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{{DiseaseDisorder infobox |
__NOTOC__
  Name        = Streptococcus, group A, as the cause of diseases classified to other chapters |
  ICD10      = {{ICD10|B|95|0|b|95}} |
  ICD9        = |
}}
{{Group A streptococcal infection}}
{{Group A streptococcal infection}}
{{CMG}}
{{CMG}}; {{AE}} {{AEL}}


==[[Group A streptococcal infection overview|Overview]]==
==Overview==
Group A streptcocci or streptoccus pyogenes causes a wide range of diseases in many organs in the body. It is important to classify the [[infections]] caused by the [[Bacterial|bacteria]] in order to understand every disease separately. Classification of the group A streptococcal infections will be based on the pathogenesis of the infection and the organ infected. According to the pathogenesis of the infection, they can be classified into [[pyogenic]], toxogenic or [[Immunogenicity|immunogenic]] infections. Based on the location, the streptococcus pyogenes affects the [[lungs]], [[ear]], [[nose]], [[throat]], [[blood]], female genital system and the [[central nervous system]].


==[[Group A streptococcal infection historical perspective|Historical perspective]]==
The pathophysiology of the disease depends on various virulence factors. These factors include protein M, streptolysins O and S, hyalourinidase and C5a peptidase.


==[[Group A streptococcal infection pathophysiology|Pathophysiology]]==
==Classification==
Group A streptococcal infections can be classified according to the pathogenesis of the infection and the organ infected. According to the pathogenesis of the infection, they can be classified into pyogenic, toxogenic or immunogenic infections. Based on the location, the streptococcus pyogenes affects the lungs, ear, nose, throat, blood, female genital system and the central nervous system.
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{{Family tree | | | | | | C01 | | | | | | | | | | | | | | | | C02 | | | | | | | | C03 | | | | | | | | C04 | | | | | | C05 | | | | | | C06 | | | C07 | | | | C08 | | | | | | C09 | |C01= [[Pyogenic]]|C02= Toxogenic|C03= Immunogenic|C04= [[Lungs]]|C05= [[Ear]], [[nose]] and [[throat]]|C06=[[Bone]]|C07= [[Blood]] |C08= Female genital system |C09= [[Brain]]|}}
{{Family tree | | | | | | |!| | | | | | | | | | | | | | | | | |!| | | | | | | | | |!| | | | | | | | | |!| | | | | | | |!| | | | | | | |!| | | | |!| | | | | |!| | | | | | | |!| | |}}
{{Family tree | | |,|-|-|-|+|-|-|-|v|-|-|-|.| | | | | |,|-|-|-|+|-|-|-|.| | | |,|-|^|-|.| | | | | | | D01 | | |,|-|-|-|+|-|-|-|.| | | D02 | | | D03 | | |,|-|^|-|.| | | |,|-|^|-|.| |D01=[[Pneumonia]]|D02=[[Osteomyelitis]]|D03=[[Bacteremia]]|}}
{{Family tree | | E01 | | E02 | | E03 | | E04 | | | | E05 | | E06 | | E07 | | E08 | | E09 | | | | | | | | | | E10 | | E11 | | E12 | | | | | | | | | | | E13 | | E14 | | E15 | | E16 ||E01=[[Pharyngitis]] ([[Strep throat]])|E02=[[Cellulitis]]|E03=[[Impetigo]]|E04=[[Erysipelas]]|E05=[[Scarlet fever]]|E06=[[Toxic shock like syndrome]]|E07=[[Necrotizing fasciitis]]|E08=[[Rheumatic fever]]|E09=[[Glomerulonephritis]]|E10=[[Sinusitis]]|E11=[[Tonsilitis]]|E12=[[Otitis media]]|E13=[[Postpartum]] [[endometritis]]|E14=[[Vaginitis]]|E15=[[Meningitis]]|E16=[[Brain abscess]]|}}


==[[Group A streptococcal infection epidemiology and demographics|Epidemiology & Demographics]]==
{{Family tree/end}}
</small></small></small>


