{{Short description|Species of bacterium}} {{Speciesbox | image = Streptococcus agalactiae.tif | image_caption = | taxon = Streptococcus agalactiae | authority = Lehmann and Neumann, 1896 }}
'''''Streptococcus agalactiae''''' (also known as '''group B streptococcus''' or '''GBS''') is a gram-positive coccus (round bacterium) with a tendency to form chains (as reflected by the genus name ''Streptococcus''). It is a beta-hemolytic, catalase-negative, and facultative anaerobe.<ref name=whiley2009>{{cite book|vauthors=Whiley RA, Hardie JM|title=Genus I. Streptococcus Rosenbach 1884. Bergey's Manual of Systematic Bacteriology: Vol 3: The Firmicutes|date=2009|publisher=Springer|isbn=978-0-387-95041-9|pages=655–711|edition=2nd}}</ref><ref name=Sherris>{{cite book | veditors = Ryan KJ, Ray CG | display-editors = etal | title = Sherris Medical Microbiology | url = https://archive.org/details/sherrismedicalmi00ryan | url-access = limited | edition = 4th | publisher = McGraw Hill | year = 2004 | isbn = 978-0-8385-8529-0 | pages=[https://archive.org/details/sherrismedicalmi00ryan/page/n303 286]–8}}</ref>
''S. agalactiae'' is the most common human pathogen of streptococci belonging to group B of the Rebecca Lancefield classification of streptococci. GBS are surrounded by a bacterial capsule composed of polysaccharides (exopolysaccharide). The species is subclassified into ten serotypes (Ia, Ib, II–IX) depending on the immunologic reactivity of their polysaccharide capsule.<ref name="whiley2009"/><ref name=Edwards-Nizet2011>{{cite book|vauthors=Edwards MS, Nizet V|title=Group B streptococcal infections. Infectious Diseases of the Fetus and Newborn Infant|date=2011|publisher=Elsevier|isbn=978-0-443-06839-3|pages=419–469|edition=7th}}</ref><ref name=Slotved>{{cite journal|vauthors=Slotved HC, Kong F, Lambertsen L, Sauer S, Gilbert GL|title=Serotype IX, a proposed new Streptococcus agalactiae serotype|journal=J Clin Microbiol|date=2007|volume=45|issue=9|pages=2929–2936|doi=10.1128/jcm.00117-07|pmid=17634306|pmc=2045254}}</ref>
The plural term '''group B streptococci''' (referring to the serotypes) and the singular term '''group B streptococcus''' (referring to the single species) are both commonly used synonymously with ''S. agalactiae'' even though ''S. halichoeri'' and ''S. pseudoporcinus'' are also group B Streptococci. These species test positive as group B, but are not frequently carried by humans, and only rarely cause disease.<ref>{{Cite web|date=July 23, 2021|title=Guidelines for the Detection and Identification of Group B Streptococcus|url=https://asm.org/ASM/media/Protocol-Images/ASM-GBS-guideline.pdf?ext=.pdf|website=The American Society for Microbiology}}</ref>
In general, GBS is a harmless commensal bacterium being part of the human microbiota colonizing the gastrointestinal and genitourinary tract of up to 30% of healthy human adults (asymptomatic carriers). Nevertheless, GBS can cause severe invasive infections especially in newborns, the elderly, and people with compromised immune systems.<ref name="Edwards-Baker-Mandell" />thumb|β-hemolytic colonies of ''Streptococcus agalactiae'', blood agar 18h at 36°C
''S. agalactiae'' is also a common veterinary pathogen, because it can cause bovine mastitis (inflammation of the udder) in dairy cows. The species name ''agalactiae'' meaning "of no milk", alludes to this.<ref name="Keefe1997" />
thumb|''Streptococcus agalactiae'' on granada agar, anaerobic incubation thumb|Granadaene thumb|200px|right|Positive CAMP test indicated by the formation of an arrowhead where ''Streptococcus agalactiae'' meets the ''Staphylococcus aureus'' (white middle streak) thumb|Gram stain of ''Streptococcus agalactiae''.
