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Ulcers  2013 

Chronic Wounds, Biofilms and Use of Medicinal Larvae

DOI: 10.1155/2013/487024

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Abstract:

Chronic wounds are a significant health problem in the United States, with annual associated costs exceeding $20 billion annually. Traditional wound care consists of surgical debridement, manual irrigation, moisture retentive dressings, and topical and/or systemic antimicrobial therapy. However, despite progress in the science of wound healing, the prevalence and incidence of chronic wounds and their complications are escalating. The presence & complexity of bacterial biofilms in chronic wounds has recently been recognized as a key aspect of non-healing wounds. Bacterial biofilms are sessile colonies of polymicrobial organisms (bacteria, fungus, etc.) enclosed within a self-produced exopolymeric matrix that provides high levels of tolerance to host defenses, antibiotics and antiseptics. Thus, there is a need for alternative therapies to reduce biofilms in chronic wounds. In this report, we present initial findings from in vitro experiments which show that larval debridement therapy with disinfected blow fly larvae (Phaenicia sericata) reduced total CFUs (6-logs) of planktonic and mature biofilms of Pseudomonas aeruginosa or Staphylococcus aureus grown on dermal pig skin explants by 5-logs after 24 hours of exposure, and eliminated biofilms (no measurable CFUs) after 48 hours of exposure. 1. Introduction Chronic wounds are a significant health problem in the USA. Chronic wounds are those wounds which fail to progress as expected through the typical healing processes in a timely manner. Health care costs related to the management and treatment of chronic wounds in the USA exceeds $20 billion annually [1–7]. For many health care providers, the treatment and management of nonhealing wounds are challenging. Traditionally, basic wound care has consisted of surgical debridement, manual irrigation, moisture retentive dressings, and topical and/or systemic antimicrobial therapy. Although there has been tremendous progress in the science of wound healing, the prevalence and incidence of chronic wounds and their associated complications continue to escalate [1]. The presence and complexity of bacterial biofilms in chronic wounds have recently been recognized as key aspects of nonhealing wounds [8–20]. Bacterial biofilms are sessile colonies of polymicrobial organisms (bacterial, fungal, and possibly, viral) which are often symbiotic. These biofilm colonies produce a protective coating to protect the colonies from host defenses. The character of this protective substance unique to biofilms is dynamic, and the production of its components seems to be triggered by

