Robert R. Tanz
Pharyngitis refers to inflammation of the pharynx, including erythema, edema, exudates, or an enanthem (ulcers, vesicles). Pharyngeal inflammation can be related to environmental exposures, such as tobacco smoke, air pollutants, and allergens; from contact with caustic substances, hot food, and liquids; and from infectious agents. The pharynx and mouth can be involved in various inflammatory conditions such as the periodic fever, aphthous stomatitis, pharyngitis, adenitis (PFAPA) syndrome, Kawasaki disease, inflammatory bowel disease (IBD), Stevens-Johnson syndrome, and systemic lupus erythematous (SLE). Noninfectious etiologies are typically evident from history and physical exam, but it can be more challenging to distinguish from among the numerous infectious causes of acute pharyngitis.
Acute infections of the upper respiratory tract account for a substantial number of visits to pediatricians and many feature sore throat as a symptom or evidence of pharyngitis on physical examination. The usual clinical task is to distinguish important, potentially serious, and treatable causes of acute pharyngitis from those that are self-limited and require no specific treatment or follow-up. Specifically, identifying patients who have group A streptococcus (GAS; Streptococcus pyogenes ; see Chapter 210 ) pharyngitis and treating them with antibiotics forms the core of the management paradigm.
In North America and most industrialized countries, GAS is the most important bacterial cause of acute pharyngitis, but viruses predominate as acute infectious causes of pharyngitis. Viral upper respiratory tract infections are typically spread by contact with oral or respiratory secretions and occur most commonly in fall, winter, and spring—that is, the respiratory season. Important viruses that cause pharyngitis include influenza, parainfluenza, adenoviruses, coronaviruses, enteroviruses, rhinoviruses, respiratory syncytial virus (RSV), cytomegalovirus, Epstein-Barr virus (EBV), herpes simplex virus (HSV), and human metapneumovirus (HMPV) (Table 409.1 ). Most viral pharyngitis, except mononucleosis, is mild. Common nonspecific symptoms such as rhinorrhea and cough develop gradually before they become prominent. However, specific findings are sometimes helpful in identifying the infectious viral agent (Table 409.2 ).
Table 409.1
Infectious Agents That Cause Pharyngitis
| VIRUSES | BACTERIA |
|---|---|
|
Adenovirus Coronavirus Cytomegalovirus Epstein-Barr virus Enteroviruses Herpes simplex virus (1 and 2) Human immunodeficiency virus Human metapneumovirus Influenza viruses (A and B) Measles virus Parainfluenza viruses Respiratory syncytial virus Rhinoviruses |
Streptococcus pyogenes (Group A streptococcus) |
| Arcanobacterium haemolyticum | |
| Fusobacterium necrophorum | |
| Corynebacterium diphtheriae | |
| Neisseria gonorrhoeae | |
| Group C streptococci | |
| Group G streptococci | |
|
Francisella tularensis Yersinia pestis |
|
| Chlamydophila pneumoniae | |
| Chlamydia trachomatis | |
|
Mycoplasma pneumoniae Mixed anaerobes (Vincent angina) |
Table 409.2
Epidemiologic and Clinical Features Suggestive of Group A Streptococcal and Viral Pharyngitis
| FEATURE, BY SUSPECTED ETIOLOGIC AGENT |
| Group A Streptococcal |
| Viral |
From Shulman ST, Bisno AL, Clegg HW, et al: Clinical practice guideline for the diagnosis and management of group A streptococcal pharyngitis: 2012 update by the Infectious Diseases Society of America. Clin Infect Dis 55(10):e86–e102, 2012, Table 4, p. e91.
Gingivostomatitis and ulcerating vesicles throughout the anterior pharynx and on the lips and perioral skin are seen in primary oral HSV infection. High fever and difficulty taking oral fluids are common. This infection can last for 14 days.
