Physiological basis of wound observations, sources of contamination and antibiotic rationale for Mary's wound

This article explains the physiological basis of wound observations, sources of contamination and antibiotic rationale for Mary's wound. It also discusses the process by which Mary's wound will heal.

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Student name (LAST NAME first name): Asad, Mohammad Basel
Student number: 17800192
Campus: Parramatta
Tutorial session (time and room no.): PS-EA.1.33 (CLS)
Tutor’s name: Alexis Cunningham & Gladis Kabil
1. Physiological basis of the wound observations (Total: 10 marks)
Mary’s wound was painful and swollen, which is a symptom of inflammation (Craft &
Gordon, 2015). Inflammation is stimulated when tissues in the body become infected
by pathogens (Craft & Gordon, 2015). Inflammatory chemicals increase the
permeability of local capillaries to help transport white blood cells to the wound area
to fight invading pathogens. As a result, capillaries will leak fluid which contains
protein and plasma and this fluid is known as exudate. (Marieb & Hoehn, 2016). The
swelling of Mary’s wound is caused by the excess exudate collecting at the wound
site, and the sensation of pain is attributed to the exudate pressing and stimulating
the adjacent nerve endings. (Marieb & Hoehn, 2016).
Mary’s wound was red and hot to touch and this is also a sign of inflammation. There
are a number of inflammatory chemicals such as prostaglandins, kinins, and
chemotaxins which are released during injury (Marieb & Hoehn, 2016). These
chemicals cause capillaries to dilate which increases the blood flowing to the wound
site known as hyperaemia. Hyperaemia leads to redness and heat at the site of the
wound and increases average body temperature to promote the metabolic rate of
cells to expedite wound healing (Marieb & Hoehn, 2016).
The third observation of Mary’s wound was purulent discharge. When a wound is
infected by an invading pathogen, the inflammatory response in initiated and
neutrophils and macrophages will migrate to the wound site (Marieb & Hoehn, 2016).
Neutrophils and macrophages engulf invading pathogens and microorganisms to

destroy them and help remove them from the body known as phagocytosis (Marieb &
Hoehn, 2016). After this process is complete, purulent discharge occurs and this
discharge is a combination of dead neutrophils, living and dead pathogens and tissue
debris (Marieb & Hoehn, 2016).
2. Possible sources of contamination and modes of transmission (Total: 10 marks)
2.1 Name one endogenous source of contamination and discuss the mode of
transmission from the source to the new host. (5 marks)
Endogenous sources of contamination can occur from natural flora present in the
body (Lee & Bishop, 2016). Staphylococcus aureus (S. aureus) is found on the skin
and inside the nose and makes up the natural microbiota of the body. Natural
microbiota of the skin can become opportunistic and cause infection if they enter the
body through a wound or enter sterile parts of the body to cause endogenous
infection (Lee & Bishop, 2016) The infectious agent, S. aureus can be transported
from a source or reservoir to a vulnerable host via the infection chain (Gary, 2016). In
terms of Mary’s situation, Mary initially had a laceration to her foot. This may have
become infected when she touched her skin or nose, and then the wound. S. aureus
is a pathogen, Mary’s skin or nose is the reservoir or source of infection and her skin
is the portal of exit and her laceration is the portal of entry. Direct skin to skin contact
is the mode of transmission with Mary being a susceptible host.
2.2 Name one exogenous source of contamination and discuss the mode of
transmission from the source to the new host. (5 marks)
Exogenous sources of contamination occur from sources external to the body as
opposed to an endogenous source of contamination (Lee & Bishop, 2016). This
includes microorganisms carried by healthcare workers or fomites which are
inanimate objects that carry pathogens on their surface (Gary, 2016). S. aureus is
the most prevalent cause of infections within hospitals and it is estimated that

around half of all hospital staff carry strains of S. aureus. (Gary, 2016). When Mary
went to the hospital to have her wound cleaned and sutured, the healthcare worker
attending Mary’s wound may have touched their skin or nose and failed to wash their
hands thoroughly. The pathogens on their hand may have transferred to the
bandage used on Mary’s wound, potentially leading to infection. Thus, the pathogen
in this scenario is S. aureus and the healthcare worker’s nose or skin and the
bandage is a reservoir or source of infection. The healthcare worker’s skin or nose is
a portal of exit, the open wound a portal of entry, the mode of transmission is indirect
contact and Mary is the susceptible host.
3. Rationale for choices of antibiotics (Total 10 Marks)
3.1 Rationale for the stat dose of ceftriaxone administered IVI immediately. (3 marks)
Based on the observations of Mary’s wounds, it is clear that Mary’s laceration has
become infected. Ceftriaxone is an antibiotic from the cephalosporin family of
antibiotics used for treating and preventing bacterial infections in different parts of
the body including the skin. Cephalosporins kill bacteria and other organisms by
interfering with the production of proteins important for their cell walls and overall
synthesis (Bullock & Manias, 2017). Although at the time of administering
ceftriaxone the strain of bacteria causing Mary’s infection was unknown, ceftriaxone
is a broad-spectrum antibiotic which is active against a number of well-known
bacteria and organisms (Bullock & Manias, 2017). As the antibiotic was administered
via IVI, the antibiotic was able to be absorbed quickly and also start treating the
infection as soon as possible, before Mary could start treatment with oral cephalexin.
3.2 Rationale for the oral cephalexin. (3 marks)
Cephalexin is also an antibiotic from the cephalosporin class of antibiotics and is
active against gram-positive and some gram-negative bacteria (Bullock & Manias,

