Bacterial Pharyngitis



Pharyngitis, or sore throat, is often caused by infection. Common respiratory viruses account for the vast majority of cases (see Viral Pharyngitis), and these are usually self-limited. Bacteria are also important etiologic agents, and, when identified properly, may be treated with antibacterials, resulting in decreased local symptoms and prevention of serious sequelae.

The most common and important bacterial cause of pharyngitis is Streptococcus pyogenes (group A Streptococcus [GAS]). When suspected, bacterial pharyngitis should be confirmed with routine diagnostic tests and treated with various antibiotics. Swabbing the throat and testing for GAS pharyngitis via rapid antigen detection test (RADT) and/or culture should be performed as clinical features alone cannot reliably distinguish GAS pharyngitis from viral pharyngitis. The exceptions to these is when patients present overt clinical features of viral infection including rhinorrhea, cough, oral ulcers, and/or hoarseness, in which case a positive test result might reflect a carriage state.[1]

If left untreated, S pyogenes pharyngitis may lead to local and distant complications. To a lesser extent, bacteria other than S pyogenes are known to cause pharyngitis, and these are discussed in Causes.


Beta-hemolytic streptococci have the ability to cause large zones of hemolysis on blood agar, aiding in microbiological identification.[2] Lancefield antigens, carbohydrates in the cell wall, provide further differentiation of streptococci. S pyogenes, which contains group A antigens and displays beta-hemolysis, is the most common species referred to as a group A beta-hemolytic streptococci (GABHS). Streptococcus dysgalactiae subspecies equisimilis and some species from the Streptococcus anginosus group may share laboratory characteristics with S pyogenes but do not commonly cause human disease. See the image below.

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Picture of Streptococcus pyogenes at 100 X magnification.

Perhaps the most important virulence factor of GABHS is the M protein. This protein, located peripherally on the cell wall, is required for invasive infection. T cells exposed to this M protein are postulated to cross-react with similar epitopes on human cardiac myosin and laminin, contributing to the pathogenesis of rheumatic heart disease.[3] This protein provides a potential target for a GABHS vaccine, although successful widespread implementation of such a vaccine remains elusive.[4] More than 100 M-protein serotypes have been described. Although individuals often develop lifelong immunity to one serotype, re-infection with a different serotype may cause disease.

GABHS contains a hyaluronic acid capsule, which also plays an important role in infection.[5] Bacteria that produce large quantities of this capsule exhibit a characteristic mucoid appearance on blood agar and may be more virulent.

Certain GABHS exotoxins act as superantigens by up-regulating T cells.[6] These superantigens can prompt a release of proinflammatory cytokines and may synergize with lipopolysaccharide. It has been speculated that these superantigens evade the pharyngeal immune response, resulting in proliferation of GABHS while permitting immune-mediated elimination of commensal organisms.

Adhesins enable GABHS attachment at sites such as the pharynx. This attachment allows for colonization and competition with normal host flora.

Some strains produce erythrogenic toxins, which cause the rash of scarlet fever in susceptible hosts.

GABHS is spread from person to person through large droplet nuclei.[7] Consequently, close quarters (eg, barracks, daycares, dormitories) facilitate transmission. In temperate regions, the prevalence of GABHS infection increases in the colder months, presumably because of the tendency of people to congregate indoors. Spread within families is common. The risk of acquiring GABHS from an infected family member is 40%, and nearly one in four of infected individuals eventually exhibit symptoms. Twenty-four hours after appropriate antibiotics are initiated, the patient is no longer considered contagious.

Case reports and in vitro studies have speculated that toothbrushes, orthodontic appliances, and pets may carry and facilitate spread of GABHS,[8, 9] although these claims have not been validated by rigorous in vivo investigation.[10]

GABHS is also a common cause of erysipelas, cellulitis, and necrotizing fasciitis and has been reported as a cause of pneumonia, empyema, toxic shock syndrome, and lymphangitis. The vast majority of these manifestations do not occur in the setting of pharyngitis.



United States

Acute pharyngitis accounts for approximately 12 million annual ambulatory care visits in the United States. It ranks within the top 20 most-common primary diagnosis groups.[11]

In temperate climates, GAS pharyngitis occurs most commonly in the winter and early spring.[1]


An estimated 616 million cases of GABHS pharyngitis occur annually worldwide.[12] Rheumatic heart disease, which may be a consequence of GABHS pharyngitis, is estimated to cause about 6 million years of life lost annually. The burden of rheumatic heart disease disproportionately affects populations from developing countries. In terms of estimated global mortality, GABHS is one of the top 10 pathogens, behind HIV infection and malaria and ahead of tetanus and pertussis.


Although GABHS pharyngitis is usually a self-limited entity, on average, a single episode in a child results in 1.9 days absence from school and a parent missing 1.8 days from work to care for the child.[13] Children with GABHS pharyngitis experience symptoms for an average of 4.5 days.

In addition to symptoms localized to the oropharynx, GABHS pharyngitis may also cause suppurative and nonsuppurative complications. Invasion of nearby structures may cause suppurative complications such as otitis media, sinusitis, peritonsillar abscess, retropharyngeal abscess, and cervical adenitis. Nonsuppurative complications of bacterial pharyngitis include rheumatic heart disease and poststreptococcal glomerulonephritis. These entities are discussed in Complications.


GABHS pharyngitis affects all races.


GABHS pharyngitis has no sexual predilection.


GABHS pharyngitis is most common in individuals aged 5-15 years, although adults may also acquire the disease.[14] Streptococcal pharyngitis is very uncommon in children younger than 3 years with the exception of children with risk factors such as an older close or household contact with GAS infection. Acute rheumatic fever is also rare in children younger than 3 years and in adults.

For more information on pharyngitis in children, see the Medscape Reference article Pediatric Pharyngitis.


GABHS pharyngitis is usually a self-limited illness. Throat symptoms resolve within 3-4 days in untreated patients. Administration of penicillin shortly after disease onset may shorten symptoms by 1-2 days.[15]

Patient Education

Symptomatic relief may be provided by warm saline gargles, throat lozenges, and ibuprofen.

Acetaminophen or ibuprofen can be used for fever relief.

Patients with bacterial pharyngitis should be instructed to complete a full course of antibiotics, even if symptoms resolve.


The signs and symptoms listed below may be seen with many non-GABHS etiologies. Furthermore, individuals with GABHS pharyngitis may have only a few or mild features listed. Conjunctivitis, cough, hoarseness, coryza, diarrhea, anterior stomatitis, discrete ulcerative lesions, and a viral exanthem are all more consistent with an etiology other than GABHS, particularly viral. Recent studies have also included rhinorrhea and conjunctival infection as viral features.[16] Signs and symptoms include the following:


Physical examination may reveal the following:

Predictive models have been developed to help determine the likelihood of GABHS pharyngitis based on the presence of fever, swollen tender anterior cervical lymph nodes, and tonsillar exudates and the absence of cough. Scores have been used to distinguish which patients merit further laboratory evaluation or treatment. The use of such clinical algorithms has been the source of much debate.[1, 17] These score systems were originally developed prior to the availability of RADTs and might be helpful in determining which patients to test for GAS pharyngitis but lack sufficient specificity to decide which patients need antibiotic therapy and might result in unnecessary use of antibiotics.[1]


Viruses cause the vast majority of pharyngitis cases. Common agents include coronavirus, rhinovirus, adenovirus, parainfluenza, influenza, Epstein-Barr virus, cytomegalovirus, and HIV.

