糖尿病併發感染提昇了糖尿病患的死亡率,其中更以金黃色葡萄球菌(Staphylococcus aureus;SA)引起之感染佔大多數。對甲氧苯青黴素有抗藥性之金黃色葡萄球菌(methicillin-resistant Staphylococcus aureus;MRSA)是造成院內感染的主要病原菌之ㄧ,更是嚴重威脅糖尿病人的健康。本篇研究是以動物模式比較糖尿病感染SA及MRSA之間的差異。使用Balb/cA雄鼠經由尾靜脈注射streptozotocin以誘發糖尿病。確認糖尿病誘發成功後,分別經由尾靜脈注射SA及MRSA的菌液,感染後2天及4天犧牲。比較血液及腎臟之菌量、肝臟脂質氧化程度及血液及脾臟中細胞激素(IL-6、IL-2、TNFα、IFNγ)之濃度。結果顯示,糖尿病小白鼠感染MRSA後,在第4天犧牲時,其腎臟內的菌量有明顯增加的情形,而肝臟脂質氧化值也有增加的現象,血清IL-6及脾臟TNFα的濃度皆顯著高於控制組及DM組(p<0.05),而血清IL-2及脾臟IFNγ的濃度則無明顯之變化。根據本研究結果認為,糖尿病小白鼠感染MRSA時,其免疫功能可能因糖尿病失調,使得病程發展偏向於更嚴重的發炎反應,甚至造成死亡。
Methicillin-resistant Staphylococcus aureus (MRSA) are the major cause for the nosocomial infection occurred in Taiwan and other countries. Because of the antibiotic-resistant property, MRSA infection results in severe motility and morbidity. In this study, the difference between Staphylococcus aureus (SA) and MRSA infection in diabetic mice was examined. Diabetic mice were produced by streptozotocin (STZ) infection. Diabetic mice were killed after 2 and 4 days infection from SA and MRSA. Then, plasma, liver, kidney and spleen from each mouse were collected. The results showed that MRSA and SA significantly appeared in kidney (p<0.05), not in plasma; oxidation level in liver from MRSA infected diabetic mice was significantly elevated (p<0.05). Cytokine analysis showed that IL-6 and TNFα levels significantly increased in MRSA infected diabetic mice; however, IL-2 and IFNγ levels among these mice were not significantly different (p>0.05). These data suggest that MRSA infection in diabetic mice favors the inflammation and oxidation reactions, which causes further damage in diabetic mice.