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| species = '''''S. dysgalactiae'''''
| species = '''''S. dysgalactiae'''''
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''Streptococcus dysgalactiae'' is a [[Gram-positive|gram positive]], [[Hemolysis_(microbiology)|beta-haemolytic]], [[Coccus|coccal]] [[Bacterium|bacterium]] belonging to the family ''[[Streptococcaceae]]''. It is capable of infecting both humans and animals, but is most frequently encountered as a [[Commensalism|commensal]] of the [[Gastrointestinal_tract|alimentary tract]], [[female_reproductive_system|genital tract]], or less commonly, as a part of the [[Skin_flora|skin flora]]. The clinical manifestations in human disease range from superficial [[skin_infection|skin-infections]] and [[tonsillitis]], to severe [[Necrotizing_fasciitis|necrotising fasciitis]] and [[Bacteremia|bacteraemia]].<ref name="Brandt2009">{{cite journal|last1=Brandt|first1=CM|last2=Spellerberg|first2=B|title=Human infections due to Streptococcus dysgalactiae subspecies equisimilis.|journal=Clinical infectious diseases : an official publication of the Infectious Diseases Society of America|date=1 September 2009|volume=49|issue=5|pages=766-72|doi=10.1086/605085|pmid=19635028}}</ref> The incidence of invasive disease has been reported to be rising (2-4).<ref name="Oppegaard2015">{{cite journal|last1=Oppegaard|first1=O|last2=Mylvaganam|first2=H|last3=Kittang|first3=BR|title=Beta-haemolytic group A, C and G streptococcal infections in Western Norway: a 15-year retrospective survey.|journal=Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases|date=February 2015|volume=21|issue=2|pages=171-8|doi=10.1016/j.cmi.2014.08.019|pmid=25658557}}</ref><ref name="Sylvetsky2002">{{cite journal|last1=Sylvetsky|first1=N|last2=Raveh|first2=D|last3=Schlesinger|first3=Y|last4=Rudensky|first4=B|last5=Yinnon|first5=AM|title=Bacteremia due to beta-hemolytic Streptococcus group G: increasing incidence and clinical characteristics of patients.|journal=The American journal of medicine|date=1 June 2002|volume=112|issue=8|pages=622-6|pmid=12034411}}</ref><ref name="HPA">{{cite journal|last1=Anonymous|title=Voluntary surveillance of pyogenic and non-pyogenic streptococcal bacteraemia in England, Wales and Northern Ireland: 2014|journal=Health Protection Report: Weekly Report|date=November 2015|volume=9|url=https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/478808/hpr4115_strptcccs.pdf}}</ref> Several different animal species are susceptible to infection by ''S.dysgalactiae'', but [[Mastitis|bovine mastitis]] and [[septic_arthritis|infectious arthritis]] in lambs (joint ill) have been most frequently reported (5, 6).
''Streptococcus dysgalactiae'' is a [[Gram-positive|gram positive]], [[Hemolysis_(microbiology)|beta-haemolytic]], [[Coccus|coccal]] [[Bacterium|bacterium]] belonging to the family ''[[Streptococcaceae]]''. It is capable of infecting both humans and animals, but is most frequently encountered as a [[Commensalism|commensal]] of the [[Gastrointestinal_tract|alimentary tract]], [[female_reproductive_system|genital tract]], or less commonly, as a part of the [[Skin_flora|skin flora]]. The clinical manifestations in human disease range from superficial [[skin_infection|skin-infections]] and [[tonsillitis]], to severe [[Necrotizing_fasciitis|necrotising fasciitis]] and [[Bacteremia|bacteraemia]].<ref name="Brandt2009">{{cite journal|last1=Brandt|first1=CM|last2=Spellerberg|first2=B|title=Human infections due to Streptococcus dysgalactiae subspecies equisimilis.|journal=Clinical infectious diseases : an official publication of the Infectious Diseases Society of America|date=1 September 2009|volume=49|issue=5|pages=766-72|doi=10.1086/605085|pmid=19635028}}</ref> The incidence of invasive disease has been reported to be rising.<ref name="Oppegaard2015">{{cite journal|last2=Mylvaganam|first2=H|last3=Kittang|first3=BR|date=February 2015|title=Beta-haemolytic group A, C and G streptococcal infections in Western Norway: a 15-year retrospective survey.|url=http://www.clinicalmicrobiologyandinfection.com/article/S1198-743X(14)00043-3/fulltext|journal=Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases|volume=21|issue=2|pages=171-8|doi=10.1016/j.cmi.2014.08.019|pmid=25658557|last1=Oppegaard|first1=O}}</ref><ref name="Sylvetsky2002">{{cite journal|last1=Sylvetsky|first1=N|last2=Raveh|first2=D|last3=Schlesinger|first3=Y|last4=Rudensky|first4=B|last5=Yinnon|first5=AM|title=Bacteremia due to beta-hemolytic Streptococcus group G: increasing incidence and clinical characteristics of patients.|journal=The American journal of medicine|date=1 June 2002|volume=112|issue=8|pages=622-6|pmid=12034411}}</ref><ref name="HPA">{{cite journal|last1=Anonymous|title=Voluntary surveillance of pyogenic and non-pyogenic streptococcal bacteraemia in England, Wales and Northern Ireland: 2014|journal=Health Protection Report: Weekly Report|date=November 2015|volume=9|url=https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/478808/hpr4115_strptcccs.pdf}}</ref> Several different animal species are susceptible to infection by ''S.dysgalactiae'', but [[Mastitis|bovine mastitis]] and [[septic_arthritis|infectious arthritis]] in lambs (joint ill) have been most frequently reported.<ref name=":0">{{Cite journal|last=Whist|first=A. C.|last2=Østerås|first2=O.|last3=Sølverød|first3=L.|date=2007-02-01|title=Streptococcus dysgalactiae isolates at calving and lactation performance within the same lactation|url=https://www.ncbi.nlm.nih.gov/pubmed/17235154|journal=Journal of Dairy Science|volume=90|issue=2|pages=766–778|doi=10.3168/jds.S0022-0302(07)71561-8|issn=1525-3198|pmid=17235154}}</ref><ref name=":1">{{Cite journal|last=Rutherford|first=S. J.|last2=Rycroft|first2=A. N.|last3=Ridler|first3=A. L.|date=2014-06-07|title=Sources of Streptococcus dysgalactiae in English and Welsh sheep flocks affected by infectious arthritis (joint ill)|url=https://www.ncbi.nlm.nih.gov/pubmed/24619629|journal=The Veterinary Record|volume=174|issue=23|pages=579|doi=10.1136/vr.101753|issn=2042-7670|pmid=24619629}}</ref>
''Streptococcus dysgalactiae'' is currently divided into the [[subspecies]] ''[[Streptococcus dysgalactiae subspecies equisimilis]]'' (SDSE) and ''[[Streptococcus dysgalactiae subspecies dysgalactiae]]'' (SDSD); the former mostly associated with human disease, and the latter almost exclusively encountered in veterinary medicine (7). Their exact [[Taxonomy|taxonomic]] delineation, however, is a matter of ongoing debate (See [[#Taxonomy|taxonomy]]).
''Streptococcus dysgalactiae'' is currently divided into the [[subspecies]] ''[[Streptococcus dysgalactiae subspecies equisimilis]]'' (SDSE) and ''[[Streptococcus dysgalactiae subspecies dysgalactiae]]'' (SDSD); the former mostly associated with human disease, and the latter almost exclusively encountered in veterinary medicine.<ref name=":2">{{Cite journal|last=VIEIRA|first=VERNICA V.|last2=TEIXEIRA|first2=LÚCIA M.|last3=ZAHNER|first3=VIVIANE|last4=MOMEN|first4=HOOMAN|last5=FACKLAM|first5=RICHARD R.|last6=STEIGERWALT|first6=ARNOLD G.|last7=BRENNER|first7=DON J.|last8=CASTRO|first8=ANGELA C. D.|date=1998-01-01|title=Genetic relationships among the different phenotypes of Streptococcus dysgalactiae strains|url=http://ijs.microbiologyresearch.org/content/journal/ijsem/10.1099/00207713-48-4-1231|journal=International Journal of Systematic and Evolutionary Microbiology|volume=48|issue=4|pages=1231–1243|doi=10.1099/00207713-48-4-1231}}</ref> Their exact [[Taxonomy|taxonomic]] delineation, however, is a matter of ongoing debate (See [[#Taxonomy|taxonomy]]).
The names are derived from [[Greek_language|Greek]]; ''Streptococcus'' meaning chain forming (Streptos) rounded berry-like bodies (kokkos), referring to their usual appearance under a [[Optical_microscope|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|Streptococcus equi]]''.
The names are derived from [[Greek_language|Greek]]; ''Streptococcus'' meaning chain forming (Streptos) rounded berry-like bodies (kokkos), referring to their usual appearance under a [[Optical_microscope|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|Streptococcus equi]]''.