==[[Group A streptococcal infection risk factors|Risk Factors]]==
==Pathophysiology==
===Transmission===
Group A streptococcal infection can be transmitted by the following:<ref name="pmid27312939">{{cite journal| author=Brouwer S, Barnett TC, Rivera-Hernandez T, Rohde M, Walker MJ| title=Streptococcus pyogenes adhesion and colonization. | journal=FEBS Lett | year= 2016 | volume= 590 | issue= 21 | pages= 3739-3757 | pmid=27312939 | doi=10.1002/1873-3468.12254 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27312939  }} </ref>
*Direct inoculation transmission
*Infected airborne droplets


==[[Group A streptococcal infection screening|Screening]]==
===Virulence factors===
Group A streptococcus are responsible for various diseases ranging from mild to life threatening cases. The bacteria depends mainly on many virulence factors which are responsible for the pathogenesis of the infections.<ref name="pmid27312939">{{cite journal| author=Brouwer S, Barnett TC, Rivera-Hernandez T, Rohde M, Walker MJ| title=Streptococcus pyogenes adhesion and colonization. | journal=FEBS Lett | year= 2016 | volume= 590 | issue= 21 | pages= 3739-3757 | pmid=27312939 | doi=10.1002/1873-3468.12254 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27312939  }} </ref>


==[[Group A streptococcal infection natural history, complications, and prognosis|Natural history, Complications, and Prognosis]]==
{| class="wikitable"
!Virulence factors
!Mechanism of action
|-
|[[M protein]]
|
* The most important virulence factor.
* It prevents the [[phagocytosis]] of the [[bacteria]] by binding to the [[fibrinogen]] and prevents binding the [[complement]] to the [[bacterial]] [[cell wall]].   
|-
|Streptolysin O and S
|
* Streptolysin O works on killing the differecnt cells like the [[neutrophils]], [[platelets]] and the sub-cellular [[organelles]].
|-
|Streptococcal pyrogenic exotoxins A and C
|
* SpeA and SpeC are superantigens secreted by many strains of ''S. pyogenes''.  These pyrogenic [[exotoxins]] are responsible for the [[rash]] of [[scarlet fever]] and many of the symptoms of streptococcal [[toxic shock syndrome]].
|-
|Streptokinase
|
* Enzymatically activates [[plasminogen]] which is a [[proteolytic enzyme]] into [[plasmin]] which in turn digests [[fibrin]] and other proteins.
|-
|Hyalourinidase
|
* It helps the [[bacteria]] to spread through the tissue by destroying the [[hyaluronic acid]] which is a [[connective tissue]] component.<ref name=Starr_2006>{{cite journal |author=Starr C, Engleberg N |title=Role of hyaluronidase in subcutaneous spread and growth of group A streptococcus |journal=Infect Immun |volume=74 |issue=1 |pages=40-8 |year=2006 |id=PMID 16368955}}</ref>
|-
|Streptodornase
|
* Most strains of ''S. pyogenes'' secrete up to four different [[DNase]]s, which are sometimes called ''streptodornase''. The DNases protect the bacteria from being trapped in [[neutrophil extracellular traps]] (NETs) by digesting the NET's web of DNA, to which are bound [[neutrophil]] [[serine protease]]s that can kill the bacteria.<ref name=Buchanan_2006>{{cite journal |author=Buchanan J, Simpson A, Aziz R, Liu G, Kristian S, Kotb M, Feramisco J, Nizet V |title=DNase expression allows the pathogen group A Streptococcus to escape killing in neutrophil extracellular traps |journal=Curr Biol |volume=16 |issue=4 |pages=396-400 |year=2006 |id=PMID 16488874}}</ref>
|-
|[[C5a]] [[peptidase]]
|
*C5a peptidase cleaves a potent [[neutrophil]] chemotaxin called [[C5a]], which is produced by the complement system.<ref name=Wexler_1985>{{cite journal |author=Wexler D, Chenoweth D, Cleary P |title=Mechanism of action of the group A streptococcal C5a inactivator |journal=Proc Natl Acad Sci U S A |volume=82 |issue=23 |pages=8144-8 |year=1985 |id=PMID 3906656}}</ref>  C5a peptidase is necessary to minimize the influx of neutrophils early in infection as the bacteria are attempting to colonize the host's tissue.<ref name="Ji 1996">{{cite journal |author=Ji Y, McLandsborough L, Kondagunta A, Cleary P |title=C5a peptidase alters clearance and trafficking of group A streptococci by infected mice |journal=Infect Immun |volume=64 |issue=2 |pages=503-10 |year=1996 |id=PMID 8550199}}</ref>.
|-
|Streptococcal chemokine protease
|
*The affected tissue of patients with severe cases of [[necrotizing fasciitis]] are devoid of [[neutrophil]]s.<ref name=Hidalgo-Grass_2004>{{cite journal |author=Hidalgo-Grass C, Dan-Goor M, Maly A, Eran Y, Kwinn L, Nizet V, Ravins M, Jaffe J, Peyser A, Moses A, Hanski E |title=Effect of a bacterial pheromone peptide on host chemokine degradation in group A streptococcal necrotising soft-tissue infections |journal=Lancet |volume=363 |issue=9410 |pages=696-703 |year=2004 |id=PMID 15001327}}</ref>.  The [[serine protease]] ScpC, which is released by ''S. pyogenes'', is responsible for preventing the migration of neutrophils to the spreading infection.<ref name="Hidalgo-Grass 2006">{{cite journal |author=Hidalgo-Grass C, Mishalian I, Dan-Goor M, Belotserkovsky I, Eran Y, Nizet V, Peled A, Hanski E |title=A streptococcal protease that degrades CXC chemokines and impairs bacterial clearance from infected tissues |journal=EMBO J |volume=25 |issue=19 |pages=4628-37 |year=2006 |id=PMID 16977314}}</ref>  ScpC degrades the [[chemokine]] [[IL-8]], which would otherwise attract [[neutrophil]]s to the site of infection.  C5a peptidase, although required to degrade the neutrophil chemotaxin C5a in the early stages of infection, is not required for ''S. pyogenes'' to prevent the influx of neutrophils as the bacteria spread through the [[fascia]].<ref name="Ji 1996"/><ref name="Hidalgo-Grass 2006"/>
|}


