Case Study: Analysis of Mary's Tetanus, Wound Infection and Treatment

This case study analyzes Mary's tetanus and wound infection, exploring the rationale for a tetanus booster, the physiological basis of wound observations (redness, swelling, and purulent discharge), and the development and benefits of fever. It examines potential sources and modes of transmission of infection, including endogenous and exogenous sources like Staphylococcus aureus. The study also evaluates the appropriateness of Augmentin as an antibacterial agent, considering its benefits and the role of its ingredients in treating the infection. The analysis incorporates relevant literature and adheres to APA 6th edition referencing style, providing a comprehensive understanding of the case and its implications for healthcare practices.

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1. Rationale for giving Mary a tetanus booster(Total: 5 marks)
1.1 What is the organism that causes tetanus and why is it of concern in this
situation?
Clostridium tetani, a bacterium that can contaminate wounds presented to soil or
earth is an endospore-framing, bar molded bacterium that can cause lockjaw. For
Mary's situation she had got an open injury when working in her garden and this could
have presented her injury to the dirt and furthermore to the bacterium C. tetani.
Lockjaw is caused because of two poisons discharged by the bacterium,
tetanospasmin and tetanolysin, both of which are neurotoxins. There is however the
lockjaw supporter antibody which can be given to Mary with the goal that she gets
satisfactory assurance (Immunise.health.gov.au, 2017).
1.2 According to the guidelines in the “The Australian Immunisation Handbook” (Dept.
of health, 2017) on administering a tetanus booster, discuss the rationale for
giving Mary the tetanus booster
The method of reasoning for giving Mary a lockjaw promoter is that she is 50 years
old and all Australians over this age are suggested for a lockjaw toxoid supporter,
especially on the off chance that they have not gotten one amid the past 10 years.
Furthermore, there have been situations where a sponsor has not shielded individuals
with minor injuries from getting lockjaw, so a supporter not long after the damage is
typically given. Likewise, her presentation to cultivate soil puts Mary at a danger of
Clostridium tetani disease.
2. Physiological basis of the three wound observations (Total: 10 marks)
2.1 For each of the three wound observations indicate, and provide a rationale, as to
whether it is a sign or a symptom.
The minute the injury takes place, the intense provocative reaction swings without
hesitation. The arrival of a few biochemicals at the injury site attempt to achieve
homeostasis and control the section of pathogens that could cause a disease.

2.2 Discuss the physiological basis of the first observation.
The edges of the injury are hot to touch and red because of an arrangement of
intense incendiary reaction that is activated in case of damage. The chemicals that
reason aggravation and are discharged at the damage site are the supplement
framework segments, histamines, prostaglandins and a few kinins. The consolidated
impact of these mixes and a few cytokinins expands the blood stream to the site so
the edges seem, by all accounts, to be red in shading. Nitric oxide assumes a part in
vasodilation, so the vessels close to the cut are enlarged for expanded blood stream.
The prostaglandins, E1 amd E2 increment the vascular permeablity with the goal that
neutrophils can extravasate from the vessels into the encompassing tissue and they
likewise unwind the smooth muscles ofthe veins. An expansion in the temperature at
the damage site makes the cells metbolize at a speedier rate, so the edges seem, by
all accounts, to be hot (Craft, 2015).
2.3 Discuss the physiological basis of the second observation.
The encompassing tissue is swollen on account of the spillage of liquid from the
vessels. This prompts the development of exudate. The spaces between tissues are
loaded with the protein-rich liquid and this causes swelling of the tissue. It is likewise
alluded to as edema. Regularly the swollen tissue is difficult and limits movement in
the influenced range, along these lines driving the patient to rest. This enables the
procedure of repair to happen quicker (Marieb and Hoehn, 2014).
2.4 Discuss the physiological basis of the third observation.
A purulent and musty release is seen from the injury and by then Mary is likewise
febrile. A release of this nature is an unmistakable sign of a disease and that is the
reason the human services staff sent an injury swab for culture testing and ID of the
pathogen and its anti-infection affectability (Bowler, Duerden, and Armstrong, 2001).
Following a contamination, the resistant framework reacts by expanding the volume of
exudate and there is an expansion in the swelling and agony. An oral anti-infection
can be given to the patient keeping in mind the end goal to treat disease by a
pathogen (Craft, 2015).
3. Development and benefits of fever (Total: 5 marks).
3.1 How did Mary’s fever develop?
Mary developed fever as an outcome of the provocative reaction to the contamination