GABHS accounts for 15%-30% of pharyngitis cases in children and 5%-10% of cases in adults.[1] Bacteria other than GABHS that may cause pharyngitis are discussed below.

Group C and G streptococci

Like GABHS, these pathogenic bacteria cause beta-hemolysis, form large colonies, and produce an M protein, yet neither is detected with RADTs, as they lack the group A antigen, which is the target of the test.

Pharyngitis caused by either of these non-GABHS streptococci have a clinical presentation similar to that of GABHS pharyngitis and should be considered in patients with worsening symptoms and an initial negative RADT result. They have been reported in epidemics, particularly in semi-closed populations such as military installations or schools[18, 19, 20] and in sporadic pharyngitis in college students.[21]

These bacteria are an uncommon cause of acute pharyngitis in pediatric patients.[22, 23] They have not been associated with the development of acute rheumatic fever.[24] Diagnosis can be achieved with a bacterial throat culture and identification based on Lancefield antigens.[25]

The prevalence of group C Streptococcus infection among primary care patients presenting with sore throat was reported to be 6.1% (95% CI, 3.1%-9.2%).[26]

Arcanobacterium haemolyticum

This gram-positive rod is an uncommon cause of pharyngitis and tonsillitis and accounts for 0.5% and 3% of cases.[27] Clinical manifestations are similar to those of GABHS pharyngitis, although about half of patients with A haemolyticum pharyngitis develop a rash, which typically starts on the extensor surfaces; spares the palms, soles, and head; and moves centrally to involve the trunk with a maculopapular or scarlatiniform appearance.

A haemolyticum exhibits variable susceptibility to penicillin and is identified more easily on human or rabbit blood agar than on sheep agar, the media traditionally used to identify GABHS. It is more common in adolescents and young adults.[28] Erythromycin is the treatment drug of choice.[27]

Neisseria gonorrhoeae

Infection with this pathogen is associated with oral-genital contact and is often asymptomatic.[29] N gonorrhoeae may be identified using chocolate or Thayer-Martin agar.[30] Nucleic acid amplification tests from throat rinses appear to be a promising alternative.[31] Because of increasing rates of fluoroquinolone resistance, ceftriaxone is now the only recommended option for treatment of pharyngeal gonorrhea.[32] Treatment aimed at Chlamydia trachomatis is also recommended, since co-infection is common.

Mycoplasma pneumoniae

This atypical bacterium is increasingly being identified as an etiologic agent of pharyngitis.[33] M pneumoniae pharyngitis may be associated with pulmonary findings.[34]

Yersinia species

Both Yersinia enterocolitica and Yersinia pestis may cause disease. Pharyngeal plague has been linked to the consumption of camel meat.[35]

Chlamydia trachomatis and Chlamydophila pneumoniae

Both of these organisms are rare causes of pharyngitis.[33, 31]

Francisella tularensis (oropharyngeal tularemia)

The causative organism is a gram-negative pleomorphic coccobacillus that can be acquired by ingestion of contaminated water or inadequately cooked game meat. It is an uncommon cause of pharyngitis and tonsillitis in the United States and is usually accompanied by lymphadenitis and severe exudative stomatitis.[36]

Corynebacterium diphtheriae

Toxigenic strains of this gram-positive bacillus are common causes of croup.[37] Young patients with C diphtheriae pharyngitis often exhibit inspiratory stridor, sternal retraction, and a barking cough. In severe cases, a membrane formation may impair breathing. The incidence of C diphtheriae pharyngitis in developed countries is low because of high immunization rates.

Fusobacterium necrophorum

This is an anaerobic gram-negative bacillus that can be isolated from the oropharynx of healthy individuals but that has been associated with sore throat.[38] It can also cause life-threatening disease, including Lemierre syndrome or postanginal sepsis (internal jugular vein thrombophlebitis, septic pulmonary emboli, and bacteremia.[39] Some studies also suggest a role for this bacterium in recurrent or persistent sore throat.[40, 41] However, it should always be considered if a patient presents with severe pharyngitis.[42] It is more common in adolescents and young adults.

The prevalence of Fusobacterium necrophorum infection among primary care patients presenting with sore throat was reported to be 19.4% (95% CI, 14.7%-24.1%).[26]


GABHS infection may result in suppurative or nonsuppurative complications.

Local complications: These result from untreated infection that spreads to adjacent sites. Some of the more common of these suppurative infections include retropharyngeal abscess, peritonsillar abscess, sinusitis, cervical lymphadenitis, otitis media, and mastoiditis.

Acute rheumatic fever: This disorder usually occurs 2-4 weeks after an episode of pharyngitis. Administration of proper antibiotics up to 9 days after the onset of pharyngeal symptoms has been shown to prevent this manifestation.[43]  Major manifestations of acute rheumatic fever include carditis, polyarthritis, chorea, erythema marginatum, and subcutaneous nodules. Minor criteria include fever, polyarthralgia, elevated leukocyte count, elevated erythrocyte sedimentation rate, and prolonged P-R interval. Current incidence of this complication after endemic infection is unknown but believed to be substantially less than 1%.[44]

Rheumatic heart disease: This is the chronic valvular manifestation of acute rheumatic fever. The mitral valve is the site most often affected, and either regurgitation or stenosis may result.[45]  In individuals with rheumatic heart disease, long-term secondary prophylaxis, often with benzathine penicillin, decreases the risk of subsequent episodes of acute rheumatic fever and further heart damage.

Poststreptococcal glomerulonephritis: This usually occurs 1-3 weeks following GABHS pharyngitis. Poststreptococcal glomerulonephritis, which may also follow a GABHS skin infection, has not been shown to be preventable with proper administration of antibiotics. Patients often present with hematuria, edema, and hypertension.

Approach Considerations

The probability that beta-hemolytic streptococci is causing the tonsillopharyngitis can be estimated using a diagnostic scoring system.[46]

The Centor score is a tool that was developed to help distinguish GAS pharyngitis from viral pharyngitis, so that antibiotics can be appropriately prescribed. It is calculated by assigning one point for each of the following:[46, 47]

The Centor score can range from 0 to 4.[46, 47]

The McIsaac score modifies the Centor score by taking into account the differences in incidence of GAS infection in children versus older adults. The Centor score is used, but one point is added if the patient is younger than 15 years, while one point is subtracted if the patient is aged 45 years or older.[46, 47]

A score of 2 or more should prompt the clinician to perform a pharyngeal swab for rapid testing or bacterial culture to evaluate for beta-hemolytic streptococci. If the score is 3 or more, it would be reasonable for the clinician to treat as GAS pharyngitis. Routine blood tests for acute tonsillopharyngitis are unnecessary. Antistreptolysin O (ASO) testing and other antistreptococcal antibody testing provide no additional help in acute tonsillopharyngitis and so should not be performed.[46, 47]

The Centers for Disease Control and Prevention (CDC) and the American College of Physicians-American Society of Internal Medicine (ACP-ASIM) endorse the Centor score to determine the risk of GAS infection and to guide the management of acute pharyngitis in adults, as shown in Table 1.[47]

Table 1. CDC/ACP Acute Pharyngitis GAS Testing and Treatment Recommendations Based on Centor Score[47]

View Table

See Table

The American Academy of Family Physicians also recommend the Centor score, as well as the FeverPAIN score as another validated clinical decision tool. The FeverPAIN scale for pharyngitis is discussed in Table 2.[48]

Table 2. FeverPAIN Scale for Pharyngitis[48]

View Table

See Table

For a score of 0 or 1, no testing or treatment is recommended, although a backup throat bacterial culture can be considered if the patient is aged 3-15 years.

