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Please type your answer below with each question number clearly stated. You do NOT need to start
a new page for each question.
Question 1a
As bleeding occurs, the hemostatic mechanisms are triggered to create inflammatory response in
host with the help of granulocytes or polymorphonuclear leukocytes (PMNLs)1. It begins with
vascular changes. Vasodilation occurs at the infected site under nervous stimulation, chemical
mediators and cytokines released by blood cells, tissues and platelets, like histamines2. Since the
blood vessels dilate, more blood flows to the injured tissue, thereby, wound area becomes red and
warm to touch2-3. Released prostaglandins increase cyclic AMP level and enhance nociceptor
sensitization which irritate the neurons to bradykinin and contribute to pain sensation and fever
that Samuel is suffering which gives a protective function4. Fever can be categorized into
endogenous and exogenous. Endogenous pyrogens are liberated by granulocytes under process of
phagocytosis while exogenous pyrogens are mostly come from the products of Clostridium
perfringens which trigger fever as well2. The elevated body temperature helps to stimulate
leukocytes to deploy and kill invaders, reducing the available free plasma iron, and inducing
interleukin 1 production, which further activates lymphocytes proliferation, maturation and
activation in the immune response; reducing the bacteria’s rate of growth and kills them more
quickly5. Vasoactive mediators, like serotonin, cause endothelial cells to contract and form gaps,
accompanied with the increased permeability of vascular endothelium, allowing influx of fluid
dilutes toxic substances2,6. Accumulated leukocytes, such as neutrophils, monocytes and
macrophages infiltrate into the extracellular space, containing varying amount of plasma proteins
and form exudate2,7. Since the exudate accumulates and increases with pus into the tissue, this
creates a local swelling and firmness on the surrounding wound area, causing edema on Samuel’s
right shin. Moreover, under PMNLs activity, the complement proteins released by macrophages,
monocytes initiated a cascade of reactions including chemotaxis. Some bacterial cells were cleared
by phagocytosis to the wound surface and formed slough. Slough is a necrotic non-viable fibrous
yellow tissue and appear in greenish color as a result of infection or damaged tissue in the wound 1.
Samuel’s exudate not only appears greenish in color, but also gives a foul-smelling on the wound
due to tissue breakdown and bacterial colonization8-9. Therefore, odorous greenish discharge was
found. Besides, as inadequate local blood supply to the wound, ischemia has occurred and tissue has
died, forming eschar which shows little dark-colored necrotic tissue along the edge of Samuel’s
wound9-10. Increasing pain over the injured site of prior injury may also indicate the signs of
systemic toxicity and gas in the tissue caused by gas gangrene from C. perfringens11. Lastly, the
bacterial infection invaded the deeper layers of skin in the unproperly-treated wound, like soft
tissues and nerves, causing peripheral neuropathy12-13. The motor nerves may be affected, leading
to muscle weakness13as a result of difficulty in walking in Samuel’s case.
(Words: 448/450)
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Question 1b
The taxonomic hierarchy of Clostridium perfringens is based on the kingdom of bacteria and
phylum is firmicutes, under class of clostridia. The order, family and genus are clostridiales,
clostridiaceae and clostridium respectively. C. perfringens ended up as one of the species of
clostridium14. C. perfringens are non-motile, rod-shaped, anaerobic, spore-forming Gram-positive
pathogenic bacteria that causes gas gangrene associated with wound infections15-16. With the
characteristics of Gram-positive bacteria, heat-resistant (20-50C), spore-forming and thick
peptidoglycan with chains of teichoic and lipoteichoic acid embedded together facilitate its
survival17-18. C. perfringens can be categorized from type A to E, based on its specific toxin
production, in which type A strains cause gas gangrene and mostly associated with wound infection
as a result of cellulitis19. For infectious cycle, it is introduced to Samuel’s wound as they are mostly
found in tap water and soil14,16. After the entry of vegetative cells or spores into body, C.
perfringens grow rapidly in host tissue through reducing tissue Redox conditions20. The growing
vegetative cells secrete alpha toxins and theta toxin which are crucial virulence factors. Alpha toxin
triggers platelet aggregation, thrombosis and histamine release by breaking down host’s cell
membranes, compromising blood flow towards infectious area. Theta toxin directly promotes
vascular degradation and breakdown of leukocytes, leading to blunted host inflammatory response
to the infection21-23. They cause depletion of blood supply and create anaerobic environment that
promote growth of C. perfringens. Not only causing local necrosis in muscle, but also allowing
progressive spread of infection to systemic circulation20. In terms of prevention of infection, wound
cleansing or surgical repair of deep and contaminated wound is the most important. Hydrogels or
hydrocolloids dressings would be suitable for infected and necrotic wounds9. Antibiotic therapy
like penicillin or clindamycin would be the first-line drug choice for further clostridial wound
infection24.
