Strep throat overview

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Historical Perspective


Causes of Strep throat

Differentiating Strep throat from other Diseases

Epidemiology & Demographics

Risk Factors


Natural History, Complications & Prognosis


History & Symptoms

Physical Examination

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

Historical perspective

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.

Differentiating strep throat from other disease

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]

Epidemiology and Demographics

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]

Risk factors

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]

Natural history and complications

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.


History and Symptoms

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]

Physical Examination

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]

Laboratory Findings

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]

X ray

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.

Other diagnostic tests

There are no other diagnostic studies to diagnose strep throat.


Medical Therapy

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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  2. Joseph Ferretti & Werner Kohler (2016). "History of Streptococcal Research". PMID 26866232.
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 Accessed on October 18, 2016
  4. 4.0 4.1 Cunningham MW (2000). "Pathogenesis of group A streptococcal infections". Clin Microbiol Rev. 13 (3): 470–511. PMC 88944. PMID 10885988.
  5. Guilherme L, Faé KC, Oshiro SE, Tanaka AC, Pomerantzeff PM, Kalil J (2007). "T cell response in rheumatic fever: crossreactivity between streptococcal M protein peptides and heart tissue proteins". Curr Protein Pept Sci. 8 (1): 39–44. PMID 17305559.
  6. Fischetti VA (1989). "Streptococcal M protein: molecular design and biological behavior". Clin Microbiol Rev. 2 (3): 285–314. PMC 358122. PMID 2670192.
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  8. Ruppert SD (1996). "Differential diagnosis of common causes of pediatric pharyngitis". Nurse Pract. 21 (4): 38–42, 44, 47–8. PMID 8801491.
  9. 9.0 9.1 9.2 Shulman ST, Bisno AL, Clegg HW, Gerber MA, Kaplan EL, Lee G; et al. (2012). "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): e86–102. doi:10.1093/cid/cis629. PMID 22965026.
  10. Cohen-Poradosu R, Kasper DL (2007). "Group A streptococcus epidemiology and vaccine implications". Clin Infect Dis. 45 (7): 863–5. doi:10.1086/521263. PMID 17806050.
  11. Carapetis JR, Steer AC, Mulholland EK, Weber M (2005). "The global burden of group A streptococcal diseases". Lancet Infect Dis. 5 (11): 685–94. doi:10.1016/S1473-3099(05)70267-X. PMID 16253886.
  12. Accessed on October 18, 2016
  13. Rantz LA (1946). "THE NATURAL HISTORY OF HEMOLYTIC STREPTOCOCCUS SORE THROAT". Calif Med. 65 (6): 265–70. PMC 1642726. PMID 18731131.
  14. Langlois DM, Andreae M (2011). "Group A streptococcal infections". Pediatr Rev. 32 (10): 423–9, quiz 430. doi:10.1542/pir.32-10-423. PMID 21965709.
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  16. Kids Health
  17. Leung AK, Newman R, Kumar A, Davies HD (2006). "Rapid antigen detection testing in diagnosing group A beta-hemolytic streptococcal pharyngitis". Expert Rev Mol Diagn. 6 (5): 761–6. doi:10.1586/14737159.6.5.761. PMID 17009909.
  18. Sarikaya S, Aktaş C, Ay D, Cetin A, Celikmen F (2010). "Sensitivity and specificity of rapid antigen detection testing for diagnosing pharyngitis in the emergency department". Ear Nose Throat J. 89 (4): 180–2. PMID 20397147.
  19. Tanz RR, Gerber MA, Kabat W, Rippe J, Seshadri R, Shulman ST (2009). "Performance of a rapid antigen-detection test and throat culture in community pediatric offices: implications for management of pharyngitis". Pediatrics. 123 (2): 437–44. doi:10.1542/peds.2008-0488. PMID 19171607. Review in: Evid Based Med. 2009 Dec;14(6):183
  20. Stewart EH, Davis B, Clemans-Taylor BL, Littenberg B, Estrada CA, Centor RM (2014). "Rapid antigen group A streptococcus test to diagnose pharyngitis: a systematic review and meta-analysis". PLoS One. 9 (11): e111727. doi:10.1371/journal.pone.0111727. PMC 4219770. PMID 25369170.
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  24. Accessed on October 18, 2016

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