Streptococcus dysgalactiae

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Streptococcus dysgalactiae
Streptococcus dysgalactiae (Beta haemolytic Streptococcus Lancefield Group G) on Columbia Horse Blood Agar - Detail.jpg
Streptococcus dysgalactiae - Beta Haemolytic Group G Streptococcus on Columbia Horse Blood Agar
Scientific classification OOjs UI icon edit-ltr.svg
Domain: Bacteria
Phylum: Bacillota
Class: Bacilli
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Species:
S. dysgalactiae
Binomial name
Streptococcus dysgalactiae
(ex Diernhofer 1932) Garvie et al. 1983

Streptococcus dysgalactiae is a gram positive, beta-haemolytic, coccal bacterium belonging to the family Streptococcaceae . It is capable of infecting both humans and animals, but is most frequently encountered as a commensal of the alimentary tract, genital tract, or less commonly, as a part of the skin flora. The clinical manifestations in human disease range from superficial skin-infections and tonsillitis, to severe necrotising fasciitis and bacteraemia. [1] The incidence of invasive disease has been reported to be rising. [2] [3] [4] Several different animal species are susceptible to infection by S. dysgalactiae, but bovine mastitis and infectious arthritis in lambs (joint ill) have been most frequently reported. [5] [6]

Contents

Streptococcus dysgalactiae is currently divided into the subspecies Streptococcus dysgalactiae subsp. equisimilis and Streptococcus dysgalactiae subsp. dysgalactiae; the former mostly associated with human disease, and the latter almost exclusively encountered in veterinary medicine. [7] Their exact taxonomic delineation, however, is a matter of ongoing debate (See taxonomy).

The names are derived from Greek; Streptococcus meaning chain forming (Streptos) rounded berry-like bodies (kokkos), referring to their usual appearance under a light-microscope. Dys (bad) galactiae (milk) alludes to their propensity to cause bovine mastitis. Equi (horse) similis (like) infers similarity to the closely related species, Streptococcus equi .

Epidemiology

Streptococcus dysgalactiae was long believed to be non-pathogenic to humans. However, an increasing incidence of S. dysgalactiae infections has been documented, and in some geographic regions, the rate of invasive infection has even surpassed that of Streptococcus pyogenes . [2] [3] [4] [8] [9] The age distribution of invasive cases among humans is clearly skewed towards the elderly, whereas the healthy carrier state appears to have the inverse relation to age. People with chronic maladies, including cancer and diabetes, are also especially susceptible to infection. [1] [10] These opportunistic traits have been proposed as one of the mechanisms underlying the observed increasing frequency of invasive disease. Furthermore, a male predominance has been noted, presumably due to a higher burden of comorbidity. The incidence of non-invasive disease in human does not appear to be increasing. [2]

Role in human disease

Streptococcus dysgalactiae subspecies equisimilis is a commensal in human alimentary tract and genital tract. Occasionally it is isolated from skin, but usually in relation to a chronic skin condition or some breach of the epithelial barrier. [11]

Non-invasive disease manifestations include predominantly tonsillitis and superficial skin infections. [1] [2] Additionally, it has long been recognized as a potential cause of cellulitis/erysipelas. However, the role of Streptococcus dysgalactiae subspecies equisimilis in cellulitis might have been previously underestimated, and it was linked to a majority of the cellulitis cases in a recent study. [11]

The clinical presentation among invasive disease is also dominated by skin and soft tissue infections, including a small subset of patients presenting with severe necrotizing fasciitis. [1] [2] Moreover, it is an important cause of bone and joint infections, and this disease manifestation is reported to be increasing. [12] Less commonly it can present as pneumonia, endocarditis, genital or intra-abdominal infections. Primary bacteraemia, infection without identifiable focal origin, comprises approximately 20% of the reported cases. [1] [2] [13]

Recently, Streptococcus dysgalactiae subspecies equisimilis has been linked to post-streptococcal glomerulonephritis and acute rheumatic fever. [14] [15] These immunologic sequelae have previously only been associated with Streptococcus pyogenes . Streptococcus dysgalactiae subspecies dysgalactiae is almost exclusively an animal pathogen. However, a few casuistic reports of human zoonotic infection have been documented. [16] [17]