==Epidemiology==
==Epidemiology==
''Streptococcus dysgalactiae'' was long believed to be non-[[Pathogen|pathogenic]] to humans. However, an increasing [[incidence_(epidemiology)|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|Streptococcus pyogenes]]'' (2-4, 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_infection|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).
''Streptococcus dysgalactiae'' was long believed to be non-[[Pathogen|pathogenic]] to humans. However, an increasing [[incidence_(epidemiology)|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|Streptococcus pyogenes]]''.<ref name="Oppegaard2015" /><ref name="Sylvetsky2002" /><ref name="HPA" /><ref>{{Cite journal|last=Bramhachari|first=Pallaval V.|last2=Kaul|first2=Santosh Y.|last3=McMillan|first3=David J.|last4=Shaila|first4=Melkote S.|last5=Karmarkar|first5=Mohan G.|last6=Sriprakash|first6=Kadaba S.|date=2010-02-01|title=Disease burden due to Streptococcus dysgalactiae subsp. equisimilis (group G and C streptococcus) is higher than that due to Streptococcus pyogenes among Mumbai school children|url=https://www.ncbi.nlm.nih.gov/pubmed/19833781|journal=Journal of Medical Microbiology|volume=59|issue=Pt 2|pages=220–223|doi=10.1099/jmm.0.015644-0|issn=1473-5644|pmid=19833781}}</ref><ref>{{Cite journal|last=Wong|first=San S.|last2=Lin|first2=Yu S.|last3=Mathew|first3=Liby|last4=Rajagopal|first4=Latha|last5=Sepkowitz|first5=Douglas|date=2009-06-01|title=Increase in group G streptococcal infections in a community hospital, New York, USA|url=https://www.ncbi.nlm.nih.gov/pubmed/19523319|journal=Emerging Infectious Diseases|volume=15|issue=6|pages=991–993|doi=10.3201/eid1506.080666|issn=1080-6059|pmc=2727315|pmid=19523319}}</ref> 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.<ref name="Brandt2009" /><ref>{{Cite journal|last=Broyles|first=Laura N.|last2=Van Beneden|first2=Chris|last3=Beall|first3=Bernard|last4=Facklam|first4=Richard|last5=Shewmaker|first5=P. Lynn|last6=Malpiedi|first6=Paul|last7=Daily|first7=Pamala|last8=Reingold|first8=Arthur|last9=Farley|first9=Monica M.|date=2009-03-15|title=Population-based study of invasive disease due to beta-hemolytic streptococci of groups other than A and B|url=https://www.ncbi.nlm.nih.gov/pubmed/19187026|journal=Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America|volume=48|issue=6|pages=706–712|doi=10.1086/597035|issn=1537-6591|pmid=19187026}}</ref> These [[Opportunistic_infection|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.<ref name="Oppegaard2015" />