==[[Group A streptococcal infection classification|Classification]]==
==References==  
{{Reflist|2}}


==[[Group A streptococcal infection causes|Causes of Group A streptococcal infection]]==
==References==
{{Reflist|2}}


==[[Group A streptococcal infection differential diagnosis|Differentiating Group A streptococcal infection from other Diseases]]==
==Diagnosis==
==[[Group A streptococcal infection history and symptoms|History & Symptoms]]==
==[[Group A streptococcal infection physical examination|Physical Examination]]==
==[[Group A streptococcal infection laboratory tests|Lab Tests]]==
==[[Group A streptococcal infection chest x ray|Chest X Ray]]==
==Treatment==
==[[Group A streptococcal infection medical therapy|Medical Therapy]]==
==[[Group A streptococcal infection primary prevention|Primary Prevention]]==
== Epidemiology and Demographics ==
Approximately 9,000 cases of invasive disease (3.2/100,000 population) occurred in 2002; STSS and NF each accounted for approximately 6% of cases. Over 10 million noninvasive GAS infections (primarily throat and skin infections) occur annually.
'''National''' passive surveillance for invasive infection and STSS since 1995. Active, population-based surveillance is conducted in 10 states in the Emerging Infection Program (total population: 31.5 million).
'''Worldwide''', rates of invasive disease, STSS and NF increased from the mid-1980s to early 1990s. Rates of invasive disease have been stable over the last 5 years in the United States. Increases in the rate and severity of disease associated with increases in prevalence of M-1 and M-3 serotypes (emm types 1 and 3). Resistance to erythromycin has increased worldwide.
==Transmission==
Person to person by contact with infectious secretions. Asymptomatic pharyngeal carriage occurs among all age groups but is most common among children.
<ref> http://www.cdc.gov/ncidod/dbmd/diseaseinfo/groupastreptococcal_t.htm</ref>
== Risk Factors ==
'''Invasive disease:''' elderly, [[Immunodeficiency|immunosuppressed]], persons with chronic cardiac or respiratory disease, [[diabetes]], skin lesions (i.e. children with varicella [[chicken pox]], [[intravenous drug use]]rs) African-Americans, American Indians.
'''Noninvasive disease:''' children (especially elementary school age) at highest risk.
<ref> http://www.cdc.gov/ncidod/dbmd/diseaseinfo/groupastreptococcal_t.htm
</ref>
==Types of infection==
Infections are largely categorized by the location of infection:
* [[bacteremia]] -- [[bloodstream]]
* [[impetigo]], cellulitis, and [[erysipelas]] -- [[skin]] and underlying tissues
* focal infections -- limited to a particular site.  [[Bacteremia]] can be associated with these infections, but it is not always present. Treatment depends on the specific clinical findings. Types include:
** [[pneumonia]] -- [[pulmonary alveolus]]
** [[tonsillitis]] -- [[tonsil]]s
** [[septic arthritis]] -- [[joint]]s
** [[osteomyelitis]] -- [[bone]]s
** [[peritonitis]] -- [[peritoneum]]
** [[meningitis]] -- [[meninges]]
* [[necrotizing fasciitis]] -- [[skin]], [[fascia]] and [[muscle]]
* [[scarlet fever]] -- upper body
* [[sinusitis]] - [[nose]].
* [[strep throat]] -- [[pharynx]]
* [[toxic shock syndrome]] -- multiple systems
(Note that some of these diseases can be caused by other infectious agents as well.)
====Severe streptococcal infections====
Some strains of group A streptococci (GAS) cause severe infection. Those at greatest risk include children with [[chickenpox]]; persons with [[suppressed immune systems]]; [[burn]] victims; elderly persons with [[cellulitis]], [[diabetes]], blood vessel disease, or [[cancer]]; and persons taking [[steroid]] treatments or [[chemotherapy]]. [[Intravenous drug]] users also are at high risk. GAS is an important cause of [[puerperal fever]] world-wide, causing serious infection and, if not promptly diagnosed and treated, death in newly delivered mothers. Severe GAS disease may also occur in healthy persons with no known risk factors.