==Laboratory identification== GBS grows readily on blood agar plates as colonies surrounded by a narrow zone of β-hemolysis. GBS is characterized by the presence in the cell wall of the antigen group B of Lancefield classification (Lancefield grouping) that can be detected directly in intact bacteria using latex agglutination tests.<ref name=Tille2014>{{cite book|author=Tille P.|title=Bailey & Scott's Diagnostic Microbiology|date=2014|publisher=Elsevier|isbn=978-0-323-08330-0|edition=13th}}</ref><ref name="Rosa-Fraile 2017" /> The CAMP test is also another important test for identification of GBS. The CAMP factor produced by GBS acts synergistically with the staphylococcal β-hemolysin inducing enhanced hemolysis of sheep or bovine erythrocytes.<ref name="Tille2014"/> GBS is also able to hydrolyze hippurate and this test can also be used to identify presumptively GBS.<ref name=Tille2014 /> Hemolytic GBS strains produce an orange-brick-red non-isoprenoid polyene (ornithine rhamnolipid) pigment (granadaene)<ref name="Granadaene">{{cite journal |last1=Rosa-Fraile M, Rodríguez-Granger J, Haidour-Benamin A, Cuerva JM, Sampedro A |title=Granadaene: Proposed Structure of the Group B Streptococcus Polyenic Pigment |journal=Applied and Environmental Microbiology |date=2006 |volume=72 |issue=9 |pages=6367–6370 |doi=10.1128/AEM.00756-06 |pmid=16957264 |pmc=1563658 |bibcode=2006ApEnM..72.6367R }}</ref> when cultivated on granada medium that allows its straightforward identification.<ref name=Rosa1999>{{cite journal|vauthors=Rosa-Fraile M, Rodriguez-Granger J, Cueto-Lopez M, Sampedro A, Biel Gaye E, Haro M, Andreu A|title=Use of Granada medium to detect group B streptococcal colonization in pregnant women|journal=J Clin Microbiol|date=1999|volume=37|issue=8|pages=2674–2677|doi=10.1128/JCM.37.8.2674-2677.1999|pmid=10405420|pmc=85311|doi-access=free}}</ref> GBS can also be identified using MALDI-TOF (Matrix Assisted Laser Desorption/Ionization-Time of Flight) instruments.<ref name="To KN">{{cite journal |vauthors=To KN, Cornwell E, Daniel R, Goonesekera S, Jauneikaite E, Chalker V, Le Doare K |title=Evaluation of matrix-assisted laser desorption ionisation time-of-flight mass spectrometry (MALDI-TOF MS) for the Identification of Group B Streptococcus. |journal=BMC Res. Notes |date=2019 |volume=12 |issue=1 |page=85 |doi=10.1186/s13104-019-4119-1 |pmid=30764872 |pmc=6376729 |doi-access=free }}</ref> GBS colonies can additionally be identified tentatively after their appearance in chromogenic agar media, nevertheless GBS-like colonies that develop in chromogenic media should be confirmed as GBS using additional reliable tests (e.g.latex agglutination or the CAMP test) to avoid potential mis-identification.<ref name="Rosa-Fraile 2017" /><ref name="El Aila">{{cite journal |vauthors=El Aila NA, Tency I, Claeys G, Saerens B, Cools P, Verstraelen H, Temmerman M, Verhelst R, Vaneechoutte M |title=Comparison of different sampling techniques and of different culture methods for detection of group B streptococcus carriage in pregnant women |journal=BMC Infectious Diseases |date=2010 |volume=10 |page=285 |doi=10.1186/1471-2334-10-285 |pmid=20920213 |pmc=2956727 |doi-access=free }}</ref><ref name="ASM Guidelines 2020">{{cite web |last1=Filkins L, Hauser J, Robinson-Dunn Tibbetts R, Boyanton B, Revell P. |title=Guidelines for the Detection and Identification of Group B Streptococcus. March 10, 2020 |url=https://asm.org/ASM/media/Policy-and-Advocacy/images/ASM-GBS-guideline-031020.pdf?ext=.pdf |website=American Society for Microbiology |access-date=7 January 2021 |archive-date=27 June 2021 |archive-url=https://web.archive.org/web/20210627062706/https://asm.org/ASM/media/Policy-and-Advocacy/images/ASM-GBS-guideline-031020.pdf?ext=.pdf }}</ref> A summary of the laboratory techniques for GBS identification is depicted in Ref 7. <ref name="Rosa-Fraile 2017">{{cite journal|vauthors=Rosa-Fraile M, Spellerberg B |title=Reliable Detection of Group B Streptococcus in the Clinical Laboratory|journal=J Clin Microbiol|date=2017|volume=55|issue=9|pages=2590–2598|doi=10.1128/JCM.00582-17|pmid=28659318|pmc=5648696}}</ref>
== GBS colonization== GBS is a normal component of the intestinal and vaginal microbiota in some people; GBS is an asymptomatic (presenting no symptoms) colonizer of the gastrointestinal tract and vagina in up to 30% of otherwise healthy adults, including pregnant women.<ref name=Edwards-Nizet2011 /><ref name="Barcaite 2008">{{cite journal|vauthors=Barcaite E, Bartusevicius A, Tameliene R, Kliucinskas M, Maleckiene L, Nadisauskiene R|title=Prevalence of maternal group B streptococcal colonization in European countries|journal=Acta Obstet Gynecol Scand|date=2008|volume=87|issue=3|pages=260–271|doi=10.1080/00016340801908759|pmid=18307064|s2cid=25897076}}</ref> GBS colonization may be permanent, intermittent or temporary. In different studies, GBS vaginal colonization rate ranges from 0% to 36%, most studies reporting colonization rates in sexually active women over 20%.