==Role in human disease==
==Role in human disease==
''Streptococcus dysgalactiae subspecies equisimilis'' (SDSE) 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 [[Epithelium|epithelial]] barrier (11).
''Streptococcus dysgalactiae subspecies equisimilis'' (SDSE) 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 [[Epithelium|epithelial]] barrier.<ref name=":3">{{Cite journal|last=Bruun|first=Trond|last2=Oppegaard|first2=Oddvar|last3=Kittang|first3=Bård R.|last4=Mylvaganam|first4=Haima|last5=Langeland|first5=Nina|last6=Skrede|first6=Steinar|date=2016-01-01|title=Etiology of Cellulitis and Clinical Prediction of Streptococcal Disease: A Prospective Study|url=https://www.ncbi.nlm.nih.gov/pubmed/26734653|journal=Open Forum Infectious Diseases|volume=3|issue=1|pages=ofv181|doi=10.1093/ofid/ofv181|issn=2328-8957|pmc=4699398|pmid=26734653}}</ref>
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 SDSE in cellulitis might have been previously underestimated, and it was linked to a majority of the cellulitis cases in a recent study (11).
Non-invasive disease manifestations include predominantly tonsillitis and superficial skin infections.<ref name="Brandt2009" /><ref name="Oppegaard2015" /> Additionally, it has long been recognized as a potential cause of [[cellulitis]]/[[erysipelas]]. However, the role of SDSE in cellulitis might have been previously underestimated, and it was linked to a majority of the cellulitis cases in a recent study.<ref name=":3" />
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|necrotizing fasciitis]] (1, 2). Moreover, it is an important cause of bone and joint infections, and this disease manifestation is reported to be increasing (Oppegaard Bone in press). Less commonly it can present as [[pneumonia]], [[endocarditis]], genital or intraabdominal infections. Primary bacteraemia, infection without identifiable focal origin, comprises approximately 20% of the reported cases (1, 2, 12).
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|necrotizing fasciitis]].<ref name="Brandt2009" /><ref name="Oppegaard2015" /> Moreover, it is an important cause of bone and joint infections, and this disease manifestation is reported to be increasing (Oppegaard et al: In press). Less commonly it can present as [[pneumonia]], [[endocarditis]], genital or intraabdominal infections. Primary bacteraemia, infection without identifiable focal origin, comprises approximately 20% of the reported cases.<ref name="Brandt2009" /><ref name="Oppegaard2015" /><ref name=":4">{{Cite journal|last=Loubinoux|first=Julien|last2=Plainvert|first2=Céline|last3=Collobert|first3=Gislène|last4=Touak|first4=Gérald|last5=Bouvet|first5=Anne|last6=Poyart|first6=Claire|last7=CNR-Strep Network|date=2013-08-01|title=Adult invasive and noninvasive infections due to Streptococcus dysgalactiae subsp. equisimilis in France from 2006 to 2010|url=https://www.ncbi.nlm.nih.gov/pubmed/23698531|journal=Journal of Clinical Microbiology|volume=51|issue=8|pages=2724–2727|doi=10.1128/JCM.01262-13|issn=1098-660X|pmc=3719644|pmid=23698531}}</ref>
Recently, SDSE has been linked to [[Acute_proliferative_glomerulonephritis|post-streptococcal glomerulonephritis]] and acute [[Rheumatic_fever|rheumatic fever]] (13, 14). These immunologic sequelae have previously only been associated with ''[[Streptococcus_pyogenes|Streptococcus pyogenes]]''.
Recently, SDSE has been linked to [[Acute_proliferative_glomerulonephritis|post-streptococcal glomerulonephritis]] and acute [[Rheumatic_fever|rheumatic fever]].<ref>{{Cite journal|last=Haidan|first=A.|last2=Talay|first2=S. R.|last3=Rohde|first3=M.|last4=Sriprakash|first4=K. S.|last5=Currie|first5=B. J.|last6=Chhatwal|first6=G. S.|date=2000-09-30|title=Pharyngeal carriage of group C and group G streptococci and acute rheumatic fever in an Aboriginal population|url=https://www.ncbi.nlm.nih.gov/pubmed/11030302|journal=Lancet (London, England)|volume=356|issue=9236|pages=1167–1169|doi=10.1016/S0140-6736(00)02765-3|issn=0140-6736|pmid=11030302}}</ref><ref>{{Cite journal|last=Reid|first=H. F.|last2=Bassett|first2=D. C.|last3=Poon-King|first3=T.|last4=Zabriskie|first4=J. B.|last5=Read|first5=S. E.|date=1985-02-01|title=Group G streptococci in healthy school-children and in patients with glomerulonephritis in Trinidad|url=http://www.ncbi.nlm.nih.gov/pubmed/3882827|journal=The Journal of Hygiene|volume=94|issue=1|pages=61–68|issn=0022-1724|pmc=2129394|pmid=3882827}}</ref> These immunologic sequelae have previously only been associated with ''[[Streptococcus_pyogenes|Streptococcus pyogenes]]''.
''Streptococcus dysgalactiae subspecies dysgalactiae'' (SDSD) is almost exclusively an animal pathogen. However, a few casuistic reports of human [[zoonotic]] infection have been documented.<ref>{{Cite journal|last=Jordal|first=Stina|last2=Glambek|first2=Marte|last3=Oppegaard|first3=Oddvar|last4=Kittang|first4=Bård Reiakvam|date=2015-02-01|title=New tricks from an old cow: infective endocarditis caused by Streptococcus dysgalactiae subsp. dysgalactiae|url=https://www.ncbi.nlm.nih.gov/pubmed/25472489|journal=Journal of Clinical Microbiology|volume=53|issue=2|pages=731–734|doi=10.1128/JCM.02437-14|issn=1098-660X|pmc=4298539|pmid=25472489}}</ref><ref>{{Cite journal|last=Koh|first=T. H.|last2=Sng|first2=L.-H.|last3=Yuen|first3=S. M.|last4=Thomas|first4=C. K.|last5=Tan|first5=P. L.|last6=Tan|first6=S. H.|last7=Wong|first7=N. S.|date=2009-05-01|title=Streptococcal cellulitis following preparation of fresh raw seafood|url=https://www.ncbi.nlm.nih.gov/pubmed/19309483|journal=Zoonoses and Public Health|volume=56|issue=4|pages=206–208|doi=10.1111/j.1863-2378.2008.01213.x|issn=1863-1959|pmid=19309483}}</ref>
''Streptococcus dysgalactiae subspecies dysgalactiae'' (SDSD) is almost exclusively an animal pathogen. However, a few casuistic reports of human [[zoonotic]] infection have been documented (15, 16).


==Role in animal disease==
==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).
''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.<ref name=":1" />
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_infection|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 (17)(17). Mastitis in other animals has also been documented (18).
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_infection|subclinical mastitis]].<ref name=":0" /> ''S. dysgalactiae'' has been particularly linked to mastitis occurring during the summer time (“Summer mastitis”), and bacterial spreading by flying insects has been suggested.<ref>{{Cite journal|last=Chirico|first=J.|last2=Jonsson|first2=P.|last3=Kjellberg|first3=S.|last4=Thomas|first4=G.|date=1997-04-01|title=Summer mastitis experimentally induced by Hydrotaea irritans exposed to bacteria|url=http://www.ncbi.nlm.nih.gov/pubmed/9226651|journal=Medical and Veterinary Entomology|volume=11|issue=2|pages=187–192|issn=0269-283X|pmid=9226651}}</ref> Mastitis in other animals has also been documented.<ref>{{Cite journal|last=Scott|first=P. R.|date=2000-03-18|title=Extensive fibrinous pleurisy associated with Streptococcus dysgalactiae mastitis in two ewes|url=https://www.ncbi.nlm.nih.gov/pubmed/10777043|journal=The Veterinary Record|volume=146|issue=12|pages=347–349|issn=0042-4900|pmid=10777043}}</ref>
''S.dysgalactiae'' has been isolated from infectious polyarthritis in several animal species, including piglets, lambs, calves and goats.<ref name=":1" /><ref name=":5">{{Cite journal|last=Abdelsalam|first=M.|last2=Eissa|first2=A. E.|last3=Chen|first3=S.-C.|date=2015-03-01|title=Genetic diversity of geographically distinct Streptococcus dysgalactiae isolates from fish|url=https://www.ncbi.nlm.nih.gov/pubmed/25750757|journal=Journal of Advanced Research|volume=6|issue=2|pages=233–238|doi=10.1016/j.jare.2013.12.003|issn=2090-1232|pmc=4348444|pmid=25750757}}</ref> Furthermore, it has been implicated in [[neonatal]] [[Mortality_rate|mortality]] among puppies.<ref>{{Cite journal|last=Vela|first=Ana I.|last2=Falsen|first2=Enevold|last3=Simarro|first3=Isabel|last4=Rollan|first4=Eduardo|last5=Collins|first5=Matthew D.|last6=Domínguez|first6=Lucas|last7=Fernandez-Garayzabal|first7=Jose F.|date=2006-02-01|title=Neonatal mortality in puppies due to bacteremia by Streptococcus dysgalactiae subsp. dysgalactiae|url=https://www.ncbi.nlm.nih.gov/pubmed/16455943|journal=Journal of Clinical Microbiology|volume=44|issue=2|pages=666–668|doi=10.1128/JCM.44.2.666-668.2006|issn=0095-1137|pmc=1392640|pmid=16455943}}</ref>
''S.dysgalactiae'' has been isolated from infectious polyarthritis in several animal species, including piglets, lambs, calves and goats (6, 19). Furthermore, it has been implicated in [[neonatal]] [[Mortality_rate|mortality]] among puppies (20).
Recently, SDSD has been described as an [[emerging_infectious_disease|emerging]] pathogen in fish, causing fulminant necrotic ulcers of the [[Fish_fin#AnchCaudal|caudal peduncle]], with ensuing high mortality rates (21). The clinical presentation is dominated by severe [[sepsis]] and the formation of micro[[abscess]]es, and a relationship between disease severity and the expression of the [[Virulence_factor|virulence factors]] [[Streptolysin]] S and SPEGdys has been inferred (19).
Recently, SDSD has been described as an [[emerging_infectious_disease|emerging]] pathogen in fish, causing fulminant necrotic ulcers of the [[Fish_fin#AnchCaudal|caudal peduncle]], with ensuing high mortality rates.<ref>{{Cite journal|last=Nomoto|first=R.|last2=Munasinghe|first2=L. I.|last3=Jin|first3=D.-H.|last4=Shimahara|first4=Y.|last5=Yasuda|first5=H.|last6=Nakamura|first6=A.|last7=Misawa|first7=N.|last8=Itami|first8=T.|last9=Yoshida|first9=T.|date=2004-12-01|title=Lancefield group C Streptococcus dysgalactiae infection responsible for fish mortalities in Japan|url=https://www.ncbi.nlm.nih.gov/pubmed/15575875|journal=Journal of Fish Diseases|volume=27|issue=12|pages=679–686|doi=10.1111/j.1365-2761.2004.00591.x|issn=0140-7775|pmid=15575875}}</ref> The clinical presentation is dominated by severe [[sepsis]] and the formation of micro[[abscess]]es, and a relationship between disease severity and the expression of the [[Virulence_factor|virulence factors]] [[Streptolysin]] S and SPEGdys has been inferred.<ref name=":5" />