References

[1]  G. S. Schultz, R. G. Sibbald, V. Falanga et al., “Wound bed preparation: a systematic approach to wound management,” Wound Repair and Regeneration, vol. 11, supplement 1, pp. S1–S28, 2003.
[2]  A. K. Seth, M. R. Geringer, S. J. Hong, K. P. Leung, T. A. Mustoe, and R. D. Galiano, “In vivo modeling of biofilm-infected wounds: a review,” Journal of Surgical Research, vol. 178, no. 1, pp. 330–338, 2012.
[3]  M. D. Fogerty, N. N. Abumrad, L. Nanney, P. G. Arbogast, B. Poulose, and A. Barbul, “Risk factors for pressure ulcers in acute care hospitals,” Wound Repair and Regeneration, vol. 16, no. 1, pp. 11–18, 2008.
[4]  J. Vas, M. Modesto, C. Mendez et al., “Effectiveness of acupuncture, special dressings and simple, low-adherence dressings for healing venous leg ulcers in primary healthcare: study protocol for a cluster-randomized open-labeled trial,” BMC Complementary and Alternative Medicine, vol. 8, article 29, 2008.
[5]  M. J. Carter and R. A. Warriner III, “Evidence-based medicine in wound care: time for a new paradigm,” Advances in Skin & Wound Care, vol. 22, no. 1, pp. 12–16, 2009.
[6]  J. W. Costerton, P. S. Stewart, and E. P. Greenberg, “Bacterial biofilms: a common cause of persistent infections,” Science, vol. 284, no. 5418, pp. 1318–1322, 1999.
[7]  National Pressure Ulcer Advisory Panel (NPUAP) Website, http://www.npuap.org.
[8]  C. A. Fleck, “Fighting infection in chronic wounds,” Advances in Skin & Wound Care, vol. 19, no. 4, pp. 184–188, 2006.
[9]  F. Boutli-Kasapidou, F. Delli, N. Avgoustinaki, N. Lambrou, M. Tsatsos, and G. Karakatsanis, “What are biofilms? Evaluation and management in open skin wounds,” Journal of the European Academy of Dermatology and Venereology, vol. 20, no. 6, pp. 743–745, 2006.
[10]  W. Costerton, R. Veeh, M. Shirtliff, M. Pasmore, C. Post, and G. Ehrlich, “The application of biofilm science to the study and control of chronic bacterial infections,” Journal of Clinical Investigation, vol. 112, no. 10, pp. 1466–1477, 2003.
[11]  S. G. Jones, R. Edwards, and D. W. Thomas, “Inflammation and wound healing: the role of bacteria in the immunoregulation of wound healing,” The International Journal of Lower Extremity Wounds, vol. 3, no. 4, pp. 201–208, 2004.
[12]  L. Hall-Stoodley, J. W. Costerton, and P. Stoodley, “Bacterial biofilms: from the natural environment to infectious diseases,” Nature Reviews Microbiology, vol. 2, no. 2, pp. 95–108, 2004.
[13]  M. R. Parsek and P. K. Singh, “Bacterial biofilms: an emerging link to disease pathogenesis,” Annual Review of Microbiology, vol. 57, pp. 677–701, 2003.
[14]  R. Edwards and K. G. Harding, “Bacteria and wound healing,” Current Opinion in Infectious Diseases, vol. 17, no. 2, pp. 91–96, 2004.
[15]  G. A. James, E. Swogger, R. Wolcott et al., “Biofilms in chronic wounds,” Wound Repair and Regeneration, vol. 16, no. 1, pp. 37–44, 2008.
[16]  S. E. Dowd, Y. Sun, P. R. Secor et al., “Survey of bacterial diversity in chronic wounds using pyrosequencing, DGGE, and full ribosome shotgun sequencing,” BMC Microbiology, vol. 6, article 43, 2008.
[17]  K. Kirketery-Moller, P. O. Jensen, M. Fazli, et al., “Distribution, organization, and ecology of bacteria in chronic wounds,” Journal of Clinical Microbiology, vol. 46, no. 8, pp. 2717–2722, 2008.
[18]  T. Bjarnsholt, K. Kirketerp-M?ller, P. ?. Jensen et al., “Why chronic wounds will not heal: a novel hypothesis,” Wound Repair and Regeneration, vol. 16, no. 1, pp. 2–10, 2008.
[19]  K. Gj?dsb?l, J. J. Christensen, T. Karlsmark, B. J?rgensen, B. M. Klein, and K. A. Krogfelt, “Multiple bacterial species reside in chronic wounds: a longitudinal study,” International Wound Journal, vol. 3, no. 3, pp. 225–231, 2006.
[20]  V. W. Serralta, C. Harrison-Balestra, A. L. Cazzaniga, S. C. Davis, and P. M. Mertz, “Lifestyles of bacteria in wounds: presence of biofilms?” Wounds, vol. 13, no. 1, pp. 29–34, 2001.
[21]  E. Klein, D. L. Smith, and R. Laxminarayan, “Community-associated methicillin-resistant Staphylococcus aureus in outpatients, United States, 1999–2006,” Emerging Infectious Diseases, vol. 15, no. 12, pp. 1925–1930, 2009.