All severe GAS infections may lead to [[Shock (medical)|shock]], [[multisystem organ failure]], and [[death]]. Early recognition and treatment are critical. Diagnostic tests include [[blood counts]] and [[urinalysis]] as well as cultures of blood or fluid from a wound site. The antibiotic of choice is [[penicillin]], to which GAS is particularly susceptible and has never been found to be resistant.  [[Erythromycin]] and [[clindamycin]] are other treatment options, though resistance to these antibiotics exists.
==Pathophysiology & Etiology==
Streptococcus pyogenes or group A streptococcus.
These bacteria are spread through direct contact with mucus from the nose or throat of persons who are infected or through contact with infected wounds or sores on the skin. Ill persons, such as those who have strep throat or skin infections, are most likely to spread the infection. Persons who carry the bacteria but have no symptoms are much less contagious. Treating an infected person with an antibiotic for 24 hours or longer generally eliminates their ability to spread the bacteria. However, it is important to complete the entire course of antibiotics as prescribed. It is not likely that household items like plates, cups, or toys spread these bacteria.
===Why does invasive group A streptococcal disease occur?===
Invasive GAS infections occur when the bacteria get past the defenses of the person who is infected. This may occur when a person has sores or other breaks in the skin that allow the bacteria to get into the tissue, or when the person’s ability to fight off the infection is decreased because of chronic illness or an illness that affects the immune system. Also, some virulent strains of GAS are more likely to cause severe disease than others.
<ref>http://www.cdc.gov/ncidod/dbmd/diseaseinfo/groupastreptococcal_t.htm
http://www.cdc.gov/ncidod/dbmd/diseaseinfo/groupastreptococcal_g.htm
</ref>
== Signs and Symptoms ==
'''Early signs and symptoms of necrotizing fasciitis'''
*[[Fever]]
*Severe pain and swelling
*Redness at the wound site 
'''Early signs and symptoms of STSS'''
*[[Fever]]
*[[Dizziness]]
*[[Confusion]]
*A flat red rash over large areas of the body 
Noninvasive disease (strep throat, cellulitis, impetigo); invasive disease (necrotizing fasciitis [NF], streptococcal toxic shock syndrome [STSS], bacteremia, pneumonia); nonsuppurative sequelae (rheumatic fever, post-streptococcal glomerulonephritis). STSS is a severe illness characterized by shock, multiorgan failure. NF presents with severe local pain, destruction of tissue. Rheumatic fever is a leading cause of acquired heart disease in young people worldwide. <ref> http://www.cdc.gov/ncidod/dbmd/diseaseinfo/groupastreptococcal_g.htm
</ref>
== Risk Stratification and Prognosis==
'''What kind of illnesses are caused by group A streptococcal infection?'''
Infection with GAS can result in a range of symptoms: 
*No illness
*Mild illness (strep throat or a skin infection such as impetigo)
*Severe illness (necrotizing faciitis, '''streptococcal toxic shock syndrome''') 
Severe, sometimes life-threatening, GAS disease may occur when bacteria get into parts of the body where bacteria usually are not found, such as the blood, muscle, or the lungs. These infections are termed "invasive GAS disease." Two of the most severe, but least common, forms of invasive GAS disease are [[necrotizing fasciitis]] and Streptococcal [[Toxic Shock Syndrome]]. Necrotizing fasciitis (occasionally described by the media as "the flesh-eating bacteria") destroys muscles, fat, and skin tissue. '''Streptococcal toxic shock syndrome''' (STSS), causes blood pressure to drop rapidly and organs (e.g., kidney, liver, lungs) to fail. STSS is not the same as the "toxic shock syndrome" frequently associated with tampon usage. About 20% of patients with necrotizing fasciitis and more than half with STSS die. About 10%-15% of patients with other forms of invasive group A streptococcal disease die. <ref> http://www.cdc.gov/ncidod/dbmd/diseaseinfo/groupastreptococcal_g.htm
</ref>
== Treatment ==