==Treatment and Antimicrobial susceptibility==
==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 (12, 22, 23). [[Aminoglycoside|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 (24). ''Streptococcus dysgalactiae'' is uniformly susceptible to [[Glycopeptide_antibiotic|glycopeptides]] and [[2-Oxazolidone|oxazolidones]].
[[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.<ref name=":4" /><ref>{{Cite journal|last=Lo|first=Hsueh-Hsia|last2=Nien|first2=Hao-Hsiang|last3=Cheng|first3=Ya-Yu|last4=Su|first4=Fang-Yi|date=2015-12-01|title=Antibiotic susceptibility pattern and erythromycin resistance mechanisms in beta-hemolytic group G Streptococcus dysgalactiae subspecies equisimilis isolates from central Taiwan|url=https://www.ncbi.nlm.nih.gov/pubmed/24856419|journal=Journal of Microbiology, Immunology, and Infection = Wei Mian Yu Gan Ran Za Zhi|volume=48|issue=6|pages=613–617|doi=10.1016/j.jmii.2014.04.003|issn=1995-9133|pmid=24856419}}</ref><ref>{{Cite journal|last=de Souza|first=José Paulo|last2=Santos|first2=Amanda Ribeiro|last3=de Paula|first3=Geraldo Renato|last4=Barros|first4=Rosana Rocha|date=2016-09-01|title=Antimicrobial susceptibility and genetic relationships among Streptococcus dysgalactiae subsp. equisimilis isolates in Rio de Janeiro|url=https://www.ncbi.nlm.nih.gov/pubmed/27301015|journal=Infectious Diseases (London, England)|volume=48|issue=9|pages=676–681|doi=10.1080/23744235.2016.1192680|issn=2374-4243|pmid=27301015}}</ref> [[Aminoglycoside|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.<ref>{{Cite journal|last=Baker|first=C. N.|last2=Thornsberry|first2=C.|last3=Facklam|first3=R. R.|date=1981-05-01|title=Synergism, killing kinetics, and antimicrobial susceptibility of group A and B streptococci|url=http://www.ncbi.nlm.nih.gov/pubmed/7027921|journal=Antimicrobial Agents and Chemotherapy|volume=19|issue=5|pages=716–725|issn=0066-4804|pmc=181512|pmid=7027921}}</ref> ''Streptococcus dysgalactiae'' is uniformly susceptible to [[Glycopeptide_antibiotic|glycopeptides]] and [[2-Oxazolidone|oxazolidones]].


==Taxonomy==
==Taxonomy==
Diernhofer first used the name ''Streptococcus dysgalactiae'' in 1932, describing a streptococcus of veterinary origin (25). Subsequently, Frost reported the discovery of the human pathogen ''[[Streptococcus_equisimilis|Streptococcus equisimilis]]'' in 1936 (26). Contemporarily, though, [[Rebecca_Lancefield|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) (27, 28). The correlation of group carbohydrate specificity with the proposed species ''S.dysgalactiae'' and ''S.equisimilis'', however, were not explored in detail. The [[Lancefield_grouping|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 (29).
Diernhofer first used the name ''Streptococcus dysgalactiae'' in 1932, describing a streptococcus of veterinary origin.<ref>{{Cite journal|last=Diernhofer|first=K|year=1932|title=Aesculinbouillon als Hilfsmittel für die Differenzierung von Euter- und Milchstreptokokken bei Massenuntersuchungen|journal=Milchwirtschaftliche Forschung|volume=13|pages=368-374}}</ref> Subsequently, Frost reported the discovery of the human pathogen ''[[Streptococcus_equisimilis|Streptococcus equisimilis]]'' in 1936.<ref>{{Cite book|title=The streptococci|last=Frost|first=W.D.E.|publisher=Willdorf Co|year=1940|isbn=|location=|pages=|via=}}</ref> Contemporarily, though, [[Rebecca_Lancefield|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).<ref>{{Cite journal|last=Lancefield|first=R. C.|date=1933-03-31|title=A SEROLOGICAL DIFFERENTIATION OF HUMAN AND OTHER GROUPS OF HEMOLYTIC STREPTOCOCCI|url=http://www.ncbi.nlm.nih.gov/pubmed/19870148|journal=The Journal of Experimental Medicine|volume=57|issue=4|pages=571–595|issn=0022-1007|pmc=2132252|pmid=19870148}}</ref><ref>{{Cite journal|last=Lancefield|first=R. C.|last2=Hare|first2=R.|date=1935-02-28|title=THE SEROLOGICAL DIFFERENTIATION OF PATHOGENIC AND NON-PATHOGENIC STRAINS OF HEMOLYTIC STREPTOCOCCI FROM PARTURIENT WOMEN|url=http://www.ncbi.nlm.nih.gov/pubmed/19870362|journal=The Journal of Experimental Medicine|volume=61|issue=3|pages=335–349|issn=0022-1007|pmc=2133228|pmid=19870362}}</ref> The correlation of group carbohydrate specificity with the proposed species ''S.dysgalactiae'' and ''S.equisimilis'', however, were not explored in detail. The [[Lancefield_grouping|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.<ref>{{Cite journal|last=Skerman|first=V.B.D.M.|last2=Sneath|first2=P.H.A.|year=1980|title=Approved list of bacterial names|journal=Int J Syst Bacteriol|volume=30|pages=225-420}}</ref>
However, three years later, [[Nucleic_acid_hybridization|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 (30, 31). 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'' (32).<ref name="pmid8782689">{{cite journal |vauthors=Vandamme P, Pot B, Falsen E, Kersters K, Devriese LA |title=Taxonomic study of lancefield streptococcal groups C, G, and L (Streptococcus dysgalactiae) and proposal of S. dysgalactiae subsp. equisimilis subsp. nov |journal=Int. J. Syst. Bacteriol. |volume=46 |issue=3 |pages=774–81 |date=July 1996 |pmid=8782689 |doi= 10.1099/00207713-46-3-774|url=http://ijs.sgmjournals.org/cgi/pmidlookup?view=long&pmid=8782689}}</ref>
However, three years later, [[Nucleic_acid_hybridization|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.<ref>{{Cite journal|last=Garvie|first=E.I.F.|last2=Collins|first2=M.D.|year=1983|title=Streptococcus dysgalactiae (Diernhofer) nom. Rev|journal=Int J Syst Bacteriol|volume=33|pages=404-405}}</ref><ref>{{Cite journal|last=Farrow|first=J.A.E.C.|last2=Collins|first2=M.D.|year=1984|title=Taxonimic studies on streptococci of serological groups C, G and L and possibly related taxa|journal=Syst Appl Microbiol|volume=5|pages=840-842}}</ref> 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''.<ref name="pmid8782689">{{cite journal |vauthors=Vandamme P, Pot B, Falsen E, Kersters K, Devriese LA |title=Taxonomic study of lancefield streptococcal groups C, G, and L (Streptococcus dysgalactiae) and proposal of S. dysgalactiae subsp. equisimilis subsp. nov |journal=Int. J. Syst. Bacteriol. |volume=46 |issue=3 |pages=774–81 |date=July 1996 |pmid=8782689 |doi= 10.1099/00207713-46-3-774|url=http://ijs.sgmjournals.org/cgi/pmidlookup?view=long&pmid=8782689}}</ref>
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 [[Hemolysis_(microbiology)|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 SDSE strains of animal and human origin are genetically divergent, and future taxonomic reclassifications are conceivable (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.<ref name=":2" /> It defines ''S.dysgalactiae subspecies dysgalactiae'' solely as the [[Hemolysis_(microbiology)|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 SDSE strains of animal and human origin are genetically divergent, and future taxonomic reclassifications are conceivable.<ref name=":6">{{Cite journal|last=Jensen|first=Anders|last2=Kilian|first2=Mogens|date=2012-01-01|title=Delineation of Streptococcus dysgalactiae, its subspecies, and its clinical and phylogenetic relationship to Streptococcus pyogenes|url=http://www.ncbi.nlm.nih.gov/pubmed/22075580|journal=Journal of Clinical Microbiology|volume=50|issue=1|pages=113–126|doi=10.1128/JCM.05900-11|issn=1098-660X|pmc=3256718|pmid=22075580}}</ref>