<ref name="Pignanelli 2015">{{cite journal|vauthors=Pignanelli S, Pulcrano G, Schiavone P, Di Santo A, Zaccherini P|title=Selectivity evaluation of a new chromogenic medium to detect group B Streptococcus|journal=Indian J Pathol Microbiol|date=2015|volume=58|issue=1|pages=45–7|doi=10.4103/0377-4929.151186|pmid=25673591|doi-access=free}}</ref> It has been estimated that maternal GBS colonization worldwide is 18%, with regional variation from 11% to 35%.<ref name="Russell 2017 Col Rate">{{cite journal|vauthors=Russell NJ, Seale AC, O'Driscoll M, O'Sullivan C, Bianchi-Jassir F, Gonzalez-Guarin J, Lawn JE, Baker CJ, Bartlett L, Cutland C, Gravett MG, Heath PT, Le Doare K, Madhi SA, Rubens CE, Schrag S, Sobanjo-Ter Meulen A, Vekemans J, Saha SK, Ip M |title=Maternal Colonization With Group B Streptococcus and Serotype Distribution Worldwide: Systematic Review and Meta-analyses|journal=Clinical Infectious Diseases|date=2017|volume=65|issue=Suppl 2|pages=S100–S111|doi=10.1093/cid/cix658|pmid=29117327|pmc=5848259}}</ref> These variations in the reported prevalence of asymptomatic GBS colonization could be related to the detection methods used, and differences in populations sampled.<ref name="Barcaite 2008" /><ref name=Rodriguez-Granger2012 />
== Virulence== As other virulent bacteria, GBS harbors an important number of virulence factors (virulence factors are molecules produced by bacteria that enhances their capacity to infect and damage human tissues), the most important being the capsular polysaccharide (rich in sialic acid)<ref name="Edwards-Nizet2011" /><ref name=Rajagopal2009>{{cite journal|author=Rajagopal L|title=Understanding the regulation of Group B Streptococcal virulence factors|journal=Future Microbiol|date=2009|volume=4|issue=2|pages=201–221|doi=10.2217/17460913.4.2.201|pmid=19257847|pmc=2691590}}</ref> and a pore-forming toxin, β-hemolysin.<ref name="Rajagopal2009" /><ref name="Armistead Oler 2019">{{cite journal |last1=Armistead B, Oler E, Adams Waldorf K, Rajagopal |title=The Double Life of Group B Streptococcus: Asymptomatic Colonizer and Potent Pathogen» |journal=J. Mol. Biol. |date=2019 |volume=431 |issue=16 |pages=2914–2931 |doi=10.1016/j.jmb.2019.01.035 |pmid=30711542 |pmc=6646060 }}</ref><ref name="Armistead Whidbey 2020">{{cite journal |last1=Armistead B, Whidbey C, Iyer LM, Herrero-Foncubierta P, Quach P, Haidour A, Aravind L, Cuerva JM, Jaspan HB and Rajagopal L |title=The cyl Genes Reveal the Biosynthetic and Evolutionary Origins of the Group B Streptococcus Hemolytic Lipid, Granadaene. |journal=Front. Microbiol. |date=2020 |volume=10 |page=3123 |doi=10.3389/fmicb.2019.03123 |pmid=32038561 |pmc=6985545 |doi-access=free }}</ref> Today it is considered that GBS pigment (granadaene) and hemolysin are identical or closely related molecules.<ref name=Rosa-Fraile2014>{{cite journal|vauthors=Rosa-Fraile M, Dramsi S, Spellerberg B|title=Group B streptococcal haemolysin and pigment, a tale of twins|journal=FEMS Microbiol. Rev.|date=2014|volume=38|issue=5|pages=932–946|url= |doi=10.1111/1574-6976.12071|pmid=24617549|pmc=4315905}}</ref><ref name="Whidbey 2013">{{cite journal|vauthors=Whidbey C, Harrell MI, Burnside K, Ngo L, Becraft AK, Iyer LM, Aravind L, Hitti J, Waldorf KM, Rajagopal L|title=A hemolytic pigment of Group B Streptococcus allows bacterial penetration of human placenta|journal=J Exp Med |date=2013|volume=210|issue=6|pages=1265–1281|doi=10.1084/jem.20122753|pmid=23712433|pmc=3674703}}</ref><ref name="Whidbey 2015">{{cite journal|vauthors=Whidbey C, Vornhagen J, Gendrin C, Boldenow E, Samson JM, Doering K, Ngo L, Ezekwe EA Jr, Gundlach JH, Elovitz MA, Liggitt D, Duncan JA, Adams Waldorf KM, Rajagopal L|title=A streptococcal lipid toxin induces membrane permeabilization and pyroptosis leading to fetal injury|journal=EMBO Mol. Med.|date=2015|volume=7|issue=4|pages=488–505|doi=10.15252/emmm.201404883|pmid=25750210|pmc=4403049}}</ref><ref name="Leclercq 2016">{{cite journal|vauthors=Leclercq SY, Sullivan MJ, Ipe DS, Smith JP, Cripps AW, Ulett GC|title=Pathogenesis of Streptococcus urinary tract infection depends on bacterial strain and β-hemolysin/cytolysin that mediates cytotoxicity, cytokine synthesis, inflammation and virulence|journal=Sci. Rep.|date=2016 |doi=10.1038/srep29000|pmid=27383371|pmc=4935997|volume=6|article-number=29000|bibcode=2016NatSR...629000L}}</ref>
Sialic acid is a notable virulence factor in ''S. agalactiae'' despite being found normally in humans and many other animals. By expressing an unusually high amount of sialic acid on the bacterial cell surface, ''S. agalactiae'' can subvert the innate immune system, convincing leukocytes that the bacteria are human cells.<ref>{{Cite journal |last1=Landwehr-Kenzel |first1=Sybille |last2=Henneke |first2=Philipp |date=2014-10-29 |title=Interaction of Streptococcus agalactiae and Cellular Innate Immunity in Colonization and Disease |journal=Frontiers in Immunology |volume=5 |page=519 |doi=10.3389/fimmu.2014.00519 |doi-access=free |issn=1664-3224 |pmc=4212683 |pmid=25400631}}</ref><ref>{{Cite journal |last1=Severi |first1=Emmanuele |last2=Hood |first2=Derek W. |last3=Thomas |first3=Gavin H. |date=2007-09-01 |title=Sialic acid utilization by bacterial pathogens |journal=Microbiology |volume=153 |issue=9 |pages=2817–2822 |doi=10.1099/mic.0.2007/009480-0 |doi-access=free |pmid=17768226 |issn=1350-0872}}</ref>
