Respond to this post with 2 paragraphs and 2 sources and respectfully agree or disagree with your colleague’s assessment and explain your reasoning. In your explanation, include why their explanations make physiological sense or why they do not
POST:
The scenario in this case study has an adolescent person with strep throat presenting to the clinic for diagnosis and treatment. While the role genetics play in streptococcal infections is not fully understood, there has been a connection noted in children with chronic or recurrent group A strep infections (La Jolla Institute for Immunology, 2019). In some of these cases, researchers have discovered their tonsils had smaller germinal centers (La Jolla Institute for Immunology, 2019). They found a decreased number of B cells and helper T cells in these subjects, which, in combination with smaller germinal centers, equates to a reduced immune response (La Jolla Institute for Immunology, 2019). Group A streptococcal bacteria generates a toxin that destroys cells called streptolysin O; B cells and helper T cells work together to form an antibody called antistreptolysin O (McCance & Huether, 2019). It is this antibody that is detected in lab tests to diagnose infections with group A streptococci (McCance & Huether, 2019).
This patient is presenting with symptoms of a sore throat, localized redness, and swelling, with visible exudate on his tonsils and a low-grade fever. The swelling and redness are an immune response to infection or injury called inflammation. In this case, the inflammation is localized to the throat and tonsils because the group A streptococcal bacteria invaded the pharyngeal tissue, thus creating a localized inflammatory reaction (McCance & Huether, 2019). One of the trademark symptoms of infection is fever; in this case, the patient’s temp is 99.6 F, which may indicate the beginnings of a systemic response (McCance & Huether, 2019). However, cervical adenopathy provides further evidence of systemic involvement (McCance & Huether, 2019). The exudate is comprised of a collection of dead cells, mucous, and proteins.
The typical treatment for this condition is a 10-day course of penicillin or a penicillin-derivative such as amoxicillin (Al-Hamad, 2015). The patient experienced an allergic reaction to the antibiotic; this is an exaggerated response in which the body attacks the allergen that has bonded to the person’s cells (McCance & Huether, 2019). Allergic reactions to antibiotics such as amoxicillin are considered Type II allergic hypersensitivities (McCance & Huether, 2019). In type II reactions, the immune system attacks the drug metabolite that has bonded to the proteins on the outside of the cell, usually erythrocytes or platelets, destroying the allergen and the cell in the process (McCance & Huether, 2019). The allergen attaches to cell, the antibody (IgG or IgM) bonds to the allergen starting a complement cascade that ends in cell death (McCance & Huether, 2019). The severity of his reaction indicates a strong histamine response that affected his breathing and airway by causing bronchial constriction and edema due to increased vascular permeability (McCance & Huether, 2019). It is possible this patient had prior exposures to penicillin-derivatives that could have sensitized his system to the antibiotic; however, this is unknown.
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