The human skin microbiome is incredibly diverse and can contain up to one billion microorganisms on a single square centimeter, including bacteria, fungi, viruses, and arthropods.1 These dynamic environments often become more complicated when wounds are present, and the types of microorganisms present near the dead and damaged tissue reduce the ability to eliminate them through normal immune responses and with standard antimicrobials.2 The treatment of chronic wounds presents a persistent challenge in the nation’s health care system that is often costly and resource intensive.3 Chronic wounds have a biological or physiological reason for not healing, and it is becoming increasingly evident that microbial biofilms play a pathogenic role in the inability of chronic wounds to heal.4
Research has shown that standard skin microbiota is essential in maintaining overall health and plays a key role in metabolic and homeostatic functions.5 In recent years, interest in the relationship between microbiota and disease has grown, and as new tools are developed to analyze the large-sequence datasets, it is becoming increasingly apparent that the skin microbiome does play a role in several conditions or diseases, although much more research is needed in this field. The current data suggest that skin microbiota may have an impact on a wide variety of conditions and diseases, including colorectal cancer and bowel disease. In addition to this, it plays an even-greater role in immunologically mediated skin diseases and other cutaneous conditions such as acne, dermatitis, rosacea, psoriasis, and chronic wounds.5
Despite knowing little about the role that microbiota and skin biofilms play in healing, investigators have demonstrated that pathogenic biofilms contribute to impairment of healing and increase the risk for infection.6 When a wound is present, the skin microbiota found is often different from healthy, intact cutaneous surfaces on the same individual. Although this microbiota often protects against diseases, it can also prolong lesions and delay healing. This complex relationship is not fully understood. However, several findings suggest some of the reasons that may contribute to prolonged healing time. Advanced rRNA techniques are finding wound colonizers that were not previously detected using culture-based studies. Several significant findings have also shown that wounds generally have higher levels of anaerobic bacteria, which may contribute to a delay in healing. Moreover, the type of injury and its severity, complications, and location also influence microbiota diversity and composition. Microbiota on a wound becomes more similar to the adjacent microbiota as the wound is healing.7
Currently, the primary method of treatment for chronic wounds is antibiotic therapy, even though there is little evidence of benefit. The major drawback of this therapeutic approach is that we are seeing more antibiotic-resistant bacteria prevalent in wounds.8 These antibiotics should be used to treat only active infections and not to heal chronic wounds. Although future treatment of chronic wounds will likely be highly dependent on genetically based analyses that allow for an individualized treatment plan, our knowledge of which types of microbiota are harmful and which are beneficial is still limited. As this knowledge expands, so too will the level of sophistication for this type of treatment. Without this key knowledge, the best approach to treating pathogenic biofilms in chronic wounds lies in using a multipronged approach that includes initial wound cleansing, frequent debridement, and subsequent application of appropriate antimicrobial wound dressings.6
1. Weyrich LS, Dixit S, Farrer AG, Cooper AJ, Cooper AJ. The skin microbiome: associations between altered microbial communities and disease. Australas J Dermatol. 2015;56:268–74.
2. Vyas KS, Wong LK. Detection of biofilm in wounds as an early indicator for risk for tissue infection and wound chronicity. Ann Plast Surg. 2016;76(1):127–31.
3. Gontcharova V, Youn E, Sun Y, Wolcott RD, Dowd S. A comparison of bacterial composition in diabetic ulcers and contralateral intact skin. Open Microbiol J. 2010;4:8–19.
4. Price LB, Liu CM, Melendez JH, et al. Community analysis of chronic wound bacteria using 16s rRNA gene-based pyrosequencing: impact of diabetes and antibiotics on chronic wound microbiota. PLoS One. 2009;4(7):e6462.
5. Cho I, Blaser MJ. The human microbiome: at the interface of health and disease. Nat Rev Genet. 2012;13(4):260–70.
6. Percival SL, McCarty SM, Lipsky B. Biofilms and wounds: an overview of the evidence. Adv Wound Care (New Rochelle). 2015;4(7):373–81.
7. Hannigan GD, Hodkinson BP, McGinnis K, et al. Culture-independent pilot study of microbiota colonizing open fractures and associations with severity, mechanism, location, and complication from presentation to early outpatient follow-up. J Orthop Res. 2014;32(4):597–605.
8. O’Meara S, Al-Kurdi D, Ovington LG. Antibiotics and antiseptics for venous leg ulcers. Cochrane Database Syst Rev. 2010;(1):CD003557.
The views and opinions expressed in this blog are solely those of the author, and do not represent the views of WoundSource, HMP Global, its affiliates, or subsidiary companies.