Role in animal disease

Streptococcus dysgalactiae can infect a range of animal hosts, and both subspecies are of importance. However, the bacterium is frequently encountered as a colonizer of healthy animals, especially in the alimentary tract and genital region. [6]

In veterinary medicine, it is a well-recognized cause of bovine mastitis, hence the name dys-galactiae. In some geographic regions, it is reported only second to Staphylococcus aureus as a cause of both clinical and subclinical mastitis. [5] S. dysgalactiae has been particularly linked to mastitis occurring during the summer time ("Summer mastitis"), and bacterial spreading by flying insects has been suggested. [18] Mastitis in other animals has also been documented. [19]

S. dysgalactiae has been isolated from infectious polyarthritis in several animal species, including piglets, lambs, calves and goats. [6] [20] Furthermore, it has been implicated in neonatal mortality among puppies. [21] Recently, Streptococcus dysgalactiae subspecies dysgalactiae has been described as an emerging pathogen in fish, causing fulminant necrotic ulcers of the caudal peduncle, with ensuing high mortality rates. [22] The clinical presentation is dominated by severe sepsis and the formation of microabscesses, and a relationship between disease severity and the expression of the virulence factors Streptolysin S and SPEGdys has been inferred. [20]

Treatment and antimicrobial susceptibility

Penicillin remains the drug of choice for treating streptococcal infections, and S. dysgalactiae strains with reduced susceptibility to penicillin have never been reported. Treatment duration varies from 5 days to 3 months, depending on the clinical diagnosis. Second-line agents include macrolides and clindamycin, although increasing resistance, due to both efflux and target modification, has been documented in some geographic regions. [13] [23] [24] Aminoglycosides are not active against streptococci due to their lacking respiratory metabolism. However, administered in combination with a beta-lactam antibiotic, aminoglycosides appear to produce a synergistic effect towards streptococci. [25] Streptococcus dysgalactiae is uniformly susceptible to glycopeptides and oxazolidones.

Taxonomy

Diernhofer first used the name Streptococcus dysgalactiae in 1932, describing a streptococcus of veterinary origin. [26] Subsequently, Frost reported the discovery of the human pathogen Streptococcus equisimilis in 1936. [27] Contemporarily, though, Rebecca Lancefield devised a classification of streptococci based on their carbohydrate-antigens, and successively described streptococci belonging to group C (1933) and group G (1935). [28] [29] The correlation of group carbohydrate specificity with the proposed species S. dysgalactiae and S. equisimilis, however, were not explored in detail. The Lancefield classification soon became the preferred laboratory identification method for streptococci, and the names S. dysgalactiae and S. equisimilis fell into disuse. In 1980, they were even removed from the List of Approved Bacterial species. [30] Three years later, though, DNA hybridization studies revealed extensive similarities between the entities Streptococcus dysgalactiae, Streptococcus equisimilis, large-colony-forming group C and group G streptococcus of human origin, and certain large-colony-forming group C, G and L streptococci of animal origin. [31] [32] Accordingly, they were fused to one species, Streptococcus dysgalactiae. However, subsequent molecular investigations indicated heterogeneity within this new species, and in 1996 it was divided into S. dysgalactiae subspecies equisimilis and S. dysgalactiae subspecies dysgalactiae. [33]

The taxonomic division of Streptococcus dysgalactiae into its two subspecies has been the origin of much confusion, and a matter of ongoing debate. Although no official taxonomic gold standard exists, the most current and widely supported definition was published by Vieira et al. in 1998. [7] It defines S. dysgalactiae subspecies dysgalactiae solely as the alpha-haemolytic phenotype harbouring the Lancefield group C antigen. The rest are classified as S. dysgalactiae subspecies equisimilis, are (mostly) beta-haemolytic and can harbour carbohydrate antigens of Lancefield group A, C, G or L. However, a recent study indicates that the Streptococcus dysgalactiae subspecies equisimilis strains of animal and human origin are genetically divergent, and future taxonomic reclassifications are conceivable. [34]