Discrete papulovesicular lesions or ulcerations in the posterior oropharynx, severe throat pain, and fever are characteristic of herpangina , caused by various enteroviruses. In hand-foot-mouth disease , there are vesicles or ulcers throughout the oropharynx, vesicles on the palms and soles, and sometimes on the trunk and extremities. Coxsackie A16 is the most common agent, but Enterovirus 71 and Coxsackie A6 can also cause this syndrome. Enteroviral infections are most common in the summer.
Various adenoviruses cause pharyngitis. When there is concurrent conjunctivitis , the syndrome is called pharyngoconjunctival fever . The pharyngitis tends to resolve within 7 days but conjunctivitis may persist for up to 14 days. Pharyngoconjunctival fever can be epidemic or sporadic; outbreaks have been associated with exposure in swimming pools.
Intense, diffuse pharyngeal erythema and Koplik spots, the pathognomonic enanthem, occur in advance of the characteristic rash of measles. Splenomegaly, lymphadenopathy, or hepatomegaly may be the clue to EBV infectious mononucleosis in an adolescent with exudative tonsillitis. Primary infection with HIV can manifest as the acute retroviral syndrome , with non-exudative pharyngitis, fever, arthralgia, myalgia, adenopathy, and often a maculopapular rash.
In addition to GAS, bacteria that cause pharyngitis include group C and group G streptococcus, Arcanobacterium haemolyticum , Francisella tularensis , Neisseria gonorrhoeae , Mycoplasma pneumoniae , Chlamydophila (formerly Chlamydia ) pneumoniae , Chlamydia trachomatis , Fusobacterium necrophorum , and Corynebacterium diphtheriae . 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.
Group C and Group G streptococcus and A. haemolyticum pharyngitis have been diagnosed most commonly in adolescents and adults. They resemble group A β-hemolytic streptococcus (GAS) pharyngitis. A scarlet fever–like rash may be present with A. haemolyticum infections.
F. necrophorum has been suggested to be a fairly common cause of pharyngitis in older adolescents and adults (15-30 yr old). Prevalence in studies has varied from 10% to 48% of patients with non-GABHS pharyngitis, but large surveillance studies have not been performed. F. necrophorum was detected by PCR in 20.5% of patients with pharyngitis in a study based in a university health clinic and in 9.4% of an asymptomatic convenience sample; some patients had more than 1 bacterial species detected by PCR. Pharyngitis patients with F. necrophorum had signs and symptoms similar to GAS pharyngitis: about one third had fever, one third had tonsillar exudates, two thirds had anterior cervical adenopathy, and most did not have cough. This organism is difficult to culture from the throat, and diagnostic testing with PCR is not generally available. F. necrophorum pharyngitis is associated with the development of Lemierre syndrome (see Chapter 410 ), internal jugular vein septic thrombophlebitis. Approximately 80% of cases of Lemierre syndrome are caused by this bacterium. Patients present initially with fever, sore throat, exudative pharyngitis, and/or peritonsillar abscess. The symptoms may persist, neck pain and swelling develop, and the patient appears toxic. Septic shock may ensue, along with metastatic complications from septic emboli that can involve the lungs, bones and joints, central nervous system, abdominal organs, and soft tissues. The case fatality rate is 4–9%.
Gonococcal pharyngeal infections are usually asymptomatic but can cause acute ulcerative or exudative pharyngitis with fever and cervical lymphadenitis. Young children with proven gonococcal disease should be evaluated for sexual abuse.
Diphtheria is extremely rare in most developed countries due to extensive immunization with diphtheria toxoid. However, it remains endemic in many areas of the world, including the former Soviet bloc countries, Africa, Asia, the Middle East, and Latin America. It can be considered in patients with recent travel to or from these areas and in unimmunized patients. Key physical findings are bull neck (extreme neck swelling) and a gray pharyngeal pseudomembrane that can cause respiratory obstruction.
Ingestion of water, milk, or undercooked meat contaminated by F. tularensis can lead to oropharyngeal tularemia. Severe throat pain, tonsillitis, cervical adenitis, oral ulcerations, and a pseudomembrane (as in diphtheria) may be present. M. pneumoniae and C. pneumonia e cause pharyngitis, but other upper and lower respiratory infections are more important and more readily recognized. Development of a severe or persistent cough subsequent to pharyngitis may be the clue to infection with 1 of these organisms.