==Laboratory identification==
==Laboratory identification==
''Streptococcus dysgalactiae'' form large colonies (>0.5 cm) after 24 hours of incubation, and produce [[hemolysis_(microbiology)|haemolysis]] on blood agar; SDSD is alpha-haemolytic, whereas SDSE is predominantly beta-haemolytic. They are [[Facultative_anaerobic_organism|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° Celsius. Lancefield group C and G carbohydrate antigens are predominantly expressed, but group A and L have been documented (33). 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 ([[Matrix-assisted_laser_desorption/ionization|MALDI TOF]] MS), [[phenotype|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|Streptococcus anginosus]] group (Lancefield A, C, G or F) can be made by colony size and [[Voges-Proskauer_test|Voges Proskauer test]] (VP); the ''S.anginosus'' group being VP positive. ''Streptococcus equi'' contains Lancefield group C, and ''[[Streptococcus_canis|Streptococcus canis]]'' harbours group G, but unlike ''S.dysgalactiae'', they are both [[Hyaluronidase]] negative (33).
''Streptococcus dysgalactiae'' form large colonies (>0.5 cm) after 24 hours of incubation, and produce [[hemolysis_(microbiology)|haemolysis]] on blood agar; SDSD is alpha-haemolytic, whereas SDSE is predominantly beta-haemolytic. They are [[Facultative_anaerobic_organism|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° Celsius. Lancefield group C and G carbohydrate antigens are predominantly expressed, but group A and L have been documented.<ref name=":6" /> 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 ([[Matrix-assisted_laser_desorption/ionization|MALDI TOF]] MS), [[phenotype|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|Streptococcus anginosus]] group (Lancefield A, C, G or F) can be made by colony size and [[Voges-Proskauer_test|Voges Proskauer test]] (VP); the ''S.anginosus'' group being VP positive. ''Streptococcus equi'' contains Lancefield group C, and ''[[Streptococcus_canis|Streptococcus canis]]'' harbours group G, but unlike ''S.dysgalactiae'', they are both [[Hyaluronidase]] negative.<ref name=":6" />
The identification of ''S.dysgalactiae'' to the subspecies level is most reliably performed by [[Multilocus_sequence_typing|MultiLocus Sequence Typing]] (MLST) (34). MALDI TOF MS does currently not possess taxonomic resolution beyond the species level.
The identification of ''S.dysgalactiae'' to the subspecies level is most reliably performed by [[Multilocus_sequence_typing|MultiLocus Sequence Typing]] (MLST).<ref>{{Cite journal|last=Bishop|first=Cynthia J.|last2=Aanensen|first2=David M.|last3=Jordan|first3=Gregory E.|last4=Kilian|first4=Mogens|last5=Hanage|first5=William P.|last6=Spratt|first6=Brian G.|date=2009-01-01|title=Assigning strains to bacterial species via the internet|url=http://www.ncbi.nlm.nih.gov/pubmed/19171050|journal=BMC biology|volume=7|pages=3|doi=10.1186/1741-7007-7-3|issn=1741-7007|pmc=2636762|pmid=19171050}}</ref> MALDI TOF MS does currently not possess taxonomic resolution beyond the species level.