Laboratory identification

Streptococcus dysgalactiae form large colonies (>0.5 cm) after 24 hours of incubation, and produce haemolysis on blood agar; Streptococcus dysgalactiae subspecies dysgalactiae is alpha-haemolytic, whereas Streptococcus dysgalactiae subspecies equisimilis is predominantly beta-haemolytic. They are facultative anaerobic, incapable of respiratory metabolism, but are aerotolerant. Growth is enhanced by incubation in 5% CO2 atmosphere, but they usually grow adequately in ambient air. The optimum temperature for growth is approximately 37 °C. Lancefield group C and G carbohydrate antigens are predominantly expressed, but group A and L have been documented. [34] However, the above characteristics are not unique to S. dysgalactiae, and further testing is required to confirm the species identity. Although many laboratories currently identify bacteria by mass-spectrometry (Matrix Assisted Laser Desorption/ionization Time Of Flight MALDI TOF MS), phenotypic testing is still widely used. Unlike Streptococcus pyogenes (harbouring Lancefield group A antigen), S. dysgalactiae is PYR-negative and Bacitracin resistant. The distinction from the Streptococcus anginosus group (Lancefield A, C, G or F) can be made by colony size and Voges Proskauer test (VP); the S.anginosus group being VP positive. Streptococcus equi contains Lancefield group C, and Streptococcus canis harbours group G, but unlike S. dysgalactiae, they are both Hyaluronidase negative. [34]

The identification of S. dysgalactiae to the subspecies level is most reliably performed by multilocus sequence typing. [35] MALDI TOF MS does currently not possess taxonomic resolution beyond the species level.

Molecular typing

Several different typing systems for Streptococcus dysgalactiae have been used, the majority originally devised for the closely related species Streptococcus pyogenes. The most widely employed method is emm-typing. The emm-gene encodes the M-protein, a major virulence factor in both S. pyogenes and Streptococcus dysgalactiae. It is ubiquitous in Streptococcus dysgalactiae subspecies equisimilis of human origin, and its hypervariability in the 5'-terminal region forms the basis for categorization into separate emm-types. [36] To date, more than 100 Streptococcus dysgalactiae subspecies equisimilis emm-types have been described (CDC Strep Lab). The prevailing emm-types vary in different geographical regions, and clonal outbreaks have been reported. [37] Unlike for S. pyogenes, a correlation between emm-type and disease manifestation or severity has not been established for S. dysgalactiae. [13] [38] Pulsed-field gel electrophoresis has historically been employed for the exploration of clonal relationships among S. dysgalactiae, but with the increased availability and reduced costs of sequencing, it is likely to be replaced by multilocus sequence typing and single-nucleotide polymorphism analysis.

Pathogenesis and virulence factors

The pathogenetic pathways of Streptococcus dysgalactiae have not been explored in detail. Several virulence factors have been identified, but predominantly by screening S. dysgalactiae isolates for homologues of well-characterized S. pyogenes virulence genes. In a study of 216 S. pyogenes virulence genes, S. dysgalactiae was found to harbour approximately half of them. [39] Indeed, whole-genome comparisons reveal a 70% -genetic similarity between the two species, indicating a common genetic ancestry. [40] However, evidence of horizontal genetic transfer has also been reported. [41]

The first pivotal step in infectious pathogenesis is the attachment to the host tissues. The M-protein, the most extensively studied Streptococcus dysgalactiae subspecies equisimilis virulence factor, has been documented to facilitate both adherence to and internalization into host cells. [1] [42] Other adhesins have also been described, including the genes gfba, fnB, fbBA, fnBB, lmb and gapC; all mediating binding to fibronectin. [43] [44] [45] [46] gfba was recently shown contribute to bacterial internalization into endothelial cells and intracellular persistence. [47] [48] These properties may explain the tendency of recurrent bacteraemia observed in human cases caused by Streptococcus dysgalactiae subspecies equisimilis .