For a score of 2 or 3, a rapid antigen detection test is recommended.

For a score of 4 or 5, empiric antibiotic therapy is recommended.

Laboratory Studies

The clinical features of GABHS pharyngitis overlap significantly with that caused by non-GABHS. Microbiological testing provides data to help determine who may benefit from GABHS-directed therapy. Laboratory evaluation of pharyngitis falls into two broad categories: rapid antigen detection tests (RADT) and throat culture.[49] A throat culture is demonstrated in the video below.

View Video

Throat swab. Video courtesy of Therese Canares, MD; Marleny Franco, MD; and Jonathan Valente, MD (Rhode Island Hospital, Brown University).

RADTs offer the advantage of a speedy diagnosis, allowing for the proper administration, as well as proper withholding, of antibiotics. Drawbacks of RADTs include a higher cost and lower sensitivity compared with culture. While throat culture remains the gold standard for diagnosis of GABHS pharyngitis, it has a 24-48 hour turnaround time and entails more technical involvement. Both RADTs and throat culture cannot be used to differentiate between infection and colonization and, in some cases, may influence a physician to overuse antibiotics. For example, a child with coronavirus pharyngitis and GABHS colonization may be prescribed antibiotics based on a false–positive RADT result. No matter what type of test is used in the outpatient setting, judicious selection of patients to be screened is imperative in order to avoid a large number of false-positive results.[50]

Samples for RADT or throat culture should be obtained from the posterior pharynx or tonsils. Samples from the oral cavity result in a greatly reduced sensitivity.

Test of cure is not usually indicated except in special situations,[1] including the following:

Test of cure should also be considered in members of a family in whom "ping-pong" spread is presumed.

Antistreptococcal antibody tests have no role in the diagnosis of acute bacterial pharyngitis. However, they may be used to confirm a history of exposure to GABHS in patients with suspected poststreptococcal glomerulonephritis or acute rheumatic fever.

Rapid antigen detection tests [51]

See the image below.

View Image

Rapid antigen detection test for group A beta-hemolytic streptococci.

All RADTs yield high specificity, allowing for prompt treatment of GABHS pharyngitis without the concern of false-positive results.

Initial RADTs relied on latex agglutination to identify cell wall carbohydrates obtained after acid extraction, a method associated with low sensitivity.

Newer RADTs use optical immunoassay (OIA) technology to identify cell wall carbohydrates. These yield a sensitivity that may be similar to that of throat culture. Nevertheless, before removing confirmatory throat cultures from any given clinical practice, verification of increased sensitivity is recommended.

A newer generation of rapid tests uses nucleic acid identification to identify GABHS-specific sequences. Such assays yield a specificity of 95%-100% and sensitivity in the range of 86%-95%. Although these tests provide an answer in hours, they rely on equipment not available in most outpatient settings and often need to be performed at a location other than the office.

Recent evidence showed that, without RADT, antibacterials are prescribed inappropriately in 41.6% of cases. RADT decreases this number to 11%.[52]

Throat culture

Considered the criterion standard of GABHS pharyngitis diagnosis, throat culture involves obtaining a sample from the posterior pharynx and tonsils and plating on sheep blood agar.

Bacitracin disks aid in differentiation of GABHS from other beta-hemolytic streptococci. A large zone of inhibition is found around GABHS but not around non–beta-hemolytic streptococci.

Cell wall carbohydrate detection assays, applied directly to the cultured bacteria, may also differentiate GABHS from other streptococci.

Imaging Studies

Imaging studies have no role in the diagnosis of bacterial pharyngitis. Lateral neck films may help to confirm the diagnosis of acute epiglottitis. CT scanning may aid in the diagnosis of some of the suppurative complications of pharyngitis, including retropharyngeal or deep neck abscesses, lymphadenitis, and sinusitis.

Approach Considerations

The following are the treatment goals for tonsillopharyngitis:[46]

Conservative treatment is first-line, while surgical management should be performed only if a patient meets recommended indications (see below).[46]

Medical Care

Overzealous prescription of antibiotics for pharyngitis has been estimated to cost health payers $1.2 billion annually.[53] Therefore, treatment of GABHS pharyngitis should be initiated only after confirmation with a RADT or throat culture.[1] Alternatively, treatment in high-risk patients may be started before throat culture results are available, but antibiotics should be stopped if the culture returns negative results. Even though most cases of GABHS pharyngitis resolve after 3-4 days without treatment, antibiotics decrease the likelihood of local suppurative complications and acute rheumatic fever. Oral antibiotics should be administered for 10 days, although many recent studies show similar efficacy with shorter courses.[54, 55] Antibiotic therapy does not decrease the likelihood of poststreptococcal glomerulonephritis.

Oral penicillin V remains the preferred antibiotic to treat GABHS pharyngitis.[1] Amoxicillin is often prescribed and is an acceptable first-line agent because of its narrow spectrum, the ease of once-daily dosing, and improved palatability, especially for children. Both antibiotics are equally efficacious.[56, 57, 58]

In vitro, no isolate of GABHS has ever been resistant to penicillin. Advantages of oral penicillin include its narrow spectrum, low cost, infrequent adverse effects, and proven track record.

A recent Cochrane meta-analysis evaluating patient outcomes on different antibiotics for group A streptococcal pharyngitis concluded that there is insufficient data to show clinically meaningful differences between antibiotics for GABHS tonsillopharyngitis and that, considering the low cost and absence of resistance, penicillin can still be recommended as first choice.[59] Nevertheless, GABHS is sensitive to many other antibiotics, which can be considered as alternative choices based on numerous factors.

The ACP, American Academy of Pediatrics (AAP), and Infectious Diseases Society of America (IDSA) all agree that the antibiotics of choice for acute pharyngitis are oral penicillin V (for 10 days), intramuscular penicillin G benzathine (single dose), and oral amoxicillin (10 days), which is as efficacious as penicillin but more palatable, especially in children.[48]

Circumstances dictating that a choice other than penicillin V should be used

Compliance: Oral penicillin requires multiple daily doses and a 10-day course. In patients unlikely to adhere to this regimen, one dose of intramuscular benzathine penicillin provides a depot that releases medication over the course. Recent reports have supported the use of once-daily amoxicillin and verified its noninferiority to twice-daily penicillin[56] or twice-daily amoxicillin.[57] Azithromycin, cefdinir, and cefpodoxime may all be given in 5-day courses, although none of these medications should be considered a first-line agent given their extended spectrum and risk for promoting antibiotic resistance.[1, 60, 61] Furthermore, although no differences in treatment outcomes have been found between macrolides and penicillin, children experienced more adverse events with macrolides.[59]

Palatability: Some young children find oral penicillin unpalatable. Taste tests and many doctors’ experiences have shown amoxicillin to be much better tolerated.[62] Amoxicillin’s similar spectrum and low cost make it a reasonable substitute.

