Background: An acute wound infection might be caused by external damage to the skin including abrasions, lacerations, bites, burns, accidents, war injuries and surgical incisions. When a wound fails to heal within a week, it should be considered a chronic type. Complement system potent inflammatory cascade in wound infection, is important and altered wound healing. Complement activation leads to the generation of many potent effectors including anaphylatoxin C5a. C5a has induced synthesis of TNF-α and IL-1β in macrophage and monocyte which are all together the goal of the present paper. Methodology: This study was conducted in Al-Kindy and Al-Wasity hospitals in Baghdad on 200 patients suffering from wounds. One hundred patients were with acute wounds infection and the other 100 patients considered as control wounds i.e. without infection. The procedure method was followed according to manufacturer’s instructions (Elabscience, USA) utilizing C5a ELISA kit for conducting the test. Blood samples were taken at 24, 48, 72, 96 and 120 hours of hospitalization of the patients. Results: It was found that the highest concentration of C5a was found at 120 hours after patients hospitalization who were with wound infection, and the mean value of C5a was 4898 pg/ml. 4661 pg/ml of C5a was recorded among patients with acute-phase infection compared to 4387 pg/ml concentration of the same complement among control group without wound infection at 96 hours post residence in hospital. Conclusions: Gram-positive bacteria were more prevalent causing wound infections. Dermacoccus nishinomiyaensis, Kocuria rosea and Kocuria kristinae were isolated for the first time in this locality. A complement 5a (C5a) revealed a very high concentration in acute-phase of wound infections. It was found that C5a was serially elevated with time of hospitalization of wounded and infected patients. C5a was highly elevated with wound infection by Gram-negative bacteria compared to infections by Gram-negatives.
References
[1]
White, R.J. (2009) Wound Infection-Associated Pain. Journal of Wound Care, 18, 245-249. https://doi.org/10.12968/jowc.2009.18.6.42803
[2]
Macleod, A.S. and Mansbridage, J.N. (2004) The Innate Immune System in Acute and Chronic Wounds. Advances in Wound Care, 5, 65-78.
https://doi.org/10.1089/wound.2014.0608
[3]
Daha, N.A., Banda, N.K., Roos, A., Beurskens, F.J., Bakker, J.M. and Daha, M.R. (2011) Complement Activation by (Auto-) Antibodies. Molecular Immunology, 48, 1656-1665. https://doi.org/10.1016/j.molimm.2011.04.024
[4]
Van de Goot, F., Krjinen, P.A.J., Begieneman, M.P.V., Middelkoop, E. and Niessen, H.W.M. (2006) Acute Inflammation Is Persistent Locally in Burn Wounds: A Pivotal Role for Complement and C-Reactive Protein. Journal of Burn Care and Research, 30, 274-280. https://doi.org/10.1097/BCR.0b013e318198a252
[5]
Cunnion, K.M., Krishna, N.K., Pallera, H.K., Fernandez, A.P., Rivera, M.G., Hair, P.S., Lassiter, B.P., Mary, A.C., Hood, A.F., Rodeheaver, G.T., Cottler, P.S., Jerry, L.N. and Dobrian, A.D. (2017) Complement Activation and STAT4 Expression Are Associated with Early Inflammation in Diabetic Wounds. PLoS ONE, 12, e0170500.
https://doi.org/10.1371/journal.pone.0170500
[6]
Markiewski, M.M. and Lambis, J.D. (2007) The Role of Complement in Inflammatory Diseases From Behind the Scenes into the Spotlight. The American Journal of Pathology, 171, 715-727. https://doi.org/10.2353/ajpath.2007.070166
[7]
Burke-Gaffney, A., Blease, K., Hartnell, A. and Hellewell, P.G. (2002) TNF-α Potentiates C5a-Stimulated Eosinophil Adhesion to Human Bronchial Epithelial Cell: A Role for α5β1 Integrin. The Journal of Immunology, 168, 1380-1388.
