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Case Study Analysis
Sahil Mehta
Walden University
NURS 6051: Advanced Pathophysiology
Dr. Helene Holbrook
June 13th, 2021
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Case Study Analysis
Scenario
A 49-year-old patient with rheumatoid arthritis comes into the clinic with a chief
complaint of a fever. The patient’s current medications include atorvastatin 40 mg at night,
methotrexate 10 mg po every Friday morning and prednisone 5 mg po qam. He states that he has
had a fever up to 101 degrees F for about a week and admits to chills and sweats. He says he has
had more fatigue than usual and reports some chest pain associated with coughing. He admits to
having occasional episodes of hemoptysis. He works as a grain inspector at a large farm
cooperative. After an extensive workup, the patient was diagnosed with Invasive aspergillosis.
Background
“Aspergillosis is an infection caused by Aspergillus, a common mold (a type of fungus)
that lives indoors and outdoors.” (Centers for Disease Control and Prevention, 2020). Invasive
aspergillosis (IA) is known to be the most severe form of aspergillosis and can be fatal. Per the
CDC, it “usually affects people who have weakened immune systems, such as people who have
had an organ transplant or a stem cell transplant. Invasive aspergillosis most commonly affects
the lungs, but it can also spread to other parts of the body.” (Centers for Disease Control and
Prevention, 2020). Due to not having specific signs and symptoms, diagnosing IA is difficult,
especially in a person who is immunocompromised. IA, “is characterized by infection that starts
in the lungs and then rapidly travels through the bloodstream to affect various organs of the body
potentially including the brain, kidneys, heart and skin.” (Lass-Flörl, 2019).
Symptoms
The patient from the scenario has rheumatoid arthritis and presented with fever, chills,
sweats, fatigue, and chest pain associated with coughing. He also admits to occasional episodes
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of hemoptysis. These signs and symptoms as well as shortness of breath are all common with IA
(National Organization for Rare Disorders, 2018). IA is most likely to occur in people who have
a weakened immune system, are neutropenic, are receiving chemotherapy, or are receiving
immunosuppressive drugs (Lass-Flörl, 2019). The patient from the scenario is known to have
RA, an autoimmune disease, and is taking prednisone and methotrexate, both which are
immunosuppressants. The patient is also at risk of IA due to his occupation as a grain inspector.
“Aspergillosis is a fungal infection caused by certain types of mold. They are found throughout
nature (ubiquitous) and can be found in the soil and decaying organic matter like decaying
vegetation.” (National Organization for Rare Disorders, 2018). Aspergillus produces mycotoxins
“that induces apoptosis of many cells of the inflammatory and immune system” (McCance &
Huether, 2021, p. 302). The mold that produces mycotoxins are known to grow on nuts, beans,
and grains (McCance & Huether, 2021, p. 302).
Associated Genes
Per Lupiañez et al. (2016) suggests, “that host genetic polymorphisms within or near
immune-related genes may contribute to determine the risk of developing the infection”. The
authors go on to write that large number of “susceptibility markers identified to date for IA are
located in genes directly or indirectly implicated in the activation of the nuclear factor-kappa B
(NFκB) signaling pathway” (Lupiañez et al., 2016). Lupiañez et al. (2016) states, single
nucleotide polymorphisms (SNPs) within toll-like receptors, C-type lectins, PTX3, and tumor
necrosis factor receptors, “are pathogen recognition receptors (PRRs) that often culminate in the
activation of NFκB pathway, may render patients more susceptible to develop IA.” Based off
their findings the authors were able to hypothesize, “that the presence of common genetic
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polymorphisms within NFκB1, NFκB2, RelA, RelB, Rel, and IRF4 genes might influence the risk
of developing IA in high-risk patients.” (Lupiañez et al., 2016).
