Acute Pharyngitis

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Chapter 373 Acute Pharyngitis

Upper respiratory tract infections account for a substantial portion of visits to pediatricians. Approximately 30% of such illnesses feature a sore throat as the primary symptom.

Etiology

The most important agents causing pharyngitis are viruses, (adenoviruses, coronaviruses, enteroviruses, rhinoviruses, respiratory syncytial virus [RSV], Epstein-Barr virus [EBV], herpes simplex virus [HSV], metapneumovirus) and group A β-hemolytic streptococcus (GABHS; Chapter 176). Other organisms sometimes associated with pharyngitis include group C streptococcus (especially Streptococcus equisimilis), Arcanobacterium haemolyticum, Francisella tularensis, Mycoplasma pneumoniae, Neisseria gonorrhoeae, Fusobacterium necrophorum, and Corynebacterium diphtheriae. Other bacteria, such as Haemophilus influenzae and Streptococcus pneumoniae, may be cultured from the throats of children with pharyngitis, but their role in causing pharyngitis has not been established. Primary infection with HIV can also manifest with pharyngitis and a mononucleosis-like syndrome.

Pathogenesis

Colonization of the pharynx by GABHS can result in either asymptomatic carriage or acute infection. The M protein is the major virulence factor of GABHS and facilitates resistance to phagocytosis by polymorphonuclear neutrophils. Type-specific immunity develops following most infections and provides protective immunity to subsequent infection with that particular M serotype.

Scarlet fever is caused by GABHS that produces 1 of 3 streptococcal erythrogenic exotoxins (A, B, and C) that can induce a fine papular rash (Chapter 176). Exotoxin A appears to be most strongly associated with scarlet fever. Exposure to each exotoxin confers specific immunity only to that toxin and, therefore, scarlet fever can occur up to 3 times.

Clinical Manifestations

The onset of streptococcal pharyngitis is often rapid, with prominent sore throat and fever in the absence of cough. Headache and gastrointestinal symptoms (abdominal pain, vomiting) are common. The pharynx is red, and the tonsils are enlarged and classically covered with a yellow, blood-tinged exudate. There may be petechiae or “doughnut” lesions on the soft palate and posterior pharynx, and the uvula may be red, stippled, and swollen. The anterior cervical lymph nodes are enlarged and tender. The incubation period is 2-5 days. Some patients demonstrate the additional stigmata of scarlet fever: circumoral pallor, strawberry tongue, and a red, finely papular rash that feels like sandpaper and resembles sunburn with goose pimples (Chapter 176).

The onset of viral pharyngitis may be more gradual, and symptoms more often include rhinorrhea, cough, and diarrhea. A viral etiology is suggested by the presence of conjunctivitis, coryza, hoarseness, and cough. Adenovirus pharyngitis can feature concurrent conjunctivitis and fever (pharyngoconjunctival fever; Chapter 254). Coxsackievirus pharyngitis can produce small (1-2 mm) grayish vesicles and punched-out ulcers in the posterior pharynx (herpangina), or small (3-6 mm) yellowish-white nodules in the posterior pharynx (acute lymphonodular pharyngitis; Chapter 242). In EBV pharyngitis, there may be prominent tonsillar enlargement with exudate, cervical lymphadenitis, hepatosplenomegaly, rash, and generalized fatigue as part of the infectious mononucleosis syndrome (Chapter 246). Primary HSV infections in young children often manifest as high fever and gingivostomatitis, but pharyngitis may be present (Chapter 244).

The illnesses attributed to group C streptococcus and A. haemolyticum are generally similar to those caused by GABHS. Infections with A. haemolyticum are sometimes accompanied by a blanching, erythematous, maculopapular rash. Gonococcal pharyngeal infections are usually asymptomatic but can cause acute pharyngitis with fever and cervical lymphadenitis. Lemierre syndrome is a serious complication of F. necrophorum pharyngitis and is characterized by septic thrombophlebitis of the internal jugular veins with septic pulmonary emboli, producing hypoxia and pulmonary infiltrates (Chapters 374, 375).

Diagnosis

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