Streptococcal pharyngitis is relatively uncommon before 2-3 yr of age, is quite common among children 5-15 yr old, and declines in frequency in late adolescence and adulthood. Illness occurs throughout the year but is most prevalent in winter and spring. It is readily spread among siblings and schoolmates. GAS causes 15–30% of pharyngitis in school-age children.
Colonization of the pharynx by GAS can result in either asymptomatic carriage or acute infection. After an incubation period of 2-5 days, pharyngeal infection with GAS classically presents as rapid onset of significant sore throat and fever (see Table 409.2 ). The pharynx is red, the tonsils are enlarged and often covered with a white, grayish, or yellow exudate that may be blood-tinged. There may be petechiae or doughnut lesions on the soft palate and posterior pharynx, and the uvula may be red and swollen (see Fig. 411.1 ). The surface of the tongue can resemble a strawberry when the papillae are inflamed and prominent (strawberry tongue). Initially, the tongue is often coated white, and with the swollen papillae it is called a white strawberry tongue (see Fig. 210.1B ). When the white coating is gone after a few days, the tongue is often quite red, and is called a red strawberry tongue (see Fig. 210.1C ). Enlarged and tender anterior cervical lymph nodes are frequently present. Headache, abdominal pain, and vomiting are frequently associated with the infection, but in the absence of clinical pharyngitis, gastrointestinal signs and symptoms should not be attributed to GAS. Ear pain is a frequent complaint, but the tympanic membranes are usually normal. Diarrhea, cough, coryza, ulcerations, croup/laryngitis/hoarseness, and conjunctivitis are not associated with GAS pharyngitis and increase the likelihood of a viral etiology (see Table 409.2 ).
Patients infected with GAS that produce streptococcal pyrogenic exotoxin A, B, or C may demonstrate the fine red, papular (sandpaper) rash of scarlet fever (see Fig. 210.1A ) . It begins on the face and then becomes generalized. The cheeks are red, and the area around the mouth is less intensely red (more pale), giving the appearance of circumoral pallor. The rash blanches with pressure, and it may be more intense in skin creases, especially in the antecubital fossae, axillae, and inguinal creases (Pastia lines or sign). Pastia lines are sometimes petechial or slightly hemorrhagic. Capillary fragility can cause petechiae distal to a tourniquet or constriction from clothing, a positive tourniquet test or Rumpel-Leeds phenomenon. Erythema fades in a few days, and when the rash resolves, it typically peels like a mild sunburn. Sometimes there is sheet-like desquamation around the free margins of the finger nails. Streptococcal pyrogenic exotoxin A, encoded by the gene spe A , is the exotoxin most commonly associated with scarlet fever.
The M protein is an important GAS virulence factor that facilitates resistance to phagocytosis. The M protein is encoded by the emm gene and determines the M type (or emm type). Molecular methods have identified more than 200 emm genes (emm types, M types). The M protein is immunogenic and protects against reinfection with the homologous M type; an individual can experience multiple episodes of GAS pharyngitis in a lifetime because natural immunity is M type–specific and does not prevent infection with a new M type. Numerous GAS M types can circulate in a community simultaneously, and they enter and leave communities unpredictably and for unknown reasons.
The clinical presentations of streptococcal and viral pharyngitis often overlap. In particular, the pharyngitis of mononucleosis can be difficult to distinguish from GAS pharyngitis. Physicians relying solely on clinical judgment often overestimate the likelihood of a streptococcal etiology. Various clinical scoring systems have been described to assist in identifying patients who are likely to have GAS pharyngitis. Criteria developed for adults by Centor and modified for children by McIsaac give 1 point for each of the following criteria: history of temperature >38°C (100.4°F), absence of cough, tender anterior cervical adenopathy, tonsillar swelling or exudates, and age 3-14 yr. It subtracts a point for age ≥45 yr. At best, a McIsaac score ≥4 is associated with a positive laboratory test for GAS in less than 70% of children with pharyngitis (Table 409.3 ), so it, too, overestimates the likelihood of GAS. Consequently, laboratory testing is essential for accurate diagnosis . Clinical findings and/or scoring systems can best be used to assist the clinician in identifying patients in need of testing. Evaluating patients indiscriminately can lead to overdiagnosis and overtreatment. Streptococcal antibody tests are not useful in assessing patients with acute pharyngitis.