Allergy: In patients with an immunoglobulin E (IgE)–mediated penicillin allergy, antibiotics that contain a beta-lactam ring (cephalosporins, amoxicillin) should be used with caution. Although cross-reactivity between penicillin and cephalosporins is probably less than 10%, the risk of anaphylaxis justifies the consideration of other viable agents.[63] In patients with nonanaphylactic reactions to penicillin a first generation cephalosporin (Cephalexin, Cefadroxil) is a treatment alternative. In patients with history of severe or anaphylactic reactions to penicillin, macrolides such as azithromycin, clarithromycin, and erythromycin may be used, although resistance has been reported in the United States[64] and internationally.[65] Clindamycin is also a reasonable alternative in penicillin-allergic patients, as resistance rates remain less than 1% in the United States.[66]

The ACP, AAP, and IDSA all agree that a first-generation cephalosporin (for 10 days) should be prescribed to patients with type IV hypersensitivity to penicillin, while clindamycin (for 10 days), clarithromycin (for 10 days), or azithromycin (for 5 days) should be prescribed to patients with type I hypersensitivity to penicillin.[48] If the patient is allergic or has some form of incompatibility to penicillin, the European Archives of Otorhinolaryngology clinical practice guidelines also suggest cephalosporins or macrolides as alternatives.[46]

Recurrence: Test of cure is not indicated when pharyngitis symptoms have resolved following treatment. In patients with recurrent symptoms, retreatment with an initial first-line agent (oral penicillin, benzathine penicillin, or a first-generation cephalosporin) is reasonable. Worth noting is the difficulty in differentiating between viral pharyngitis with GABHS carriage and actual GABHS pharyngitis. This becomes even more of an issue in patients with multiple recurrences. Between 5% and 15% of children are asymptomatic carriers during seasons when GABHS pharyngitis is most prevalent.[67] A positive test result during a time of wellness may indicate GABHS carriage. When multiple recurrences are believed to be due to GABHS infection, clindamycin or amoxicillin/clavulanic acid is indicated.[1] A 2018 systematic review supports this recommendation because of the superiority of the two drugs to penicillin in terms of eradicating streptococci and nonstreptococci. However, the level of evidence was deemed of moderate quality owing to the risk of bias from two included randomized controlled trials.[68]

The European Archives of Otorhinolaryngology clinical practice guidelines also recommend oral penicillin as first-line therapy for beta-hemolytic streptococci. Oral cephalosporins (eg, cefadroxil, cephalexin) are the recommended alternatives that can be used for penicillin failure, frequent recurrences, or whenever a more reliable eradication of beta-hemolytic streptococci is needed.[46]

Pharyngeal carriage

Antimicrobial therapy is not indicated for most pharyngeal GAS carriers. Eradication for carriage may be indicated in the following situations:

Antimicrobial treatment options that have been shown to be more effective than penicillin monotherapy include clindamycin, cephalosporins, amoxicillin/clavulanic acid, azithromycin, or a combination that includes either penicillin V or G with rifampin for the last 4 days of treatment.[69]

Delayed antibiotic prescribing

When a patient presents with signs and symptoms that cannot be initially confirmed as viral or bacterial by a healthcare provider, one strategy is to provide a delayed antibiotic prescription. The delayed prescription can be filled by the patient "just in case" the sore throat does not follow the course of viral pharyngitis, instead progressing as bacterial pharyngitis. Symptom control was similar between immediate and delayed antibiotic prescription, with the latter having the potential to decrease antibiotic usage.[70]


A double-blind, placebo-controlled randomized trial conducted in 42 family practices in South and West England enrolled 576 patients who presented with acute sore throat that was deemed to not require immediate antibiotic therapy. Administration of a single 10-mg dose of oral dexamethasone significantly increased the proportion of patients with resolution of symptoms at 48 hours compared with placebo, although not at 24 hours.[71]

Nonetheless, the authors stressed that the results did not suggest that all patients presenting with sore throat should receive a corticosteroid. In fact, the question was raised: "Is it worth using corticosteroids to treat a relatively harmless disorder?" particularly since a cohort study of more than 1.5 million patients showed that the risks for fractures, venous thromboembolism, and sepsis were significantly higher in those given steroids within 30 days and despite low doses prescribed.[72, 73]

Surgical Care

In rare cases, pharyngitis spreads to adjacent structures and forms abscesses. In these cases, a drainage procedure performed by an interventional radiologist or otolaryngologist should be considered.

Tonsillectomy is one of the most frequently performed procedures in the United States[68] and United Kingdom.[74] However, the IDSA does not recommend tonsillectomy if it will be performed solely to reduce the frequency of GAS pharyngitis.[1] A systematic review showed that tonsillectomy may reduce sore throat frequency in children and adults compared with no surgery but is associated with more morbidity.[74]

Clinical practice guidelines published in the European Archives of Otorhinolaryngology state that surgical options can be either intracapsular or extracapsular tonsil surgery and can be used for the following:[75]

Of course, conservative treatment should be first-line. However, the recommendation to use of tonsillectomy for recurrent tonsillitis in children is based on moderate quality of evidence, while the evidence in adults is of low quality. Tonsillectomy in children modestly affects the number of sore throat episodes per year. Data in adults were found to be heterogenous, explaining why tonsillectomy cannot be considered effective yet in these patients. In fact, additional research is still needed to show if tonsillectomy has significant benefit over the nonsurgical treatment of tonsillitis or tonsillopharyngitis.[75]

In general, tonsillectomy positively affects quality of life, although additional research may better establish this. Conversely, tonsillotomy and similar procedures are associated with much less postoperative pain and bleeding and similar outcomes in the children and young adults. However, the Brodsky scale should be used to evaluate the patient’s tonsil volume; a grade of more than 1 indicates eligibility for tonsillotomy.[75]

The number of tonsillitis episodes in the preceding 12 months determines the indication to perform tonsillectomy or tonsillotomy. Surgery is not recommended in patients with less than 3 episodes, which means watchful waiting for 6 months is reasonable. However, a patient who has had 6 or more episodes of tonsillitis in the preceding 12 months is considered a candidate for tonsil surgery.[75]

In patients with peritonsillar abscess, the following are effective treatment methods:[75]

Before deciding which surgical method is to be performed, patient compliance and ability to cooperate must be considered. It is also recommended to prescribe antibiotic therapy simultaneously, although additional research on this subject is still being conducted.[75]

Tonsillectomy of the contralateral side should be performed only in patients who meet criteria for elective tonsillectomy or if the peritonsillar abscess is bilateral.[75]

Needle aspiration or incision and drainage is preferred if the patient has comorbidities, increased surgical risk, or a coagulation disorder.[75]

Patients with infectious mononucleosis (viral rather than bacterial pharyngitis) should not undergo routine tonsillectomy for symptom control. Tonsillectomy becomes indicated if clinically significant upper airway obstruction results from inflammatory tonsillar hyperplasia. If the patient has no signs of a concomitant bacterial infection, antibiotics should not be prescribed. In contrast, a steroid may be prescribed to relieve symptoms in patients with infectious mononucleosis.


An otolaryngologist should be consulted for local suppurative complications such as peritonsillar abscess and mastoiditis. Tonsillectomy may be considered in recurrent GABHS infection.[76, 77]

An infectious diseases expert may be consulted for patients with immunocompromising conditions or when an agent other than GABHS (eg, HIV) is suspected or confirmed.


Allow a regular diet as tolerated in patients with bacterial pharyngitis. Warm liquids may provide symptomatic relief.


Encourage rest during the acute illness.


Patients with bacterial pharyngitis should be kept out of daycare, school, or work until 24 hours after the initiation of antibiotics.


