Streptococcus pyogenes


Streptococcus pyogenes

Taxobox
color = lightblue
name = "Streptococcus pyogenes"



image_width = 240px
image_caption = "S. pyogenes" bacteria @ 900x magnification.
regnum = Bacteria
phylum = Firmicutes
classis = Bacilli
ordo = Lactobacillales
familia = Streptococcaceae
genus = "Streptococcus"
species = "S. pyogenes"
binomial = "Streptococcus pyogenes"
binomial_authority = Rosenbach 1884

"Streptococcus pyogenes" is a spherical gram-positive bacteria that grows in long chains cite book | author = Ryan KJ; Ray CG (editors) | title = Sherris Medical Microbiology | edition = 4th ed. | publisher = McGraw Hill | year = 2004 | id = ISBN 0-8385-8529-9 ] and is the cause of Group A streptococcal infections. "S. pyogenes" displays group A antigen on its cell wall and beta-hemolysis when cultured on blood agar plate. "S. pyogenes" typically produces large zones of beta-hemolysis, the complete disruption of erythrocytes and the release of hemoglobin, and it is therefore called Group A (beta-hemolytic) "Streptococcus" (abbreviated "GAS"). Streptococci are catalase-negative. In ideal conditions, Streptococcus pyogenes has an incubation period of approximately 10 days.

erotyping

In 1928, Rebecca Lancefield published a method for serotyping "S. pyogenes" based on its "M protein", a virulence factor that is displayed on its surface.cite journal | author = Lancefield RC| title = The antigenic complex of "Streptococcus hemolyticus" | journal = J Exp Med | year = 1928 | volume = 47 | pages = 9–10 | url=http://www.jem.org/cgi/content/abstract/47/1/91| doi = 10.1084/jem.47.1.91 ] Later in 1946, Lancefield described the serologic classification of "S. pyogenes" isolates based on their surface "T antigen".cite journal | author = Lancefield RC, Dole VP | title = The properties of T antigen extracted from group A hemolytic streptococci | journal = J Exp Med | year = 1946 | volume = 84 | pages = 449–71 | doi= 10.1084/jem.84.5.449 ] Four of the 20 T antigens have been revealed to be pili, which are used by bacteria to attach to host cells.cite journal |author=Mora M, Bensi G, Capo S, Falugi F, Zingaretti C, Manetti A, Maggi T, Taddei A, Grandi G, Telford J |title=Group A Streptococcus produce pilus-like structures containing protective antigens and Lancefield T antigens |journal=Proc Natl Acad Sci U S A |volume=102 |issue=43 |pages=15641–6 |year=2005 |pmid=16223875 |doi=10.1073/pnas.0507808102] Currently, over 100 M serotypes and approximately 20 T serotypes are known.

Pathogenesis

"S. pyogenes" is the cause of many important human diseases ranging from mild superficial skin infections to life-threatening systemic diseases. Infections typically begin in the throat or skin. Examples of mild "S. pyogenes" infections include pharyngitis ("strep throat") and localized skin infection ("impetigo"). Erysipelas and cellulitis are characterized by multiplication and lateral spread of "S. pyogenes" in deep layers of the skin. "S. pyogenes" invasion and multiplication in the fascia can lead to necrotizing fasciitis, a potentially life-threatening condition requiring surgical treatment.

Infections due to certain strains of "S. pyogenes" can be associated with the release of bacterial toxins. Throat infections associated with release of certain toxins lead to scarlet fever. Other toxigenic "S. pyogenes" infections may lead to streptococcal toxic shock syndrome, which can be life-threatening.

"S. pyogenes" can also cause disease in the form of post-infectious "non-pyogenic" (not associated with local bacterial multiplication and pus formation) syndromes. These autoimmune mediated complications follow a small percentage of infections and include rheumatic fever and acute poststreptococcal glomerulonephritis. Both conditions appear several weeks following the initial streptococcal infection. Rheumatic fever is characterised by inflammation of the joints and/or heart following an episode of Streptococcal pharyngitis. Acute glomerulonephritis, inflammation of the renal glomerulus, can follow Streptococcal pharyngitis or skin infection.

This bacterium remains acutely sensitive to penicillin. Failure of treatment with penicillin is generally attributed to other local commensal organisms producing β-lactamase or failure to achieve adequate tissue levels in the pharynx. Certain strains have developed resistance to macrolides, tetracyclines and clindamycin.

