PhysiologyThe pathophysiology of infection, inflammatory response, and sepsis leading to septic shock (the cascade) is a major area of ​​interest in the literature. Under normal circumstances, when a pathogen enters a human host and tissue damage occurs, the host initiates an inflammatory response to repair the tissues. The main types of pathogens include viruses, bacteria and parasites (Porth & Matfin, 2009; Raghavan & Marik, 2006). Cellulitis is an example of an acute infection that affects the skin and/or subcutaneous tissues, often in the lower extremities. Cellulitis is caused by Streptococcus pyogenes and Staphylococcus aureus (multi-drug resistant bacteria) and is transmitted by direct contact, entering the body via skin lesions such as ulcers and/or following trauma. The presentation of cellulitis often includes (localized) pain, erythema, fever, and swelling. Infections such as cellulitis tend to become systemic through distribution into the blood and lymph (Hadzovic-Cengic et al., 2012). The inflammatory response to infection involves the release of pro- and anti-inflammatory mediators. When excessive pro-inflammatory mediators such as cytokines are released, they cause inflammation systemically which can cause sepsis or systemic inflammatory response syndrome (which is a non-specific response to a non-infectious cause) (Sagy, Al- Qaqaa and Kim, 2013). Pro-inflammatory mediators also activate the complement system, resulting in increased inflammation and upregulation of specific receptors leading to cell damage and apoptosis seen in severe sepsis and organ dysfunction (Ward , 2008). Organ dysfunction can occur in one or more organs such as the lungs, liver, kidneys and/or heart and often results from a lack of...... middle of paper ..... .. (2012). Severe sepsis in prehospital emergency care: analysis of incidence, care and outcomes. American Journal of Respiratory and Critical Care Medicine, 186(12), 1264-1271. doi:10.1164/rccm.201204-0713OC Trautmann, M., Scheibe, C., Wellinghausen, N., Holst, O., & Lepper, P. M. (2010). Low release of endotoxins from Escherichia coli and Bacteroides fragilis upon exposure to moxifloxacin. Chemotherapy, 56(5), 364-370. doi:10.1159/000321622 Vincent, J. L. & De Backer, D. (2013). Circulatory shock. New England Journal of Medicine, 369(18), 1726-1734. doi:10.1056/NEJMc1314999Ward, P.A. (2008). Sepsis, apoptosis and complement. Biochemical Pharmacology, 76(11), 1383-1388. doi:10.1016/j.bcp.2008.09.017Zawistowski, Calif. (2013). Management of sepsis. Current Issues in Pediatric and Adolescent Health Care, 43(10), 285. doi:10.1016/j.cppeds.2013.10.005