Despite the massive disease burden caused by S pyogenes (GAS) infection, no licensed vaccine is available to prevent GAS infection and its complications, particularly rheumatic fever and rheumatic heart disease.[78, 79, 80]

GAS vaccines can be classified into two groups: M-protein–based and non–M-protein–based vaccines. The vaccines undergoing clinical investigation are the N-terminal M-protein–based 26- and 30-valent vaccines and the conserved M-protein vaccines, J8 and StreptInCor vaccines.[78, 79]

GAS vaccines are considered "impeded vaccines" for multiple reasons, including the following:[78, 79]

Further Inpatient Care

Droplet precautions should be observed until 24 hours after the initiation of antibiotics.

Medication Summary

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications.

Penicillin G benzathine (Bicillin L-A, Permapen)

Clinical Context:  Interferes with synthesis of cell wall by binding to penicillin-binding proteins. Penicillin is the drug of choice to treat GABHS pharyngitis, as recommended by expert committees of the American Heart Association, American Academy of Pediatrics, and the Infectious Disease Society of America, because of proven efficacy, safety, narrow spectrum, and low cost. Preferred for patients unlikely to complete a full 10-d PO course. S pyogenes remains universally sensitive to penicillin.

Penicillin VK (Beepen VK)

Clinical Context:  Treatment of choice for GAS pharyngitis, as recommended by expert committees of the American Heart Association, American Academy of Pediatrics, and the Infectious Disease Society of America, because of its proven efficacy, safety, narrow spectrum, and low cost. Inhibits biosynthesis of cell wall by binding to penicillin-binding proteins. Bactericidal against sensitive organisms when adequate concentrations are reached and most effective during stage of active multiplication. Inadequate concentrations may be ineffective. GABHS remains uniformly susceptible in vitro.

Amoxicillin (Amoxil, Biomox, Trimox)

Clinical Context:  Interferes with synthesis of cell wall mucopeptides by binding to penicillin-binding proteins. Often used in place of oral penicillin VK in young children. Efficacy equal to penicillin, and often chosen because of the unpalatability of the penicillin susp.

Azithromycin (Zithromax)

Clinical Context:  Inhibits RNA-dependent protein synthesis at the 50s ribosome. Can be given as a single daily dose, is better tolerated than erythromycin in patients who are allergic to penicillin, and is effective in a 5-d course. However, much more expensive and should be avoided as first-line therapy in patients with streptococcal pharyngitis. Sporadic resistance has been reported.

Clindamycin (Cleocin)

Clinical Context:  Belongs to the lincosamide class of antibiotics. Binds to the 50s ribosome and prevents bacterial protein synthesis. Is an option for symptomatic patients with multiple, recurrent episodes of pharyngitis proven by culture or rapid antigen testing.

Erythromycin (E.E.S., E-Mycin, Ery-Tab, Erythrocin)

Clinical Context:  Inhibits RNA-dependent protein synthesis at the 50s ribosome. An option in those with severe allergic reactions to beta-lactam antibiotics. Sporadic resistance has been reported.

Cephalexin (Keflex)

Clinical Context:  First-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms. Oral cephalosporins are highly effective for streptococcal pharyngitis, and several studies have found them to have slightly higher eradication rates than those of penicillin. Second-line agents in the treatment of patients with GABHS pharyngitis.

Clarithromycin (Biaxin, Biaxin XL)

Clinical Context:  Semisynthetic macrolide antibiotic that reversibly binds to P site of 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl t-RNA from ribosomes, causing bacterial growth inhibition.

Similar susceptibility profile to erythromycin but has fewer adverse effects.

Cefadroxil (Duricef, Ultracef)

Clinical Context:  First generation semi-synthetic cephalosporin, that arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms.

Class Summary

Oral penicillin is currently the drug of choice for GABHS pharyngitis.[1] Amoxicillin remains a reliable alternative and offers advantages in terms of easier dosing and increased palatability.

Tetracyclines and trimethoprim/sulfamethoxazole should not be used to treat GABHS pharyngitis owing to higher rates of resistance.

Macrolides have poor anaerobic in vitro activity  so should be avoided if an anaerobe (eg, Fusobacterium) is the suspected pathogen.[42]

What is bacterial pharyngitis?What is the pathophysiology of bacterial pharyngitis?What is the prevalence of bacterial pharyngitis in the US?What is the global prevalence of bacterial pharyngitis?What is the morbidity associated with bacterial pharyngitis?What are the racial predilections of bacterial pharyngitis?What are the sexual predilections of bacterial pharyngitis?Which age groups have the highest prevalence of bacterial pharyngitis?What is the prognosis of bacterial pharyngitis?What is included in patient education about bacterial pharyngitis?What are the signs and symptoms of bacterial pharyngitis?Which physical findings are characteristic of bacterial pharyngitis?What is the role of clinical algorithms in the diagnosis of bacterial pharyngitis?What causes bacterial pharyngitis?What is the role of group C and G streptococci to the etiology of bacterial pharyngitis?How is Arcanobacterium haemolyticum pharyngitis diagnosed and treated?How is Neisseria gonorrhoeae pharyngitis diagnosed and treated?How is Mycoplasma pneumoniae pharyngitis diagnosed?Which Yersinia species cause bacterial pharyngitis?Which Chlamydia species cause bacterial pharyngitis?What is the role of Francisella tularensis (oropharyngeal tularemia) in the etiology of bacterial pharyngitis?What is the role of Corynebacterium diphtheriae in the etiology of bacterial pharyngitis?What is the role of Fusobacterium necrophorum in the etiology of bacterial pharyngitis?What are the possible complications of bacterial pharyngitis?What are the differential diagnoses for Bacterial Pharyngitis?What is the role of Centor score in the workup of bacterial pharyngitis?What is the role of the McIsaac score in the workup of bacterial pharyngitis?What are the CDC/ACP acute bacterial pharyngitis testing and treatment recommendations based on the Center Score?What is the FeverPAIN scale for bacterial pharyngitis?Which lab studies are performed in the workup of bacterial pharyngitis?When is test of cure in indicated in the management of bacterial pharyngitis?What is the role of antistreptococcal antibody tests in the diagnosis of bacterial pharyngitis?What is the role of rapid antigen detection tests (RADTs) in the workup of bacterial pharyngitis?What is the role of throat culture in the workup of bacterial pharyngitis?What is the role of imaging studies in the workup of bacterial pharyngitis?What are the goals for treatment of bacterial pharyngitis?How is bacterial pharyngitis treated?What is the role of antibiotics in the treatment of bacterial pharyngitis?What is the role of penicillin V in the treatment of bacterial pharyngitis?Which antibiotics are recommended by the ACP, AAP and IDSA for the treatment of bacterial pharyngitis?Which medications are used in the treatment of bacterial pharyngitis in noncompliant patients?Which medication is used to treat bacterial pharyngitis in young children?Which medication is used to treat bacterial pharyngitis in patients with an allergy to penicillin?Which medication is used to treat recurrent bacterial pharyngitis?What is the role of antimicrobial therapy of GAS carriers in the treatment of bacterial pharyngitis?What is the role of delayed antibiotic prescribing in the treatment of bacterial pharyngitis?What is the role of corticosteroids in the treatment of bacterial pharyngitis?What is the role of surgery in the treatment of bacterial pharyngitis?What are clinical guidelines for the surgical management of bacterial pharyngitis?How is peritonsillar abscess treated in bacterial pharyngitis?When is tonsillectomy contraindicated in the treatment of bacterial pharyngitis?Which specialist consultations are beneficial to patients with bacterial pharyngitis?Which dietary modifications are used in the treatment of bacterial pharyngitis?Which activity modifications are used in the treatment of bacterial pharyngitis?How is bacterial pharyngitis prevented?What is the role of vaccination in the prevention of bacterial pharyngitis?What is included in inpatient care of bacterial pharyngitis?What is the goal of drug treatment for bacterial pharyngitis?Which medications in the drug class Antibiotics are used in the treatment of Bacterial Pharyngitis?