Virulence factors

"S. pyogenes" has several virulence factors that enable it to attach to host tissues, evade the immune response, and spread by penetrating host tissue layers.cite book | author = Patterson MJ | title = Streptococcus. "In:" Baron's Medical Microbiology "(Baron S "et al", eds.)| edition = 4th ed. | publisher = Univ of Texas Medical Branch | year = 1996 | id = [http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.824 (via NCBI Bookshelf)] ISBN 0-9631172-1-1 ] A carbohydrate capsule composed of hyaluronic acid surrounds the bacterium, protecting it from phagocytosis by neutrophils. In addition, the capsule and several factors embedded in the cell wall, including M protein, lipoteichoic acid, and protein F (SfbI) facilitate attachment to various host cells.cite journal | author=Bisno AL, Brito MO, Collins CM | title=Molecular basis of group A streptococcal virulence | journal=Lancet Infect Dis | year=2003 | pages=191–200 | volume=3 | issue=4 | pmid=12679262 | doi=10.1016/S1473-3099(03)00576-0] M protein also inhibits opsonization by the alternative complement pathway by binding to host complement regulators. M protein found on some serotypes are also able to prevent opsonization by binding to fibrinogen. However, the M protein is also the weakest point in this pathogen's defense as antibodies produced by the immune system against M protein target the bacteria for engulfment by phagocytes. M proteins are unique to each strain, and identification can be used clinically to confirm the strain causing an infection.

"S. pyogenes" releases a number of proteins, including several virulence factors, into its host:

;Streptolysin O and S:These are toxins which are the basis of the organism's beta-hemolytic property. Streptolysin O is a potent cell poison affecting many types of cell including neutrophils, platelets, and sub-cellular organelles. It causes an immune response and detection of antibodies to it; antistreptolysin O (ASO) can be clinically used to confirm a recent infection. Streptolysin O is cardiotoxic.

;Streptococcal pyogenic exotoxins (Spe) A and C:SpeA and SpeC are superantigens secreted by many strains of "S. pyogenes". These pyogenic exotoxins are responsible for the rash of scarlet fever and many of the symptoms of streptococcal toxic shock syndrome.

;Streptokinase:Enzymatically activates plasminogen, a proteolytic enzyme, into plasmin which in turn digests fibrin and other proteins.

;Hyaluronidase:It is widely assumed that hyaluronidase facilitates the spread of the bacteria through tissues by breaking down hyaluronic acid, an important component of connective tissue. However, very few isolates of "S. pyogenes" are capable of secreting active hyaluronidase due to mutations in the gene that encode the enzyme. Moreover, the few isolates that are capable of secreting hyaluronidase do not appear to need it to spread through tissues or to cause skin lesions.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 |pmid=16368955 |doi=10.1128/IAI.74.1.40-48.2006] Thus, the true role of hyaluronidase in pathogenesis, if any, remains unknown.

;Streptodornase:Most strains of "S. pyogenes" secrete up to four different DNases, 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 proteases that can kill the bacteria.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 |pmid=16488874 |doi=10.1016/j.cub.2005.12.039]

;C5a peptidase:C5a peptidase cleaves a potent neutrophil chemotaxin called C5a, which is produced by the complement system.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 |pmid=3906656 |doi=10.1073/pnas.82.23.8144] C5a peptidase is necessary to minimize the influx of neutrophils early in infection as the bacteria are attempting to colonize the host's tissue.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 |pmid=8550199]

;Streptococcal chemokine protease:The affected tissue of patients with severe cases of necrotizing fasciitis are devoid of neutrophils.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 |pmid=15001327 |doi=10.1016/S0140-6736(04)15643-2] The serine protease ScpC, which is released by "S. pyogenes", is responsible for preventing the migration of neutrophils to the spreading infection.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 |pmid=16977314 |doi=10.1038/sj.emboj.7601327] 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.

Diagnosis

Usually, a throat swab is taken to the laboratory for testing. A Gram stain is performed to show Gram positive, cocci, in chains. Then, culture the organism on blood agar with added bacitracin antibiotic disk to show beta-haemolytic colonies and sensitivity (zone of inhibition around the disk) for the antibiotic. Then, perform catalase test, which should show a negative reaction for all "Streptococci". "S. pyogenes" is cAMP and hippurate tests negative. Serological identification of the organism involves testing for the presence of group A specific polysaccharide in the bacterium's cell wall using the Phadebact test.

Treatment

The treatment of choice is penicillin, however in the absence of readily available penicillin, small incisions made to the infected area will relieve swelling and discomfort until proper medical assistance can be sought. There is no reported instance of penicillin-resistance reported to date, although since 1985 there have been many reports of penicillin-tolerance. [cite journal|journal=J Pediatr|year=1985|volume=107|issue=5|pages=681–4|title=Association of penicillin tolerance with failure to eradicate group A streptococci from patients with pharyngitis|author=Kim KS, Kaplan EL|pmid=3903089|doi=10.1016/S0022-3476(85)80392-9]

Macrolides, chloramphenicol, and tetracyclines may be used if the strain isolated has been shown to be sensitive, but resistance is much more common.

References

Other reading

* Gladwin, Mark and Bill Trattler. "Clinical Microbiology Made Ridiculously Simple, 3rd edition", 2004.
* Brooks, Geo F., Janet S. Butel, and Stephen A. Morse. "Jawetz, Melnick, and Adelberg's Medical Microbiology, 22nd edition", 2001.


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