Streptococcus dysgalactiae

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A Microbial Biorealm page on the genus Streptococcus dysgalactiae

Classification

Higher order taxa

Bacteria; Firmicutes; Bacilli; Lactobacillales; Streptococcaceae; Streptococcus


Species

NCBI: Taxonomy

Streptococcus dysgalactiae

Description and significance

Streptococcus dysgalactiae is a member of group C streptococci (GCS). This gram-positive bacteria is commonly found on the animal and can be isolated from udders of cows with mild mastitis, an inflammation of the mammalian breast, and from blood and tissues of lambs with polyarthritis, an inflammation of five or more joints (1). Although it is extremely rare to be found on human, it can cause meningitis, an inflammation of the protective membrane covering the central nervous system (2,3). The virulence factors of group C streptococci were not studied as extensively as much as other streptococci group; as a result, researchers sequenced the whole genome of one strain, NS3396 (4). The study of the sequence revealed a number of similarities between Streptococcus pyogenes, a group A streptococci (GAS), and Streptococcus dysgalactiae. This allows researchers to understand the pathology of Streptococcus dysgalactiae (4).

Genome structure

The genome of Streptococcus dysgalactiae (strain NS3396) includes a linear chromosome of 38,528 bp and has an average of 37.48% GC content, also known as guanine-cytosine content (4). This was completed just recently in the year 2007.

Comparative genomic analysis has revealed many significant similarities between the genomes of Streptococcus dysgalactiae and those of group A streptococci (GAS). In addition, a large proportion of the open reading frames (ORFs), 83%, corresponds to hypothetical phage proteins and well- known phage proteins (4). This reveals that not only Streptococcus dysgalactiae and GAS are closely related, but they are also part of the lactic acid bacteria, bacteria that uses lactic acid metabolism (5).

While the genomes between both groups have close resemblance, there are four regions on Streptococcus dysgalactiae that shows little or no similarities with GAS. The first region, contains ORF3 to ORF7, which codes the lysogeny module. Researchers concluded that this region shows high levels of nucleotide diversity (5). The second region contains ORF12 to ORF22, which codes for the whole DNA replication module. It is concluded that there might have been potential modular recombination events (5). The bacteria might also have a unique methlase. The third region contains ORF45 that codes for ClustralW alignment at protein level. Researchers observed that while the first 639 amino acids are identical between S. dysgalactiae and GAS, the remaining 736 amino acids show more variation. This suggests that there might have been a level of evolutionary adaptation for the cell wall (5). The fourth region codes for tail fiber, host lysis, and lysogenic conversion modules, which suggests that S. dysgalactiae might have evolved a number of special proteins for the ability to attach to bacterial surface and lysis (5).

The genome structures between Streptococcus dysgalactiae and GAS also show that there are lateral gene transfer between both groups, which makes the species a remarkable adaptor (5).

Cell structure and metabolism

Role of Cell Surface Protein

The bacteria contain proteins known as the M protein on cell surfaces that specifically bind to tissue proteins of the host. It can also resist phagocytosis, which helps resisting against immune cells (6).

In a study of Streptococcus dysgalactiae using strain 8215, researchers isolated a gene called demA that encode for protein DemA. This protein shares many homologous features of M and M-like protein (6). The significance of this protein is that it can completely inhibit the binding of fg (fibrinogen). Fibrinolytic system is used by human body to control level of inflamation (21). Therefore, by inhibiting fg, the microbe is capabable of resisting human body immune system (6).

Further analysis reveals that dmgA, an order reading frame (ORF), is encoded before demA. dmgA codes for the protein DmgA, which exhibits many features of Mga Protein in Streptococcus pyogenes. Both the Mga Protein and DmgA are known to take part in microbe's pathogenesis (6).