https://doi.org/10.4049/jimmunol.168.3.1380
[8]
Amara, U., Flierl, M.A., Rittirsch, D., Klos, A., Chen, H., Acker, B., Bruckner, U.B., Nilsson, B., Gebhard, F., Lambris, J.D. and Huber-Lang, M. (2010) Molecular Intercommunication between the Complement and Coagulation System. Journal of Immunology, 185, 5628-5636. https://doi.org/10.4049/jimmunol.0903678
[9]
Oikonomopoulou, K. and Ricklin, D. (2012) Interactions between Coagulation and Complement-Their Role in Inflammation. Seminars in Immunopathology, 34, 151-165. https://doi.org/10.1007/s00281-011-0280-x
[10]
Angel, D.E., Lioyd, P., Carville, K. and Santamaria, N. (2011) The Clinical Efficacy of Two Semi-Quantitative Wound-Swabbing Techniques in Identifying the Causative Organisms in Infected Cutaneous Wounds. International Wound Journal, 8, 176-185. https://doi.org/10.1111/j.1742-481X.2010.00765.x
[11]
Bonham, P.A. (2009) Swab Cultures for Diagnosis Wound Infections: A Literature Review and Clinical Guideline. Journal of Wound Ostomy and Continence Nursing, 36, 389-395. https://doi.org/10.1097/WON.0b013e3181aaef7f
[12]
Forbes, B.A., Sahm, D.F. and Weissfeld, A.S. (2007) Bailey and Scott’s Diagnostic Microbiology. 12th Edition, Mosby, Maryland Heights, MO, 108.
[13]
Kamlage, B., Neuber, S., Bethan, B., Maldonado, S.G., Wagner-Golbs, A., Peter, E. and Schatz, P. (2018) Impact of Prolonged Blood Incubation and Extended Serum Storage at Room Temperature on the Human Serum Metabolome. Journal of Metabolites, 8, 1-13. https://doi.org/10.3390/metabo8010006
[14]
Scales, B. and Huffnagle, G. (2013) The Microbime in Wound Repair and Tissue Fibrosis. The Journal of Pathology, 229, 323-331. https://doi.org/10.1002/path.4118
[15]
Nagoba, B., Raju, R., Wadher, B., Gandhi, R., Rao, A.K., Selkar, S. and Hartalkar, A. (2011) Citric Acid Treatment of Surgical Site Infections: A Prospective Open Study. Wound Practice and Research: Journal of the Australian Wound Management Association, 19, 82-86.
[16]
Yin, H., Li, X., Hu, S., Liu, T., Yuan, B., Ni, Q., Lan, F., Luo, X., Gu, H. and Zheng, F. (2013) IL-33 Promotes Staphylococcus aureus-Infected Wound Healing in Mice. International Immunopharmacology, 17, 432-438.
https://doi.org/10.1016/j.intimp.2013.07.008
[17]
Rajan, S. (2012) Skin and Soft-Tissue Infections: Classifying and Treating a Spectrum. Cleveland Clinic Journal of Medicine, 79, 57-66.
https://doi.org/10.3949/ccjm.79a.11044
[18]
Alwan, M.J., Lafta, I.J. and Hamzah, A.M. (2011) Bacterial Isolation from Burn Wound Infections and Studying Their Antimicrobial Susceptibility. Kufa Journal for Veterinary Medical Sciences, 2, 121-131.
