Strep throat

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]

Strep throat (also know as “Streptococcal pharyngitis” or “Streptococcal sore throat”) is a form of Group A streptococcal infection that affects the pharynx.

In the 4th century BC, Hippocrates described the cause of the scarlet fever epidemic as S. pyogenes (GAS). In 1874, Billroth described streptococcal infection for the first time. In 1879, Louis Pasteur isolated the bacteria from a pregnant woman’s blood who was septic.n that had contracted Perpueral Fever. In the late 19th century, Rosenbach designated it as S.pyogenes. Blood agar patterns of streptococcal hemolysis was described by the Brown in 1919. Rebecca Lancefield identified distinct serogroups of beta-hemolytic streptococci in the 1930s.^[1][2]

Group A strep pharyngitis is most commonly spread through direct person-to-person transmission, typically through saliva or nasal secretions from an infected person. Rarely, contaminated food, especially milk and milk products, can result in outbreaks.^[3] The incubation period of group A strep pharyngitis is approximately 2 to 5 days.^[3] Pathogenesis of GAS throat involves adhesion of bacteria to pharyngeal mucosa with the help of adhesins on the surface of organism. It then invades the mucosal tissue by producing various proteases and cytolysins causing inflammation manifesting as signs and symptoms of pharyngitis.^[4] M protein on the surface of group A streptococcal infection plays important role in the pathogenesis of rheumatic fever.^[5]

Strep throat is caused by B hemolytic Group A streptococcal infection. Human skin and mucous membrane are the only known reservoir. More than 80 serotypes identified based on M protien. GAS strep throat may be associated with serotypes such as M types 1, 3, 5, 6, 14, 18, 19, and 24.^[4][6][7] GAS is a gram-positive coccus (grows in chains), non-motile, non-spore forming, 0.5-1.2µm in size, catalase-negative, facultative anaerobes or obligate (strict) anaerobes, is capsulated (hyaluronic acid capsule) and requires enriched media (blood agar) to grow.

Strep throat must be differentiated from other diseases that cause sore throat and fever such as epiglottitisperitonsillar abscessretropharyngeal abscess, coxsackie virus, herpangina, influenza, EBV, adenovirus, HIV, measles, rubella, herpes simplex virus, parainfluenza viruses, coronaviruses, rhinoviruses, respiratory syncytial virus gonorrhea, diphtheria, tularemia mycoplasma pneumoniae and other causes such as foreign body (e.g., fish bone), chemical exposure, and GERD.^[8][9]

GAS pharyngitis is the most common bacterial cause of pharyngitis.^[10] Worldwide, the incidence of group A stretococcal pharyngitis (GAS) is estimated to be above 616 million cases annually. ^[11] It commonly affects children aged 5-15 years and is rare in children age less than 3 years.^[3] GAS pharyngitis is common in winter and early spring season.^[3]

Common risk factors in the development of strep throat are younger age (5-15 years), being in close contact with other people afflicted with streptococcal pharyngitis, and over-crowding.^[3]

There are no specific screening guidelines for strep throat.^[3][12]

If left untreated, group A streptococcal pharyngitis may be self-limiting. In some cases, complications such as peritonsillar abscess, retropharyngeal abscess, mastoiditis, and cervical lymphadenitis may develop in untreated patients.^[3][13][14] Less commonly, post-streptococcal glomerulonephritis, rheumatic fever, and toxic shock syndrome may develop as delayed complications. Rarely, vasculitis may occur. The prognosis of strep throat is good with treatment; complications rarely develop with adequate treatment.

The hallmark of strep throat is sudden onset of sore throat. A positive history of ill contact with strep throat and overcrowding (school, military recruit) may be suggestive of group A streptococcal pharyngitis. The most common symptoms of Strep throat include high grade fever, difficulty swallowing, headache, abdominal pain, nausea, vomiting, tender cervical lymphadenopathy, red and enlarged tonsils, red and black patches in the throat, halitosis, rash, frequent cold chills, and absence of cough. ^{[3][9][15][16]}

Common physical examination findings of strep throat include fever (101F), pharyngeal erythema, tonsillar erythema, tonsillar hypertrophy with or without exudates, palatal petechiae, anterior cervical lymphadenopathy, inflamed uvula and scarlatiniform rash.^[3][9][15]

History and clinical examination can be used to diagnosis viral pharyngitis when clear viral symptoms (e.g., cough, rhinorrhea, hoarseness, oral ulcers, conjunctivitis) are present; these patients do not need testing for group A strep. However, clinical examination cannot be used to differentiate viral and group A strep pharyngitis in the absence of viral symptoms, even for experienced clinicians. Group A streptococcal pharyngitis may be diagnosed with the help of rapid antigen detection test (RADT) and throat culture. Throat culture is the gold standard diagnostic test for group A streptococcal pharyngitis. Individuals with negative rapid antigen detection test and high clinical suspicion of strep throat must be confirmed with throat culture.^[3] RADTs have higher specificity for group A streptococcal throat but lower sensitivity than throat culture.^{[17][18][19][20][21]}

A lateral neck x-ray may be used to diagnose complications of strep throat infection such as retropharyngeal abscess. It shows widening of prevertebral space.^[22][23]

Echocardiography may have a role in diagnosing the rheumatic fever carditis, one of the complication of strep throat infection. It may be helpful in monitoring the progress of valve defects present in the rheumatic fever.