==Molecular typing==
==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_(Streptococcus)|M-protein]], a major virulence factor in both ''S.pyogenes'' and ''Streptococcus dysgalactiae''. It is ubiquitous in SDSE of human origin, and its hypervariability in the 5’-terminal region forms the basis for categorization into separate ''emm''-types (35). To date, more than 100 SDSE ''emm''-types have been described ([http://www2a.cdc.gov/ncidod/biotech/strepblast.asp CDC Strep Lab]). The prevailing ''emm''-types vary in different geographical regions, and clonal outbreaks have been reported (36). Unlike for ''S.pyogenes'', a correlation between ''emm''-type and disease manifestation or severity has not been established for ''S. dysgalactiae'' (12, 37).
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_(Streptococcus)|M-protein]], a major virulence factor in both ''S.pyogenes'' and ''Streptococcus dysgalactiae''. It is ubiquitous in SDSE of human origin, and its hypervariability in the 5’-terminal region forms the basis for categorization into separate ''emm''-types.<ref>{{Cite journal|last=Beall|first=B.|last2=Facklam|first2=R.|last3=Thompson|first3=T.|date=1996-04-01|title=Sequencing emm-specific PCR products for routine and accurate typing of group A streptococci|url=http://www.ncbi.nlm.nih.gov/pubmed/8815115|journal=Journal of Clinical Microbiology|volume=34|issue=4|pages=953–958|issn=0095-1137|pmc=228924|pmid=8815115}}</ref> To date, more than 100 SDSE ''emm''-types have been described ([http://www2a.cdc.gov/ncidod/biotech/strepblast.asp CDC Strep Lab]). The prevailing ''emm''-types vary in different geographical regions, and clonal outbreaks have been reported.<ref>{{Cite journal|last=Wang|first=Xiaohui|last2=Zhang|first2=Xiaoxia|last3=Zong|first3=Zhiyong|date=2016-01-01|title=Genome sequence and virulence factors of a group G Streptococcus dysgalactiae subsp. equisimilis strain with a new element carrying erm(B)|url=http://www.ncbi.nlm.nih.gov/pubmed/26843282|journal=Scientific Reports|volume=6|pages=20389|doi=10.1038/srep20389|issn=2045-2322|pmc=4740735|pmid=26843282}}</ref> Unlike for ''S.pyogenes'', a correlation between ''emm''-type and disease manifestation or severity has not been established for ''S. dysgalactiae''.<ref name=":4" /><ref name=":7">{{Cite journal|last=Kittang|first=B. R.|last2=Skrede|first2=S.|last3=Langeland|first3=N.|last4=Haanshuus|first4=C. G.|last5=Mylvaganam|first5=H.|date=2011-03-01|title=emm gene diversity, superantigen gene profiles and presence of SlaA among clinical isolates of group A, C and G streptococci from western Norway|url=http://www.ncbi.nlm.nih.gov/pubmed/21103900|journal=European Journal of Clinical Microbiology & Infectious Diseases: Official Publication of the European Society of Clinical Microbiology|volume=30|issue=3|pages=423–433|doi=10.1007/s10096-010-1105-x|issn=1435-4373|pmc=3034890|pmid=21103900}}</ref>
[[Pulsed-field_gel_electrophoresis|Pulsed Field Gel Electrophoresis]] (PFGE) 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 MLST and [[Single-nucleotide_polymorphism|Single Nucleotide Polymorphism-analysis]] (SNP).
[[Pulsed-field_gel_electrophoresis|Pulsed Field Gel Electrophoresis]] (PFGE) 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 MLST and [[Single-nucleotide_polymorphism|Single Nucleotide Polymorphism-analysis]] (SNP).