==GBS infection in newborns== {{Main|Group B streptococcal infection}}
GBS colonization of the vagina usually does not cause problems in healthy women, nevertheless during pregnancy it can sometimes cause serious illness for the mother and the newborn. GBS is the leading cause of bacterial neonatal infection in the baby during gestation and after delivery with significant mortality rates in premature infants. GBS infections in the mother can cause chorioamnionitis (a severe infection of the placental tissues) infrequently, postpartum infections (after birth) and it had been related with prematurity and fetal death.<ref name="Muller 2006">{{cite journal |vauthors=Muller AE, Oostvogel PM, Steegers EA, Dörr PJ |title=Morbidity related to maternal group B streptococcal infections |journal=Acta Obstet Gynecol Scand |date=2006 |volume=85 |issue=9 |pages=1027–1037 |doi=10.1080/00016340600780508|pmid=16929406 |s2cid=11745321 |doi-access=free }}</ref> GBS urinary tract infections (UTI) may also induce labor and cause premature delivery.<ref name="Edwards-Nizet2011" /> In the western world, GBS (in the absence of effective prevention measures) is the major cause of several bacterial infections of the newborn neonatal infection sepsis, pneumonia, and meningitis, which can lead to death or long-term sequelae.<ref name="Edwards-Nizet2011" /> GBS neonatal infection typically originates in the lower reproductive tract of infected mothers. GBS infections in newborns are separated into two clinical syndromes, early-onset disease (EOD) and late-onset disease (LOD).<ref name="Puopolo 2019">{{cite journal |last1=Puopolo KM, Lynfield R, Cummings JJ, AAP COMMITTEE ON FETUS AND NEWBORN, AAP COMMITTEE ON INFECTIOUS DISEASES. |title=Management of Infants at Risk for Group B Streptococcal Disease. |journal=Pediatrics |date=2019 |volume=144 |issue=2 |pages=e20191881 |doi=10.1542/peds.2019-1881 |pmid=31285392 |s2cid=195843897 |url=https://pediatrics.aappublications.org/content/pediatrics/144/2/e20191881.full.pdf |access-date=7 January 2021|doi-access=free }}</ref> EOD manifests from 0 to 7 living days in the newborn, most of the cases of EOD being apparent within 24h of birth.<ref name="Edwards-Nizet2011" /><ref name=Verani2010>{{cite journal|vauthors=Verani JR, McGee L, Schrag SJ|title=Prevention of perinatal group B streptococcal disease: revised guidelines from CDC, 2010|journal=MMWR Recomm Rep|date=2010|volume=59(RR-10)|pages=1–32|url=https://www.cdc.gov/mmwr/pdf/rr/rr5910.pdf}}</ref><ref name="ACOG">{{cite journal |last1=ACOG. The American College of Obstetricians and Gynecologists |title=Prevention of Group B Streptococcal Early-Onset Disease in Newborns: ACOG Committee Opinion, Number 782 |journal=Obstetrics & Gynecology |date=2019 |volume=134 |issue=1 |pages=e19–e40 |doi=10.1097/AOG.0000000000003334 |pmid=31241599 |s2cid=195659363 |doi-access=free }}</ref> The most common clinical syndromes of EOD are sepsis without apparent focus, pneumonia, and less frequently meningitis. EOD is acquired vertically (vertical transmission), through exposure of the fetus or the baby to GBS from the vagina of a colonized woman, either intrautero or during birth after rupture of membranes. Infants can be infected during passage through the birth canal, nevertheless newborns that acquire GBS through this route can become only colonized, and these colonized infants habitually do not develop EOD. Roughly 50% of newborns to GBS colonized mothers are also GBS colonized and (without prevention measures) 1–2% of these newborns will develop EOD.<ref name=Boyer1985>{{cite book|vauthors=Boyer KM, Gotoff SP|title=Neonatal Group B Streptococcal Infections |chapter=Strategies for Chemoprophylaxis of GBS Early-Onset Infections|date=1985|volume=35|pages=267–280|doi=10.1159/000410380|pmid=3931544|series=Antibiotics and Chemotherapy|isbn=978-3-8055-3953-1}}</ref>
In the past, the incidence of EOD ranged from 0.7 to 3.7 per thousand live births in the US<ref name="Edwards-Nizet2011" /> and from 0.2 to 3.25 per thousand in Europe.<ref name=Rodriguez-Granger2012>{{cite journal|vauthors=Rodriguez-Granger J, Alvargonzalez JC, Berardi A, Berner R, Kunze M, Hufnagel M, Melin P, Decheva A, Orefici G, Poyart C, Telford J, Efstratiou A, Killian M, Krizova P, Baldassarri L, Spellerberg B, Puertas A, Rosa-Fraile M|title=Prevention of group B streptococcal neonatal disease revisited. The DEVANI European project|journal=Eur J Clin Microbiol Infect Dis|date=2012|volume=31|issue=9|pages=2097–2114|doi=10.1007/s10096-012-1559-0|pmid=22314410|s2cid=15588906|hdl=11380/1168706|hdl-access=free}}</ref> In 2008, after widespread use of antenatal screening and intrapartum antibiotic prophylaxis (IAP), the CDC reported an incidence of 0.28 cases of EOD per thousand live births in the US.<ref name=CDC2014>{{cite web|last1=CDC|title=Group B Strep (GBS)-Clinical Overview|url=https://www.cdc.gov/groupbstrep/clinicians/clinical-overview.html|access-date=27 Oct 2015}}</ref> Multistate surveillance 2006-2015 shows a decline in EOD from 0.37 to 0.23 per 1000 live births in the US but LOD remains steady at 0.31 per 1000 live births.