Metabolism

Streptococcus dysgalactiae is part of the Lactic Acid Bacteria (LAB); therefore, its metabolism is essentially the same as LAB. Their metabolism of carbohydrates consists of homolactic or heterolactic (5). The homolactic fermentation is similar to Embden-Meyerhof-Oarnas (EMP) pathway for glycolysis. They are, however, different from the animal carbohydrate metabolism in that they can form D (-)- or L (+)- lactic acid or both lactic acid. There are three main sugar metabolisms in LAB (5). The first one is glycolysis: Glucose->Fru-1,6 P->Triose-3P->Pyruvate->Lactate. The second one is bifidus pathway: Glucose->Fru-6P->AcetylP+Erythrose-4P->Acetate+ Lactate. The third one is 6P-Gluconate pathway: Glucose->Glc-6P->6P-Gluconate->Xylulose5P->Triose 3P+ Acetyl-P -> Lactate+ Acetate(Ethanol) (5).

Ecology

Streptococcus dysgalactiae is usually found on animals. It can be found in the mouth, vagina, and skin of healthy animals. It can also be find in bedding and pastures. Because of its habitat, it is hard to prevent Streptococcus dysgalactiae infections by hygiene methods and antibiotic therapy. However, researchers have worked to develop therapy based on the M-protein and receptors on Streptococcus dysgalactiae (7). On human, Streptococcus dysgalactiae can be found on skins, blood cultures, throat, and genital tract (8). There is also evidence of Streptococcus dysgalactiae interacting with different pathogens, mostly species from the same genus (9). The interaction involves with horizontal gene transfer, which explains why Streptococcus dysgalactiae share similar M protein and M-like protein with group A streptococci (GAS) (9). In the interaction with eukaryotes cells, Streptococcus dysgalactiae enters the host, epithelial cells, to colonize (10).

Pathology

Streptococcus dysgalactiae is a common pathogen that causes mastits and polyarthritis in animals, and in rare cases, it can cause meningitis in humans (6, 3, 11, 12). It has been determined that group C streptococci have two of the same virulence components as Streptococcus pyogenes: M protein and hyaluronate capsule (13). The M protein is known for its resistant to phagocytosis, while hyaluronate capsule is known for its ability to bind to epithelial surfaces (14).

Like most of the pathogens infections, the Streptococcus dysgalactiae binds to the mucosal surface, and begins to attack the epithelial cells (10). The importance of this step is that, the bacteria need to have the access to the host cell and the ability to avoid host defense mechanisms in order to colonize and invade (for mechanism to evade defense system, see “Role of Cell Surface Protein”)(10).

In a case study of Streptococcus dysgalactia’s invasion on cow’s mammary epithelial cell line (Mac-T cell), it is revealed that the microbe is capable of surviving inside the Mac-T cell. In response to the invading microbes, the Mac-T cell engulfs the microbe by endocytosis. This suggests that the microfilaments of the Mac-T cell play an important role of Streptococcus dysgalactia’s entry (10). After the microbe gains entry into the Mac-T cell, it affects the eukaryotic cell membrane by using its ligands to interact with the surface of Mac-T cell. The result triggers more cytoskeleton reactions that allow entry for other invasive bacteria, which explains why Streptococcus dysgalactia infection often makes the host vulnerable to other infectious bacteria as well. However, more experiments are needed to further confirm this process (10).

In another study, the defense mechanism of Streptococcus dysgalactia in response to the immune system was studied. According to the researchers, there are two plasma protein-binding receptors produced from the mig gene, α2-macroglobulin (α2-M) and immunoglobulin G (IgG). These two receptors are responsible for the entry of the host cell by binding to the plasma protein α2-M or IgG, which prevent phagocytosis by bovine neutrophils (PMN), a type of white blood cell. These traits are also share by other members of the streptococcus species (7).

Recently a new bacterial superantigen, Streptococcus dysgalactiae-derived mitogen (SDM), was discovered (8). This superantigen is a powerful T cell mitogen, which can make T lymphocytes out of control resulting in serious illness such as fever and shock and even death (15). Superantigen can interact with human immune system by binding to MHC class II molecules and T cell receptors; as a result, immune system responses by releasing large amount of cytokines. This produces a catastrophic effect on human body that causes acute condition toxic shock, which can be fatal (15).

Common antibiotics that are subject to resistance in group C streptococci and Streptococcus dysgalactiae include third-generation cephalosporins, the newer semisynthetic penicillins, and erythromycin. There have been few evidences of increasing resistance of group C streptococci to penicillin and other antibodies (16, 17).