==Pathogenesis and virulence factors==
==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 [[Homology_(biology)|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 (38). Indeed, whole-genome comparisons reveal a 70% -genetic similarity between the two species, indicating a common genetic ancestry (39). However, evidence of [[horizontal_gene_transfer|horizontal genetic transfer]] has also been reported (40).
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 [[Homology_(biology)|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.<ref name=":8">{{Cite journal|last=Davies|first=Mark R.|last2=McMillan|first2=David J.|last3=Beiko|first3=Robert G.|last4=Barroso|first4=Vanessa|last5=Geffers|first5=Robert|last6=Sriprakash|first6=Kadaba S.|last7=Chhatwal|first7=Gursharan S.|date=2007-06-01|title=Virulence profiling of Streptococcus dysgalactiae subspecies equisimilis isolated from infected humans reveals 2 distinct genetic lineages that do not segregate with their phenotypes or propensity to cause diseases|url=http://www.ncbi.nlm.nih.gov/pubmed/17479940|journal=Clinical Infectious Diseases: An Official Publication of the Infectious Diseases Society of America|volume=44|issue=11|pages=1442–1454|doi=10.1086/516780|issn=1537-6591|pmid=17479940}}</ref> Indeed, whole-genome comparisons reveal a 70% -genetic similarity between the two species, indicating a common genetic ancestry.<ref>{{Cite journal|last=Shimomura|first=Yumi|last2=Okumura|first2=Kayo|last3=Murayama|first3=Somay Yamagata|last4=Yagi|first4=Junji|last5=Ubukata|first5=Kimiko|last6=Kirikae|first6=Teruo|last7=Miyoshi-Akiyama|first7=Tohru|date=2011-01-01|title=Complete genome sequencing and analysis of a Lancefield group G Streptococcus dysgalactiae subsp. equisimilis strain causing streptococcal toxic shock syndrome (STSS)|url=http://www.ncbi.nlm.nih.gov/pubmed/21223537|journal=BMC genomics|volume=12|pages=17|doi=10.1186/1471-2164-12-17|issn=1471-2164|pmc=3027156|pmid=21223537}}</ref> However, evidence of [[horizontal_gene_transfer|horizontal genetic transfer]] has also been reported.<ref>{{Cite journal|last=McNeilly|first=Celia L.|last2=McMillan|first2=David J.|date=2014-01-01|title=Horizontal gene transfer and recombination in Streptococcus dysgalactiae subsp. equisimilis|url=http://www.ncbi.nlm.nih.gov/pubmed/25566202|journal=Frontiers in Microbiology|volume=5|pages=676|doi=10.3389/fmicb.2014.00676|issn=1664-302X|pmc=4266089|pmid=25566202}}</ref>
The first pivotal step in infectious [[pathogenesis]] is the attachment to the host tissues. The M-protein, the most extensively studied SDSE virulence factor, has been documented to facilitate both adherence to and [[Endocytosis|internalization]] into host cells.<ref name="Brandt2009" /><ref>{{Cite journal|last=Bisno|first=A. L.|last2=Craven|first2=D. E.|last3=McCabe|first3=W. R.|date=1987-03-01|title=M proteins of group G streptococci isolated from bacteremic human infections|url=http://www.ncbi.nlm.nih.gov/pubmed/3102380|journal=Infection and Immunity|volume=55|issue=3|pages=753–757|issn=0019-9567|pmc=260406|pmid=3102380}}</ref> Other adhesins have also been described, including the genes ''gfba'', ''fnB'', ''fbBA'', ''fnBB'', ''lmb'' and ''gapC''; all mediating binding to [[fibronectin]].<ref>{{Cite journal|last=Kline|first=J. B.|last2=Xu|first2=S.|last3=Bisno|first3=A. L.|last4=Collins|first4=C. M.|date=1996-06-01|title=Identification of a fibronectin-binding protein (GfbA) in pathogenic group G streptococci|url=http://www.ncbi.nlm.nih.gov/pubmed/8675316|journal=Infection and Immunity|volume=64|issue=6|pages=2122–2129|issn=0019-9567|pmc=174045|pmid=8675316}}</ref><ref>{{Cite journal|last=Lindgren|first=P. E.|last2=McGavin|first2=M. J.|last3=Signäs|first3=C.|last4=Guss|first4=B.|last5=Gurusiddappa|first5=S.|last6=Höök|first6=M.|last7=Lindberg|first7=M.|date=1993-06-15|title=Two different genes coding for fibronectin-binding proteins from Streptococcus dysgalactiae. The complete nucleotide sequences and characterization of the binding domains|url=http://www.ncbi.nlm.nih.gov/pubmed/8319691|journal=European journal of biochemistry / FEBS|volume=214|issue=3|pages=819–827|issn=0014-2956|pmid=8319691}}</ref><ref>{{Cite journal|last=Lindgren|first=P. E.|last2=Signäs|first2=C.|last3=Rantamäki|first3=L.|last4=Lindberg|first4=M.|date=1994-08-01|title=A fibronectin-binding protein from Streptococcus equisimilis: characterization of the gene and identification of the binding domain|url=http://www.ncbi.nlm.nih.gov/pubmed/7975149|journal=Veterinary Microbiology|volume=41|issue=3|pages=235–247|issn=0378-1135|pmid=7975149}}</ref><ref>{{Cite journal|last=Lo|first=Hsueh-Hsia|last2=Cheng|first2=Wei-Shan|date=2015-01-01|title=Distribution of virulence factors and association with emm polymorphism or isolation site among beta-hemolytic group G Streptococcus dysgalactiae subspecies equisimilis|url=http://www.ncbi.nlm.nih.gov/pubmed/25244428|journal=APMIS: acta pathologica, microbiologica, et immunologica Scandinavica|volume=123|issue=1|pages=45–52|doi=10.1111/apm.12305|issn=1600-0463|pmid=25244428}}</ref> ''gfba'' was recently shown contribute to bacterial internalization into [[endothelial]] cells and intracellular persistence.<ref>{{Cite journal|last=Rohde|first=Manfred|last2=Talay|first2=Susanne R.|last3=Rasmussen|first3=Magnus|date=2012-04-01|title=Molecular mechanisms of Streptococcus dysgalactiae subsp equisimilis enabling intravascular persistence|url=http://www.ncbi.nlm.nih.gov/pubmed/22100875|journal=Microbes and Infection / Institut Pasteur|volume=14|issue=4|pages=329–334|doi=10.1016/j.micinf.2011.10.008|issn=1769-714X|pmid=22100875}}</ref><ref>{{Cite journal|last=Gherardi|first=Giovanni|last2=Imperi|first2=Monica|last3=Palmieri|first3=Claudio|last4=Magi|first4=Gloria|last5=Facinelli|first5=Bruna|last6=Baldassarri|first6=Lucilla|last7=Pataracchia|first7=Marco|last8=Creti|first8=Roberta|date=2014-01-01|title=Genetic diversity and virulence properties of Streptococcus dysgalactiae subsp. equisimilis from different sources|url=http://www.ncbi.nlm.nih.gov/pubmed/24149625|journal=Journal of Medical Microbiology|volume=63|issue=Pt 1|pages=90–98|doi=10.1099/jmm.0.062109-0|issn=1473-5644|pmid=24149625}}</ref> These properties may explain the tendency of recurrent bacteraemia observed in human SDSE-cases.
The first pivotal step in infectious [[pathogenesis]] is the attachment to the host tissues. The M-protein, the most extensively studied SDSE virulence factor, has been documented to facilitate both adherence to and [[Endocytosis|internalization]] into host cells (1, 41). Other adhesins have also been described, including the genes ''gfba'', ''fnB'', ''fbBA'', ''fnBB'', ''lmb'' and ''gapC''; all mediating binding to [[fibronectin]] (42-45). ''gfba'' was recently shown contribute to bacterial internalization into [[endothelial]] cells and intracellular persistence (46, 47). These properties may explain the tendency of recurrent bacteraemia observed in human SDSE-cases.
In order to establish infection, the bacteria need to escape the host [[immune_system|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|complement system]] (1). Furthermore, ''Streptococcus dysgalactiae'' possesses [[Protein_G|Protein G]], a virulence factor binding circulating [[immunoglobulin]]s, and thus interfering with the host [[antibody]] response (48). DrsG, a virulence protein abrogating the effect of [[Antimicrobial_peptides|antimicrobial peptides]] secreted by human immune cells, is also harboured by a subset of SDSE-strains (49, 50).
In order to establish infection, the bacteria need to escape the host [[immune_system|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|complement system]].<ref name="Brandt2009" /> Furthermore, ''Streptococcus dysgalactiae'' possesses [[Protein_G|Protein G]], a virulence factor binding circulating [[immunoglobulin]]s, and thus interfering with the host [[antibody]] response.<ref>{{Cite journal|last=Sjöbring|first=U.|last2=Björck|first2=L.|last3=Kastern|first3=W.|date=1991-01-05|title=Streptococcal protein G. Gene structure and protein binding properties|url=http://www.ncbi.nlm.nih.gov/pubmed/1985908|journal=The Journal of Biological Chemistry|volume=266|issue=1|pages=399–405|issn=0021-9258|pmid=1985908}}</ref> DrsG, a virulence protein abrogating the effect of [[Antimicrobial_peptides|antimicrobial peptides]] secreted by human immune cells, is also harboured by a subset of SDSE-strains.<ref>{{Cite journal|last=Smyth|first=Danielle|last2=Cameron|first2=Ainslie|last3=Davies|first3=Mark R.|last4=McNeilly|first4=Celia|last5=Hafner|first5=Louise|last6=Sriprakash|first6=Kadaba S.|last7=McMillan|first7=David J.|date=2014-06-01|title=DrsG from Streptococcus dysgalactiae subsp. equisimilis inhibits the antimicrobial peptide LL-37|url=http://www.ncbi.nlm.nih.gov/pubmed/24664506|journal=Infection and Immunity|volume=82|issue=6|pages=2337–2344|doi=10.1128/IAI.01411-13|issn=1098-5522|pmc=4019180|pmid=24664506}}</ref><ref>{{Cite journal|last=Oppegaard|first=O.|last2=Mylvaganam|first2=H.|last3=Skrede|first3=S.|last4=Langeland|first4=N.|last5=Kittang|first5=B. R.|date=2014-02-01|title=Sequence diversity of sicG among group C and G Streptococcus dysgalactiae subspecies equisimilis isolates associated with human infections in western Norway|url=http://www.ncbi.nlm.nih.gov/pubmed/24019161|journal=European Journal of Clinical Microbiology & Infectious Diseases: Official Publication of the European Society of Clinical Microbiology|volume=33|issue=2|pages=273–277|doi=10.1007/s10096-013-1955-0|issn=1435-4373|pmid=24019161}}</ref>
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 (51). ''speGdys'', a homolog of the ''S.pyogenes'' [[superantigen]] ''speG'', has been documented in some ''S.dysgalactiae'' strains (37, 52). However, it only appears to possess superantigen-capabilities in animals, and its relevance in human disease has yet to be elucidated (53). [[Streptokinase]] appears to be ubiquitous in ''S.dysgalactiae'', enabling [[fibrinolysis]] and aiding in bacterial spreading through tissues (1, 38).
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.<ref>{{Cite journal|last=Watanabe|first=Shinya|last2=Shimomura|first2=Yumi|last3=Ubukata|first3=Kimiko|last4=Kirikae|first4=Teruo|last5=Miyoshi-Akiyama|first5=Tohru|date=2013-11-01|title=Concomitant regulation of host tissue-destroying virulence factors and carbohydrate metabolism during invasive diseases induced by group g streptococci|url=http://www.ncbi.nlm.nih.gov/pubmed/23901096|journal=The Journal of Infectious Diseases|volume=208|issue=9|pages=1482–1493|doi=10.1093/infdis/jit353|issn=1537-6613|pmid=23901096}}</ref> ''speGdys'', a homolog of the ''S.pyogenes'' [[superantigen]] ''speG'', has been documented in some ''S.dysgalactiae'' strains.<ref name=":7" /><ref>{{Cite journal|last=Sachse|first=Svea|last2=Seidel|first2=Peter|last3=Gerlach|first3=Dieter|last4=Günther|first4=Elisabeth|last5=Rödel|first5=Jürgen|last6=Straube|first6=Eberhard|last7=Schmidt|first7=Karl-Hermann|date=2002-10-11|title=Superantigen-like gene(s) in human pathogenic Streptococcus dysgalactiae, subsp equisimilis: genomic localisation of the gene encoding streptococcal pyrogenic exotoxin G (speG(dys))|url=http://www.ncbi.nlm.nih.gov/pubmed/12381468|journal=FEMS immunology and medical microbiology|volume=34|issue=2|pages=159–167|issn=0928-8244|pmid=12381468}}</ref> However, it only appears to possess superantigen-capabilities in animals, and its relevance in human disease has yet to be elucidated.<ref>{{Cite journal|last=Zhao|first=Jizi|last2=Hayashi|first2=Tomohito|last3=Saarinen|first3=Susanna|last4=Papageorgiou|first4=Anastassios C.|last5=Kato|first5=Hidehito|last6=Imanishi|first6=Ken'ichi|last7=Kirikae|first7=Teruo|last8=Abe|first8=Ryo|last9=Uchiyama|first9=Takehiko|date=2007-04-01|title=Cloning, expression, and characterization of the superantigen streptococcal pyrogenic exotoxin G from Streptococcus dysgalactiae|url=http://www.ncbi.nlm.nih.gov/pubmed/17283088|journal=Infection and Immunity|volume=75|issue=4|pages=1721–1729|doi=10.1128/IAI.01183-06|issn=0019-9567|pmc=1865666|pmid=17283088}}</ref> [[Streptokinase]] appears to be ubiquitous in ''S.dysgalactiae'', enabling [[fibrinolysis]] and aiding in bacterial spreading through tissues<ref name="Brandt2009" /><ref name=":8" />.
Recently, a capacity to form [[biofilm]] was reported, facilitating survival and proliferation in hostile environments (54). Although this potentially could have implications for the treatment of ''S.dysgalactiae''-infections, its clinical significance has not yet been determined.
Recently, a capacity to form [[biofilm]] was reported, facilitating survival and proliferation in hostile environments.<ref>{{Cite journal|last=Genteluci|first=Gabrielle Limeira|last2=Silva|first2=Ligia Guedes|last3=Souza|first3=Maria Clara|last4=Glatthardt|first4=Thaís|last5=de Mattos|first5=Marcos Corrêa|last6=Ejzemberg|first6=Regina|last7=Alviano|first7=Celuta Sales|last8=Figueiredo|first8=Agnes Marie Sá|last9=Ferreira-Carvalho|first9=Bernadete Teixeira|date=2015-12-01|title=Assessment and characterization of biofilm formation among human isolates of Streptococcus dysgalactiae subsp. equisimilis|url=http://www.ncbi.nlm.nih.gov/pubmed/26558847|journal=International journal of medical microbiology: IJMM|volume=305|issue=8|pages=937–947|doi=10.1016/j.ijmm.2015.10.004|issn=1618-0607|pmid=26558847}}</ref> Although this potentially could have implications for the treatment of ''S.dysgalactiae''-infections, its clinical significance has not yet been determined.