RA is “a chronic, systemic inflammatory autoimmune disease” which involves
inflammation of the synovial, “joint swelling, and ankylosis and destruction of articular
cartilage.” (McCance & Huether, 2021, p. 1450). “Genetic factors including class II major histo-
compatibility antigens/human leukocyte antigens (HLA-DR), as well as non-HLA genes have
been implicated in the pathogenesis of RA” (Yap et al., 2018). Kurkó et al. (2013) states that,
the “heritability of RA has been estimated to be about 60 %, while the contribution of HLA to
heritability has been estimated to be 11–37 %. Apart from known shared epitope (SE) alleles,
such as HLA-DRB1*01 and DRB1*04, other HLA alleles, such as HLA-DRB1*13 and
DRB1*15 have been linked to RA susceptibility.” Disease-modifying antirheumatic drugs
(DMARDs) are the first line of treatment for RA. Biological DMARDs (bDMARDs) are
medications that “affect specific processes in the development of RA and include tumor necrosis
factor inhibitors” (McCance & Huether, 2021, p. 1454).
Process of Immunosuppression
Immunosuppression is the suppression of the body’s immune system and its ability to
fight infections or diseases. Per Wilson (2018), “suppression may be the result of a disease that
targets the immune system, such as the human immunodeficiency virus (HIV), or as a
consequence of pharmaceutical agents used to fight certain conditions, like cancer.”
Immunosuppressant medications are necessary to use to treat autoimmune disorders and to
prevent the body from rejecting an organ transplant. In autoimmune disorders, the body is
attacking healthy cells and tissues, and the use of these medications prevents it from doing so.
“Antiproliferatives such as methotrexate (an inhibitor of T-cell folate metabolism) and
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leflunomide (an inhibitor of T & B-cell purine synthesis)” are used for the treatment of
autoimmune disorders like RA (Yap et al., 2018).
The patient from the scenario appears to have common signs and symptoms of an
immunocompromised patient who has IA. Due to having RA, being on immunosuppressant
medications, and his occupation, the patient is higher risk of developing IA and his symptoms
are consistent with the diagnosis. His medications may need to be adjusted and he should be
closely monitored due to the potential fatality of the disease.
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References
American Lung Association. (2021, January 25). Aspergillosis Symptoms and Diagnosis.
https://www.lung.org/lung-health-diseases/lung-disease-lookup/aspergillosis/symptoms-
diagnosis
Centers for Disease Control and Prevention. (2020, November 18). Symptoms of Aspergillosis.
https://www.cdc.gov/fungal/diseases/aspergillosis/symptoms.html
Kurkó, J., Besenyei, T., Laki, J., Glant, T. T., Mikecz, K., & Szekanecz, Z. (2013). Genetics of
rheumatoid arthritis - a comprehensive review. Clinical reviews in allergy &
immunology, 45(2), 170–179. https://doi.org/10.1007/s12016-012-8346-
Lass-Flörl, C. (2019, April). How to make a fast diagnosis in invasive aspergillosis. Oxford
Academic. https://academic.oup.com/mmy/article/57/Supplement_2/S155/5366892?
login=true#
Lupiañez, C. B., Villaescusa, M. T., Carvalho, A., Springer, J., Lackner, M., Sánchez-
Maldonado, J. M., Canet, L. M., Cunha, C., Segura-Catena, J., Alcazar-Fuoli, L., Solano,
C., Fianchi, L., Pagano, L., Potenza, L., Aguado, J. M., Luppi, M., Cuenca-Estrella, M.,
Lass-Flörl, C., Einsele, H., Vázquez, L., … Sainz, J. (2016). Common Genetic
Polymorphisms within NFκB-Related Genes and the Risk of Developing Invasive
Aspergillosis. Frontiers in microbiology, 7, 1243.
https://doi.org/10.3389/fmicb.2016.01243
McCance, K. L., & Huether, S. E. (2021). Pathophysiology: The Biologic Basis for Disease in
Adults and Children 8th Edition (8th ed.). Elsevier.
National Organization for Rare Disorders. (2018, September 21). Aspergillosis. NORD (National
Organization for Rare Disorders). https://rarediseases.org/rare-diseases/aspergillosis/
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Yap, H. Y., Tee, S. Z., Wong, M. M., Chow, S. K., Peh, S. C., & Teow, S. Y. (2018). Pathogenic
Role of Immune Cells in Rheumatoid Arthritis: Implications in Clinical Treatment and
Biomarker Development. Cells, 7(10), 161. https://doi.org/10.3390/cells7100161