GAS infections can be treated with many different antibiotics. Early treatment may reduce the risk of death from invasive group A streptococcal disease. However, even the best medical care does not prevent death in every case. For those with very severe illness, supportive care in an intensive care unit may be needed.
====Surgery and Device Based Therapy ====
For persons with necrotizing fasciitis, surgery often is needed to remove damaged tissue.
==Complications==
====Acute rheumatic fever====
[[Acute rheumatic fever]] (ARF) is a complication of a strep throat caused by particular strains of GAS. Although common in developing countries, ARF is rare in the United States, with small isolated outbreaks reported only occasionally. It is most common among children between 5-15 years of age. A family history of ARF may predispose an individual to the disease. Symptoms typically occur 18 days after an untreated strep throat. An acute attack lasts approximately 3 months. The most common clinical finding is a migratory arthritis involving multiple joints. The most serious complication is carditis, or heart inflammation (rheumatic heart disease), as this may lead to chronic heart disease and disability or death years after an attack. Less common findings include bumps or nodules under the skin (usually over the spine or other bony areas) and a red expanding rash on the trunk and extremities that recurs over weeks to months. Because of the different ways ARF presents itself, the disease may be difficult to diagnose. A neurological disorder, [[Chorea (disease)|chorea]], can occur months after an initial attack, causing jerky involuntary movements, muscle weakness, slurred speech, and personality changes. Initial episodes of ARF as well as recurrences can be prevented by treatment with appropriate antibiotics.
====Post-streptococcal glomerulonephritis====
[[Post-streptococcal glomerulonephritis]] (PSGN) is an uncommon complication of either a strep throat or a streptococcal skin infection. Symptoms of PSGN develop within 10 days following a strep throat or 3 weeks following a GAS skin infection. PSGN involves inflammation of the kidney. Symptoms include pale skin, lethargy, loss of appetite, headache and dull back pain. Clinical findings may include dark-colored urine, swelling of different parts of the body (edema), and high blood pressure. Treatment of PSGN consists of supportive care.
==Primary Prevention ==
The spread of all types of GAS infection can be reduced by good hand washing, especially after coughing and sneezing and before preparing foods or eating. Persons with sore throats should be seen by a doctor who can perform tests to find out whether the illness is strep throat. If the test result shows strep throat, the person should stay home from work, school, or day care until 24 hours after taking an antibiotic. All wounds should be kept clean and watched for possible signs of infection such as redness, swelling, drainage, and pain at the wound site. A person with signs of an infected wound, especially if fever occurs, should seek medical care. It is not necessary for all persons exposed to someone with an invasive group A strep infection (i.e. necrotizing fasciitis or strep toxic shock syndrome) to receive antibiotic therapy to prevent infection. However, in certain circumstances, antibiotic therapy may be appropriate. That decision should be made after consulting with a physician. <ref> http://www.cdc.gov/ncidod/dbmd/diseaseinfo/groupastreptococcal_g.htm
</ref>
==Source==
* The original text of this article is taken from the [[National Institutes of Health|NIH]] Fact Sheet "Group A Streptococcal Infections", dated March 1999. As a work of the U.S. Federal Government without any other copyright notice, this is assumed to be a public domain resource.
== References ==
{{Reflist}}
== Acknowledgements ==
The content on this page was first contributed by: C. Michael Gibson, M.S., M.D.
List of contributors:
Pilar Almonacid
==External links==
*[http://www.niaid.nih.gov/factsheets/strep.htm Group A streptococcal infection] at [[National Institutes of Health]]
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Latest revision as of 06:52, 20 October 2020