Joseph Adrian L Buensalido, MD, Clinical Associate Professor, Division of Infectious Diseases, Department of Medicine, Philippine General Hospital, University of the Philippines Manila College of Medicine; Specialist in Infectious Diseases, Private Practice

Disclosure: Nothing to disclose.


Marisse J Nepomuceno, MD, Chief Fellow, External Affairs, Section of Infectious Diseases, Department of Medicine, University of the Philippines-Philippine General Hospital

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Disclosure: Nothing to disclose.

Additional Contributors

Maria A Carrillo-Marquez, MD, Assistant Professor, Department of Pediatrics, Division of Infectious Diseases, Le Bonheur Children's Hospital, University of Tennessee Health Science Center College of Medicine

Disclosure: Nothing to disclose.


Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Kenneth C Earhart, MD Deputy Head, Disease Surveillance Program, United States Naval Medical Research Unit #3

Kenneth C Earhart, MD is a member of the following medical societies: American College of Physicians, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

Eric S Halsey, MD Head, Virology Department, Naval Medical Research Unit No. 6, Lima, Peru; Assistant Professor of Medicine, Uniformed Services University of the Health Sciences

Eric S Halsey, MD is a member of the following medical societies: Armed Forces Infectious Diseases Society, HIV Medicine Association of America, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Kelley Struble, DO Fellow, Department of Infectious Diseases, University of Oklahoma College of Medicine

Kelley Struble, DO is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Gordon L Woods, MD Consulting Staff, Department of Internal Medicine, University Medical Center

Gordon L Woods, MD is a member of the following medical societies: Society of General Internal Medicine

Disclosure: Nothing to disclose.


The authors wish to thank Donald Minnich and Dennis Clark for the preparation and photography of the microbiology specimens.


