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Streptococcus

Streptococcus is a genus of spherical Gram-positive bacteria belonging to the phylum Firmicutes 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.

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Streptococcus

Not to be confused with Staphylococcus.

Streptococcus is a genus of coccus (spherical) Gram-positive bacteria belonging to the phylum Firmicutes[2] and the Lactobacillales (lactic acid bacteria) order. Cellular division occurs along a single axis in these bacteria, and thus they grow in chains or pairs, hence the name—from Greek στρεπτός 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] Currently, over 50 species are recognised in this genus.

Pathogenesis and classification[edit]

Streptococcal classification.

In addition to streptococcal pharyngitis (strep throat), certain Streptococcus species are responsible for many cases of pink eye,[4] meningitis, bacterial pneumonia, endocarditis, erysipelas, and necrotizing fasciitis (the 'flesh-eating' bacterial infections). However, many streptococcal species are not pathogenic, and form part of the commensal human microbiome of the mouth, skin, intestine, and upper respiratory tract. Furthermore, streptococci are a necessary ingredient in producing Emmentaler ("Swiss") cheese.

Species of Streptococcus are classified based on their hemolytic properties.[5] Alpha-hemolytic species cause oxidization of iron in hemoglobin molecules within red blood cells, giving it a greenish color on blood agar. Beta-hemolytic species cause complete rupture of red blood cells. On blood agar, this appears as wide areas clear of blood cells surrounding bacterial colonies. Gamma-hemolytic species cause no hemolysis.

Beta-hemolytic streptococci are further characterised by Lancefield serotyping, which describes specific carbohydrates present on the bacterial cell wall.[6] The 20 described serotypes are named Lancefield groups A to V (excluding I and J).

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”).

Alpha-hemolytic[edit]

Pneumococci[edit]

  • S. pneumoniae (sometimes called pneumococcus), is a leading cause of bacterial pneumonia and occasional etiology of otitis media, sinusitis, meningitis, and peritonitis. Inflammation is thought to be the major cause of how pneumococci cause disease, hence the tendency of diagnoses associated with them to involve inflammation.

The viridans group: alpha-hemolytic[edit]

Table: Medically relevant streptococci[5]

SpeciesHostDisease
S. pyogeneshumanpharyngitis
S. agalactiaehuman, cattleneonatal meningitis and sepsis
S. equisimilishuman, animalsendocarditis, bacteremia, pneumonia, meningitis, respiratory infections
S. bovishuman, animalsbiliary or urinary tract infections, endocarditis
S. anginosushuman, animalssubcutaneous/organ abscesses, meningitis, respiratory infections
S. sanguinishumanendocarditis, dental caries
S. suisswinemeningitis
S. mitishumanendocarditis
S. mutanshumandental caries
S. pneumoniaehumanpneumonia

Beta-hemolytic[edit]

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

Group A[edit]

S. pyogenes, also known as group A Streptococcus (GAS), is the causative agent in a wide range of group A streptococcal infections. These infections may be noninvasive or invasive. The noninvasive infections tend to be more common and less severe. The most common of these infections include streptococcal pharyngitis (strep throat) and impetigo.[7] Scarlet fever is also a noninvasive infection, but has not been as common in recent years.

The invasive infections caused by group A β-hemolytic streptococci tend to be more severe and less common. This occurs when the bacterium is able to infect areas where it is not usually found, such as the blood and the organs.[8] The diseases that may be caused include streptococcal toxic shock syndrome, necrotizing fasciitis, pneumonia, and bacteremia.[7]

Additional complications may be caused by GAS, namely acute rheumatic fever and acute glomerulonephritis. 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. Globally, GAS has been estimated to cause more than 500,000 deaths every year, making it one of the world's leading pathogens.[7] Group A Streptococcus infection is generally diagnosed with a rapid strep test or by culture.

