[2] Cell division in streptococci occurs along a single axis, thus when growing they tend to form pairs or chains, which may appear bent or twisted.
This differs from staphylococci, which divide along multiple axes, thereby generating irregular, grape-like clusters of cells.
The term was coined in 1877 by Viennese surgeon Albert Theodor Billroth (1829–1894),[3] by combining the prefix "strepto-" (from Ancient Greek: στρεπτός, romanized: streptós, lit.
'easily twisted, pliant'[4]), together with the suffix "-coccus" (from Modern Latin: coccus, from Ancient Greek: κόκκος, romanized: kókkos, lit.
However, many streptococcal species are not pathogenic, and form part of the commensal human microbiota of the mouth, skin, intestine, and upper respiratory tract.
[11] Beta-hemolytic streptococci are further classified by Lancefield grouping, a serotype classification (that is, describing specific carbohydrates present on the bacterial cell wall).
Table: Medically relevant streptococci[10] When alpha-hemolysis (α-hemolysis) is present, the agar under the colony will appear dark and greenish due to the conversion of hemoglobin to green biliverdin.
Streptolysin, an exotoxin, is the enzyme produced by the bacteria which causes the complete lysis of red blood cells.
Streptolysin O is an oxygen-sensitive cytotoxin, secreted by most group A Streptococcus (GAS), and interacts with cholesterol in the membrane of eukaryotic cells (mainly red and white blood cells, macrophages, and platelets), and usually results in beta-hemolysis under the surface of blood agar.
Streptolysin S is an oxygen-stable cytotoxin also produced by most GAS strains which results in clearing on the surface of blood agar.
[14] The diseases that may be caused include streptococcal toxic shock syndrome, necrotizing fasciitis, pneumonia, and bacteremia.
[13] Globally, GAS has been estimated to cause more than 500,000 deaths every year, making it one of the world's leading pathogens.
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, but due to the antibodies created by the immune system to fight off the infection cross-reacting with other proteins in the body.
S. agalactiae, or group B streptococcus, GBS, causes pneumonia and meningitis in newborns 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.
[15] Group III polysaccharide vaccines have been proven effective in preventing the passing of GBS from mother to infant.
Group C streptococcal bacteria are considered zoonotic pathogens, meaning infection can be passed from animal to human.
Streptococci have been divided into six groups on the basis of their 16S rDNA sequences: S. anginosus, S. gallolyticus, S. mitis, S. mutans, S. pyogenes and S.
[30] In 2018, the evolutionary relationships within Streptococcus was re-examined by Patel and Gupta through the analysis of comprehensive phylogenetic trees constructed based on four different datasets of proteins and the identification of 134 highly specific molecular signatures (in the form of conserved signature indels) that are exclusively shared by the entire genus or its distinct subclades.
The second main clade, the "Pyogenes-Equinus-Mutans", includes the Pyogenes, Mutans, Salivarius, Equinus, Sobrinus, Halotolerans, Porci, Entericus and Orisratti subclades.
[30] A summary diagram showing the overall relationships among the Streptococcus based on these studies is depicted in a figure on this page.
[33] 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%.
[37][38][39] In 1981 the Cp (Complutense phage 1, officially Streptococcus virus Cp1, Picovirinae) family was discovered with Cp-1 as its first member.
S. pneumoniae, S. mitis and S. oralis can become competent, and as a result actively acquire homologous DNA for transformation by a predatory fratricidal mechanism [42] This fratricidal mechanism mainly exploits non-competent siblings present in the same niche [43] Among highly competent isolates of S. pneumoniae, Li et al.[44] showed that nasal colonization fitness and virulence (lung infectivity) depend on an intact competence system.