  1. [Guideline] 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. 2012 Nov 15. 55(10):1279-82. [View Abstract]
  2. Spellerberg B, Brandt C. Streptococcus. Manual of Clinical Microbiology. 9th edition. 2007. 412-29.
  3. Guilherme L, Kalil J, Cunningham M. Molecular mimicry in the autoimmune pathogenesis of rheumatic heart disease. Autoimmunity. 2006 Feb. 39(1):31-9. [View Abstract]
  4. Dale JB. Current status of group A streptococcal vaccine development. Adv Exp Med Biol. 2008. 609:53-63. [View Abstract]
  5. Stollerman GH, Dale JB. The importance of the group a streptococcus capsule in the pathogenesis of human infections: a historical perspective. Clin Infect Dis. 2008 Apr 1. 46(7):1038-45. [View Abstract]
  6. Sriskandan S, Faulkner L, Hopkins P. Streptococcus pyogenes: Insight into the function of the streptococcal superantigens. Int J Biochem Cell Biol. 2007. 39(1):12-9. [View Abstract]
  7. Musher DM. How contagious are common respiratory tract infections?. N Engl J Med. 2003 Mar 27. 348(13):1256-66. [View Abstract]
  8. Brook I, Gober AE. Persistence of group A beta-hemolytic streptococci in toothbrushes and removable orthodontic appliances following treatment of pharyngotonsillitis. Arch Otolaryngol Head Neck Surg. 1998 Sep. 124(9):993-5. [View Abstract]
  9. Roos K, Lind L, Holm SE. Beta-haemolytic streptococci group A in a cat, as a possible source of repeated tonsillitis in a family. Lancet. 1988 Nov 5. 2(8619):1072. [View Abstract]
  10. Wilson KS, Maroney SA, Gander RM. The family pet as an unlikely source of group A beta-hemolytic streptococcal infection in humans. Pediatr Infect Dis J. 1995 May. 14(5):372-5. [View Abstract]
  11. Schappert SM, Rechtsteiner EA. Ambulatory medical care utilization estimates for 2006. Natl Health Stat Report. 2008 Aug 6. 1-29. [View Abstract]
  12. Carapetis JR, Steer AC, Mulholland EK, Weber M. The global burden of group A streptococcal diseases. Lancet Infect Dis. 2005 Nov. 5(11):685-94. [View Abstract]
  13. Pfoh E, Wessels MR, Goldmann D, Lee GM. Burden and economic cost of group A streptococcal pharyngitis. Pediatrics. 2008 Feb. 121(2):229-34. [View Abstract]
  14. Alter SJ, Vidwan NK, Sobande PO, Omoloja A, Bennett JS. Common childhood bacterial infections. Curr Probl Pediatr Adolesc Health Care. 2011 Nov. 41(10):256-83. [View Abstract]
  15. Dagnelie CF, van der Graaf Y, De Melker RA. Do patients with sore throat benefit from penicillin? A randomized double-blind placebo-controlled clinical trial with penicillin V in general practice. Br J Gen Pract. 1996 Oct. 46(411):589-93. [View Abstract]
  16. Shapiro DJ, Lindgren CE, Neuman MI, Fine AM. Viral Features and Testing for Streptococcal Pharyngitis. Pediatrics. 2017 May. 139 (5):[View Abstract]
  17. Centor RM, Allison JJ, Cohen SJ. Pharyngitis management: defining the controversy. J Gen Intern Med. 2007 Jan. 22(1):127-30. [View Abstract]
  18. Gerber MA, Randolph MF, Martin NJ, Rizkallah MF, Cleary PP, Kaplan EL. Community-wide outbreak of group G streptococcal pharyngitis. Pediatrics. 1991 May. 87(5):598-603. [View Abstract]
  19. Cohen D, Ferne M, Rouach T, Bergner-Rabinowitz S. Food-borne outbreak of group G streptococcal sore throat in an Israeli military base. Epidemiol Infect. 1987 Oct. 99(2):249-55. [View Abstract]
  20. Stryker WS, Fraser DW, Facklam RR. Foodborne outbreak of group G streptococcal pharyngitis. Am J Epidemiol. 1982 Sep. 116(3):533-40. [View Abstract]
  21. Turner JC, Hayden FG, Lobo MC, Ramirez CE, Murren D. Epidemiologic evidence for Lancefield group C beta-hemolytic streptococci as a cause of exudative pharyngitis in college students. J Clin Microbiol. 1997 Jan. 35(1):1-4. [View Abstract]
  22. Zaoutis T, Attia M, Gross R, Klein J. The role of group C and group G streptococci in acute pharyngitis in children. Clin Microbiol Infect. 2004 Jan. 10(1):37-40. [View Abstract]
  23. Llor C, Madurell J, Balagué-Corbella M, Gómez M, Cots JM. Impact on antibiotic prescription of rapid antigen detection testing in acute pharyngitis in adults: a randomised clinical trial. Br J Gen Pract. 2011 May. 61(586):e244-51. [View Abstract]
  24. Gerber MA, Baltimore RS, Eaton CB, Gewitz M, Rowley AH, Shulman ST. Prevention of rheumatic fever and diagnosis and treatment of acute Streptococcal pharyngitis: a scientific statement from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young, the Interdisciplinary Council on Functional Genomics and Translational Biology, and the Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation. 2009 Mar 24. 119(11):1541-51. [View Abstract]
  25. Shah M, Centor RM, Jennings M. Severe acute pharyngitis caused by group C streptococcus. J Gen Intern Med. 2007 Feb. 22(2):272-4. [View Abstract]
  26. Marchello C, Ebell MH. Prevalence of Group C Streptococcus and Fusobacterium Necrophorum in Patients With Sore Throat: A Meta-Analysis. Ann Fam Med. 2016 Nov. 14 (6):567-574. [View Abstract]
  27. American Academy of Pediatrics. Arcanobacterium haemolyticum Infections. Red Book: Report of the Committee on Infectious Diseases. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012. 238-9.
  28. Miller RA, Brancato F, Holmes KK. Corynebacterium hemolyticum as a cause of pharyngitis and scarlatiniform rash in young adults. Ann Intern Med. 1986 Dec. 105(6):867-72. [View Abstract]
  29. Morris SR, Klausner JD, Buchbinder SP, et al. Prevalence and incidence of pharyngeal gonorrhea in a longitudinal sample of men who have sex with men: the EXPLORE study. Clin Infect Dis. 2006 Nov 15. 43(10):1284-9. [View Abstract]
  30. Holder NA. Gonococcal infections. Pediatr Rev. 2008 Jul. 29(7):228-34. [View Abstract]
  31. Papp JR, Ahrens K, Phillips C, Kent CK, Philip S, Klausner JD. The use and performance of oral-throat rinses to detect pharyngeal Neisseria gonorrhoeae and Chlamydia trachomatis infections. Diagn Microbiol Infect Dis. 2007 Nov. 59(3):259-64. [View Abstract]
  32. Centers for Disease Control and Prevention. Press Release. First-line Oral Gonorrhea Treatment Available Again in United States. April 25, 2008.
  33. Esposito S, Blasi F, Bosis S, et al. Aetiology of acute pharyngitis: the role of atypical bacteria. J Med Microbiol. 2004 Jul. 53:645-51. [View Abstract]
  34. Sendi P, Graber P, Lepere F, Schiller P, Zimmerli W. Mycoplasma pneumoniae infection complicated by severe mucocutaneous lesions. Lancet Infect Dis. 2008 Apr. 8(4):268. [View Abstract]
  35. Arbaji A, Kharabsheh S, Al-Azab S, et al. A 12-case outbreak of pharyngeal plague following the consumption of camel meat, in north-eastern Jordan. Ann Trop Med Parasitol. 2005 Dec. 99(8):789-93. [View Abstract]
  36. American Academy of Pediatrics. Tularemia. Red Book: Report of the Committee on Infectious Diseases. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012. 768-9.
  37. American Academy of Pediatrics. Diphtheria. Red Book: Report of the Committee on Infectious Diseases. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012. 307-11.
  38. Amess JA, O'Neill W, Giollariabhaigh CN, Dytrych JK. A six-month audit of the isolation of Fusobacterium necrophorum from patients with sore throat in a district general hospital. Br J Biomed Sci. 2007. 64(2):63-5. [View Abstract]
  39. American Academy of Pediatrics. Fusobacterium Infections. Red Book: Report of the Committee on Infectious Diseases. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012. 331-2.
  40. Batty A, Wren MW. Prevalence of Fusobacterium necrophorum and other upper respiratory tract pathogens isolated from throat swabs. Br J Biomed Sci. 2005. 62(2):66-70. [View Abstract]
  41. Jensen A, Hagelskjaer Kristensen L, Prag J. Detection of Fusobacterium necrophorum subsp. funduliforme in tonsillitis in young adults by real-time PCR. Clin Microbiol Infect. 2007 Jul. 13(7):695-701. [View Abstract]
  42. Lundin MS, Bastakoti S, Havlichek D, Laird-Fick H. Lemierre's syndrome and 2016 American College of Physician guidelines for pharyngitis: no to empiric coverage for bacterial pharyngitis. While no role for routine Fusobacterium PCR, keep suspicion for this pathogen. BMJ Case Rep. 2018 Jul 19. 2018:[View Abstract]
  43. Catanzaro FJ, Stetson CA, Morris AJ, et al. The role of the streptococcus in the pathogenesis of rheumatic fever. Am J Med. 1954 Dec. 17(6):749-56. [View Abstract]
  44. American Academy of Pediatrics. Group A Streptococcal Infections. Red Book: Report of the Committee on Infectious Diseases. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012. 668-80.
