Background
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.
Pathophysiology
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.
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.
Epidemiology
Frequency
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]
International
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.
Mortality/Morbidity
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.
Race
GABHS pharyngitis affects all races.
Sex
GABHS pharyngitis has no sexual predilection.
Age
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.
Prognosis
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.
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Picture of Streptococcus pyogenes at 100 X magnification.
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Rapid antigen detection test for group A beta-hemolytic streptococci.
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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.
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Throat swab. Video courtesy of Therese Canares, MD; Marleny Franco, MD; and Jonathan Valente, MD (Rhode Island Hospital, Brown University).
Tables
Centor score |
Recommendation |
|---|---|
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. OR Option 2: Treat empirically. |
4 |
Treat empirically. |
Feature |
Points |
Fever within the past 24 hours |
1 |
Markedly inflamed tonsils |
1 |
No coryza or cough |
1 |
Presented within 3 days symptom onset |
1 |
Purulence of tonsils |
1 |
