Mucormycosis Infection: Analysis of Lab Results and Treatment Options

This assignment provides a detailed overview of mucormycosis (mucor), a rare fungal infection caused by mucormycetes, primarily affecting individuals with weakened immune systems. The document highlights the fungi's ability to thrive by obtaining iron from the host, making diabetic patients with ketoacidosis particularly susceptible. The analysis includes an interpretation of laboratory blood test results, noting deviations from normal ranges in pH, oxygen and carbon dioxide levels, and white blood cell counts, which are indicative of the infection's impact on the host's immune system. Therapeutic interventions discussed range from first-line antifungal therapies like AmB deosycholate and Posaconazole to second-line therapies and salvage options, emphasizing the importance of surgical removal of affected parts and combination antifungal approaches. The assignment concludes by referencing studies that support the efficacy of treatments like liposomal amphotericin B and combination polyene caspofungin therapy in improving patient survival rates.

Running head: MUCOR
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Title: Mucormycosis Infection

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The Centers for Disease Control and Prevention (2015) describe mucor (also
mucormycosis or zygomycosis) as a rare fungal disease caused by mucormycetes. Mucor can
occur in any part of the body and mainly affects people with weak immunity. In most cases,
mucor affect the lungs after an individual inhales the fungal spores. It also affects the skin
after the fungi penetrates into the skin through an opening like a burn or a cut. Actor (2012)
claims that the mucor fungi is found in decomposing fruits, in plants and the soil. Mucor
infection has currently been associated with increased morbidity and mortality rates among
diabetic patients as it cause no-resolving pneumonia (Muqeetadnan et al. 2012).
Iron is essential for growth and development of cells and the mucor fungi has the
ability to obtain this element from the host, hence enabling its growth. According to clinical
observations, patients suffering from diabetic ketoacidosis (DKA) are highly susceptible to
mucor due to their elevated iron levels in their serum (Ibrahim, Spellberg, Walsh and
Kontoyiannis, 2012). Ibrahim et al. (2012) also claim that patients treated with iron chelator
deferoxamine are at a higher risk of contracting mucor infection. The fungi have a high
affinity iron permeases which they use to obtain the iron by reducing iron in to a high soluble
ferrous material. The reduced iron is obtained by a complex protein made of multi copper
oxidase. The fungi can also use heme to obtain iron from the host. Research shows that the
fungi attaches itself on umbilical endothelial cells and then attack them through induced
endocytosis, hence damaging the cells (Spellberg, Edwards and Ibrahim, 2005).
Normal arterial blood pH ranges between 7.35 and 7.45, partial oxygen pressure (PO2)
ranges between 80 and 100 mmHg while partial carbon IV oxide (PCO2) between 35 and 45
mmHg (Luo and Zhang, 2017). White blood cells count, for a normal person should range
between 4.0 and 10.0 x 109/l, hematocrit (hct) should be between 37% and 52%;
haemoglobin, ranging from 110 to 160 g/l, lymphocytes ranging between 20 and 40% and
glucose level of between 6 and 7.1 mmol/l. the laboratory blood test results indicate a pH

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higher than the normal, which favors growth of mucor fungi. Comparing the normal partial
oxygen and carbon dioxide levels with those of the laboratory test, the results have low
values. The white blood cell count from the lab results have a large deviation from the
normal. This could be explained from the fact that mucor fungi attacks and damages the
immune system of the host. The low lymphocytes level is because the fungi attacks and
weakens the immunity of the host.
Therapeutic intervention for mucor is multimodal, which not only includes antifungal
agents but also surgically removing affected parts. For the first line of mucormycosis
treatment the following antifungal therapy can be administered: AmB deosycholate, ABCD,
ABLC 5-7mg/kg and Posaconazole 400 mg bid. If in case the first line therapy fails, a second
line therapy is administered which includes combination of lipid AmB and caspofungin or
posaconazole. Currently, amphotericin B bas become the drugs of choice in treatment of
mucor. Due to scarcity of mucor cases, it has been difficult to compare studies on antifungal
agents (Skiada et al. 2013). Lipid formaulation of AmB are highly considered as they can be
administered at higher doses and for a longer time than AmB. They are also associated with
reduced death rates (Spellberg and Ibrahim, 2010). Liposomal amphotericin B is associated
with 67 percent chances of the patient surviving this infection, and therefore the LAmB
treatment is more effective.
Another therapy for mucor infection is combining antifungal therapy, where
caspofungin plus ABLC therapy has showed improved results in treatment of mucor.
According to Spellberg and Ibrahim (2010), combination polyene caspofungin therapy
showed improved results as compared to polyene monotherapy. Salvage therapy is an option
for patients whom polyene therapy becomes intolerant. Posaconazole, though administered
for a long time is a safer option used in salvage therapy. Deferasirox is also used in salvage
therapy, although there is little information concerning its use. Patients administered with

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deferasirox registered improved outcomes. Deferasirox should be used carefully with a steady
hepatic and renal function monitoring.it should be administered at a dose of 20 mg/kg/d for
about four weeks.

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References
Actor, J. K. (2012). Mycology: Mucor. Retrieved from:
https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/mucor
Centers for Disease control and Prevention. (2015). Mucormycosis. Retrieved from:
https://www.cdc.gov/fungal/diseases/mucormycosis/index.html
Ibrahim, A. S., Spellberg, B., Walsh, T. J., & Kontoyiannis, D. P. (2012). Pathogenesis of
mucormycosis. Clinical infectious diseases: an official publication of the Infectious
Diseases Society of America, 54 Suppl 1(Suppl 1), S16-22.
Luo, Z., & Zhang, L. (2017). Diagnosis and treatment of pulmonary mucormycosis: A case
report. Experimental and therapeutic medicine, 14(4), 3788-3791.
Muqeetadnan, M., Rahman, A., Amer, S. Nusrat, S., Hassan, S. and Hashmi, S. (2012).
Pulmonary Mucormycosis: An Emerging Infection. Case Reports on Pulmonology,
Vol. 2012, Article ID 120803, pp. 3. Doi: 10.1155/2012/120809.
Spellberg, B., & Ibrahim, A. S. (2010). Recent advances in the treatment of mucormycosis.
Current infectious disease reports, 12(6), 423-9.
Skiada, A., Lanternier, F., Groll, A. H., Pagano, L., Zimmerli, S., Herbrecht, R., Lortholary,
O., Petrikkos, G. L., European Conference on Infections in Leukemia (2013).
Diagnosis and treatment of mucormycosis in patients with hematological
malignancies: guidelines from the 3rd European Conference on Infections in
Leukemia (ECIL 3). Haematologica, 98(4), 492-504.
Spellberg, B., Edwards, J., & Ibrahim, A. (2005). Novel perspectives on mucormycosis:
pathophysiology, presentation, and management. Clinical microbiology reviews,
18(3), 556-69.