<ref name="Nanduri">{{cite journal |last1=Nanduri SA, Petit S, Smelser C, Apostol M, Alden NB, Harrison LH, Lynfield R, Vagnone PS, Burzlaff K, Spina NL, Dufort EM, Schaffner W, Thomas AR, Farley MM, Jain JH, Pondo T, McGee L, Beall BW, Schrag SJ. |title=Epidemiology of Invasive Early-Onset and Late-Onset Group B Streptococcal Disease in the United States, 2006 to 2015: Multistate Laboratory and Population-Based Surveillance |journal=JAMA Pediatr. |date=2019 |volume=173 |issue=3 |pages=224–233 |doi=10.1001/jamapediatrics.2018.4826 |pmid=30640366 |pmc=6439883 |doi-access=free }}</ref> In 2021 had been estimated a total of 1970 deaths ((0.59/100,000 population) in the US caused by GBS neonatal infections. It was estimated that 226 infants (49 per 100,000) in the United States had a clinically significant GBS infection, and that approximately 11 (2.4%) of those cases resulted in death.<ref name="ABCS 2021">{{cite web |last1=Centers for Disease Control and Prevention |title=Active Bacterial Core Surveillance Report, Emerging Infections Program Network, Group B Streptococcus, 2021 |url=https://www.cdc.gov/abcs/downloads/GBS_Surveillance_Report_2021.pdf |access-date=14 July 2024}}</ref>
It has been indicated that where there was a policy of providing IAP for GBS colonized mothers the overall risk of EOGBS is 0.3%.<ref name="Russell 2017">{{cite journal|vauthors=Russell NJ, Seale AC, O'Sullivan C, Le Doare K, Heath PT, Lawn JE, Bartlett L, Cutland C, Gravett M, Ip M, Madhi SA, Rubens CE, Saha SK, Schrag S, Sobanjo-Ter Meulen A, Vekemans J, Baker CJ |title=Risk of Early-Onset Neonatal Group B Streptococcal Disease With Maternal Colonization Worldwide: Systematic Review and Meta-analyses|journal=Clin Infect Dis|date=2017|volume=65, Suppl 2|issue=suppl_2|pages=S152–S159|doi=10.1093/cid/cix655|pmid=29117325|pmc=5850448}}</ref>
Though maternal GBS colonization is the key determinant for EOD, other factors also increase the risk. These factors include onset of labor before 37 weeks of gestation (premature birth), prolonged rupture of membranes (≥18h before delivery), intra-partum fever (>38 °C, >100.4 °F), amniotic infections (chorioamnionitis), young maternal age, and low levels of GBS anticapsular polysaccharide antibodies in the mother.<ref name="Edwards-Nizet2011" /><ref name="Verani2010" /><ref name="ACOG" /> Nevertheless, most babies who develop EOD are born to GBS colonized mothers without any additional risk factor.<ref name="Verani2010" /><ref name="ACOG" /> A previous sibling with EOD is also an important risk factor for development of the infection in subsequent deliveries, probably reflecting a lack of GBS polysaccharides protective antibodies in the mother. Heavy GBS vaginal colonization is also associated with a higher risk for EOD.<ref name=Verani2010 /> Overall, the case–fatality rates from EOD have declined, from 50% observed in studies from the 1970s to 2 to 10% in recent years, mainly as a consequence of improvements in therapy and management. Fatal neonatal infections by GBS are more frequent among premature infants.<ref name="Edwards-Nizet2011"/><ref name="Verani2010"/><ref name="ACOG" /><ref name=Edmond2012>{{cite journal|vauthors=Edmond KM, Kortsalioudaki C, Scott S, Schrag SJ, Zaidi AK, Cousens S, Heath PT|title=Group B streptococcal disease in infants aged younger than 3 months: systematic review and meta-analysis|journal=Lancet|date=2012|volume=379|issue=9815|pages=547–556|url=http://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(11)61651-6.pdf|doi=10.1016/s0140-6736(11)61651-6|pmid=22226047|s2cid=15438484}}</ref>
GBS LOD affects infants from 7 days to 3 months of age and is more likely to cause bacteremia or meningitis. LOD can be acquired from the mother or from environmental sources. Hearing loss and mental impairment can be a long-term sequela of GBS meningitis.<ref name="Edwards-Nizet2011" /><ref name=Libster2012>{{cite journal|last1=Libster|first1=R|last2=Edwards|first2=KM|last3=Levent|first3=F|last4=Edwards|first4=MS|last5=Rench|first5=MA|last6=Castagnini|first6=LA|last7=Cooper|first7=T|last8=Sparks|first8=RC|last9=Baker|first9=CJ|last10=Shah|first10=PE|title=Long-term outcomes of group B streptococcal meningitis|journal=Pediatrics|date=July 2012|volume=130|issue=1|pages=e8–15|doi=10.1542/peds.2011-3453|pmid=22689869|s2cid=1013682}}</ref><ref name="Kohli 2017">{{cite journal|vauthors=Kohli-Lynch M, Russell NJ, Seale AC, Dangor Z, Tann CJ, Baker CJ, Bartlett L, Cutland C, Gravett MG, Heath PT, Ip M, Le Doare K, Madhi SA, Rubens CE, Saha SK, Schrag S, Sobanjo-Ter Meulen A, Vekemans J, O'Sullivan C, Nakwa F, Ben Hamouda H, Soua H, Giorgakoudi K, Ladhani S, Lamagni T, Rattue H, Trotter C, Lawn JE |title=Neurodevelopmental Impairment in Children After Group B Streptococcal Disease Worldwide: Systematic Review and Meta-analyses|journal=Clinical Infectious Diseases|date=2017|volume=65|issue=Suppl. 2|pages=S190–S199|doi=10.1093/cid/cix663|pmid=29117331|pmc=5848372}}</ref> In contrast with EOD, the incidence of LOD has remained unchanged at 0.26 per 1000 live births in the US.<ref name=Baker2013vaccine>{{cite journal|author=Baker CJ|title=The spectrum of perinatal group B streptococcal disease|journal=Vaccine|date=2013|volume=31 |issue=Suppl 4|doi=10.1016/j.vaccine.2013.02.030|pages=D3–D6|pmid=23973344}}</ref> ''S. agalactiae'' neonatal meningitis does not present with the hallmark sign of adult meningitis, a stiff neck; rather, it presents with nonspecific symptoms, such as fever, vomiting and irritability, and can consequently lead to a late diagnosis.<ref name=Sherris/>