Group B[edit]

S. agalactiae, or group B Streptococcus, 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 during pregnancy, and transmission of the organism 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 to be tested for GBS. Women who test positive should be given prophylactic antibiotics during labor, which will usually prevent transmission to the infant.[9]

The United Kingdom has chosen to adopt a risk factor-based protocol, rather than the culture-based protocol followed in the US. Current guidelines state that if one or more of the following risk factors are present, then women should be treated with intrapartum antibiotics:

- Preterm labour (<37 weeks)- Prolonged rupture of membranes (>18 hours)- Intrapartum fever (>38C)- Prior GBS affected infant- GBS bacteriuria during this pregnancy

This protocol results in treatment of 15–20% of pregnant women and prevention of 65–70% of cases of early onset GBS sepsis. [10]

Group C[edit]

This group includes S. equi, which causes strangles in horses,[11] and S. zooepidemicusS. equi is a clonal descendent or biovar of the ancestral S. zooepidemicus—which causes infections in several species of mammals, including cattle and horses. S. dysgalactiae is also a member of group C, β-haemolytic streptococci that can cause pharyngitis and other pyogenic infections similar to group A streptococci.

Group D (enterococci)[edit]

Many former group D streptococci have been reclassified and placed in the genus Enterococcus (including E. faecalis, E. faecium, E. durans, and E. 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.

Group F streptococci[edit]

Group F streptococci were first described in 1934 by Long and Bliss amongst the "minute haemolytic streptococci".[13] 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[edit]

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

Group H streptococci[edit]

Group H streptococci cause infections in medium-sized canines. Group H streptococci rarely cause illness unless a human has direct contact with the mouth of a canine. One of the most common ways this can be spread is human-to-canine, mouth-to-mouth contact. However, the canine may lick the human's hand and infection can be spread, as well.

[14]

Molecular taxonomy and phylogenetics[edit]

Phylogenetic tree of Streptococcus species, based on data from PATRIC.[15] 16S groups are indicated by brackets and their key members are highlighted in red.

Streptococci have been divided into six groups on the basis of their 16S rDNA sequences: S. anginosus, S.bovis, S. mitis, S. mutans, S. pyogenes and S. salivarius.[16] The 16S groups have been confirmed by whole genome sequencing (see figure). The important pathogens S. pneumoniae and S. pyogenes belong to the S. mitis and S. pyogenes groups, respectively, while the causative agent of dental caries,Streptococcus mutans, is basal to the Streptococcus group.

Genomics[edit]

Common and species-specific genes among Streptococcus sanguinis, S. mutans, and S. pneumoniae. Modified after Xu et al. (2007) [17]

The genomes of hundreds of species have been sequenced.[18] Most Streptococcus genomes are 1.8 to 2.3 Mb in size and encode 1,700 to 2,300 proteins. Some important genomes are listed in the table.[19] The four species shown in the table (S. pyogenes, S. agalactiae, S. pneumoniae, and S. mutans) have an average pairwise protein sequence identity of about 70%.[19]

featureS. pyogenesS. agalactiaeS. pneumoniaeS. mutans
bp1,852,4422,211,4882,160,8372,030,921
ORFs1792211822361963
prophagesyesnonono

Treatment[edit]

Main article: List of antibiotics

See also[edit]

References[edit]

