ALTERATIONS IN CELLULAR PROCESSES NURS 6501

In this week’s case study, the patient presents with a chief complaint of a sore throat and multiple other symptoms that resulted in a positive strep test. Strep throat, also known as bacterial pharyngitis, is caused by the presence of Streptococcus group A bacteria that is spread by respiratory droplets and is the most common cause of pharyngitis in children (Chauhan, et al., 2016). In a recent meta-analysis, 37% of children less than 18 years old were diagnosed with Group A Strep and presented to an outpatient center for treatment for a sore throat in comparison to only 15% of adults (Ashurst & Edgerley-Gibb, 2022).

The patient presented with a sore throat, reddened posterior pharynx with white exudate, and 3+ tonsils- all due to the presence and colonization of the streptococcus bacteria. The positive sign of anterior and posterior cervical adenopathy is due to the infection and the body’s response to try and fight the infection. The patient was prescribed ten days’ worth of amoxicillin and after consumption, immediately experienced swelling of the tongue and lips, difficulty breathing, and wheezing. The patient was having an anaphylaxis reaction to the antibiotics. An anaphylaxis response is IgE mediated and results in mast cells releasing a large amount of histamine and leukotrienes that cause bronchospasm and edema (Vaillant, Vashisht, & Zito, 2022).

Even after antibiotic treatment, some children get recurrent strep throat due to a genetic basis. A study performed by Dr. Shane Crotty and Dr. Jennifer Dan (2019), explored the germinal centers of both children with a normal rate of infection and those with recurrent tonsillitis. Their findings suggested that children with recurring strep throat had smaller germinal centers with fewer B and helper T cells which are responsible for producing antibodies and fighting invading pathogens. Upon further research, it was discovered that the genetic component was identified as two variants in the HLA genomic region which are associated with increased susceptibility to recurrent tonsillitis as well as protecting against the disease. If a child presented with recurring group A streptococcus pharyngitis, it may warrant a different response than treating with just antibiotics, such as referring them to an ENT for a tonsillectomy.

References

Ashurst, J. V., & Edgerley-Gibb, L. (2022). Streptococcal Pharyngitis. National Library of Medicine. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK525997/

Chauhan, S., Kashyap, N., Kanga, A., Thakur, K., Sood, A., & Chandel, L. (2016). Genetic diversity among group A streptococcus isolated from throats of healthy and symptomatic children. Journal of Tropical Pediatrics, 62(2), 152-157. doi:10.1093/tropej/fmv092

Crotty, S., & Dan, J. (2019). Recurrent group A streptococcus tonsillitis is an immunosusceptibility disease involving antibody deficiency and aberrant TFH cells. Science Translational Medicine, 11(478). doi:DOI: 10.1126/scitranslmed.aau3776

Vaillant, A. A., Vashisht, R., & Zito, P. M. (2022). Immediate hypersensitivity reactions. StatPearls. doi:https://www.ncbi.nlm.nih.gov/books/NBK513315/

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Case Discussion 1

In this scenario, an otherwise healthy 16-year-old boy is diagnosed with strep pharyngitis (strep throat) via an in-office rapid strep test, which tests for group A streptococcus bacteria (Cohen et al., 2016). He was prescribed penicillin, which is the antibiotic of choice for a patient with no known allergy to penicillin given that there is no strain of group A streptococcus bacteria that is resistant to it (“Centers for Disease Control,” 2022). Unfortunately for this young man, upon taking his first dose of penicillin he experienced an anaphylactic response, as evidenced by lip and oral swelling and breathing difficulties. This response is the most rapid and severe, and characteristic of a Type I hypersensitivity reaction, or IgE-mediated response resulting from the sensitization of mast cells by the binding of IgE to Fc protein receptors on the plasma membranes (McCance & Huether, 2019). Once sensitized, further exposure results in degranulation and release of histamine causing bronchial constriction and increased vascular permeability producing the breathing difficulties and lip and oral swelling respectively seen in this patient (Patterson & Stankewicz, 2020; McCance & Huether, 2019). Though type IV (IgG-mediated) hypersensitivity reactions are found in penicillin allergies, the primary result of this would be related to a delayed hypersensitivity mechanism resulting in dermatologic symptoms, not reported in this case (McCance & Huether, 2019).

ALTERATIONS IN CELLULAR PROCESSES NURS 6501

Of note, Type I allergic responses can only occur with prior sensitization of the Fc proteins on mast cells. This patient was presented as having no known drug allergies, and while he could have taken penicillin in the past, which could have resulted in sensitization without evidence of allergic reaction, consideration should be given to the possibility that the patient carries a genetic erroneous beta (b)-lactam allergy. This could result in the allergic reaction without previously having taken the drug (Bhattacharya, 2010). Knowing the patient has a serious sensitivity to penicillins, the clinician should be aware of a cross-sensitivity to cephalosporins due to similarities in the chemical structure (Patterson & Stankewicz, 2020). Though research has shown females have a greater predisposition to penicillin allergy than males, the case presentation demonstrates a clear hypersensitivity reaction in this patient (Park et al., 2007).

References

Bhattacharya, S. (2010). The Facts About Penicillin Allergy: A Review. Journal of Advanced Pharmaceutical Technology and Research, 1(1), 11–17.

Centers for Disease Control and Prevention. (2022, June 27). Pharyngitis (strep throat): Information for clinicians. Centers for Disease Control and Prevention. https://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html#:~:text=Penicillin%20or%20amoxicillin%20is%20the,that%20is%20resistant%20to%20penicillin.