== Prevention of neonatal infection == The only reliable way to prevent EOD currently is intrapartum antibiotic prophylaxis (IAP), that is to say administration of antibiotics during delivery. It has been proved that intravenous penicillin or ampicillin administered for at least 4 hours before delivery to GBS colonized women is very effective at preventing vertical transmission of GBS from mother to baby and EOD. Intravenous penicillin remains the agent of choice for IAP, with intravenous ampicillin as an acceptable alternative.<ref name="Edwards-Nizet2011" /><ref name="Verani2010" /><ref name="ACOG" /> For penicillin allergic women, the laboratory requisitions for ordering antepartum GBS screening cultures should indicate clearly the presence of penicillin allergy.<ref name="ACOG" />
Cefazolin, clindamycin, and vancomycin are used to prevent EOD in infants born to penicillin-allergic mothers.<ref name="Verani2010" /><ref name="ACOG"/> Intravenous vancomycin is recommended for IAP in women colonized with a clindamycin-resistant Group B Streptococcus strain and a severe penicillin allergy.<ref name="Puopolo 2019" /><ref name="ACOG" /> There are two ways to identify female candidates to receive intrapartum antibiotic prophylaxis: a risk-based approach or a culture-based screening approach. The culture-based screening approach identifies candidates to receive IAP using lower vaginal and rectal cultures obtained between 36 and 37 weeks' gestation<ref name="Verani2010" /><ref name="ACOG" /> (32–34 weeks of gestation for women with twins<ref name="RCOG 2017" />) and IAP is administered to all GBS colonized women. The risk-based strategy identifies candidates to receive IAP by the aforementioned risk factors known to increase the probability of EOD without considering if the mother is or is not a GBS carrier.<ref name="Edwards-Nizet2011" /><ref name=Cliford2011>{{cite journal|vauthors=Clifford V, Garland SM, Grimwood K|title=Prevention of neonatal group B streptococcus disease in the 21st century|journal=J Paediatr Child Health|date=2011|volume=48|issue=9|pages=808–815|doi=10.1111/j.1440-1754.2011.02203.x|pmid=22151082|s2cid=36906520}}</ref>
IAP is also recommended for women with intrapartum risk factors if their GBS carrier status is not known at the time of delivery, for women with GBS bacteriuria during their pregnancy, and for women who have had an infant with EOD previously.{{citation needed|date=February 2023}}
The risk-based approach for IAP is in general less effective than the culture-based approach because in most of the cases EOD develops among newborns, which are born to mothers without risk factors.<ref name="Rodriguez-Granger2012" />
In 2010, the Centers for Disease Control and Prevention (CDC), in collaboration with several professional groups, issued its revised GBS prevention guidelines.<ref name="Verani2010" />
In 2018, the task of revising and updating the GBS prophylaxis guidelines was transferred from the CDC <ref name="CDC 2019">{{cite web |last1=CDC |title=Prevention Guidelines. 2019 Guidelines Update. |url=https://www.cdc.gov/groupbstrep/guidelines/index.html |access-date=4 March 2021}}</ref> to American College of Obstetricians and Gynecologists (ACOG), the American Academy of Pediatrics, and to the American Society for Microbiology.<ref name="ASM Guidelines 2020" /><ref name="Puopolo 2019" /><ref name="ACOG" />
The ACOG committee issued an update document on Prevention of Group B Streptococcal Early-Onset Disease in Newborns in 2019.<ref name="ACOG" /> This document does not introduce important changes from the CDC guidelines. The key measures necessary for preventing neonatal GBS early onset disease continue to be universal prenatal screening by culture of GBS from swabs collected from the lower vagina and rectum, correct collection and microbiological processing of the samples, and proper implementation of intrapartum antibiotic prophylaxis. The ACOG now recommends performing universal GBS screening between 36 and 37 weeks of gestation. This new recommendation provides a five-week window <ref name="Yancey">{{cite journal |vauthors=Yancey MK, Schuchat A, Brown LK, Ventura VL, Markenson GR |title=The accuracy of late antenatal screening cultures in predicting genital group B streptococcal colonization at delivery |journal= Obstetrics & Gynecology|date=1996 |volume=88 |issue=5 |pages=811–815 |doi=10.1016/0029-7844(96)00320-1|pmid=8885919 }}</ref> for valid culture results that includes births that occur up to a gestational age of at least 41 weeks.