  1. ^ "Result of detail taxonomy information". TXSearch Taxonomy Retrieval. DNA Data Bank of Japan. 19 February 2010. Retrieved 30 March 2010. 
  2. ^ a b 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. 
  4. ^ http://www.medicinenet.com/pink_eye/article.htm
  5. ^ a b 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. 
  6. ^ 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. 
  7. ^ a b c 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. 
  8. ^ "Streptococcal Infections (Invasive Group A Strep)". New York City Department of Health and Mental Hygiene. Retrieved 21 November 2012. 
  9. ^ 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. 
  10. ^ Obstetrics and Gynaecology at a Glance, 4e; Norwitz E.R, Schorge J.O; 2013 John Wiley & Sons LTD.
  11. ^ Harrington DJ, Sutcliffe IC, 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. 
  12. ^ Köhler W (June 2007). "The present state of species within the genera Streptococcus and Enterococcus". International Journal of Medical Microbiology 297 (3): 133–50. doi:10.1016/j.ijmm.2006.11.008. PMID 17400023. 
  13. ^ Whitworth JM (November 1990). "Lancefield group F and related streptococci" (PDF). J. Med. Microbiol. 33 (3): 135–51. doi:10.1099/00222615-33-3-135. PMID 2250284. 
  14. ^ http://www.petmd.com/dog/conditions/respiratory/c_multi_streptococcal_infections.  Missing or empty |title= (help)
  15. ^ http://patricbrc.org/portal/portal/patric/Phylogeny?cType=taxon&cId=1301
  16. ^ Kawamura Y, Hou XG, Sultana F, Miura H, Ezaki T (1995) Determination of 16S rRNA sequences of Streptococcus mitis and Streptococcus gordonii and phylogenetic relationships among members of the genus Streptococcus. Int J Syst Bacteriol 45: 406–408
  17. ^ Xu, P; Alves, J. M.; Kitten, T; Brown, A; Chen, Z; Ozaki, L. S.; Manque, P; Ge, X; Serrano, M. G.; Puiu, D; Hendricks, S; Wang, Y; Chaplin, M. D.; Akan, D; Paik, S; Peterson, D. L.; MacRina, F. L.; Buck, G. A. (2007). "Genome of the opportunistic pathogen Streptococcus sanguinis". Journal of Bacteriology 189 (8): 3166–75. doi:10.1128/JB.01808-06. PMC 1855836. PMID 17277061.  edit
  18. ^ Streptococcus genomes and related information at PATRIC
  19. ^ a b Ferretti JJ, Ajdic D, McShan WM (2004). "Comparative genomics of streptococcal species". The Indian journal of medical research. 119 Suppl: 1–6. PMID 15232152. 
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Viridans streptococci

The viridans streptococci are a large group of commensal streptococcal bacteria species that are either α-hemolytic, producing a green coloration on blood agar plates (hence the name "viridans", from Latin "vĭrĭdis", green), or nonhemolytic. The pseudotaxonomic non-Linnean term Streptococcus viridans is often used to refer to this group of species, but writers that do not like to use the pseudotaxonomic term (which treats a group of species as if they were one species) prefer the terms viridans streptococci[1] or viridans streptococcal species.

These species possess no Lancefield antigens.[2] In general, pathogenicity is low.[3]

Identification[edit]

Viridans streptococci can be differentiated from Streptococcus pneumoniae using an optochin test, as viridans streptococci are optochin-resistant; they also lack either the polysaccharide-based capsule typical of S. pneumoniae or the Lancefield antigens of the pyogenic members of the genus.[4]

Viridans streptococciStreptococcus pneumoniae
Solubility in bileInsolubleSoluble
Fermentation of inulinNot a fermenterFermenter with acid production
Sensitivity to optochinNot sensitiveSensitive
Pathogenicity to miceNonpathogenicPathogenic
Quellung testNegativePositive

Pathology[edit]

The organisms are most abundant in the mouth, and one member of the group, S. mutans, is the etiologic agent of dental caries in most cases and populations. S. sanguinis is also another potential cause. Others may be involved in other mouth or gingival infections as pericoronitis.

If they are introduced into the bloodstream, they have the potential of causing endocarditis, in particular in individuals with damaged heart valves. They are the most common causes of subacute bacterial endocarditis.

Viridans streptococci have the unique ability to synthesize dextrans from glucose, which allows them to adhere to fibrin-platelet aggregates at damaged heart valves. This mechanism underlies their ability to cause subacute valvular heart disease following their introduction into the bloodstream (e.g., following dental extraction).

Treatment[edit]

References[edit]

  1. ^ Dorland's Illustrated Medical Dictionary, headword "streptococcus", subentry "viridans streptococci".
  2. ^ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 293–4. ISBN 0-8385-8529-9. 
  3. ^ Viridans Streptococci at the US National Library of Medicine Medical Subject Headings (MeSH)
  4. ^ Patterson MJ (1996). "Streptococcus". Baron's Medical Microbiology (Baron S et al., eds.) (4th ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1. 