Cohen, J. F., Bertille, N., Cohen, R., & Chalumeau, M. (2016). Rapid antigen detection test for group A streptococcus in children with pharyngitis. Cochrane Database of Systematic Reviews. https://doi.org/10.1002/14651858.cd010502.pub2

McCance, K., & Huether, S. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier.

Park, M. A., Matesic, D., Markus, P. J., & Li, J. T.-C. . (2007). Female sex as a risk factor for penicillin allergy. Annals of Allergy, Asthma & Immunology, 99(1), 54–58. https://doi.org/10.1016/s1081-1206(10)60621-7

Patterson, R. A., & Stankewicz, H. A. (2020). Penicillin Allergy. PubMed; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK459320/

Great explanation of the type I hypersensitivity presented in this week’s case study. I was interested to learn about the genetic component and the possibility of the beta (b)-lactam allergy you spoke of and did not consider it when I was reviewing this patient. My assumption was that the patient likely took penicillin before making him hypersensitive to it now. Upon further research, I found an article that studied the prediction of penicillin allergy through genome mapping. This study researched 387 patients with immediate allergic reactions to B-lactams and found significant associations between gene variants HLA-DRA and an allergy to penicillin (Gueant, et al., 2015). It is important to note that this study confirmed predictors of penicillin allergies but not to cephalosporins. Although rare, it is interesting to understand that there could be a genetic component to those with allergies to penicillin. Another aspect to consider with this case study is how recurring strep throat could be a genetic component. Germinal centers of individuals with recurrent strep were found to be smaller, there were fewer B and helper T cells and two variants in the HLA genomic region could make them more susceptible to tonsillitis (Crotty & Dan, 2019).

References

Gueant, J.-L., Romano, A., Cornejo-Garci, J.-A., Oussalah, A., Chery, C., Blanca-Lopez, N., . . . Gaeta, F. (2015). HLA-DRA variants predict penicillin allergy in genome-wide fine-mapping genotyping. Journal of Allergy and Clinical Immunology, 135(1), 253-259. doi:https://doi.org/10.1016/j.jaci.2014.07.047

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Collapse SubdiscussionMercy Wendy Muthoni

Mercy Wendy Muthoni

YesterdayNov 28 at 11:23pm

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The role genetics plays in the disease.

According to McCance (2019), humans have approximately 20,000-25,000 genes. An error in one of the genes can be the cause of an identifiable genetic disease (McCance et al., 2019). Variations in DNA and differences in how DNA functions on its own or in combination with the environment can be a contributing factors to disease processes (Jackson et al., 2018).

Why the patient is presenting with the specific symptoms described

The patient is presenting the symptoms of a reddened posterior pharynx with white exudate on tonsils that are enlarged to 3+. Positive anterior and posterior cervical adenopathy. A rapid strep test performed in the office was positive. The patient has been infected either through a respiratory droplet or by direct contact with someone who had the disease. The symptoms the patient is presenting are from a bacteria called group A Streptococcus (group A strep). Among the symptoms presented by a patient infected by Streptococcus are Sore throat, fever, pain when swallowing, red and swollen tonsils, headache swollen lymph nodes.

The physiologic response to the stimulus presented in the scenario and why you think this response occurred.

The physiologic response to the stimulus in this case is the way the body reacted to amoxicillin 500 mg when the patient took it. The patient complained of difficulty breathing with audible wheezing. He had an allergic reaction to amoxicillin. This may have happened because the patient’s immune system became hypersensitive to the drug and mistook the drug as a harmful substance or as if the amoxicillin was a viral or bacterial infection. Seems the patient had never been exposed to the medication before

The cells that are involved in this process

The cells involved are Helper T-cells αβT cells. These cells can be divided into, CD4⁺ and CD8⁺ T cells. T cell-mediated immunity can be invoked upon recognition of foreign or non-self peptides (eg viral) presented by the human leukocyte antigen (HLA) molecules of an antigen-presenting cell (APC) (Goh et al, 2021). This was a type 1 hypersensitivity reaction.

How another characteristic (e.g., gender, genetics) would change your response?

Genetics would change my response by analyzing how immunodeficiency may affect this patient. Immunodeficiency emerges from the absence of elements of the immune system, such as the phagocytes, lymphocytes, and the complement system. These are classified as primary and secondary immunodeficiencies. The primary immunodeficiency cause deficiencies such as T-cell deficiency, B-cell deficiency, phagocyte deficiency, immunoglobulin A deficiency, and complement deficiency. The secondary immunodeficiency is caused by obesity, steroids, AIDS, nutrient deficiency, and viral infections. If this patient lacks the Helper T-cells due to immunodeficiency, this would be a life-or-death situation.

References:

Goh, SJR, Tuomisto, JEE, Purcell, AW, Mifsud, NA, Illing, PT. (2021). The complexity of T cell–mediated penicillin hypersensitivity reaction Allergy. 76: 150– 167. https://doi.org/10.1111/all.14355Links to an external site.

Jackson M, Marks L, May GHW, Wilson JB. (2018). The genetic basis of disease. Biochem. ;62(5):643-723. doi: 10.1042/EBC20170053. Erratum in: Essays Biochem. 2020 Oct 8;64(4):681. PMID: 30509934; PMCID: PMC6279436.

McCance K. L. Huether S. E. Brashers V. L. & Rote N. S. (2019). Pathophysiology : the biologic basis for disease in adults and children (Eighth). Elsevier.

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