The culture-based screening approach is followed in most developed countries<ref name="Le Doare 2017">{{cite journal|vauthors=Le Doare K, O'Driscoll M, Turner K, Seedat F, Russell NJ, Seale AC, Heath PT, Lawn JE, Baker CJ, Bartlett L, Cutland C, Gravett MG, Ip M, Madhi SA, Rubens CE, Saha SK, Schrag S, Sobanjo-Ter Meulen A, Vekemans J, Kampmann B |collaboration=GBS Intrapartum Antibiotic Investigator Group|title=Intrapartum Antibiotic Chemoprophylaxis Policies for the Prevention of Group B Streptococcal Disease Worldwide: Systematic Review|journal=Clin Infect Dis|date=2017|volume=65|issue=Suppl.2|pages=S143–S151|doi=10.1093/cid/cix654|pmid=29117324|pmc=5850619}}</ref> such as the United States,<ref name="Puopolo 2019" /><ref name="Verani2010" /><ref name="ACOG" /> France,<ref name="France">{{cite web|last1=Agence Nationale d'Accreditation et d'Evaluation en Santé.|title=Prévention anténatale du risque infectieux bactérien néonatal précoce. 2001|url=https://www.has-sante.fr//portail/upload/docs/application/pdf/prevention_antenatale_du_risque_infectieux_bacterien_-_rec.pdf|access-date=22 December 2017}}</ref> Spain,<ref name="Rec España">{{cite journal |vauthors=Alós Cortés JI, Andreu Domingo A, Arribas Mir L, Cabero Roura L, Cueto Lopez M, López Sastre J, Melchor Marcos JC, Puertas Prieto A, de la Rosa Fraile M, Salcedo Abizanda S, Sánchez Luna M, Sánchez Pérez MJ, Torrejón Cardoso R |title=Prevención de la infección perinatal por estreptococo del grupo B. Recomendaciones españolas revisadas 2012 |journal=Rev Esp Quimioter |date=2012 |volume=25 |issue=1 |pages=79–88 |pmid=22488547 |url=https://seq.es/seq/0214-3429/25/1/alos.pdf |access-date=1 December 2019}}</ref> Belgium,<ref name="Belgium">{{cite web|last1=Belgian Health Council|title=PREVENTION OF PERINATAL GROUP B STREPTOCOCCAL INFECTIONS. Guidelines from the Belgian Health Council, 2003|url=https://orbi.ulg.ac.be/bitstream/2268/8652/1/GBS_CSH%20english%202003.pdf|access-date=22 December 2017}}</ref> Canada, Argentina,<ref name="Argentina">{{cite web|last1=Ministerio de Salud de la Nación. Dirección Nacional de Salud Materno Infantil. Argentina|title=Recomendaciones para la prevención, diagnóstico y tratamiento de la infección neonatal precoz por Estreptococo β Hemolítico del Grupo B (EGB)|url=http://www.ms.gba.gov.ar/sitios/tocoginecologia/files/2014/09/Consenso-Estreptococo-B-Hemol%C3%ADtico.pdf|access-date=2 December 2019}}</ref> and Australia. The risk-based strategy is followed in the United Kingdom,<ref name="RCOG 2017">{{cite journal|vauthors=Huges RG, Brocklehurst P, Steer PJ, Heath P, Stenson BM |publisher=Royal College of Obstetricians and Gynaecologists |title=Prevention of Early-onset Neonatal Group B Streptococcal Disease Green-top Guideline No. 36 September 2017|journal=BJOG|date=2017|volume=124|issue=12|pages=e280–e305|doi=10.1111/1471-0528.14821|pmid=28901693|doi-access=free}}</ref><ref name="GBS UK">{{cite web |last1=RCOG and GBSS UK |title=Group B Streptococcus (GBS) in pregnancy and newborn babies |url=https://www.rcog.org.uk/globalassets/documents/patients/patient-information-leaflets/pregnancy/pi-gbs-pregnancy-newborn-booklet.pdf |access-date=7 January 2021}}</ref> and the Netherlands.<ref name="Rodriguez-Granger2012" /><ref name="Trijbels">{{cite journal |last1=M Trijbels-Smeulders, G A de Jonge, P C M Pasker-de Jong, L J Gerards, A H Adriaanse, R A vanLingen, L A A Kolle´e |title=Epidemiology of neonatal group B streptococcal disease in theNetherlands before and after introduction of guidelines for prevention |journal=Archives of Disease in Childhood - Fetal and Neonatal Edition |date=2007 |volume=92 |issue=4 |pages=F271–F276 |doi=10.1136/adc.2005.088799|pmid=17227807 |pmc=2675425 }}</ref>
=== Screening for GBS colonization === Though the GBS colonization status of women can change during pregnancy, cultures to detect GBS carried out ≤5 weeks before delivery predict quite accurately the GBS carrier status at delivery.{{citation needed|date=February 2023}}
In contrast, if the prenatal culture is performed more than five weeks before delivery it is unreliable for predicting accurately the GBS carrier status at delivery.<ref name="Verani2010" /><ref name="ACOG" /><ref name="Yancey" /><ref name=Valkenburg2010>{{cite journal|vauthors=Valkenburg-van den Berg AW, Houtman-Roelofsen RL, Oostvogel PM, Dekker FW, Dorr PJ, Sprij AJ|title=Timing of group B streptococcus screening in pregnancy: a systematic review|journal= Gynecologic and Obstetric Investigation |date=2010|volume=69|issue=3|pages=174–183 |url=https://karger.com/goi/article-abstract/69/3/174/149395/Timing-of-Group-B-Streptococcus-Screening-in |doi=10.1159/000265942|pmid=20016190|s2cid=26709882|url-access=subscription}}</ref><ref name="Virranniemi 2019">{{cite journal |vauthors=Virranniemi M, Raudaskoski T, Haapsamo M, Kauppila J, Renko M, Peltola J, Risteli L, Laatio L |title=The effect of screening-to-labor interval on the sensitivity of late-pregnancy culture in the prediction of group B streptococcus colonization at labor: A prospective multicenter cohort study |journal=Acta Obstetricia et Gynecologica Scandinavica |date=2019 |volume=98 |issue=4 |pages=494–499 |doi=10.1111/aogs.13522 |pmid=30578547 |s2cid=58106301 |doi-access=free }}</ref>
