Pharyngitis is defined as inflammation of the mucous membranes and underlying structures of the throat. The peak incidence occurs in children aged from 4 to 7 years, and approximately 10% of children seek medical care for pharyngitis annually. Most cases occur during colder months of the year when viruses are prevalent, and spread among family members is a prominent feature.13 Although bacteria, spirochetes, Chlamydia, Mycoplasma, mycobacteria, fungi, and parasites can all cause pharyngitis, 40% to 60% of cases are viral. Commonly involved viruses include adenovirus, parainfluenza virus, rhinovirus, herpes simplex, respiratory syncytial virus, Epstein–Barr virus, influenza virus, Coxsackie virus, echo virus, coronavirus, and cytomegalovirus.
Group A β-hemolytic Streptococcus (S. pyogenes, GAS) is the most common bacterial cause of pharyngitis in children, responsible for 15% to 30% of cases.13 Other, less common bacterial causes to consider include groups C and G streptococci, Mycoplasma pneumoniae, and Corynebacterium diphtheriae. Corynebacterium hemolyticum causes pharyngitis accompanied by a scarlatiniform rash similar to GAS. Pneumococcus, Staphylococcus aureus, Neisseria meningitides, and Haemophilus influenzae are thought to cause pharyngitis, usually after a viral upper respiratory infection. Fusobacterium necrophorum (FN) is both part of the normal oral flora and a pharyngeal pathogen implicated in Lemmiere syndrome.14 Consider Neisseria gonorrhoeae, Chlamydia trachomatis, and syphilis in sexually active adolescents.
Noninfectious causes of pharyngitis include postnasal drip, sinusitis, and respiratory irritants such as tobacco smoke or caustic ingestions. Agranulocytosis, lymphoma, and lymphocytic leukemia, though rare, can present with pharyngeal inflammation and symptoms.
Uvular inflammation may result from bacterial infection, trauma (usually medical instrumentation), and allergy. Uvulitis is most worrisome when associated with epiglottitis or angioneurotic edema, both potentially life-threatening conditions. GAS, H. influenzae type B, and Streptococcus pneumoniae can cause uvulitis.
Children with acute GAS pharyngitis commonly present with sore throat, fever, odynophagia, and tonsillopharyngeal erythema with or without exudate. Headache, vomiting, abdominal pain, and scarlatiniform rash (fine, erythematous, sandpaper-like) commonly accompany streptococcal pharyngitis. Non-GAS infections have a similar presentation. Rhinorrhea, cough, hoarseness, or mucosal ulcers, suggest a viral etiology. Epstein–Barr virus and cytomegalovirus infection present with fever, pharyngitis, and lymphadenopathy. Fatigue, abdominal pain, splenomegaly, and bilateral upper eyelid edema may also be noted. Low-grade fever, follicular conjunctivitis, sore throat, and cervical lymphadenopathy characterize pharyngoconjunctival fever. Pharyngitis accompanied by rash, joint pain, and urethral or vaginal discharge may indicate gonorrhea. Syphilis in the primary stage may present with diffuse pharyngeal erythema and a chancre. Secondary syphilis may manifest with gray oropharyngeal patches and a rash. Diphtheria presents as an adherent, grayish pharyngeal membrane with bull neck and toxic appearance.
Scoring systems for the diagnosis of GAS have not demonstrated adequate sensitivity or specificity in children. Testing for GAS by rapid antigen detection tests (RADT) is recommended except when overt viral features are present.14 False-positives with RADT are uncommon, however negative RADT should be confirmed by throat culture. The Infectious Diseases Society of America does not recommend GAS testing in children younger than 3 years.15 Diagnosis of infectious mononucleosis is largely clinical although viral capsid antigen IgM level may be helpful. Syphilis screening tests and/or cultures for N. gonorrhoeae are indicated for unusual presentations or recurrent disease.
Suppuration can spread to contiguous tissues causing PTA, Lemmiere postanginal sepsis (aerobic or anaerobic bacteremia from septic thrombophlebitis of the tonsillar vein), and Ludwig angina. Hematologic spread may result in mesenteric adenitis, meningitis, brain abscess, cavernous sinus thrombosis, suppurative arthritis, endocarditis, osteomyelitis, sepsis, and septic embolization to the lung.
Nonsuppurative complications of GAS include scarlet fever, acute rheumatic fever (ARF), and glomerulonephritis (PSGN). ARF typically begins 1 to 5 weeks after GAS infection and is suggested by clinical features outlined in the Jones criteria (see Chapter 110). PSGN tends to occur in outbreaks associated with virulent strains of GAS. Symptoms typically appear 1 to 3 weeks after pharyngitis, and 3 to 6 weeks after scarlet fever or impetigo. The most common presentation is dark urine, edema, and hypertension. Treatment of GAS pharyngitis within 10 days of the illness can prevent ARF, however, there is no evidence that treatment prevents PSGN.
Current recommendations for GAS pharyngitis support treatment of cases where clinical suspicion is high or the diagnosis is confirmed by RADT or culture. Penicillin (oral or IM) is the first-line agent. Advanced macrolide antibiotics, clindamycin, or first-generation cephalosporins may be used in penicillin-allergic patients.15 Treatment of group C and G streptococci should be considered in patients with severe symptoms and negative RADT culture. FN is treated with penicillin and metronidazole. Other bacterial causes require specific and supportive management. If diphtheria is suspected, diphtheria antitoxin is given along with penicillin or erythromycin to eradicate the organism.