In Taiwan, liver abscess is usually caused by Klebsiella pneumoniae (KP). Diabetes mellitus (DM) is a known risk factor for the development of KP infection. KP is a common resident bacterium in human intestinal lumen. To investigate the establishment of colonization and infection by KP in the intestinal tract, normal and streptozotocin-induced DM C57BL/6J mice were employed. Hyper-mucoid KP1112 and hypo-mucoid KP1084 were used and were transformed by pGFPuv plasmid and were infected into mice via oral route. The mice were sacrificed at different time points, and organ and blood samples were collected for bacterial culture. The blood culture results demonstrated that KP entered the systemic circulation of the normal and DM mice at 24 to 32 hours. Furthermore, liver and spleen were the main targets of KP infection. Additional result on intestine histopathology by H & E staining, the severity of intestine was time dependent. To investigate if DM and antibiotic metronidazole (MTZ) affect the colonization and infection of KP in the intestinal tracts, normal and DM mice were injected with MTZ intra-peritoneally. Thereafter, mice were infected with 105 CFU KP via oral feeding, stool, blood, and organs were cultured for KP. In the stool, the amount of hypo-mucoid KP 1084 was less than that of hyper-mucoid KP 1112. KP was shown to reside in the intestine up to 2 days and was eradicated at 4-7 days. DM mice were not infected with orally administrated 105 CFU KP after 1 week. These data revealed that DM and intestinal anaerobes were not likely the major factors for KP to be colonized in the intestine. As well, we did not establish a model of KP colonization in the intestine of mice .
