Tonsillitis, Its Mechanism and Organism Response

As the name of the disorder suggests, tonsillitis usually affects the tonsils because they are located at the junction of the respiratory and digestive tracts and, compared to other lymphoid formations of the pharynx, they are most exposed to infection when streptococci enter the body through the air or with food. ß-hemolytic streptococcus easily attaches to the surface of tonsils and other clusters of lymphoid tissue due to the similarity of the microbe’s antigenic structures (i.e., lipoteichoic acid) with the epithelium of the lymphoid apparatus of the oropharynx (Walker et al., 2014). M-protein of streptococci reduces the phagocytic activity of leukocytes at the site of the entrance gate and, thereby, contributes to the child’s susceptibility to this disease.

The introduction of a sufficiently large number of virulent streptococci into the amygdala provokes the suppression of immunity factors which, in turn, causes the proliferation of microbes. As a result, the tonsils become damaged. Their capillary permeability increases. Tonsils start swelling and become infiltrated with neutrophils, purulent melting of lymphoid follicles by macrophage enzymes (Walker et al., 2014). The toxins released by streptococci pose the biggest threat to the patient because they are absorbed into the blood, exerting a general toxic effect on the entire body. In this case, the cardiovascular system may become severely affected as this pathophysiological alteration leads to the blockage of tissue respiration in the heart muscle and the disturbing of cardiac impulses (James, Nelson, & Ashwill, 2014).

In the case of tonsilitis, the protective responses of the organism, which usually are developed within a few days after infection, are as follows: an increase in the speed of circulation, an improved supply of damaged tissues with nutrients, a better removal of metabolic products, an increased activity of phagocytosis, and a decreased production of glucocorticoids (Walker et al., 2014). The latter reaction reduces the permeability of blood vessels and cell membranes and has an anti-inflammatory effect. It also prevents the damage to tissues caused by pathogens and the products of their life activity.

References

Huether, S. E., & McCance, K. L. (2015). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby/Elsevier.

James, S., Nelson, K., & Ashwill, J. (2014). Nursing care of children: Principles and practice (4th ed.). St. Louis, MO: Elsevier.

Lee, H. Y., Stieger, M., Yawalkar, N., & Kakeda, M. (2013). Cytokines and chemokines in irritant contact dermatitis. Mediators of Inflammation, 916497, 1-7.

McEwen, B. S., Bowles, N. P., Gray, J. D., Hill, M. N., Hunter, R. G., Karatsoreos, I. N., & Nasca, C. (2015). Mechanisms of stress in the brain. Nature Neuroscience, 18(10), 1353–1363.

Rogers, H. (2016). Heart disease and the stress hypothesis in the mid-twentieth century: A historical review. Psicologia: Reflexão e Crítica, 29(47), 1-8.

Walker, M. J., Barnett, T. C., McArthur, J. D., Cole, J. N., Gillen, C. M., Henningham, A., … Nizet, V. (2014). Disease manifestations and pathogenic mechanisms of group A streptococcus. Clinical Microbiology Reviews, 27(2), 264–301.

Wiegner, L., Hange, D., Björkelund, C., & Ahlborg, G. (2015). Prevalence of perceived stress and associations to symptoms of exhaustion, depression and anxiety in a working age population seeking primary care ̶ An observational study. BMC Family Practice, 16, 38.

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