of her injury. Arrival of exogenous pyrogens as endotoxins discharged by the
pathogenic living being can invigorate the arrival of endogenous pyrogens or
cytokines, for example, tumor putrefaction factor-α, interleukin-1, interleukin-6 and
interferons. Prostaglandin E2 and endothelin I alongside corticotrophin-discharging
factor are discharged in light of the pyrogens. These follow up on the preoptic region,
a locale of the foremost hypothalamus and trigger a febrile reaction. The temperature
adjust point is then raised to a more elevated amount than it regularly is. Warmth
creation in the body takes after joined by protection of the warmth and the body
temperature starts to rise, bringing about fever (Craft, 2015).
3.2 Discuss two ways in which fever is beneficial.
Fever is beneficial in light of the fact that it can stop the increase of the pathogenic
microorganisms. Fever exhausts three minerals, copper, iron and zinc that are key for
bacterial replication and lessens the rate at which bacterial pathogens duplicate.
Phagocytosis additionally happens at a quicker rate and the disposal of pathogens
happens significantly speedier (Marieb and Hoehn, 2014).
4. Possible sources of contamination and modes of transmission (Total: 10 marks)
4.1 Name one endogenous source of contaminationand discuss the mode of
transmission from the source to the new host.
Endogenous wellsprings of tainting with Staphylococcus aureus is the skin and the
mucosal surfaces. The living being is a commensal and lives on these surfaces
without making any damage the human body. Be that as it may, in the internal spans
of an injury, the earth is great for it to duplicate and offers more dampness, an ideal
temperature and sufficient sustenance. In any case, once it enters the injury, it winds
up noticeably pathogenic and defers the tissue repair and causes fever. The
Stapylococci can be exchanged to the injury site through the patient's hand that have
been sullied because of nasal mucosa or the oropharyngeal mucosa (Lee, 2016).
4.2 Name one exogenous source of contamination and discuss the mode of
transmission from the source to the new host.
At the point when exchange of a life form to the patient happens through contact
with different surfaces or people, the source is said to be exogenous. An exogenous
wellspring of the Staphylococus aureus could be sullying of hands of medicinal
services staff. Since S. aureus tainting from soil is very improbable, exogenous

contact through hands of individuals around Mary could be a probable source.
Sullying through articles that been touched by other individuals is another
plausibility.
5. Appropriateness of Augmentin as the antibacterial agent prescribed to Mary
(Total: 5 marks)
5.1 Given the colonizing organism wasStaphylococcus aureus, discuss why
Augmentin is an appropriate prescription?
Mary's injury swab report affirmed that she experienced a S. aureus disease on the
injury. The report additionally expressed that the way of life was delicate to
Amoxycillin. However, a few strains of Staphylococcus are known to be impervious
to beta lactam anti-toxins and Augmentin is an anti-infection that is viable against
anti-microbial safe S Aureus.So it is a proper decision of an anti-microbial to treat
her condition (Bullock and Manias, 2017).
5.2 Describe the added benefits that Augmentin provides, with reference to the role of
the major ingredients in Augmentin.
Staphylococcus aureus is regularly impervious to the anti-microbial Amoxycillin
which is a penicillin subordinate. Amoxycillin can hinder bacterial development in
light of the fact that the beta lactam ring in its structure represses the arrangement of
the peptidoglycan cell divider in microbes. However, the wrong utilization of anti-
toxins has prompted the improvement of anti-microbial resistance in microscopic
organisms. S. aureus can deliver the catalyst beta lactamase which renders the beta
lactam anti-microbials unequipped for blocking cell divider arrangement. Augmentin
is a blend of amoxycillin and clavulenic corrosive. Clavulenic corrosive is a beta
lactamase inhibitor and in this manner in its essence amoxycillin can keep on
inhibitting the augmentation of S. aureus and cure the contamination (Bullock and
Manias, 2017).
6. Presentation (Total: 5 marks)
6.1 Referencing in-text and in reference list conforms to APA 6th Ed. referencing
style.
6.2 Critique supported by relevant literature as prescribed.
6.3 Correct sentence structure, paragraph, grammatical construction, spelling,
punctuation and presentation.

References
Bowler, P. G., Duerden, B. I., & Armstrong, D. G. (2001). Wound Microbiology and
Associated Approaches to Wound Management . Clinical Microbiology Reviews,
14(2), 244–269. http://doi.org/10.1128/CMR.14.2.244-269.2001.
Bullock, S., & Manias, E. (2017). Fundamentals of pharmacology (8th ed.). Frenchs Forest,
Australia: Pearson Australia.
Craft, J. &. (2015). Understanding pathophysiology (2nd Australian and New Zealand ed.). .
Chatswood, Australia: Elsevier.
Demidova-Rice, T. N., Hamblin, M. R., & Herman, I. M. (2012). Acute and Impaired Wound
Healing: Pathophysiology and Current Methods for Drug Delivery, Part 1: Normal
and Chronic Wounds: Biology, Causes, and Approaches to Care. Advances in Skin
& Wound Car.
Immunise.health.gov.au. (2017, August 1). /Aus-Imm-Handbook.pdf. Retrieved from
http://immunise.health.gov.au:
http://immunise.health.gov.au/internet/immunise/publishing.nsf/Content/
7B28E87511E08905CA257D4D001DB1F8/$File/Aus-Imm-Handbook.pdf
Lee, G. &. (2016). Microbiology and infection control for health professionals (6th ed.). .
Melbourne, Victoria : Pearson Australia.
Marieb, E., & Hoehn, K. (2014). Human Anatomy & Physiology, Global Edition. Pearson
Education Limited.