Division of Infectious Diseases, Department of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Arch Dermatol Res. 2010 Jul;302(5):375-82. doi: 10.1007/s00403-010-1030-y. Epub 2010 Feb 4.
Staphylococcal skin infections are quite common in human patients. These infections often clear spontaneously, but may also progress locally and/or disseminate to cause serious and sometimes fatal deep infections. The present studies were undertaken to examine the clearance phase of experimental cutaneous Staphylococcus aureus infections in a mouse model system. Previous work in this system has shown that staphylococci applied to the skin rapidly disseminate to the spleen and kidney. In the present experiments the bacteria were found to persist at the skin infection site at a time (8 days after inoculation) when they had disappeared from the spleen and kidney. Examination of the infected skin at earlier times revealed rapid (within 6 h) invasion into the stratum corneum, stratum Malpighii, and dermis, but subsequent redistribution of bacteria (at 1-2 days) to more superficial sites, particularly crusts located just above the skin surface. The crusts seen in these infections were of two distinct types, which were termed type 1 and type 2. Type 1 crusts appeared first, consisted of bacteria, inflammatory cells, and debris, and developed over an intact epidermis. Type 2 crusts arose from the process of dermal necrosis previously reported to take place at 2 days in this model system. In the latter situation the bacteria were not really cleared from the epidermis and dermis; rather those layers were transformed into a superficial crust that contained the bacteria. Deep hair follicle infections in the dermis were found in these infections, but they did not persist and did not seem to be a reservoir for organisms in the dermis. Resolution of these experimental infections appeared to involve redistribution of invading bacteria to more superficial locations in crusts above the skin surface, marked proliferation of the epidermis, loss of the bacteria-laden crusts from the skin, and eventual healing of the cutaneous damage.
葡萄球菌皮肤感染在人类患者中很常见。这些感染通常会自行清除,但也可能在局部进展和/或传播,导致严重且有时致命的深部感染。本研究旨在检查小鼠模型系统中实验性皮肤金黄色葡萄球菌感染的清除阶段。该系统之前的工作表明,应用于皮肤的葡萄球菌迅速扩散到脾脏和肾脏。在本实验中,发现细菌在感染部位持续存在,而此时它们已经从脾脏和肾脏中消失(接种后 8 天)。对感染皮肤的早期检查显示,细菌迅速(在 6 小时内)侵入角质层、表皮和真皮,但随后细菌重新分布(在 1-2 天)到更浅表的部位,特别是位于皮肤表面上方的结痂。在这些感染中看到的结痂有两种不同的类型,分别称为 1 型和 2 型。1 型结痂首先出现,由细菌、炎症细胞和碎片组成,覆盖在完整的表皮上。2 型结痂是由之前在该模型系统中 2 天发生的真皮坏死过程引起的。在后一种情况下,细菌并没有真正从表皮和真皮中清除;相反,这些层被转化为包含细菌的浅表结痂。真皮深部毛囊感染在这些感染中被发现,但它们不会持续存在,也似乎不是真皮中细菌的储存库。这些实验性感染的解决似乎涉及到入侵细菌向更浅表的皮肤表面结痂处重新分布,表皮大量增殖,细菌负载的结痂从皮肤脱落,以及最终皮肤损伤的愈合。