In order to establish infection, the bacteria need to escape the host immune response, and in streptococci, a varied arsenal of bacterial strategies have been described. The M-protein aids in immune evasion by inhibiting phagocytosis and inactivating the complement system. [1] Furthermore, Streptococcus dysgalactiae possesses protein G, a virulence factor binding circulating immunoglobulins, and thus interfering with the host antibody response. [49] DrsG, a virulence protein abrogating the effect of antimicrobial peptides secreted by human immune cells, is also harboured by a subset of strains of Streptococcus dysgalactiae subspecies equisimilis. [50] [51]

Several toxins and secreted enzymes have been identified in Streptococcus dysgalactiae, including the haemolysins Streptolysin O (SLO) and Streptolysin S (SLS), and a correlation between the expression of SLO and SLS and disease severity has been inferred. [52] speGdys, a homolog of the S. pyogenes superantigen speG, has been documented in some S. dysgalactiae strains. [38] [53] However, it only appears to possess superantigen-capabilities in animals, and its relevance in human disease has yet to be elucidated. [54] Streptokinase appears to be ubiquitous in S. dysgalactiae, enabling fibrinolysis and aiding in bacterial spreading through tissues. [1] [39]

Recently, a capacity to form biofilm was reported, facilitating survival and proliferation in hostile environments. [55] Although this potentially could have implications for the treatment of S. dysgalactiae-infections, its clinical significance has not yet been determined.

Related Research Articles

<i>Streptococcus</i> Genus of bacteria

Streptococcus is a genus of gram-positive coccus or spherical bacteria that belongs to the family Streptococcaceae, within the order Lactobacillales, in the phylum Bacillota. Cell division in streptococci occurs along a single axis, so as they grow, they tend to form pairs or chains that may appear bent or twisted. This differs from staphylococci, which divide along multiple axes, thereby generating irregular, grape-like clusters of cells. Most streptococci are oxidase-negative and catalase-negative, and many are facultative anaerobes.

<span class="mw-page-title-main">Group A streptococcal infection</span> Medical condition

Group A streptococcal infections are a number of infections with Streptococcus pyogenes, a group A streptococcus (GAS). S. pyogenes is a species of beta-hemolytic Gram-positive bacteria that is responsible for a wide range of infections that are mostly common and fairly mild. If the bacteria enter the bloodstream an infection can become severe and life-threatening, and is called an invasive GAS (iGAS).

<i>Streptococcus pyogenes</i> Species of bacterium

Streptococcus pyogenes is a species of Gram-positive, aerotolerant bacteria in the genus Streptococcus. These bacteria are extracellular, and made up of non-motile and non-sporing cocci that tend to link in chains. They are clinically important for humans, as they are an infrequent, but usually pathogenic, part of the skin microbiota that can cause Group A streptococcal infection. S. pyogenes is the predominant species harboring the Lancefield group A antigen, and is often called group A Streptococcus (GAS). However, both Streptococcus dysgalactiae and the Streptococcus anginosus group can possess group A antigen as well. Group A streptococci, when grown on blood agar, typically produce small (2–3 mm) zones of beta-hemolysis, a complete destruction of red blood cells. The name group A (beta-hemolytic) Streptococcus (GABHS) is thus also used.

<span class="mw-page-title-main">Scarlet fever</span> Infectious disease caused by Streptococcus pyogenes

Scarlet fever, also known as scarlatina, is an infectious disease caused by Streptococcus pyogenes, a Group A streptococcus (GAS). The infection is a type of Group A streptococcal infection. It most commonly affects children between five and 15 years of age. The signs and symptoms include a sore throat, fever, headache, swollen lymph nodes, and a characteristic rash. The face is flushed and the rash is red and blanching. It typically feels like sandpaper and the tongue may be red and bumpy. The rash occurs as a result of capillary damage by exotoxins produced by S.pyogenes. On darker-pigmented skin the rash may be hard to discern.

<i>Streptococcus agalactiae</i> Species of bacterium

Streptococcus agalactiae is a gram-positive coccus with a tendency to form chains. It is a beta-hemolytic, catalase-negative, and facultative anaerobe.

