Hirsch Tobias, Spielmann Malte, Zuhaili Baraa, Koehler Till, Fossum Magdalena, Steinau Hans-Ulrich, Yao Feng, Steinstraesser Lars, Onderdonk Andrew B, Eriksson Elof
Division of Plastic Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
BMC Surg. 2008 Feb 29;8:5. doi: 10.1186/1471-2482-8-5.
Wound infection is a common complication in diabetic patients. The progressive spread of infections and development of drug-resistant strains underline the need for further insights into bacterial behavior in the host in order to develop new therapeutic strategies. The aim of our study was to develop a large animal model suitable for monitoring the development and effect of bacterial infections in diabetic wounds.
Fourteen excisional wounds were created on the dorsum of diabetic and non-diabetic Yorkshire pigs and sealed with polyurethane chambers. Wounds were either inoculated with 2 x 108 Colony-Forming Units (CFU) of Staphylococcus aureus or injected with 0.9% sterile saline. Blood glucose was monitored daily, and wound fluid was collected for bacterial quantification and measurement of glucose concentration. Tissue biopsies for microbiological and histological analysis were performed at days 4, 8, and 12. Wounds were assessed for reepithelialization and wound contraction.
Diabetic wounds showed a sustained significant infection (>105 CFU/g tissue) compared to non-diabetic wounds (p < 0.05) over the whole time course of the experiment. S. aureus-inoculated diabetic wounds showed tissue infection with up to 8 x 107 CFU/g wound tissue. Non-diabetic wounds showed high bacterial counts at day 4 followed by a decrease and no apparent infection at day 12. Epidermal healing in S. aureus-inoculated diabetic wounds showed a significant delay compared with non-inoculated diabetic wounds (59% versus 84%; p < 0.05) and were highly significant compared with healing in non-diabetic wounds (97%; p < 0.001).
Diabetic wounds developed significantly more sustained infection than non-diabetic wounds. S. aureus inoculation leads to invasive infection and significant wound healing delay and promotes invasive co-infection with endogenous bacteria. This novel wound healing model provides the opportunity to closely assess infections during diabetic wound healing and to monitor the effect of therapeutical agents in vivo.
伤口感染是糖尿病患者常见的并发症。感染的逐步扩散和耐药菌株的出现凸显了进一步深入了解宿主中细菌行为以制定新治疗策略的必要性。我们研究的目的是建立一个适合监测糖尿病伤口细菌感染发展及影响的大型动物模型。
在糖尿病和非糖尿病约克夏猪的背部制造14个切除伤口,并用聚氨酯腔室封闭。伤口要么接种2×10⁸个金黄色葡萄球菌菌落形成单位(CFU),要么注射0.9%无菌盐水。每天监测血糖,并收集伤口液体进行细菌定量和葡萄糖浓度测量。在第4、8和12天进行组织活检以进行微生物学和组织学分析。评估伤口的再上皮化和伤口收缩情况。
在整个实验过程中,与非糖尿病伤口相比,糖尿病伤口显示出持续的显著感染(>10⁵CFU/g组织)(p<0.05)。接种金黄色葡萄球菌的糖尿病伤口显示组织感染,伤口组织中CFU高达8×10⁷/g。非糖尿病伤口在第4天细菌计数较高,随后下降,在第12天无明显感染。接种金黄色葡萄球菌的糖尿病伤口的表皮愈合与未接种的糖尿病伤口相比有显著延迟(59%对84%;p<0.05),与非糖尿病伤口的愈合相比差异极显著(97%;p<0.001)。
糖尿病伤口比非糖尿病伤口发生更持续的显著感染。接种金黄色葡萄球菌会导致侵袭性感染和显著的伤口愈合延迟,并促进与内源性细菌的侵袭性合并感染。这种新型伤口愈合模型为在糖尿病伤口愈合期间密切评估感染以及监测体内治疗药物的效果提供了机会。