Further Reading[edit]

Naveen Kumar, Venkatesan; van der Linden, Mark; Menon, Thangam; Patric Nitsche-Schmitz, D. (May 2014). "Viridans and bovis group streptococci that cause infective endocarditis in two regions with contrasting epidemiology". International Journal of Medical Microbiology 304 (3-4): 262–268. doi:10.1016/j.ijmm.2013.10.004. Retrieved 31 October 2014. 

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Streptococcus mitis

Streptococcus mitis, previously known as Streptococcus mitior, is a mesophilic alpha-hemolytic species of Streptococcus that inhabits the human mouth. It is a Gram positive, coccus, facultative anaerobe and catalase negative. It can cause endocarditis.[1] It has been widely reported that this organism survived for over two years on the Surveyor 3 probe on the moon; but some NASA scientists suggest this may be a result of contamination during or after return of Surveyor parts to Earth, as the person assembling the camera may have sneezed.[2]

See also[edit]

References[edit]

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Streptococcus milleri group

Streptococcus milleri group
Classification and external resources
MeSHB03.510.400.800.872.875.475, B03.510.550.737.872.875.475, B03.510.400.800.872.875.475,

Streptococcus milleri is an unofficial name applied to a group of basically similar viridans streptococci species[1] showing various hemolytic, serological, and physiological characteristics. The species name Streptococcus anginosus has recently been recognized as the approved name for these organisms. They have been implicated as etiologic agents in a variety of serious purulent infections, but because of their heterogeneous characteristics, these organisms may be unrecognized or misidentified by clinical laboratorians.[2] The unique characteristic of them from other pathogenic streptococci, such as S. pyogenes and S. agalactiae, is their ability to cause abscesses.[3][4]

Further information: Streptococcus anginosus

Species[edit]

Members include:[2]

Nomenclature[edit]

These non-hemolytic viridans streptococci were first described by Guthof in 1956 after being isolated from dental abscesses. He named these organisms "Streptococcus milleri" in honor of the microbiologist W. D. Miller.[5][6] Ehy UOu Pnis

Occurrence[edit]

The organisms were subsequently recognized as normal flora of the human oral cavity and gastrointestinal tract with the ability to cause abscesses and systemic infections.[7]

References[edit]

  1. ^ Streptococcus milleri group at the US National Library of Medicine Medical Subject Headings (MeSH)
  2. ^ a b Ruoff, K L (Jan 1988). "Streptococcus anginosus ("Streptococcus milleri"): the unrecognized pathogen". Clinical Microbiology Reviews 1 (1): 102–108. doi:10.1128/CMR.1.1.102. PMC 358032. PMID 3060239. 
  3. ^ Gossling, J (Mar–Apr 1988). "Occurrence and pathogenicity of the Streptococcus milleri group". Reviews of infectious diseases 10 (2): 257–85. doi:10.1093/clinids/10.2.257. PMID 3287560. 
  4. ^ Rashid, R. M.; Salah, W.; Parada, J. P. (1 February 2007). "'Streptococcus milleri' aortic valve endocarditis and hepatic abscess". Journal of Medical Microbiology 56 (2): 280–282. doi:10.1099/jmm.0.46781-0. 
  5. ^ Whiley, RA; Beighton, D (January 1991). "Emended descriptions and recognition of Streptococcus constellatus, Streptococcus intermedius, and Streptococcus anginosus as distinct species". International journal of systematic bacteriology 41 (1): 1–5. doi:10.1099/00207713-41-1-1. PMID 1995029. 
  6. ^ Verrall, R (November 1986). "The Streptococcus milleri group". Infection Control and Hospital Epidemiology 7 (11): 558–60. JSTOR 30146431. PMID 3640746. 
  7. ^ Mejàre, B; Edwardsson, S (November 1975). "Streptococcus milleri (Guthof); an indigenous organism of the human oral cavity". Archives of oral biology 20 (11): 757–62. doi:10.1016/0003-9969(75)90048-5. PMID 1061530. 


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