Pharyngitis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Venkata Sivakrishna Kumar Pulivarthi M.B.B.S [2]Delband Yekta Moazami, M.D.[3]

The pathogenesis of the sore throat due to pharyngitis is poorly understood. The pharynx is often the first site of infection for many contagious diseases such as pharyngitis because pathogens such as viruses and bacteria often settle in the nasopharynx through inhalation or through droplets. Viral pharyngitis usually transmits from person to person through direct touch or through droplets transmission. The foreign invader reproduces rapidly after settling on the nasopharynx. Generally, pharyngitis is a primary disease, but may be associated with systemic disorders such as the acute retroviral syndrome, or part of a more generalized upper respiratory tract infection.

• Most viruses, such as adenovirus or coxsackie virus, can cause inflammation of the pharyngeal mucosa by direct invasion of the mucosa or by secondary to suprapharyngeal secretions.^[1] Other viruses, such as rhinoviral infections produce bradykinin and lysyl bradykinin, which are known inflammatory mediators that can excite nerve endings in the pharynx to cause pain.^{[2] [3] [4]}
• Pathogenesis of bacterial pharyngitis varies with etiology. In streptococcal pharyngitis (which is the most common bacterial pharyngitis), the bacteria release exotoxins and proteases. Erythrogenic exotoxins are responsible for the development of the scarlatiniform exanthem. Secondary antibody cross react against M2-protein of the myocardial tissue that may result in rheumatic fever and valvular heart diseasea(type II hypersensitivity reaction)nd the antigen-antibody complexes can lead to acute poststreptococcal glomerulonephritis (type 3 hypersensitivity reaction).^[5][6][7]