[19]
Chen, H.M., Chi, H., Chiu, N.C. and Huang, F.Y. (2015) Kocuria kristinae: A True Pathogen in Pediatric Patients. Journal of Microbiology, Immunology and Infection, 48, 80-84. https://doi.org/10.1016/j.jmii.2013.07.001
[20]
Horino, T., Shimamura, Y., Ogata, K., Inoue, K. and Terada, Y. (2016) Kocuria kristinae Septic Arthritis Associated with Infectious Endocarditis in a Hemodialysis Patients with Diabetic Mellitus: A Case Report and Literature Review. Renal Replacement Therapy, 2, 32-41. https://doi.org/10.1186/s41100-016-0041-3
[21]
Ma, E.S., Wong, C.L., Lai, K.T., Chan, E.C., Yam, W. and Chan, A.C. (2005) Kocuria kristinae Infection Associated with Acute Cholecystitis. BMC Infectious Diseases, 5, 60-66. https://doi.org/10.1186/1471-2334-5-60
[22]
Kandi, V., Palange, P., Vaish, R., Bhatti, A.B., Kale, V., Kandi, M.R. and Bhoomagiri, M.R. (2016) Emerging Bacterial Infection: Identification and Clinical Significance of Kocuria Spp. Cureus, 8, 73-81. https://doi.org/10.7759/cureus.731
[23]
Shah, P., Ostwal, K., Jadhav, A. and Shaikh, N. (2015) Post Hysterectomy Wound Infection by Dermacoccus Nishinomiyaensis—A First Case Report in India. European Journal of Biomedical and Pharmaceutical Sciences, 2, 329-335.
[24]
Valen, A. (2011) Characterization of Airborne Microorganism at National Theatre Subway Station. Master’s Thesis, Norwegian University of Science and Technology, Gjøvik, Norway.
[25]
Al-Ali, K.Y. (2016) Microbial Profile of Burn Wound Infections in Burn Patients, Taif, Saudi Arabia. Archives of Clinical Microbiology, 7, 1-9.
[26]
Rashid, K.J., Babakir-Mina, M. and Abdilkarim, D.A. (2017) Characteristics of Burn Injury and Factors in Relation to Infection among Pediatric Patients. MOJ Gerontology and Geriatrics, 1, 1-13.
[27]
Idomir, M., Pirau, R., Nemet, C. and Badea, M. (2012) Evaluation of Microbiological Spectrum of Burn Wound Infections. Bulletin of the Transilvania University of Brasov, 5, 7-11.
[28]
Datta, S., Ghosh, T., Sarkar, D., Tudu, N.K., Chatterjee, T.K. and Jana, A. (2016) Bacteriological Profile of Burn Wounds and Their Antibiotic Susceptibility Pattern in a Tertiary Care Hospital. International Journal of Scientific Study, 4, 141-145.
[29]
Orban, C. (2012) Diagnostic Criteria for Sepsis in Burns Patients. Chirurgia (Bucur), 107, 697-700.
[30]
Rafail, S., Kourtzelis, I., Foukas, P.G., Markiewski, M.M., De Angelis, R.A., Guariento, M., Ricklin, D., Grice, E.A. and Lambris, J.D. (2015) Complement Deficiency Promotes Cutaneous Wound Healing in Mice. The Journal of Immunology, 194, 1285-1291. https://doi.org/10.4049/jimmunol.1402354
[31]
Triplett, A. and Hurwitz, A.A. (2014) Complement and Adaptive Immunity: Roles for the Anaphylatoxins C3a and C5a in Regulating Tumor Immunity. International Trends in Immunity, 2, 78-82.
[32]
Jang, J.H., Liang, D., Kido, K., Sun, Y., Clark, D.J. and Brennan, T.J. (2011) Increased Local Concentration of Complement C5a Contributes to Incisional Pain in Mice. Journal of Neuroinflammation, 8, 1-17.
https://doi.org/10.1186/1742-2094-8-80
[33]
Morris, A.C., Kefala, K., Wilkinson, T.S., Dhaliwal, K., Farrell, L., Walsh, T., Mackenzie, S.J., Reid, H., Davidson, D.J., Haslett, C., Rossi, A.G., Sallenave, J.M. and Simpso, A.J. (2009) C5a Mediates Peripheral Blood Neutrophil Dysfunction in Critically III Patients. American Journal of Respiration and Critical Care Medicine, 180, 19-28. https://doi.org/10.1164/rccm.200812-1928OC
[34]
Cazander, G., Jukema, G.N. and Nibbering, P.H. (2012) Complement Activation and Inhibition in Wound Healing. Clinical and Developmental Immunology, 2012, Article ID: 534291. https://doi.org/10.1155/2012/534291