Table 409.3
Positive Predictive Value of McIsaac Score in Children in Clinical Studies*
| SCORE | McISAAC, 2004 (N = 454) (%) | EDMONSON, 2005 (N = 1184) (%) | TANZ, 2009 (N = 1848) (%) | FINE, 2012 (N = 64,789) (%) |
|---|---|---|---|---|
| 0 | — | — | 7 | 17 |
| 1 | — | 0.5 | 19 | 23 |
| 2 | 20.5 | 8.9 | 20 | 34 |
| 3 | 27.5 | 42.4 | 29 | 50 |
| ≥4 | 67.8 | 48.2 | 49 | 68 |
| GAS prevalence | 34 | 38 | 30 | 37 |
* One point is given for each of the following criteria: history of temperature >38°C (100.4°F); absence of cough; tender anterior cervical adenopathy; tonsillar swelling or exudates; and age 3-14 yr. Note that the Centor score lacks only the age criterion. Positive predictive value refers to the proportion of patients with documented GAS by rapid antigen-detection test and/or throat culture.
Throat culture and rapid antigen-detection tests (RADTs) are the diagnostic tests for GAS most available in routine clinical care. Throat culture plated on blood agar remains the gold standard for diagnosing streptococcal pharyngitis. There are both false-negative cultures as a consequence of sampling errors or prior antibiotic treatment and false-positive cultures as a consequence of misidentification of other bacteria as GAS. Streptococcal RADTs detect the group A carbohydrate of GAS. They are used by the vast majority of office-based pediatricians. All RADTs have very high specificity, generally ≥95%, so when a RADT is positive it is assumed to be accurate and throat culture is unnecessary. Because RADTs are generally much less sensitive than culture, confirming a negative rapid test with a throat culture is recommended. RADTs and throat culture exhibit spectrum bias: they are more sensitive when the pretest probability of GAS is high (signs and symptoms are typical of GAS infection, higher McIsaac scores) and less sensitive when the pretest probability is low. Avoidance of testing when patients have signs and symptoms more suggestive of a viral infection is recommended by expert guidelines.
Many laboratories have replaced throat culture with one of the highly sensitive and specific GAS molecular tests . A variety of methods are available to amplify the DNA of a specific GAS gene from a throat swab in less than 1 hr. In studies both sensitivity and specificity are reported to be ≥98% when compared with standard throat culture. Polymerase chain reaction (PCR) usually matches the molecular test when used to adjudicate discrepancies between the culture and molecular test results. Some of these nucleic acid amplification tests are approved by the FDA for use in physician office laboratories and can be used as the initial test for GAS or as a confirmatory test when the RADT is negative. Unlike throat culture and RADTs, molecular tests may not exhibit spectrum bias—that is, although test sensitivity is extremely high, it is independent of the pretest probability that GAS are the cause of illness (using signs and symptoms, McIsaac score), thus increasing the potential to identify a chronic GAS carrier who actually has an intercurrent illness not due to GAS (discussed later). However, the ability of these stand-alone tests to deliver a definitive result in less than 1 hr makes them attractive (there is one test that takes 15 min)—the potential to swab symptomatic children, have them wait or send them home, and electronically prescribe an antibiotic when the test is positive can speed initiation of therapy and subsequent return to school and activities. The role of molecular tests in diagnosis of GAS pharyngitis is currently unclear because of 3 concerns: (1) they are so sensitive they may cause unnecessary treatment of more patients who are carriers than would ordinarily occur with RADT and/or culture; (2) unless rigorous technique is followed, they may be prone to contamination with exogenous GAS DNA from other swabs, a particular concern in physician offices when performed by staff who are not trained laboratory technologists; and (3) they are much more expensive than throat culture.
