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




Group A streptococci is an extracellular bacterial pathogen that produce various infections when exposed to areas such as the mucous membrane, tonsils, throat, skin, and deeper tissue  (Cunningham. 2000).  In the case study mentioned above, this pathogen invades the pharynx and bacterial pharyngitis is diagnosed. This discussion will explore the patients’ symptoms, the physiological response to the infection and the cellular mechanisms involved. Additionally the role of genetics will be explored as part of the disease process.

The physiologic response as it relates to the patient’s symptoms

For successful invasion of a host and subsequent tissue damage, the bacteria must breach multiple lines of defense. The first is via breach of natural barriers. The bacterium enters the body and attempts to make contact with the infection source (physical barrier breach)(Mc Chance. Heuther. 2019). Then goblet cells produce mucus; making a barrier on the epithelial surface. The cilia then move the organisms trapped in the mucus upward and outward via coughing and expulsion (mechanism barrier).  Biochemically, epithelial cells secrete proteins responsible for eradicating multiple pathogens.  Known as antimicrobial peptides, these do not appear to be sufficient in killing the extracellular exotoxins of streptococci  (biochemical barrier breach). As a result tissue damage begins and the second line of defense is activated.

To prevent additional damage, the inflammatory defense is then activated (Mc Chance. Heuther. 2019). This occurs on a vascular and cellular level; activating multiple responses to prevent further tissue injury.  On a vascular level, the tetrad signs of inflammation is present- redness, heat, swelling and pain. As presented in the case study, the patient’s sore throat (pain), reddened posterior pharynx (erythema), positive anterior and posterior cervical adenopathy (swelling) and low grade temperature of 99.6 (heat), fit the cardinal signs (Mc Chance. Heuther. 2019). On a cellular level, neutrophils and macrophages migrate to the damaged tissue with the intent of devouring bacterial organisms. Eisonophils and plasma proteins work together to contain the injured tissue; preventing spread of the infection to healthy regions.

Genetics and the disease process

The normal flora of the oral mucousa includes a species of harmless streptococci such as S. sanguis, S. mutans  and S. salivarius (Cvitkovich. 2001). Through horizontal transmission of genetic information amongst various Streptococci bacterium, evolution of the pyrogenic Streptococci A strain can occur (Cvitkovich. 2001). This may be a key factor in why the first line of defense was breached.  As tissue damage occurs, DNA synthesis is halted as the cell enters the repair phase (Mc Chance. Heuther. 2019).  This process prohibits spread of disease and promotes cellular repair.

Upon initiation of penicillin therapy, an inflammatory response is activated as the patient’s tongue and lips are notably swollen. When the penicillin enters the body, it is perceived as a threat (City Allergy. 2017). The body then sends IgE antibodies to the allergen as a form of defense. Once two IgE mediators run concomitantly along the mast cell, the membrane begins to break down; releasing histamines and leukotrienes. This biochemical response leads to the immediate reaction and angioedema is seen in the patient.


The disease process and the mechanism of action to restrict the spread of the bacteria is an intricate one. As a complete process, the body implements the first and second line of defense with the hopes of eradicating the disease.