Rahim Kashif, Saleha Shamim, Zhu Xudong, Huo Liang, Basit Abdul, Franco Octavio Luiz
Institute of Biochemistry and Molecular Biology, College of Life Sciences, Beijing Normal University, Beijing, 100875, China.
Department of Biotechnology and Genetic Engineering, Kohat University of Science and Technology (KUST), Khyber Pakhtunkhwa Kohat, 26000, Pakistan.
Microb Ecol. 2017 Apr;73(3):710-721. doi: 10.1007/s00248-016-0867-9. Epub 2016 Oct 14.
A wound is damage of a tissue usually caused by laceration of a membrane, generally the skin. Wound healing is accomplished in three stages in healthy individuals, including inflammatory, proliferative, and remodeling stages. Healing of wounds normally starts from the inflammatory phase and ends up in the remodeling phase, but chronic wounds remain in an inflammatory stage and do not show progression due to some specific reasons. Chronic wounds are classified in different categories, such as diabetic foot ulcer (DFU), venous leg ulcers (VLU) and pressure ulcer (PU), surgical site infection (SSI), abscess, or trauma ulcers. Globally, the incidence rate of DFU is 1-4 % and prevalence rate is 5.3-10.5 %. However, colonization of pathogenic bacteria at the wound site is associated with wound chronicity. Most chronic wounds contain more than one bacterial species and produce a synergetic effect that results in previously non-virulent bacterial species becoming virulent and causing damage to the host. While investigating bacterial diversity in chronic wounds, Staphylococcus, Pseudomonas, Peptoniphilus, Enterobacter, Stenotrophomonas, Finegoldia, and Serratia were found most frequently in chronic wounds. Recently, it has been observed that bacteria in chronic wounds develop biofilms that contribute to a delay in healing. In a mature biofilm, bacteria grow slowly due to deficiency of nutrients that results in the resistance of bacteria to antibiotics. The present review reflects the reasons why acute wounds become chronic. Interesting findings include the bacterial load, which forms biofilms and shows high-level resistance toward antibiotics, which is a threat to human health in general and particularly to some patients who have acute wounds.
伤口是组织的损伤,通常由膜(一般为皮肤)的撕裂引起。在健康个体中,伤口愈合分三个阶段完成,包括炎症期、增殖期和重塑期。伤口愈合通常从炎症期开始,到重塑期结束,但慢性伤口由于某些特定原因会停留在炎症阶段且不会进展。慢性伤口分为不同类别,如糖尿病足溃疡(DFU)、下肢静脉溃疡(VLU)、压疮(PU)、手术部位感染(SSI)、脓肿或创伤性溃疡。在全球范围内,DFU的发病率为1%-4%,患病率为5.3%-10.5%。然而,伤口部位病原菌的定植与伤口慢性化有关。大多数慢性伤口含有不止一种细菌,会产生协同效应,导致原本无毒的细菌变得有毒并对宿主造成损害。在研究慢性伤口中的细菌多样性时,发现葡萄球菌、假单胞菌、嗜胨菌、肠杆菌、嗜麦芽窄食单胞菌、菲氏菌和沙雷氏菌在慢性伤口中最为常见。最近,人们观察到慢性伤口中的细菌会形成生物膜,这会导致愈合延迟。在成熟的生物膜中,由于营养物质缺乏,细菌生长缓慢,这导致细菌对抗生素产生耐药性。本综述反映了急性伤口转变为慢性伤口的原因。有趣的发现包括细菌载量,其形成生物膜并表现出对抗生素的高度耐药性,这对一般人类健康构成威胁,尤其对一些有急性伤口的患者。