Streptococcus bovis is a species of Gram-positive bacteria that in humans is associated with urinary tract infections, endocarditis, sepsis, and colorectal cancer. S. gallolyticus is commonly found in the alimentary tract of cattle, sheep, and other ruminants, and may cause ruminal acidosis or feedlot bloat. It is also associated with spontaneous bacterial peritonitis, a frequent complication occurring in patients affected by cirrhosis. Equivalence with Streptococcus equinus has been contested.

<span class="mw-page-title-main">Group B streptococcal infection</span> Medical condition

Group B streptococcal infection, also known as Group B streptococcal disease or just Group B strep, is the infection caused by the bacterium Streptococcus agalactiae. GBS infection can cause serious illness and sometimes death, especially in newborns, the elderly, and people with compromised immune systems.

<span class="mw-page-title-main">Rebecca Lancefield</span> 20th-century American microbiologist

Rebecca Craighill Lancefield was a prominent American microbiologist. She joined the Rockefeller Institute for Medical Research in New York in 1918, and was associated with that institute throughout her long and outstanding career. Her bibliography comprises more than 50 publications published over 60 years.

Streptolysins are two hemolytic exotoxins from Streptococcus pyogenes. Types include streptolysin O, which is oxygen-labile, and streptolysin S, which is oxygen-stable.

M protein is a virulence factor that can be produced by certain species of Streptococcus.

Streptococcus constellatus is a species of Streptococcus that is part of the normal flora in the oral cavity, urogenital region, and intestinal tract. However, it can frequently cause purulent infections in other parts of the body. DNA homology studies and 16S rRNA sequence analysis demonstrate S. constellatus belongs to the Streptococcus anginosus group along with Streptococcus intermedius and Streptococcus anginosus.

<i>Streptococcus anginosus</i> group Species of bacterium

The Streptococcus anginosus group (SAG), also known as the anginosus group streptococci (AGS) or the milleri group streptococci (MGS), are a group of several species of streptococci with clinical similarities. The group is named after a principal member species, Streptococcus anginosus. The older name Streptococcus milleri is now pseudotaxonomic, as the idea that these streptococci constituted a single species was incorrect. The anginosus group streptococci are members of the viridans streptococci group. 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. The unique characteristic of them from other pathogenic streptococci, such as S. pyogenes and S. agalactiae, is their ability to cause abscesses.

<i>Streptococcus canis</i> Species of bacterium

Streptococcus canis is a group G beta-hemolytic species of Streptococcus. It was first isolated in dogs, giving the bacterium its name. These bacteria are characteristically different from Streptococcus dysgalactiae, which is a human-specific group G species that has a different phenotypic chemical composition. S. canis is important to the skin and mucosal health of cats and dogs, but under certain circumstances, these bacteria can cause opportunistic infections. These infections were known to afflict dogs and cats prior to the formal description of the species in Devriese et al., 1986. However, additional studies revealed cases of infection in other mammal species, including cattle and even humans. Instances of mortality from S. canis in humans are very low with only a few reported cases, while actual instances of infection may be underreported due to mischaracterizations of the bacteria as S. dysgalactiae. This species, in general, is highly susceptible to antibiotics, and plans to develop a vaccine to prevent human infections are currently being considered.

<i>Streptococcus zooepidemicus</i> Species of bacterium

Streptococcus zooepidemicus is a Lancefield group C streptococcus that was first isolated in 1934 by P. R. Edwards, and named Animal pyogens A. It is a mucosal commensal and opportunistic pathogen that infects several animals and humans, but most commonly isolated from the uterus of mares. It is a subspecies of Streptococcus equi, a contagious upper respiratory tract infection of horses, and shares greater than 98% DNA homology, as well as many of the same virulence factors.

Streptococcus dysgalactiae subsp. equisimilis is a species of Streptococcus, initially described by Frost in 1936. As a result of several DNA hybridization studies in 1983, the species was merged into Streptococcus dysgalactiae. Subsequently, S. dysgalactiae was divided into the subspecies Streptococcus dysgalactiae subsp. equisimilis and Streptococcus dysgalactiae subsp. dysgalactiae. Although the name Streptococcus equisimilis is no longer valid, it is still encountered both in clinical practice, and in scientific journals.

