Streptococcus

Streptococcus
Streptococcus
Scientific classification
Kingdom: Bacteria
Phylum: Firmicutes
Class: Bacilli[1]
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Rosenbach, 1884
Species

S. agalactiae
S. anginosus
S. bovis
S. canis
S. constellatus
S. dysgalactiae
S. equi
S. equinus
S. iniae
S. intermedius
S. mitis
S. mutans
S. oralis
S. parasanguinis
S. peroris
S. pneumoniae
S. pyogenes
S. ratti
S. salivarius
S. salivarius ssp. thermophilus
S. sanguinis
S. sobrinus
S. suis
S. uberis
S. vestibularis
S. viridans
S. zooepidemicus

Streptococcus is a genus of spherical Gram-positive bacteria belonging to the phylum Firmicutes[2] and the lactic acid bacteria group. Cellular division occurs along a single axis in these bacteria, and thus they grow in chains or pairs, hence the name — from Greek στρεπτος streptos, meaning easily bent or twisted, like a chain (twisted chain). Contrast this with staphylococci, which divide along multiple axes and generate grape-like clusters of cells. Most streptococci are oxidase- and catalase-negative, and many are facultative anaerobes.

In 1984, many organisms formerly considered Streptococcus were separated out into the genera Enterococcus and Lactococcus.[3]

Contents

Pathogenesis

Streptococcal classification.

In addition to streptococcal pharyngitis (strep throat), certain Streptococcus species are responsible for many cases of meningitis, bacterial pneumonia, endocarditis, erysipelas and necrotizing fasciitis (the 'flesh-eating' bacterial infections). However, many streptococcal species are nonpathogenic. Indeed, streptococci are a necessary ingredient in Emmentaler ("Swiss") cheese. Streptococci are also part of the normal commensal microbiome of the mouth, skin, intestine, and upper respiratory tract of humans.

As a rule, individual species of Streptococcus are classified based on their hemolytic properties.[4] Alpha hemolysis is caused by an oxidation of iron in hemoglobin, giving it a greenish color on blood agar. Beta hemolysis is complete rupture of red blood cells, giving distinct, wide, clear areas around bacterial colonies on blood agar. Other streptococci are labeled as gamma-hemolytic, actually a misnomer, as no hemolysis takes place.

In the medical setting, the most important groups are the alpha-hemolytic streptococci, S. pneumoniae and Streptococcus Viridans-group, and the beta-hemolytic streptococci of Lancefield groups A and B (also known as “Group A strep” and “Group B strep”). Beta-hemolytic streptococci are further characterised via the Lancefield serotyping – based on specific carbohydrates in the bacterial cell wall.[5] These are named Lancefield groups A to V (except I and J).

Alpha-hemolytic

Pneumococci

Inflammation is thought to be the major cause of how pneumococcus causes disease, hence the inflammatory nature of the diagnoses assocaited with it [ above ].

The Viridans group: alpha-hemolytic

Beta-hemolytic

Alpha-hemolytic S. viridans (right) and beta-hemolytic S. pyogenes (left) streptococci growing on blood agar

Group A

S. pyogenes, also known as Group A Streptococcus (GAS), is the causative agent in Group A streptococcal infections, including streptococcal pharyngitis ("strep throat" AmE), acute rheumatic fever, scarlet fever, acute glomerulonephritis and necrotizing fasciitis. Strep. pyogenes is the other major cause of streptococcal infection in humans, after pneumococcus. However rather than being directly invasive and inflammatory, it seems to cause local infection, but then it's other actions are via toxins: whether affecting kidneys in post strep glomerulonephritis, heart valves in rheumatic fever, the scarlet skin of scarlet fever or dissolving tissue in necrotizing fasciitis. Other Streptococcus species may also possess the Group A antigen, but human infections by non-S. pyogenes GAS strains (some S. dysgalactiae subsp. equisimilis and S. anginosus Group strains) appear to be uncommon.

Group A Streptococcus infection is generally diagnosed with a Rapid Strep Test (AmE) or by culture. Rheumatic fever, a disease that affects the joints, kidneys and heart valves, is a consequence of untreated strep A infection caused not by the bacterium itself. Rheumatic fever is caused by the antibodies created by the immune system to fight off the infection cross-reacting with other proteins in the body. This cross-reaction causes the body to essentially attack itself and leads to the damage above.