Testing for bacteria other than GAS is performed infrequently, and should be reserved for patients with persistent symptoms and symptoms suggestive of a specific non-GAS bacterial pharyngitis—for example, when there is concern for gonococcal infection or sexual abuse. Special culture media and a prolonged incubation are required to detect A. haemolyticum. A complete blood cell count showing many atypical lymphocytes and a positive mononucleosis slide agglutination test can help confirm a clinical suspicion of EBV infectious mononucleosis. Viral cultures are often unavailable and are generally too expensive and slow to be clinically useful. PCR is more rapid and multiplex PCR (respiratory viral panel) testing for respiratory pathogens can identify a variety of viral and bacterial agents within a few hours. This may be useful in determining the isolation needs of hospitalized patients, assisting in patient prognosis, and epidemiology, but in the absence of specific treatment for most viral infections such testing is usually not necessary or useful. In fact, interpreting such tests can be difficult unless the patient has signs or symptoms characteristic of a specific pathogen.
Specific therapy is unavailable for most viral pharyngitis. However, nonspecific, symptomatic therapy can be an important part of the overall treatment plan. An oral antipyretic/analgesic agent (acetaminophen or ibuprofen) can relieve fever and sore throat pain. Anesthetic sprays and lozenges (often containing benzocaine, phenol, or menthol) can provide local relief in children who are developmentally appropriate to use them. Systemic corticosteroids are sometimes used in children who have evidence of upper airway compromise due to mononucleosis. Although corticosteroids are used commonly in adults with pharyngitis, large-scale studies capable of providing safety and efficacy data are lacking in children. Corticosteroids cannot be recommended for treatment of most pediatric pharyngitis.
Antibiotic therapy of bacterial pharyngitis depends on the organism identified. On the basis of in vitro susceptibility data, oral penicillin is often suggested for patients with group C streptococcal isolates, and oral erythromycin is recommended for patients with A. haemolyticum , but the clinical benefit of such treatment is uncertain.
Most untreated episodes of GAS pharyngitis resolve uneventfully within a few days, but early antibiotic therapy hastens clinical recovery by 12-24 hr and also reduces suppurative complications of GAS pharyngitis such as peritonsillar abscess and cervical adenitis. The primary benefit and intent of antibiotic treatment is the prevention of acute rheumatic fever (ARF) ; it is highly effective when started within 9 days of onset of illness. Antibiotic therapy does not prevent acute poststreptococcal glomerulonephritis (APSGN). Antibiotic treatment should not be delayed for children with symptomatic pharyngitis and a positive test for GAS. Presumptive antibiotic treatment can be started when there is a clinical diagnosis of scarlet fever, a symptomatic child has a household contact with documented streptococcal pharyngitis, or there is a history of ARF in the patient or a family member, but a diagnostic test should be performed to confirm the presence of GAS and antibiotics should be discontinued if GAS are not identified.
A variety of antimicrobial agents are effective for GAS pharyngitis (Table 409.4 ). Group A streptococci are universally susceptible to penicillin and all other β-lactam antibiotics. Penicillin is inexpensive, has a narrow spectrum of activity, and has few adverse effects. Amoxicillin is often preferred for children because of taste, availability as chewable tablets and liquid, and the convenience of once-daily dosing. The duration of oral penicillin and amoxicillin therapy is 10 days. A single intramuscular dose of benzathine penicillin or a benzathine-procaine penicillin G combination is effective and ensures compliance. Follow-up testing for GAS is unnecessary after completion of therapy and is not recommended unless symptoms recur.