Group A streptococcal infection Microchapters

Home

Overview

Classification

Impetigo
Strep throat
Rheumatic heart disease
Poststreptococcal glomerulonephritis
Sinusitis
Scarlet fever
Tonsilitis
Otitis
Osteomyelitis
Meningitis
Brain abscess
Endometritis
Cellulitis
Erysipelas
Toxic Shock Syndrome

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

Overview

Group A streptcocci or streptoccus pyogenes causes a wide range of diseases in many organs in the body. It is important to classify the infections caused by the bacteria in order to understand every disease separately. Classification of the group A streptococcal infections will be based on the pathogenesis of the infection and the organ infected. According to the pathogenesis of the infection, they can be classified into pyogenic, toxogenic or immunogenic infections. Based on the location, the streptococcus pyogenes affects the lungs, ear, nose, throat, blood, female genital system and the central nervous system.

The pathophysiology of the disease depends on various virulence factors. These factors include protein M, streptolysins O and S, hyalourinidase and C5a peptidase.

Classification

Group A streptococcal infections can be classified according to the pathogenesis of the infection and the organ infected. According to the pathogenesis of the infection, they can be classified into pyogenic, toxogenic or immunogenic infections. Based on the location, the streptococcus pyogenes affects the lungs, ear, nose, throat, blood, female genital system and the central nervous system.