  45. Steer AC, Danchin MH, Carapetis JR. Group A streptococcal infections in children. J Paediatr Child Health. 2007 Apr. 43(4):203-13. [View Abstract]
  46. Windfuhr JP, Toepfner N, Steffen G, Waldfahrer F, Berner R. Clinical practice guideline: tonsillitis I. Diagnostics and nonsurgical management. Eur Arch Otorhinolaryngol. 2016 Apr. 273 (4):973-87. [View Abstract]
  47. Fine AM, Nizet V, Mandl KD. Large-scale validation of the Centor and McIsaac scores to predict group A streptococcal pharyngitis. Arch Intern Med. 2012 Jun 11. 172 (11):847-52. [View Abstract]
  48. Kalra MG, Higgins KE, Perez ED. Common Questions About Streptococcal Pharyngitis. Am Fam Physician. 2016 Jul 1. 94 (1):24-31. [View Abstract]
  49. Gerber MA. Diagnosis and treatment of pharyngitis in children. Pediatr Clin North Am. 2005 Jun. 52(3):729-47, vi. [View Abstract]
  50. Tanz RR, Gerber MA, Kabat W, Rippe J, Seshadri R, Shulman ST. Performance of a rapid antigen-detection test and throat culture in community pediatric offices: implications for management of pharyngitis. Pediatrics. 2009 Feb. 123(2):437-44. [View Abstract]
  51. Gerber MA, Shulman ST. Rapid diagnosis of pharyngitis caused by group A streptococci. Clin Microbiol Rev. 2004 Jul. 17(3):571-80, table of contents. [View Abstract]
  52. Dodd M, Adolphe A, Parada A, Brett M, Culbreath K, Mercier RC. Clinical Impact of a Rapid Streptococcal Antigen Test on Antibiotic Use in Adult Patients. Diagn Microbiol Infect Dis. 2018 Aug. 91 (4):339-344. [View Abstract]
  53. Salkind AR, Wright JM. Economic Burden of Adult Pharyngitis: The Payer's Perspective. Value Health. 2007 Dec 17. [View Abstract]
  54. Altamimi S, Khalil A, Khalaiwi KA, Milner R, Pusic MV, Al Othman MA. Short versus standard duration antibiotic therapy for acute streptococcal pharyngitis in children. Cochrane Database Syst Rev. 2009 Jan 21. CD004872. [View Abstract]
  55. Moore M, Stuart B, Hobbs FR, Butler CC, Hay AD, Campbell J, et al. Influence of the duration of penicillin prescriptions on outcomes for acute sore throat in adults: the DESCARTE prospective cohort study in UK general practice. Br J Gen Pract. 2017 Sep. 67 (662):e623-e633. [View Abstract]
  56. Lennon DR, Farrell E, Martin DR, Stewart JM. Once-daily amoxicillin versus twice-daily penicillin V in group A beta-haemolytic streptococcal pharyngitis. Arch Dis Child. 2008 Jun. 93(6):474-8. [View Abstract]
  57. Clegg HW, Ryan AG, Dallas SD, et al. Treatment of streptococcal pharyngitis with once-daily compared with twice-daily amoxicillin: a noninferiority trial. Pediatr Infect Dis J. 2006 Sep. 25(9):761-7. [View Abstract]
  58. Shvartzman P, Tabenkin H, Rosentzwaig A, Dolginov F. Treatment of streptococcal pharyngitis with amoxycillin once a day. BMJ. 1993 May 1. 306(6886):1170-2. [View Abstract]
  59. van Driel ML, De Sutter AI, Keber N, Habraken H, Christiaens T. Different antibiotic treatments for group A streptococcal pharyngitis. Cochrane Database Syst Rev. 2010 Oct 6. CD004406. [View Abstract]
  60. Pichichero ME, Casey JR. Bacterial eradication rates with shortened courses of 2nd- and 3rd-generation cephalosporins versus 10 days of penicillin for treatment of group A streptococcal tonsillopharyngitis in adults. Diagn Microbiol Infect Dis. 2007 Oct. 59(2):127-30. [View Abstract]
  61. Lakoš AK, Gašparic M, Kovacic D, Pangercic A, Kukuruzovic MM, Baršic B. Safety and effectiveness of azithromycin in the treatment of respiratory infections in children. Curr Med Res Opin. 2011 Dec 1. [View Abstract]
  62. Chan DS, Demers DM, Bass JW. Antimicrobial liquid formulations: a blind taste comparison of three brands of penicillin VK and three brands of amoxicillin. Ann Pharmacother. 1996 Feb. 30(2):130-2. [View Abstract]
  63. Gruchalla RS, Pirmohamed M. Clinical practice. Antibiotic allergy. N Engl J Med. 2006 Feb 9. 354(6):601-9. [View Abstract]
  64. Richter SS, Heilmann KP, Beekmann SE, et al. Macrolide-resistant Streptococcus pyogenes in the United States, 2002-2003. Clin Infect Dis. 2005 Sep 1. 41(5):599-608. [View Abstract]
  65. Malhotra-Kumar S, Lammens C, Chapelle S, et al. Macrolide- and telithromycin-resistant Streptococcus pyogenes, Belgium, 1999-2003. Emerg Infect Dis. 2005 Jun. 11(6):939-42. [View Abstract]
  66. Tanz RR, Shulman ST, Shortridge VD, et al. Community-based surveillance in the united states of macrolide-resistant pediatric pharyngeal group A streptococci during 3 respiratory disease seasons. Clin Infect Dis. 2004 Dec 15. 39(12):1794-801. [View Abstract]
  67. Kaplan EL. The group A streptococcal upper respiratory tract carrier state: an enigma. J Pediatr. 1980 Sep. 97(3):337-45. [View Abstract]
  68. Munck H, Jørgensen AW, Klug TE. Antibiotics for recurrent acute pharyngo-tonsillitis: systematic review. Eur J Clin Microbiol Infect Dis. 2018 Jul. 37 (7):1221-1230. [View Abstract]
  69. American Academy of Paediatrics. Group A Streptococcal Infections. Kimberlin DW, Brady MT, Jackson MA, Long SS. Red Book: 2018 Report of the Committee on Infectious Diseases. 31st. Itasca, IL: American Academy of Pediatrics; 2018. 755-756.
  70. Moore M, Stuart B, Hobbs FR, Butler CC, Hay AD, Campbell J, et al. Symptom response to antibiotic prescribing strategies in acute sore throat in adults: the DESCARTE prospective cohort study in UK general practice. Br J Gen Pract. 2017 Sep. 67 (662):e634-e642. [View Abstract]
  71. Hayward GN, Hay AD, Moore MV, Jawad S, Williams N, Voysey M, et al. Effect of Oral Dexamethasone Without Immediate Antibiotics vs Placebo on Acute Sore Throat in Adults: A Randomized Clinical Trial. JAMA. 2017 Apr 18. 317 (15):1535-1543. [View Abstract]
  72. Francis DO, Merati AL. Dexamethasone Without Antibiotics for Sore Throat. JAMA. 2017 Aug 22. 318 (8):753. [View Abstract]
  73. Sardovski S. Dexamethasone Without Antibiotics for Sore Throat. JAMA. 2017 Aug 22. 318 (8):752-753. [View Abstract]
  74. Georgalas CC, Tolley NS, Narula PA. Tonsillitis. BMJ Clin Evid. 2014 Jul 22. 2014:[View Abstract]
  75. Windfuhr JP, Toepfner N, Steffen G, Waldfahrer F, Berner R. Clinical practice guideline: tonsillitis II. Surgical management. Eur Arch Otorhinolaryngol. 2016 Apr. 273 (4):989-1009. [View Abstract]
  76. Orvidas LJ, St Sauver JL, Weaver AL. Efficacy of tonsillectomy in treatment of recurrent group A beta-hemolytic streptococcal pharyngitis. Laryngoscope. 2006 Nov. 116(11):1946-50. [View Abstract]
  77. [Guideline] Baugh RF, Archer SM, Mitchell RB, et al. Clinical practice guideline: tonsillectomy in children. Otolaryngol Head Neck Surg. 2011 Jan. 144(1 Suppl):S1-30. [View Abstract]
  78. Steer AC, Dale JB, Carapetis JR. Progress toward a global group a streptococcal vaccine. Pediatr Infect Dis J. 2013 Feb. 32 (2):180-2. [View Abstract]
  79. Steer AC, Carapetis JR, Dale JB, Fraser JD, Good MF, Guilherme L, et al. Status of research and development of vaccines for Streptococcus pyogenes. Vaccine. 2016 Jun 3. 34 (26):2953-2958. [View Abstract]
  80. Wozniak A, Scioscia N, García PC, Dale JB, Paillavil BA, Legarraga P, et al. Protective immunity induced by an intranasal multivalent vaccine comprising 10 Lactococcus lactis strains expressing highly prevalent M-protein antigens derived from Group A Streptococcus. Microbiol Immunol. 2018 Jun. 62 (6):395-404. [View Abstract]
  81. Kassutto S, Rosenberg ES. Primary HIV type 1 infection. Clin Infect Dis. 2004 May 15. 38(10):1447-53. [View Abstract]

Picture of Streptococcus pyogenes at 100 X magnification.

Throat swab. Video courtesy of Therese Canares, MD; Marleny Franco, MD; and Jonathan Valente, MD (Rhode Island Hospital, Brown University).

Rapid antigen detection test for group A beta-hemolytic streptococci.

Picture of Streptococcus pyogenes at 100 X magnification.

Rapid antigen detection test for group A beta-hemolytic streptococci.

Posterior pharynx with petechiae and exudates in a 12-year-old girl. Both the rapid antigen detection test and throat culture were positive for group A beta-hemolytic Streptococcus.

Throat swab. Video courtesy of Therese Canares, MD; Marleny Franco, MD; and Jonathan Valente, MD (Rhode Island Hospital, Brown University).

Centor score


0 Do not test. Do not treat.
1 Do not test. Do not treat.
2 Treat if rapid test result is positive for GAS.
3 Option 1: Treat if rapid test result is positive for GAS.


Option 2: Treat empirically.

4 Treat empirically.
Feature Points
Fever within the past 24 hours1
Markedly inflamed tonsils1
No coryza or cough1
Presented within 3 days symptom onset1
Purulence of tonsils1