Table 409.4
Recommended Treatment for Acute Streptococcal Pharyngitis
| MOST PATIENTS | ||||
| WEIGHT <27 kg | WEIGHT ≥27 kg | ROUTE | DURATION | |
| Amoxicillin | 50 mg/kg once daily (maximum 1,000 mg) | Oral | 10 days | |
| Penicillin V | 250 mg bid | 500 mg bid | Oral | 10 days |
| Benzathine penicillin G | 600,000 units | 1.2 million units | IM | Once |
| Benzathine penicillin G + procaine penicillin G | 900,000 units + 300,000 units | 900,000 units + 300,000 units | IM | Once |
| PENICILLIN-ALLERGIC PATIENTS | ||||
| ORAL DOSE | FREQUENCY | DURATION | ||
| Cephalosporins* | Varies with agent chosen | 10 days | ||
|
Erythromycins Ethylsuccinate Estolate |
||||
| 40 mg/kg/day up to 1,000 mg/day | bid | 10 days | ||
| 20-40 mg/kg/day up to 1,000 mg/day | bid | 10 days | ||
| Clarithromycin | 15 mg/kg/day up to 500 mg/day | bid | 10 days | |
| Azithromycin † | 12 mg/kg day 1; 6 mg/kg days 2-5 | qd | 5 days | |
| Clindamycin | 20 mg/kg/day up to 1.8 g/day | tid | 10 days | |
* First-generation cephalosporins are preferred; dosage and frequency vary among agents. Do not use in patients with history of immediate (anaphylactic) hypersensitivity to penicillin or other β-lactam antibiotics.
† Maximum dose is 500 mg the 1st day, 250 mg subsequent days.
Patients allergic to the penicillins can be treated with a 10-day course of a narrow-spectrum, 1st-generation cephalosporin (cephalexin or cefadroxil) if the previous reaction to penicillin was not an immediate, type I hypersensitivity reaction. Frequently, penicillin-allergic patients are treated for 10 days with erythromycin, clarithromycin, or clindamycin, or for 5 days with azithromycin.
The increased use of macrolides and related antibiotics for a variety of infections, especially the azalide, azithromycin, is associated with increased rates of resistance to these drugs among GAS in many countries. Approximately 5% of GAS in the United States and more than 10% in Canada are macrolide-resistant (macrolide resistance includes azalide resistance), but there is considerable local variation in both countries. Rates are much higher in many European and Asian countries. Some macrolide-resistant GAS isolates are also resistant to clindamycin. Although not a major hindrance for treatment of pharyngitis, clindamycin resistance may be important in management of invasive GAS infections. The use of macrolides and related antibiotics should be restricted to patients who cannot safely receive a β-lactam drug for GAS pharyngitis. Tetracyclines, fluoroquinolones, or sulfonamides should not be used to treat GAS pharyngitis.
Streptococcal carriers are patients who continue to harbor GAS in the pharynx despite appropriate antibiotic therapy or when they are well. They have little or no evidence of an inflammatory response to the organism. The pathogenesis of chronic carriage is not known; it is assuredly not related to penicillin resistance or nonadherence to therapy, and there is little direct evidence to support the concept of co-pathogenicity (presence of β-lactamase-producing organisms in the pharynx). Carriage generally poses little risk to patients and their contacts, but it can confound testing in subsequent episodes of sore throat. A child who is chronically colonized with GAS (streptococcal carrier) can have a positive test for GAS if it is obtained when the child is evaluated for pharyngitis that is actually caused by a viral infection. Patients with repeated test-positive pharyngitis create anxiety among their families and physicians. It is usually unnecessary to attempt to eliminate chronic carriage. Instead, evaluation and treatment of clinical pharyngitis should be undertaken without regard for chronic carriage, using clinical criteria to determine the need for testing, treating test-positive patients in routine fashion, and avoiding antibiotics in patients who have negative tests. This approach often requires considerable effort to reassure the patient and family that chronic carriage is not a significant health risk. Expert opinion suggests that eradication might be attempted in select circumstances: a community outbreak of ARF or APSGN; personal or family history of ARF; an outbreak of GAS pharyngitis in a closed or semiclosed community, nursing home, or healthcare facility; repeated episodes of symptomatic GAS pharyngitis in a family with ping pong spread among family members despite adequate therapy; when tonsillectomy is being considered because of chronic carriage or recurrent streptococcal pharyngitis; and extreme, unmanageable anxiety related to GAS carriage (“streptophobia”) among family members. Clindamycin given by mouth for 10 days is effective therapy (20 mg/kg/day divided in 3 doses; adult dose 150-450 mg tid). Amoxicillin-clavulanate (40 mg amoxicillin/kg/day up to 2,000 mg amoxicillin/day divided tid for 10 days), and 4 days of oral rifampin (20 mg/kg/day up to 600 mg divided in 2 doses) plus either intramuscular benzathine penicillin given once or oral penicillin given for 10 days have also been used (rifampin is started on the 1st day of penicillin therapy).