Group B

S. agalactiae, or GBS, causes pneumonia and meningitis in neonates and the elderly, with occasional systemic bacteremia. They can also colonize the intestines and the female reproductive tract, increasing the risk for premature rupture of membranes and transmission to the infant. The American College of Obstetricians and Gynecologists, American Academy of Pediatrics and the Centers for Disease Control recommend all pregnant women between 35 and 37 weeks gestation should be tested for GBS. Women who test positive should be given prophylactic antibiotics during labor, which will usually prevent transmission to the infant.[6] In the UK, clinicians have been slow to implement the same standards as the US, Australia and Canada. In the UK, only 1% of maternity units test for the presence of Group B Streptococcus.[7] Although the Royal College of Obstetricians and Gynaecologists issued risk-based guidelines in 2003 (due for review 2006), the implementation of these guidelines has been patchy. As a result, over 75 infants in the UK die each year of GBS-related disease, and another 600 or so suffer serious infection, most of which could be prevented;[8] however, this is yet to be substantiated by randomized, controlled trial in the UK setting and, given the evidence for the efficacy of testing and treating from other countries, it may be that the large-scale trial necessary would receive neither funding nor ethics approval.[9]

Group C

This group includes S. equi, which causes strangles in horses,[10] and S. zooepidemicus - S. equi is a clonal descendent or biovar of the ancestral S. zooepidemicus - which causes infections in several species of mammals, including cattle and horses.

Group F streptococci

Group F streptococci were first described in 1934 by Long and Bliss amongst the "minute haemolytic streptococci".[11] They are also known as Streptococcus anginosus (according to the Lancefield classification system) or as members of the S. milleri group (according to the European system).

Group G streptococci

These streptococci are usually, but not exclusively, beta-hemolytic. Streptococcus canis is an example of a GGS which is typically found on animals, but can cause infection in humans.

Nonhemolytic

Group D (enterococci)

Many former Group D streptococci have been reclassified and placed in the genus Enterococcus (including S. faecalis, S. faecium, S. durans, and S. avium).[12] For example, Streptococcus faecalis is now Enterococcus faecalis.

The remaining nonenterococcal Group D strains include Streptococcus bovis and Streptococcus equinus.

Nonhemolytic streptococci rarely cause illness. However, weakly hemolytic group D beta-hemolytic streptococci and Listeria monocytogenes (which is actually a Gram-positive bacillus) should not be confused with nonhemolytic streptococci.

Treatment

See also

References

  1. ^ "Result of detail taxonomy information". TXSearch Taxonomy Retrieval. DNA Data Bank of Japan. 19 February 2010. http://txsearch.ddbj.nig.ac.jp/txsearch/txsearch.TXSearch?tx_Clas=scientific+name&tx_Name=Streptococcus&tx_Rank=All&tx_Rmax=10&tx_Dcls=yes&tx_Lang=en&tx_Mode=DETAIL&tx_Id=1301&tx_R_Id=0. Retrieved 30 March 2010. 
  2. ^ Ryan KJ, Ray CG, ed (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 0-8385-8529-9. 
  3. ^ Facklam R (October 2002). "What happened to the streptococci: overview of taxonomic and nomenclature changes". Clin. Microbiol. Rev. 15 (4): 613–30. doi:10.1128/CMR.15.4.613-630.2002. PMC 126867. PMID 12364372. http://cmr.asm.org/cgi/pmidlookup?view=long&pmid=12364372. 
  4. ^ Patterson MJ (1996). Streptococcus. In: Baron's Medical Microbiology (Baron S et al., eds.) (4th ed.). Univ of Texas Medical Branch. (via NCBI Bookshelf) ISBN 0-9631172-1-1. 
  5. ^ Facklam R (2002). "What happened to the streptococci: overview of taxonomic and nomenclature changes". Clin Microbiol Rev 15 (4): 613–30. doi:10.1128/CMR.15.4.613-630.2002. PMC 126867. PMID 12364372. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=126867. 
  6. ^ Schrag S, Gorwitz R, Fultz-Butts K, Schuchat A (2002). "Prevention of perinatal group B streptococcal disease. Revised guidelines from CDC". MMWR Recomm Rep 51 (RR-11): 1–22. PMID 12211284. 
  7. ^ Hughes, RG, et al.. Prevention of Early Onset Neonatal Group B Streptococcal Disease. Royal College of Obstetricians and Gynaecologists. http://www.rcog.org.uk/index.asp?PageID=520. 
  8. ^ "Group B Strep Support Home Page". Group B Strep Support. 2007-01-09. http://www.gbss.org.uk/. 
  9. ^ "RCOG: Preventing group B streptococcus infection in new born babies". RCOG. 2006-02. http://www.rcog.org.uk/index.asp?PageID=1400#national. 
  10. ^ Harrington D, Sutcliffe I, Chanter N (2002). "The molecular basis of Streptococcus equi infection and disease". Microbes Infect 4 (4): 501–10. doi:10.1016/S1286-4579(02)01565-4. PMID 11932201. 
  11. ^ Withworth JM (1990). "Lancefield group F and related streptococci". J Med Microbiol 33: 131–51. 
  12. ^ Ruoff KL (1990). "Recent taxonomic changes in the genus Enterococcus". Eur J Clin Microbiol Infect Dis 9 (2): 75–9. doi:10.1007/BF01963630. PMID 2108030. 

External links


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