Application to Biotechnology

Streptococcus dysgalactiae is use in biotechnology lab for its enzyme, S. dysgalactiae hyaluronidase. This enzyme degrades hyaluronic acid and chondroitin results in disaccharides with nonreducing 4,5-unsaturated uronic acid residue (18). Many labs use this enzyme to produce larger oligosaccharides. Since this enzyme does not degrade chondroitiin sulfate, researchers use it to determine the distribution of sulfate group in certain biochemical compounds (18). S. dysgalactiae hyaluronidase is also stable and can be stored for 2 years at - 20 degree Celsius, which makes it an ideal commercial product of biotechnology (18).

Current Research

First study

Group C streptococci (GCS) are not studied as extensively as group A streptococci (GAS) until recent years. The study of GCS is important in that the species within GCS have obtained many methods to fight against immune response. Whole-genome sequencing of Streptococcus dysgalactiae is a first important step to fight this problem. The information provided by the genome sequence will allow researchers to understand the virulence factors behind the microbe and ways to deal with them. The recent genome sequencing of strain 3396 reveals that Streptococcus dysgalactiae has 87% of homologous gene with GAS (4). This is a significant discovery, which further supports the evidence that phage is the source of intraspecies genetic variation of other microbe species. It is also suggested from the research that progenitor strain 3396 may have arisen in GAS first then lacteral transfer to group G streptococci (GGS). This is helpful information that allows researchers to trace back the origins of the species (4).

Second study

The recent discover of superantigen on Streptococcus dysgalactiae, has made it a serious threat to worldwide health care facilities. Superantigen can cause serious illness and death in a short period of time. There are already several clinical cases involving animals getting toxic shock syndrome. To find a solution to prevent these illness, the first step is to identify and understand the superantigens of Streptococcus dysgalactiae (19). A group of researchers of Japan has taken the step to identify the superantigens. They identified 7 new variants of streptococcal pyrogenic exotoxin G (SPEGG) superantigen from Streptococcus dysgalactiae subsp. dysgalactiae and equisimilis. While these superantigens are effectively at stimulating animal peripheral blood mononuclear cells (PBMCs), it is not as effectively at stimulating human PBMCs. Thus, it is suggested that Streptococcus dysgalactiae is more threatening to animals than human as of now (19).

Third study

Streptococcus dysgalactiae always have contributed to the economic lose of dairy products and herd. Therefore, a study was done in Estonia concerning what factors will cause Streptococcus dysgalactiae infection in calved heifers, and what common pathogen is responsible for clinical mastitis (20). This study proceeded on for about a year. The researches conclude that in tiestall farm, teat injuries, short stalls, and shortage of bedding materials are factors that increase clinical mastitis. Because of this discover, cows in one of the Sweden tiestall farm were moved to freestall farm (20). Researchers also took record of clinical mastitis during the movement of herds from one farm to another. The result was that the movement increases the risk of clinical mastitis (20).It is suggested that because the herd had a change of environments, the stress level of herd increases, which decreases the defense level of immune system. This results in higher risk of clinical mastitis (20). It is also discovered that the most common pathogen responsible for the clinical mastitis is not Streptococcus dysgalactiae as previously thought, but it is Staphylococcus aureus (20).

