Strep throat overview: Difference between revisions
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==Screening== | ==Screening== | ||
There are no specific screening guidelines for Strep throat.<ref name=cdcp>http://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html Accessed on October 18, 2016</ref><ref name=USPSTF2>https://www.uspreventiveservicestaskforce.org/BrowseRec/Search?s=Streptococcal+pharyngitis Accessed on October 18, 2016</ref> | |||
==Natural history and complications== | ==Natural history and complications== | ||
==Diagnosis== | ==Diagnosis== | ||
Revision as of 16:57, 21 October 2016
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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]
Overview
Strep throat (or "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 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.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]
Pathophysiology
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]
Causes
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 typhoid fever 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 (eg, 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 strept throat are younger age 5-15 years, close contact with the other person having streptococcal pharyngitis, and crowding.[3]
Screening
There are no specific screening guidelines for Strep throat.[3][12]
Natural history and complications
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
X ray
Other diagnostic tests
Treatment
References
- ↑ Alouf JE, Horaud T (1997). "Streptococcal research at Pasteur Institute from Louis Pasteur's time to date". Adv Exp Med Biol. 418: 7–14. PMID 9331588.
- ↑ Joseph Ferretti & Werner Kohler (2016). "History of Streptococcal Research". PMID 26866232.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 http://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html Accessed on October 18, 2016
- ↑ 4.0 4.1 Cunningham MW (2000). "Pathogenesis of group A streptococcal infections". Clin Microbiol Rev. 13 (3): 470–511. PMC 88944. PMID 10885988.
- ↑ 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.
- ↑ Fischetti VA (1989). "Streptococcal M protein: molecular design and biological behavior". Clin Microbiol Rev. 2 (3): 285–314. PMC 358122. PMID 2670192.
- ↑ Stanley J, Desai M, Xerry J, Tanna A, Efstratiou A, George R (1996). "High-resolution genotyping elucidates the epidemiology of group A streptococcus outbreaks". J Infect Dis. 174 (3): 500–6. PMID 8769606.
- ↑ Ruppert SD (1996). "Differential diagnosis of common causes of pediatric pharyngitis". Nurse Pract. 21 (4): 38–42, 44, 47–8. PMID 8801491.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ https://www.uspreventiveservicestaskforce.org/BrowseRec/Search?s=Streptococcal+pharyngitis Accessed on October 18, 2016