True recurrent GAS pharyngitis can occur for several reasons: reinfection with the same M type if type-specific antibody has not developed; poor compliance with oral antibiotic therapy; macrolide resistance if a macrolide was used for treatment; and infection with a new M type. Unfortunately, determining the GAS M type in an acute infection is not available to the clinician. Treatment with intramuscular benzathine penicillin eliminates nonadherence to therapy. Apparent recurrences can represent pharyngitis of another cause in the presence of streptococcal carriage. Chronic GAS carriage is particularly likely if the illnesses are mild and otherwise atypical for GAS pharyngitis.
Tonsillectomy may lower the incidence of pharyngitis for 1-2 yr among children with frequent episodes of documented pharyngitis (≥7 episodes in the previous year or ≥5 in each of the preceding 2 yr, or ≥3 in each of the previous 3 yr). However, the frequency of pharyngitis (GAS and non-GAS) generally declines over time. By 2 yr posttonsillectomy, the incidence of pharyngitis in severely affected children is similar among those who have tonsillectomy and those who do not. Few children are so severely affected, and the limited clinical benefit of tonsillectomy for most must be balanced against the risks of anesthesia and surgery. Undocumented history of recurrent pharyngitis is an inadequate basis for recommending tonsillectomy.
Recurrent GAS pharyngitis is rarely, if ever, a sign of an immune disorder. However, recurrent pharyngitis can be part of a recurrent fever or autoinflammatory syndrome such as PFAPA syndrome. Prolonged pharyngitis (>1 wk) can occur in infectious mononucleosis and Lemierre syndrome, but it also suggests the possibility of another disorder such as neutropenia, a recurrent fever syndrome, or an autoimmune disease such as SLE or IBD. In such instances, pharyngitis would be 1 of a number of clinical findings that together should suggest the underlying diagnosis.
Viral respiratory tract infections can predispose to bacterial middle ear infections and bacterial sinusitis. The complications of GAS pharyngitis include local suppurative complications, such as parapharyngeal abscess, and subsequent nonsuppurative illnesses, such as ARF, APSGN, poststreptococcal reactive arthritis, and possibly PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococci) (sometimes referred to as CANS [childhood acute neuropsychiatric symptoms] or PANS [pediatric acute-onset neuropsychiatric syndrome], recognizing that many infections other than GAS may predispose to these syndromes).
Vaccines intended to prevent infection with various viruses (e.g., RSV) and GAS are being developed. A recombinant multivalent GAS M-type vaccine uses the terminal portions of various M proteins to take advantage of their immunogenicity. Other GAS vaccines are based on more conserved epitopes in order to avoid the necessity of matching the vaccine with the M types prevalent in a community or target population. None of the investigational GAS vaccines are near licensing for use. A recent comprehensive study of the immune response to childhood GAS pharyngeal acquisition raises questions about how to best design effective vaccines. This is complicated by the variety of clinical scenarios and clinical syndromes associated with GAS and the need to determine the intended clinical benefit(s) of vaccination. Antimicrobial prophylaxis with daily oral penicillin prevents recurrent GAS infections but is recommended only to prevent recurrences of ARF.