There are no other diagnostic studies to diagnose strep throat.

The mainstay of therapy for strep throat is antibiotic therapy. Treatment will help reduce symptoms, minimize transmission, and reduce the likelihood of complications.^[24]

Surgery is not indicated for the treatment of strep throat.

There are no available vaccines against Group A streptococcal infection. Primary prevention strategies include good hand hygiene, especially after coughing and sneezing, washing hands before preparing foods or eating, respiratory etiquette (e.g., covering your cough or sneeze, and staying home from work, school, or daycare until afebrile and until at least 24 hours after starting appropriate antibiotic therapy.^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]

In the 4th century BC, Hippocrates described the cause of a Scarlet fever epidemic as S. pyogenes (GAS). In 1874, Billroth described streptococcal infection for the first time. In 1879, Louis Pasteur isolated the bacteria from a pregnant woman’s blood who was septic.n that had contracted perpueral fever. In the late 19th century, Rosenbach designated it as S.pyogenes. Blood agar patterns of streptococcal hemolysis was described by the Brown in 1919. Rebecca Lancefield identified distinct serogroups of beta-hemolytic streptococci in the 1930s.^[1][2]

• In the 4th century BC, Hippocrates described the scarlet fever epidemic cause as S. pyogenes (GAS). In 1874, Billroth described streptococcal infection for the first time.
• In 1879, Louis Pasteur isolated the bacteria from a pregnant woman’s blood who was septic and had contracted perpueral fever.
• In the late 19th century, Rosenbach designated it as S. pyogenes.
• Blood agar patterns of streptococcal hemolysis was described by the Brown in 1919.
• Rebecca Lancefield identified distinct serogroups of beta-hemolytic streptococci in the 1930s.^[1][3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]

Group A strep pharyngitis is most commonly spread through direct person-to-person transmission, typically through saliva or nasal secretions from an infected person. Rarely, contaminated food, especially milk and milk products, can result in outbreaks.The incubation period of group A strep pharyngitis is approximately 2 to 5 days. The pathogenesis of GAS throat involves adhesion of bacteria to pharyngeal mucosa with the help of adhesins on the surface of organism. It then invades the mucosal tissue by producing various proteases and cytolysins causing inflammation, which manifests as the signs and symptoms of pharyngitis.^[1][2]

Pathophysiology of GAS throat infection may be described in the following steps:^{[1][2][3][4][5]}

Group A strep pharyngitis is most commonly spread through direct person-to-person transmission, typically through saliva or nasal secretions from an infected person. Rarely, contaminated food, especially milk and milk products, can result in outbreaks.^[1]

The incubation period of group A strep pharyngitis is approximately 2 to 5 days.^[1]

• The pathogenesis of GAS in the throat involves adhesion of bacteria to pharyngeal mucosa with the help of adhesins on the surface of organism.
• It then invades the mucosal tissue by producing various proteases and cytolysins causing inflammation manifesting as signs and symptoms of pharyngitis.^[2]
• M protein on the surface of group A streptococcal infection plays important role in the pathogenesis of rheumatic fever.^[6]

• HLA-DRB1*07 allele may have a role in recurrent streptococcal pharyngitis and rheumatic heart disease.^[7]
• HLA-DRB1*11 allele may have a protective role in rheumatic heart disease.^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]

Strep throat is caused by B hemolytic Group A streptococcal infection. More than 80 serotypes are identified based on M protien. GAS strep throat may be associated with serotypes such as M types 1, 3, 5, 6, 14, 18, 19, and 24.^[1]

Strep throat is caused by B hemolytic Group A streptococcal infection.