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Group A streptococcal infections
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Pathogenesis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Organ based
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Pyogenic
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Toxogenic
 
 
 
 
 
 
 
Immunogenic
 
 
 
 
 
 
 
Lungs
 
 
 
 
 
Ear, nose and throat
 
 
 
 
 
Bone
 
 
Blood
 
 
 
Female genital system
 
 
 
 
 
Brain
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Pneumonia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Osteomyelitis
 
 
Bacteremia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Pharyngitis (Strep throat)
 
Cellulitis
 
Impetigo
 
Erysipelas
 
 
 
Scarlet fever
 
Toxic shock like syndrome
 
Necrotizing fasciitis
 
Rheumatic fever
 
Glomerulonephritis
 
 
 
 
 
 
 
 
 
Sinusitis
 
Tonsilitis
 
Otitis media
 
 
 
 
 
 
 
 
 
 
Postpartum endometritis
 
Vaginitis
 
Meningitis
 
Brain abscess

Pathophysiology

Transmission

Group A streptococcal infection can be transmitted by the following:[1]

  • Direct inoculation transmission
  • Infected airborne droplets

Virulence factors

Group A streptococcus are responsible for various diseases ranging from mild to life threatening cases. The bacteria depends mainly on many virulence factors which are responsible for the pathogenesis of the infections.[1]

Virulence factors Mechanism of action
M protein
Streptolysin O and S
Streptococcal pyrogenic exotoxins A and C
Streptokinase
Hyalourinidase
Streptodornase
C5a peptidase
  • C5a peptidase cleaves a potent neutrophil chemotaxin called C5a, which is produced by the complement system.[4] C5a peptidase is necessary to minimize the influx of neutrophils early in infection as the bacteria are attempting to colonize the host's tissue.[5].
Streptococcal chemokine protease
  • The affected tissue of patients with severe cases of necrotizing fasciitis are devoid of neutrophils.[6]. The serine protease ScpC, which is released by S. pyogenes, is responsible for preventing the migration of neutrophils to the spreading infection.[7] ScpC degrades the chemokine IL-8, which would otherwise attract neutrophils to the site of infection. C5a peptidase, although required to degrade the neutrophil chemotaxin C5a in the early stages of infection, is not required for S. pyogenes to prevent the influx of neutrophils as the bacteria spread through the fascia.[5][7]

References

  1. ↑ 1.0 1.1 Brouwer S, Barnett TC, Rivera-Hernandez T, Rohde M, Walker MJ (2016). "Streptococcus pyogenes adhesion and colonization". FEBS Lett. 590 (21): 3739–3757. doi:10.1002/1873-3468.12254. PMID 27312939.
  2. ↑ Starr C, Engleberg N (2006). "Role of hyaluronidase in subcutaneous spread and growth of group A streptococcus". Infect Immun. 74 (1): 40–8. PMID 16368955.
  3. ↑ Buchanan J, Simpson A, Aziz R, Liu G, Kristian S, Kotb M, Feramisco J, Nizet V (2006). "DNase expression allows the pathogen group A Streptococcus to escape killing in neutrophil extracellular traps". Curr Biol. 16 (4): 396–400. PMID 16488874.
  4. ↑ Wexler D, Chenoweth D, Cleary P (1985). "Mechanism of action of the group A streptococcal C5a inactivator". Proc Natl Acad Sci U S A. 82 (23): 8144–8. PMID 3906656.
  5. ↑ 5.0 5.1 Ji Y, McLandsborough L, Kondagunta A, Cleary P (1996). "C5a peptidase alters clearance and trafficking of group A streptococci by infected mice". Infect Immun. 64 (2): 503–10. PMID 8550199.
  6. ↑ Hidalgo-Grass C, Dan-Goor M, Maly A, Eran Y, Kwinn L, Nizet V, Ravins M, Jaffe J, Peyser A, Moses A, Hanski E (2004). "Effect of a bacterial pheromone peptide on host chemokine degradation in group A streptococcal necrotising soft-tissue infections". Lancet. 363 (9410): 696–703. PMID 15001327.
  7. ↑ 7.0 7.1 Hidalgo-Grass C, Mishalian I, Dan-Goor M, Belotserkovsky I, Eran Y, Nizet V, Peled A, Hanski E (2006). "A streptococcal protease that degrades CXC chemokines and impairs bacterial clearance from infected tissues". EMBO J. 25 (19): 4628–37. PMID 16977314.

References


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