Perianal cellulitis, also known as perianitis or perianal streptococcal dermatitis, is a bacterial infection affecting the lower layers of the skin (cellulitis) around the anus. It presents as bright redness in the skin and can be accompanied by pain, difficulty defecating, itching, and bleeding. This disease is considered a complicated skin and soft tissue infection (cSSTI) because of the involvement of the deeper soft tissues.

<span class="mw-page-title-main">Streptococcal pyrogenic exotoxin</span>

Streptococcal pyrogenic exotoxins also known as erythrogenic toxins, are exotoxins secreted by strains of the bacterial species Streptococcus pyogenes. SpeA and speC are superantigens, which induce inflammation by nonspecifically activating T cells and stimulating the production of inflammatory cytokines. SpeB, the most abundant streptococcal extracellular protein, is a cysteine protease. Pyrogenic exotoxins are implicated as the causative agent of scarlet fever and streptococcal toxic shock syndrome. There is no consensus on the exact number of pyrogenic exotoxins. Serotypes A-C are the most extensively studied and recognized by all sources, but others note up to thirteen distinct types, categorizing speF through speM as additional superantigens. Erythrogenic toxins are known to damage the plasma membranes of blood capillaries under the skin and produce a red skin rash. Past studies have shown that multiple variants of erythrogenic toxins may be produced, depending on the strain of S. pyogenes in question. Some strains may not produce a detectable toxin at all. Bacteriophage T12 infection of S. pyogenes enables the production of speA, and increases virulence.

Bacteriophage T12 is a bacteriophage that infects Streptococcus pyogenes bacteria. It is a proposed species of the family Siphoviridae in the order Caudovirales also known as tailed viruses. It converts a harmless strain of bacteria into a virulent strain. It carries the speA gene which codes for erythrogenic toxin A. speA is also known as streptococcal pyogenic exotoxin A, scarlet fever toxin A, or even scarlatinal toxin. Note that the name of the gene "speA" is italicized; the name of the toxin "speA" is not italicized. Erythrogenic toxin A converts a harmless, non-virulent strain of Streptococcus pyogenes to a virulent strain through lysogeny, a life cycle which is characterized by the ability of the genome to become a part of the host cell and be stably maintained there for generations. Phages with a lysogenic life cycle are also called temperate phages. Bacteriophage T12, proposed member of family Siphoviridae including related speA-carrying bacteriophages, is also a prototypic phage for all the speA-carrying phages of Streptococcus pyogenes, meaning that its genome is the prototype for the genomes of all such phages of S. pyogenes. It is the main suspect as the cause of scarlet fever, an infectious disease that affects small children.

In molecular biology, the FasX small RNA (fibronectin/fibrinogen-binding/haemolytic-activity/streptokinase-regulator-X) is a non-coding small RNA (sRNA) produced by all group A Streptococcus. FasX has also been found in species of group D and group G Streptococcus. FasX regulates expression of secreted virulence factor streptokinase (SKA), encoded by the ska gene. FasX base pairs to the 5' end of the ska mRNA, increasing the stability of the mRNA, resulting in elevated levels of streptokinase expression. FasX negatively regulates the expression of pili and fibronectin-binding proteins on the bacterial cell surface. It binds to the 5' untranslated region of genes in the FCT-region in a serotype-specific manner, reducing the stability of and inhibiting translation of the pilus biosynthesis operon mRNA by occluding the ribosome-binding site through a simple Watson-Crick base-pairing mechanism.

<span class="mw-page-title-main">Lancefield grouping</span>

Lancefield grouping is a system of classification that classifies catalase-negative Gram-positive cocci based on the carbohydrate composition of bacterial antigens found on their cell walls. The system, created by Rebecca Lancefield, was historically used to organize the various members of the family Streptococcaceae, which includes the genera Lactococcus and Streptococcus, but now is largely superfluous due to explosive growth in the number of streptococcal species identified since the 1970s. However, it has retained some clinical usefulness even after the taxonomic changes, and as of 2018, Lancefield designations are still often used to communicate medical microbiological test results.

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