(Words: 298/300)
Question 2a
First, doctor must evaluate Mrs Wong’s overall medical condition. Diabetes mellitus is a common
comorbid illness to pneumonia patient25. Normally, a germinated community-acquired pneumonia
will prescribe beta-lactamase inhibitor combined with macrolide to patient as initial empiric
therapy until the test results are ready, such as ampicillin-sulbactam with clarithromycin26-27.
Simultaneously, doctor should assess for any allergic reaction to beta-lactam drugs to prevent more
severe complications. A fluroquinolone and clindamycin would be replaced if Mrs. Wong allergic
to beta-lactam drugs. However, since Mrs Wong is administering a drug for controlling diabetes
every day, this increased risk of drug-drug interactions that causes alteration in pharmacokinetic or
pharmacodynamic of drugs, like adverse drug reactions, toxicity and transmutation of drug
efficacy28. For example, fluroquinolones would cause fluctuation in blood sugars. Sulfonylureas,
the major diabetes pills for older adults, tends to develop hypoglycaemia when it administered with
clarithromycin or ciprofloxacin which is a type of broad-spectrum combination antibiotics for
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treating pneumonia29. Another type of diabetes medication is thiazolidinedione. It neither impedes
community-acquired pneumonia, nor decrease the susceptibility to the host30. Therefore, if the
doctor has discovered this diabetes medication is continuously administering, it should be impeded
for other replacement. Second, the degree of microorganism’s susceptibility to those drugs should
be evaluated by using Kirby-Bauer disk-diffusion susceptibility test. It helps to determine which
drug is the most effective in treating the infection. For example, the most common communityacquired pneumonia is due to Streptococcus pneumoniae which has high resistance to most
antibiotics31. Though old studies found penicillin and macrolides were effective in treating, the
modern research have discovered 80% of S. pneumoniae were resistant to both drugs, where 65.2%
of S. pneumoniae were resistant to ciprofloxacin. But only 21% of 3rd generation of cephalosporins,
ceftriaxone, has the resistance to S. pneumoniae. So, considering ceftriaxone is the most effective
treatment in curing community-acquired pneumonia27,32,33. Therefore, the suspected infectious
agent must have a certain level of sensitivity to drugs for achieving its optimal antimicrobial
therapy. Third, since the identity of microorganism causing the infection has no result yet, doctor
can direct to the efficacy at the site of infection and evaluate the age of patient that may affect the
drug activity in body34. Geriatric patients have poorer liver and kidney function causing reduction
in first-pass metabolism and deteriorated drug clearance respectively. She may have lower blood
flow, thereby the bioavailability of drugs may undergo extensive first-pass metabolism. Also, Mrs.
Wong’s serum creatinine level may have slightly reduced. For example, aminoglycoside antibiotics
will have a narrower therapeutic index in elderly and causing severe adverse effects if the drug
accumulates34,35. Therefore, the age that reflects her liver and kidney function should be assessed to
determine the drug dosage and route of administration.
(Words: 450/450)
Question 2b
Broad-spectrum antibiotics inhibit both gram-positive and gram-negative bacteria, such as
tetracyclines or ampicillin, while narrow-spectrum antibiotics only inhibit either gram-positive or
gram-negative bacteria, such as erythromycin or gentamycin36. However, as broad-spectrum target
general groups of bacteria, it is easier to create antibiotic-resistant, like azithromycin which has
longer half-life and increases resistance to S. pneumoniae37. More side effects and adverse reactions
will be found in broad-spectrum antibiotics. For broad-spectrum beta-lactam antibiotics’
mechanism of action, they are bactericidal agents which effectively disrupts the bacterial
peptidoglycan formation by binding penicillin-binding proteins (PBPs) into beta-lactam. The
rendering of beta-lactam ring of antibiotics bind to different PBPs, causing inability of crosslinking of bacteria for cell wall synthesis, leading to cell death due to osmotic instability or
autolysis38. The preferred antibiotics for Mrs Wong is ceftriaxone since it has lower resistance
strength39 and up to 95% of sensitivity to the typical pneumonia bacteria40.
(Words: 147/150)
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Question 2c
The most common infectious agent is Streptococcus pneumoniae which causes bacterial meningitis,
a kind of systemic infection41. The invasion of S. pneumoniae to bloodstream after colonization on
nasopharyngeal mucosa will be transmitted to alveoli through inhalation41-42. Fluid surrounding the
brain or spine will be infected as S. pneumoniae has entered into system of host. The meningeal
vascular endothelial cells are mediated by pneumococcal adhesion to platelet-activating factor
which specifically attack meninges. Clinical presentation will be shown nonspecifically42-43, like
fever, irritability, anorexia. Neurological abnormality will also be resulted, like delirium, lethargy43.
Polysaccharide capsule and hyaluronate lyase are the virulence factors44. When S. pneumoniae has
introduced to alveoli, it competes with resident microbes to replicate. The capsule of S. pneumoniae
prevents immunoglobulins from interacting with phagocytic cells of host and the degradation of
hyaluronic acid that promotes bacterial spread and colonization. With increased pathogenicity and
weakened immune system, pneumonia will be resulted42,44.
(Words: 150/150)
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