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1. The physiological appearance of the wound.

Deep – the wound appeared to be deep due affecting both the epidermis and dermis of the patient. This indicated that the cut was a vital one. The injury was long, covering an approximated length of 2 cm and was situated on the left foot of the patient. Besides, the wound appeared swollen and filled with infected discharge. This could be possibly brought forward by the infection the could either be acquired from the disinfected handkerchief that was used to dress the wound or from the glass that caused the cutting on the patient (Atiyeh, Costagliola, Hayek, & Dibo, 2007).

2. Sources of injury infection

a. Staphylococci

Most wounds acquired through the deep cutting of the skin are contaminated by the patient's endogenous flora, which is present on the surface, mucous membranes, or hollow viscera. The traditional microbial concentration quoted as being highly associated with SSIs is that of bacterial counts higher than 10,000 organisms per gram of tissue (or in the case of burned sites, organisms per cm²of wound). The common pathogens on the skin and mucosal surfaces are gram-positive cocci (notably staphylococci). This could have been present on the handkerchief that the patient used in dressing the wound or on the skin of the patient (Tong, Davis, Eichenberger, Holland, & Fowler, 2015).

Erysipelothrix b.rhusiopathiae

This is found in the aquatic marketing environment. Since the patient was on a beach a couple of days ago, it means that this bacterial species could have been present on the surface of the glass that cat the patient (Guo, & DiPietro, 2010). The recent researches have indicated that, Lacerations and puncture wounds sustained in an aquatic environment (e.g., oceans, lakes, streams) may be contaminated with bacteria not typically found in land-based injuries, including Aeromonas hydrophila, Pseudomonas and Plesiomonas species, Vibrio species, Erysipelothrix rhusiopathiae, and Mycobacterium marinum (Guo, & DiPietro, 2010).

3. Antibiotics.

At first, when the patient visits the healthcare facility concerning her wound, the wound appearance is evidence enough that there has been an infection on the same. It is however impossible to look at the wound site with bear eyes and determine what is the microorganism behind the poisoning. For that matter, it is imperative to use a cephalosporin class of antibiotics on the patient (Kohira et al., 2016). This types of drugs are known to have an impact on a wide range of microorganisms. These antibiotics help in stopping further growth and spreading of the infection by such bacteria. The most commonly used antibiotic such cases are the ceftriaxone. For that matter, this drug is used in the case study presented since the causal microorganism is not yet determined (Lipsky, Dryden, Gottrup, Nathwani, Seaton, & Stryja, 2016).

When using cephalosporin class antibiotics, it is highly recommended that a tetanus injection is included in the therapeutic process. This I however not crucial in the case presented as the patient had had a tetanus injection, a couple of week before the instance. For that matter it was important to introduce another cephalosporin class of antibiotics in the therapeutic process, to supplement the one that was induced before (Kohira et al., 2016). This second antibiotic would be necessary for initializing the healing process for the wounds caused by a wide range of bacteria. This was essential as the first drag used was to stop further infections. The most appropriate drug for this case was cephalexin, as the causal bacteria was not yet determined (Heal, Banks, Lepper, Kontopantelis, & van Driel, 2016).

Upon the determination of the actual microorganism behind the infection, another antibiotic was introduced (dicloxacillin). This antibiotic was introduced to replace cephalexin since the real bacteria was found. Just Like other β-lactam anti-infection agents, dicloxacillin acts by restraining the amalgamation of bacterial cell dividers. It hinders cross-linkage between the direct peptidoglycan polymer ties that make up a noteworthy segment of the cell mass of Gram-positive microorganisms. This drug is one of the most effective antibiotics of this class; however, it has two significant side effects that may include, heartburn, nausea, vomiting, diarrhea; blisters or ulcers in your mouth, red or swollen gums, trouble swallowing;

4. The healing process of the wound

Wound-healing is a range of complicated interrelated biologic processes at the molecular level. For descriptive purposes, healing may be divided into the following three phases:

1. Inflammatory phase
2. Proliferative phase
3. Maturation phase

Inflammatory phase

The incendiary stage initiates when tissue trustworthiness is upset by damage; this starts the coagulation course to constrain dying. Platelets are the first of the cell parts that total to the injury, and, because of their degranulation (platelet response), they discharge a few cytokines (or paracrine development factors) (Martin, & Nunan, 2015). These cytokines incorporate platelet-determined development factor (PDGF), insulin-like development factor-1 (IGF-1), epidermal development factor (EGF), and fibroblast economic development factor (FGF) (SA, Muftah, & Jude, 2018). Serotonin is likewise discharged, which, together with histamine (released by pole cells), incites a reversible opening of the intersections between the endothelial cells, permitting the entry of neutrophils and monocytes (which progress toward becoming macrophages) to the site of damage (Takagi et al., 2017).