References

[1]Bisno, Alan L. and Gaviria, J.Milton. "Group C and G Streptococci". Streptococcal Infections: Taxonomy. New York; Oxford University Press, 2000.
[2]Quinn RJ, Hallett AF, Appelbaum PC, Cooper RC. "Meningitis caused by Streptococcus dysgalactiae in a preterm infant". PubMed Central. 1978.p. 948-50
[3]Mollison LC, Donaldson E. Group C streptococcal meningitis. PubMed Central. 1990.p. 319-20
[4]Mark R. Davies, David J. McMillan,1 Gary H. Van Domselaar, Malcolm K. Jones, and Kadaba S. Sriprakash "Phage 3396 from a Streptococcus dysgalactiae subsp. equisimilis Pathovar May Have Its Origins in Streptococcus pyogenes"PubMed Central. 2007.p. 2646–2652
[5]W.H. Holzapfel and B.J.B Wood "Lactic acid bacteria in contemporary perspective"The Genera of Lactic Acid Bacteria.1992.p.1-4
[6]József Vasi, Lars Frykberg, Lena E. Carlsson, Martin Lindberg, and Bengt Guss "M-Like Proteins of Streptococcus dysgalactiae"PubMed Central.2000.p.294-302
[7]Xin-Ming Song,nJose Perez-Casal, Alexandra Bolton, and Andrew A. Potter "Surface-Expressed Mig Protein Protects Streptococcus dysgalactiae against Phagocytosis by Bovine Neutrophils"PubMed Central.2001.p.6030-6037
[8]Claudia M. Brandt, Gerhard Haase, Norbert Schnitzler, Reinhard Zbinden, and Rudolf Lütticken1 "Characterization of Blood Culture Isolates of Streptococcus dysgalactiae subsp. equisimilis Possessing Lancefield's Group A Antigen"PubMed Central.1999.p.4194-4197
[9]W J Simpson, J M Musser and P P Cleary "Evidence consistent with horizontal transfer of the gene (emm12) encoding serotype M12 protein between group A and group G pathogenic streptococci. "Infect Immun.1992.p.1890-1893
[10]Raul A. Almeida and Stephen P. Oliver "Invasion of Bovine Mammary Epithelial Cells by Streptococcus dysgalactiae " Journal of Dairy Science.1994.p.1310-1317
[11]Cheeseman M, Genain C, Smith CD. "Group C streptococcal meningitis with favorable recovery. A case report." PubMed Central.1990.p.545-6
[12]Quinn RJ, Hallett AF, Appelbaum PC, Cooper RC. "Meningitis caused by Streptococcus dysgalactiae in a preterm infant." PubMed Central.1978.p.948-50
[13]Jean-François MJ ; Poskitt DC ; Turnbull SJ ; Macdonald LM ; Yasmeen D. "Protection against Streptococcus equi infection by monoclonal antibodies against an M-like protein."MedScape.1991.p.2125-33
[14]Per-Eric LINDGREN, Martin J. McGAVIN, Christer SIGNÄS, Bengt GUSS, Sivashankarappa GURUSIDDAPPA, Magnus HÖÖK, Martin LINDBERG. "Two different genes coding for fibronectin-binding proteins from Streptococcus dysgalactiae. The complete nucleotide sequences and characterization of the binding domains."blackwell-synergy.1993.p.1432-1033
[15]T PROFT and J D FRASER. "Bacterial superantigens"PubMed Central.2003.p.1365-2249
[16]Barnham M, Kerby J, Chandler RS, Millar MR. "Group C streptococci in human infection: a study of 308 isolates with clinical correlations."PubMed Central.1989.p.379-90
[17]K V Rolston, J L LeFrock and R F Schell. "Activity of nine antimicrobial agents against Lancefield group C and group G streptococci. "Antimicrob Agents Chemother.1982.p.930-932
[18]Rajeshwara N. Achur, Manojkumar Valiyaveettil, and D. Channe Gowda. "The Low Sulfated Chondroitin Sulfate Proteoglycans of Human Placenta Have Sulfate Group-clustered Domains That Can Efficiently Bind Plasmodium falciparum-infected Erythrocytes" J. Biol. Chem.2002.
[19]Jizi Zhao, Tomohito Hayashi, Susanna Saarinen, Anastassios C. Papageorgiou, Hidehito Kato, Ken'ichi Imanishi, Teruo Kirikae, Ryo Abe, Takehiko Uchiyama, and Tohru Miyoshi-Akiyama1. "Cloning, Expression, and Characterization of the Superantigen Streptococcal Pyrogenic Exotoxin G from Streptococcus dysgalactiae"PubMed Central.2007.p.1721–1729
[20]Piret Kalmus, Arvo Viltrop, Birgit Aasmäe, and Kalle Kask. "Occurrence of clinical mastitis in primiparous Estonian dairy cows in different housing conditions"PubMed Central.2006.p.10.1186/1751-0147-48-21
[21]Cesarman-Maus G, Hajjar KA. "Molecular mechanisms of fibrinolysis."PubMed Central.2005.p.307-21

Edited by student of Rachel Larsen

Edited by KLB