[22]  S. L. Percival and P. G. Bowler, “Biofilms and their potential role in wound healing,” Wounds, vol. 16, no. 7, pp. 234–240, 2004.
[23]  L. Hall-Stoodley and P. Stoodley, “Evolving concepts in biofilm infections,” Cellular Microbiology, vol. 11, no. 7, pp. 1034–1043, 2009.
[24]  R. D. Wolcott, D. D. Rhoads, M. E. Bennett et al., “Chronic wounds and the medical biofilm paradigm,” Journal of Wound Care, vol. 19, no. 2, pp. 45–52, 2010.
[25]  P. L. Phillips, R. D. Wolcott, J. Fletcher, and G. S. Schultz, “Biofilms made easy,” Wounds International, vol. 1, no. 3, pp. 1–6, 2010.
[26]  R. D. Wolcott, J. W. Costerton, D. Raoult, and S. J. Cutler, “The polymicrobial nature of biofilm infection,” Clinical Microbiology and Infection. In press.
[27]  E. Veiga, J. A. Guttman, M. Bonazzi et al., “Invasive and adherent bacterial pathogens co-opt host clathrin for infection,” Cell Host and Microbe, vol. 2, no. 5, pp. 340–351, 2007.
[28]  D. Gibson, B. Cullen, R. Legerstee, K. G. Harding, and G. Schultz, “MMPs made easy,” Wounds International, vol. 1, no. 1, pp. 1–6, 2010.
[29]  V. C. Tam, D. Serruto, M. Dziejman, W. Brieher, and J. J. Mekalanos II, “A type III secretion system in Vibrio cholerae translocates a formin/spire hybrid like actin nucleator to promote intestinal colonization,” Cell Host and Microbe, vol. 1, no. 2, pp. 95–107, 2007.
[30]  Y. Iizumi, H. Sagara, Y. Kabe et al., “The enteropathogenic E.coli effector EspB facilitates microvillus effacing and antiphagocytosis by inhibiting myosin function,” Cell Host and Microbe, vol. 2, no. 6, pp. 383–392, 2007.
[31]  G. M. Preston, “Metropoliitan microbes: type III secretion in multihost symbionts,” Cell Host and Microbe, vol. 2, no. 5, pp. 291–294, 2007.
[32]  E. Mills, K. Baruch, X. Charpentier, S. Kobi, and I. Rosenshine, “Real-time analysis of effector translocation by the type III secretion system of enteropathogenic Escherichia coli,” Cell Host and Microbe, vol. 3, no. 2, pp. 104–113, 2008.
[33]  H. Mimuro, T. Suzuki, S. Nagai et al., “Helicobacter pylori dampens gut epithelial self-renewal by inhibiting apoptosis, a bacterial strategy to enhance colonization of the stomach,” Cell Host and Microbe, vol. 2, no. 4, pp. 250–263, 2007.
[34]  H. K. Kuramitsu, X. He, R. Lux, M. H. Anderson, and W. Shi, “Interspecies interactions within oral microbial communities,” Microbiology and Molecular Biology Reviews, vol. 71, no. 4, pp. 653–670, 2007.
[35]  R. D. Wolcott, D. D. Rhoads, and S. E. Dowd, “Biofilms and chronic wound inflammation,” Journal of Wound Care, vol. 17, no. 8, pp. 333–341, 2008.
[36]  S. Elias and E. Banin, “Multi-species biofilms: living with friendly neighbors,” FEMS Microbiology Reviews. In press.
[37]  M. M. Manring and J. H. Calhoun, “Biographical sketch: William S. Baer (1872–1931),” Clinical Orthopaedics and Related Research, vol. 469, no. 4, pp. 917–919, 2011.
[38]  M. L. Marineau, M. T. Herrington, K. M. Swenor, and L. J. Eron, “Maggot debridement therapy in the treatment of complex diabetic wounds,” Hawaii Medical Journal, vol. 70, pp. 121–124, 2011.
[39]  W. S. Baer, “The treatment of chronic osteomyelitis with the maggot (larva of the blow fly),” The Journal of Bone & Joint Surgery, vol. 13, pp. 438–475, 1931.
[40]  C. A. Acton, “Know-how guide to using larval therapy for wound debridement,” Wound Essentials, vol. 2, pp. 156–159, 2007.
[41]  R. A. Sherman, “Maggot therapy takes us back to the future of wound care: new and improved maggot therapy for the 21st century,” Journal of Diabetes Science and Technology, vol. 3, no. 2, pp. 336–344, 2009.
[42]  H. Evans, “A treatment of last resort,” Nursing Times, vol. 93, no. 23, pp. 62–65, 1997.
[43]  P. E. Prete, “Growth effects of Phaenicia sericata larval extracts on fibroblasts: mechanism for wound healing by maggot therapy,” Life Sciences, vol. 60, no. 8, pp. 505–510, 1997.
[44]  Medical MaggotsTM package insert, http://www.monarchlabs.com/maggotpi.pdf.
[45]  BioTherapeutics, Education and Research Foundation, 2009, Draft Policies and Procedures for Maggot Debridement Therapy (MDT) http://www.BTERFoundation.org.

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