Revision as of 13:00, 27 September 2016

Streptococcus dysgalactiae
Scientific classification
Kingdom:
Bacteria
Phylum:
Firmicutes
Class:
Bacilli
Order:
Lactobacillales
Family:
Streptococcaceae
Genus:
Streptococcus
Species:
S. dysgalactiae

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] Streptococcus dysgalactiae is currently divided into the subspecies Streptococcus dysgalactiae subspecies equisimilis (SDSE) and Streptococcus dysgalactiae subspecies dysgalactiae (SDSD); 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 (SDSE) 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 SDSE 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 (Oppegaard et al: In press). Less commonly it can present as pneumonia, endocarditis, genital or intraabdominal infections. Primary bacteraemia, infection without identifiable focal origin, comprises approximately 20% of the reported cases.[1][2][12] Recently, SDSE has been linked to post-streptococcal glomerulonephritis and acute rheumatic fever.[13][14] These immunologic sequelae have previously only been associated with Streptococcus pyogenes. Streptococcus dysgalactiae subspecies dysgalactiae (SDSD) is almost exclusively an animal pathogen. However, a few casuistic reports of human zoonotic infection have been documented.[15][16]

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.[17] Mastitis in other animals has also been documented.[18] S.dysgalactiae has been isolated from infectious polyarthritis in several animal species, including piglets, lambs, calves and goats.[6][19] Furthermore, it has been implicated in neonatal mortality among puppies.[20] Recently, SDSD has been described as an emerging pathogen in fish, causing fulminant necrotic ulcers of the caudal peduncle, with ensuing high mortality rates.[21] 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.[19]

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.[12][22][23] 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.[24] 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.[25] Subsequently, Frost reported the discovery of the human pathogen Streptococcus equisimilis in 1936.[26] 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).[27][28] 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.[29] However, three years later, 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.[30][31] 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.[32] 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 SDSE strains of animal and human origin are genetically divergent, and future taxonomic reclassifications are conceivable.[33]

Laboratory identification

Streptococcus dysgalactiae form large colonies (>0.5 cm) after 24 hours of incubation, and produce haemolysis on blood agar; SDSD is alpha-haemolytic, whereas SDSE 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° Celsius. Lancefield group C and G carbohydrate antigens are predominantly expressed, but group A and L have been documented.[33] 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.[33] The identification of S.dysgalactiae to the subspecies level is most reliably performed by MultiLocus Sequence Typing (MLST).[34] 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 SDSE of human origin, and its hypervariability in the 5’-terminal region forms the basis for categorization into separate emm-types.[35] To date, more than 100 SDSE emm-types have been described (CDC Strep Lab). The prevailing emm-types vary in different geographical regions, and clonal outbreaks have been reported.[36] Unlike for S.pyogenes, a correlation between emm-type and disease manifestation or severity has not been established for S. dysgalactiae.[12][37] Pulsed Field Gel Electrophoresis (PFGE) 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 MLST and Single Nucleotide Polymorphism-analysis (SNP).

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.[38] Indeed, whole-genome comparisons reveal a 70% -genetic similarity between the two species, indicating a common genetic ancestry.[39] However, evidence of horizontal genetic transfer has also been reported.[40] The first pivotal step in infectious pathogenesis is the attachment to the host tissues. The M-protein, the most extensively studied SDSE virulence factor, has been documented to facilitate both adherence to and internalization into host cells.[1][41] Other adhesins have also been described, including the genes gfba, fnB, fbBA, fnBB, lmb and gapC; all mediating binding to fibronectin.[42][43][44][45] gfba was recently shown contribute to bacterial internalization into endothelial cells and intracellular persistence.[46][47] These properties may explain the tendency of recurrent bacteraemia observed in human SDSE-cases. 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.[48] DrsG, a virulence protein abrogating the effect of antimicrobial peptides secreted by human immune cells, is also harboured by a subset of SDSE-strains.[49][50] 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.[51] speGdys, a homolog of the S.pyogenes superantigen speG, has been documented in some S.dysgalactiae strains.[37][52] However, it only appears to possess superantigen-capabilities in animals, and its relevance in human disease has yet to be elucidated.[53] Streptokinase appears to be ubiquitous in S.dysgalactiae, enabling fibrinolysis and aiding in bacterial spreading through tissues[1][38]. Recently, a capacity to form biofilm was reported, facilitating survival and proliferation in hostile environments.[54] Although this potentially could have implications for the treatment of S.dysgalactiae-infections, its clinical significance has not yet been determined.




References

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