This massive cell development to the damage site is prompted by cytokines discharged by the platelets (chemotaxis) and promote chemotactic cytokines emitted by the macrophages themselves once at the location of damage. These incorporate changing development factor alpha (TGF-α) and evolving development factor beta (TGF-β). Subsequently, a provocative exudate that contains red platelets, neutrophils, macrophages, and plasma proteins, including coagulation course proteins and fibrin strands, fills the injury in a matter of hours. Macrophages search as well as our key to the injury mending process in light of their cytokine discharge (SA, Muftah, & Jude, 2018).

Proliferative phase

The proliferative stage starts as the cells that relocate to the site of damage, for example, fibroblasts, epithelial cells, and vascular endothelial cells, begin to multiply and the cellularity of the injury increments. The cytokines associated with this stage incorporate FGFs, especially FGF-2 (already known as fundamental FGF), which empowers angiogenesis and epithelial cell and fibroblast multiplication. The minor basal cells at the edge of the injury move over the damage, and, inside 48 hours, the whole twisted is epithelialized. In the profundity of the accident, the quantity of fiery cells diminishes with the expansion of stromal cells, for example, fibroblasts and endothelial cells, which, this way, keep on emitting cytokines. Cell expansion proceeds with the development of extracellular lattice proteins, including collagen and new vessels (angiogenesis). This procedure is variable length and may most recent a little while (Martin, & Nunan, 2015).

Maturation phase

In the development stage, the predominant element is collagen. The thick heap of strands, regular for collagen, is the characteristic constituent of the scar. Wound compression jumps out at some degree in essential shut injuries yet is an articulated component in wounds left to near to auxiliary expectation. The phones in charge of wound constriction are called myofibroblasts, which look like fibroblasts yet have cytoplasmic actin fibers in the cost of compression. The injury ceaselessly experiences redesigning to attempt to accomplish a state like that before damage. The injury has 70-80% of its different elasticity at 3-4 months after activity (Barchitta, Matranga, & Quattrocchi, 2012).

References

1. Atiyeh, B. S., Costagliola, M., Hayek, S. N., & Dibo, S. A. (2007). Effect of silver on burn wound infection control and healing: a review of the literature. Burns, 33(2), 139-148.
2. Barchitta M, Matranga D, Quattrocchi A, (2012). Prevalence of surgical site infections before and after the implementation of a multimodal infection control programme. J Antimicrob Chemother. 67(3):749-55. 
3. Guo, S. A., & DiPietro, L. A. (2010). Factors affecting wound healing. Journal of dental research, 89(3), 219-229.
4. Heal, C. F., Banks, J. L., Lepper, P. D., Kontopantelis, E., & van Driel, M. L. (2016). Topical antibiotics for preventing surgical site infection in wounds healing by primary intention. Cochrane Database of Systematic Reviews, (11).
5. Kohira, N., West, J., Ito, A., Ito-Horiyama, T., Nakamura, R., Sato, T., ... & Yamano, Y. (2016). In the vitro antimicrobial activity of a siderophore cephalosporin, S-649266, against Enterobacteriaceae clinical isolates, including carbapenem-resistant strains. Antimicrobial agents and chemotherapy, 60(2), 729-734.
6. Krausz, A. E., Adler, B. L., Cabral, V., Navati, M., Doerner, J., Charafeddine, R. A., ... & Harper, S. (2015). Curcumin-encapsulated nanoparticles as an innovative antimicrobial and wound healing agent. Nanomedicine: Nanotechnology, Biology and Medicine, 11(1), 195-206.
7. Lipsky, B. A., Dryden, M., Gottrup, F., Nathwani, D., Seaton, R. A., & Stryja, J. (2016). Antimicrobial stewardship in wound care: a position paper from the British Society for Antimicrobial Chemotherapy and European Wound Management Association. Journal of Antimicrobial Chemotherapy, 71(11), 3026-3035.
8. Martin, P., & Nunan, R. (2015). Cellular and molecular mechanisms of repair in acute and chronic wound healing. British Journal of Dermatology, 173(2), 370-378.
9. SA, A. E. A., Muftah, A. A., & Jude, E. B. (2018). Immunohistochemical Characterization of the Inflammatory Responses in Wound Healing and the Use of the Subcutaneous Polyvinyl Alcohol (PVA) Sponge Implantation Model for Evaluation of the Healing Process. J Cytol Histol, 9(519), 2.
10. Takagi, N., Kawakami, K., Kanno, E., Tanno, H., Takeda, A., Ishii, K., ... & Tachi, M. (2017). IL?17A promotes neutrophilic inflammation and disturbs acute wound healing in skin. Psychology Experimental Dermatology, 26(2), 137-144.
11. Tong, S. Y., Davis, J. S., Eichenberger, E., Holland, T. L., & Fowler, V. G. (2015). Staphylococcus aureus infections: epidemiology, pathophysiology, clinical manifestations, and management. Clinical microbiology reviews, 28(3), 603-661.