2017). It is used for treating bacterial infections in different parts of the body
including the skin, which is why it was prescribed for Mary’s infection as most skin
infections are caused by gram-positive bacteria such as Staphylococcus,
Streptococcus or other organisms (Bullock & Manias, 2017).
3.3 Rationale for the change to oral dicloxacillin. (3 marks)
The culture test confirmed the infection-causing bacteria was S. aureus. A sensitivity
test would have also confirmed which antibiotic would be the most effective in
treating the infection. S. aureus produces the enzyme beta-lactamase which breaks
down the structure of several antibiotics, rendering them ineffective, including
cephalexin (Bullock & Manias, 2017). Dicloxacillin is a narrow-spectrum antibiotic of
the penicillin class used for treating gram-positive bacteria and it works by
obstructing bacteria from synthesizing cell walls, similar to cephalexin (Bullock &
Manias, 2017). However, Dicloxacillin is insensitive to beta-lactamase and therefore
active against S. aureus, rendering it the most effective antibiotic treatment for
Mary’s infection.
3.4 State two adverse reactions to dicloxacillin. (1 mark)
Taking dicloxacillin can have several side effects. The most common adverse
reactions to dicloxacillin include diarrhoea and stomach pain (Bullock & Manias,
2017).
4. Process by which Mary’s wound will heal (Total: 5 marks)
Mary’s wound will heal in four phases (Marieb & Hoehn, 2016). In the first phase,
hemostasis, the body attempts to close the wound and stop blood flow by clotting.
Initially, the chemical epinephrine is released into the blood to constrict blood

vessels and reduce blood flow (Marieb & Hoehn, 2016). Platelet cells will then travel
to the site of injury and aggregate to seal the wound. Platelets also release key
cytokines that signal other cells to participate in the next phases of wound healing
(Marieb & Hoehn, 2016).
The inflammatory phase is the next phase of wound healing and is characterized by
swelling, pain, heat and redness at the site of injury and this phase helps prevent
infection (Marieb & Hoehn, 2016). Mary’s injury was at the inflammatory stage when
she arrived at the hospital. During this phase capillaries are dilated and permeability
is increased to allow healing and repair cells such as white blood cells, growth
factors, nutrients and enzymes to move to the wound site, and bacteria, pathogens
and dead tissue are removed from the site (Marieb & Hoehn, 2016).
The third phase of wound healing is the proliferative phase. During this phase,
granulation tissue consisting of collagen and extracellular matrix is formed and
begins to fill the wound (Marieb & Hoehn, 2016).The granulation tissue will gradually
proliferate and fill the wound. In doing so, the edges of the wound will contract to
reduce the wound’s size and to allow the surrounding epithelial cells to divide,
migrate and seal the wound (Marieb & Hoehn, 2016).
In the fourth and final phase, the maturation phase, collagen fibres in the granular
tissue will be reorganized, remodeled and will mature to gain tensile strength.
However, the tensile strength of the repaired tissue is typically 80% of unwounded
tissue (Marieb & Hoehn, 2016).

References
Bishop, P. (2016). Epidemiology: How diseases are spread. In G. Lee & P. Bishop
(Eds.). Microbiology and infection control for health professionals (6th ed., pp.
161-183). Melbourne, Australia: Pearson.
Bullock, S., & Manias, E. (2017). Fundamentals of pharmacology (8th ed.). Melbourne,
Australia: Pearson.
Craft, J., & Gordon, C. (2015). Introduction to clinical science. In J. A. Craft, C. J.
Gordon, E. S. Huether, K. L. McCance, L. V. Brashers & N. S. Rote (Eds).
Understanding pathophysiology (2nd Australian and New Zealand ed., pp. 4-19).
Sydney, Australia: Elsevier.
Gary, L. (2016). Infection control in healthcare facilities. In G. Lee & P. Bishop (Eds.).
Microbiology and infection control for health professionals (6th ed., pp. 295-324).
Melbourne, Australia: Pearson.
Lee, G., & Bishop, P. (Eds.). (2016). Microbiology and infection control for health
professionals (6th ed., pp. 161-183). Melbourne, Australia: Pearson.
Marieb, E. N. & Hoehn, K. (2016). Human anatomy and physiology (10th ed.). Essex,
England: Pearson.