• Members of the normal flora
• Human skin and mucous membrane are the only known reservoirs

• More than 80 serotypes identified based on M protien
• GAS strep throat may be associated with serotypes such as M types 1, 3, 5, 6, 14, 18, 19, and 24.^[1][2][3]

• Gram-positive coccus (grows in chains)
• Non-motile
• Non-spore forming
• 0.5-1.2µm in size
• Catalase-negative
• Facultative anaerobes or obligate (strict) anaerobes
• Requires enriched media (blood agar) to grow
• Capsulated (hyaluronic acid capsule)

• According to the Lancefield classification, based on the group A antigen in the cell wall, it is named group A streptococcus
• Based on the hemolysis on blood agar, the GAS is β-hemolytic (clear, complete lysis of red cells)

Virulence factors of group A streptococci include:^[4][5]

• A hyaluronic acid capsule (outermost covering inhibits phagocytosis)
• Peptidoglycan cell wall
• Cell membrane
• Adhesion molecules

• M protein PMC358122
• Lipoteichoic acid (located in cell membrane)

• Toxins

• Pyrogenic (erythrogenic) toxin (rash of scarlet fever)

• Cytolysins

• Streptokinase
• Streptodornase (DNase B)
• Streptolysins
• Hyaluronidase

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]

Streptococcal throat infection must be differentiated from epiglottitis, peritonsillar abscess, retropharyngeal abscess, viral pharyngitis, coxsackie virus (herpangina), influenza and EBV.

Strep throat must be differentiated from other diseases that cause sore throat and fever:^[1][2]

• Epiglottitis
• Peritonsillar abscess
• Retropharyngeal abscess
• Viral pharyngitis

• Coxsackie virus (herpangina)
• Influenza
• EBV
• Adenovirus
• HIV
• Measles
• Rubella
• Herpes simplex virus
• Parainfluenza viruses
• Coronaviruses
• Rhinoviruses
• Respiratory syncytial virus

• Bacterial pharyngitis

• Gonorrhea
• Diphtheria
• Tularemia
• Mycoplasma pneumoniae

• Other causes of pharyngitis

• Foreign body (e.g., fish bone)
• Chemical exposure
• Referred pain (e.g., dental abscess, otitis media)
• GERD

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]

GAS pharyngitis is the most common bacterial cause of pharyngitis.^[1] Worldwide, the incidence of group A stretococcal pharyngitis (GAS) is estimated to be above 616 million cases annually.^[2] It commonly affects children aged 5-15 years and is rare in children age less than 3 years.^[3] GAS pharyngitis is common in winter and early spring season.^[3]

• GAS pharyngitis is the most common bacterial cause of pharyngitis.^[1]
  • Worldwide, the incidence of group A stretococcal pharyngitis (GAS) is estimated to be above 616 million cases annually.^[2][3]
  • It accounts for 20-30% cases of acute bacterial pharyngitis in children and 5-15% in adults.^[3][1]
  • The CDC does not track the incidence of GAS pharyngitis.^[3]

The following demographic factors may affect the incidence and prevalence of GAS pharyngitis.^[3]

Group A streptococcal pharyngitis commonly affects children aged 5-15 years and is rare in children aged less than 3 years.^[3]

Men and women are affected equally by Group A streptococcal pharyngitis.^[3]

There is no racial predilection to Group A streptococcal pharyngitis.^[3]

GAS pharyngitis is common in winter and early spring.^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]

Common risk factors in the development of strep throat include youth (especially between 5 and 15 years of age), close contact with others who are infected with streptococcal pharyngitis, and crowded conditions.^[1]

Common risk factors in the development of strep throat are:^[1]

• Younger age (5-15 years)
• Close contact with others infected with streptococcal pharyngitis
• Crowded conditions (such as in schools, military barracks, and daycare centers)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S[2]

There are no specific screening guidelines for strep throat.^[1][2]

There are no specific screening guidelines for strep throat.^[1][2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Tarek Nafee, M.D. [2]; Aysha Anwar, M.B.B.S[3]

If left untreated, group A streptococcal pharyngitis may be self-limiting. In some cases, complications such as peritonsillar abscess, retropharyngeal abscess, mastoiditis, and cervical lymphadenitis may develop in untreated patients.^[1][2][3] Less commonly, post-streptococcal glomerulonephritis, rheumatic fever, and toxic shock syndrome may develop as delayed complications. Rarely, vasculitis may occur. The prognosis of strep throat is good with treatment; complications rarely develop with adequate treatment.

If left untreated, group A streptococcal pharyngitis may be self-limiting. In some cases, complications such as peritonsillar abscess, retropharyngeal abscess, mastoiditis, and cervical lymphadenitis may develop in untreated patients which may results in septic shock or death if they are not managed appropriately.^[1][2][3] Less commonly, delayed chronic complications such as post-streptococcal glomerulonephritis, rheumatic fever, and toxic shock syndrome may develop. Rarely, vasculitis may occur.

Complications that can develop as a result of strep throat may be divided into suppurative and non-suppurative types:^[1][3]

• Peritonsillar abscess
• Retropharyngeal abscess
• Otitis media
• Sinusitis
• Cervical lymphadenitis
• Mastoiditis
• Vasculitis

Images of vasculitis after Streptococcal throat infection

• Rheumatic fever
• Acute glomerulonephritis
• Toxic shock syndrome

The prognosis of strep throat is good with treatment. Complications rarely develop with adequate treatment.^[1]

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