The clinical specimens recommended for culture of GBS at 36–37 weeks' gestation, this recommendation provides a 5-week window for valid culture results that includes births that occur up to a gestational age of at least 41 weeks <ref name="ACOG" /> (32–34 weeks of gestation for women with twins<ref name="RCOG 2017" />) are swabs collected the lower vagina (near the introitus) and then from the rectum (through the anal sphincter) without use of a speculum.<ref name="Verani2010" /><ref name="ACOG" /> Vaginal-rectal samples should be collected using a flocked swab preferably, since flocked swabs releases samples and microorganisms more effectively than fiber swabs.<ref name="ASM Guidelines 2020" />
Following the recommendations of the Centers for Disease Control and Prevention of United States (CDC) these swabs should be placed into a non-nutritive transport medium and later inoculated into a selective enrichment broth, Todd Hewitt broth with selective antibiotics (enrichment culture).<ref name="Verani2010" /> After incubation the enrichment broth is subcultured to blood agar plates and GBS like colonies are identified by the CAMP test or using latex agglutination with GBS antisera. After incubation the enrichment broth can also be subcultured to granada medium agar <ref name="Rosa1999" /> where GBS grows as pink-red colonies or to chromogenic agars, where GBS grows as colored colonies.<ref name="Rosa-Fraile 2017" /><ref name="Verani2010" /> GBS-like colonies that develop in chromogenic media should be confirmed as GBS using additional reliable tests to avoid mis-identification.<ref name="Rosa-Fraile 2017" />
Nucleic acid amplification tests (NAAT) such as polymerase chain reaction (PCR) and DNA hybridization probes have been developed for identifying GBS directly from recto-vaginal samples, but they have a high false negative rate, and still cannot replace antenatal culture for the most accurate detection of GBS carriers. This technology to detect GBS must be improved and simplified to make the method cost-effective and useful as a point-of-care test. Nevertheless These tests can also be used to detect GBS directly from broth media, after the enrichment step, avoiding the subculture of the incubated enrichment broth to an appropriate agar plate.<ref name="ASM Guidelines 2020" />
thumb|Red colonies of ''S.agalactiae'' in granada agar. Vagino-rectal culture 18h incubation 36°C anaerobiosis thumb|''Streptococcus agalactiae'' colonies in chromogenic medium (ChromID CPS chromogenic agar)
=== Vaccination === Though IAP for EOD prevention is associated with a large decline in the incidence of the disease, there is, however, no effective strategy for preventing late-onset neonatal GBS disease.<ref name=Jordan2008>{{cite journal|vauthors=Jordan HT, Farley MM, Craig A, Mohle-Boetani J, Harrison LH, Petit S, Lynfield R, Thomas A, Zansky S, Gershman K, Albanese BA, Schaffner W, Schrag SJ|title=Revisiting the need for vaccine prevention of late-onset neonatal group B streptococcal disease: a multistate, population-based analysis|journal=Pediatr Infect Dis J|date=2008|volume=27|issue=12|pages=1057–1064|doi=10.1097/inf.0b013e318180b3b9|pmid=18989238|s2cid=1533957|url=https://zenodo.org/record/1234885}}</ref>
Vaccination is considered an ideal solution to prevent not only EOD and LOD but also GBS infections in adults at risk.<ref name="Edwards-Rench 2016">{{cite journal|vauthors=Edwards MS, Rench MA, Rinaudo CD, Fabbrini M, Tuscano G, Buffi G, Bartolini E, Bonacci S, Baker CJ, Margarit I |title=Immune Responses to Invasive Group B Streptococcal Disease in Adults|journal=Emerg Infect Dis|date=2016|volume=22|issue=11|pages=1877–1883|doi=10.3201/eid2211.160914|pmid=27767008|pmc=5088039}}</ref> Nevertheless, though research and clinical trials for the development of an effective vaccine to prevent GBS infections are underway, no vaccine was available in 2023.<ref name="Heath 2016" /><ref name="Davies, Carreras 2019">{{cite journal |vauthors=Davies HG, Carreras-Abad C, Le Doare K, Heath PT |title=Group B Streptococcus: Trials and Tribulations |journal=Pediatr Infect Dis J |date=2019 |volume=38 |issue=6S Suppl 1 |pages=S72–S76 |doi=10.1097/INF.0000000000002328|pmid=31205250 |url=http://openaccess.sgul.ac.uk/111031/6/Trials%20and%20tribulations%20Revised.pdf |doi-access=free }}</ref><ref name="Carreras-Abad 2020">{{cite journal |last1=Carreras-Abad C, Ramkhelawon L, Heath PT, Le Doare K. |title=A Vaccine Against Group B Streptococcus: Recent Advances. |journal=Infect Drug Resist |date=2020 |volume=13 |pages=1263–1272 |doi=10.2147/IDR.S203454 |pmid=32425562 |pmc=7196769 |doi-access=free }}</ref><ref name ="Mahdi 2023">{{cite journal | vauthors = Madhi SA | title = Potential for Maternally Administered Vaccines for Infant Group B Streptococcus. | journal = New England Journal of Medicine | volume = 389 | issue = 3 | pages = 215–227 | date = June 2023|doi=10.1056/NEJMoa2116045| pmid = 37467497 | s2cid = 259995252 | doi-access = free | hdl = 2263/94684 | hdl-access = free }}</ref> The capsular polysaccharide of GBS is not only an important GBS virulence factor but it is also an excellent candidate for the development of an effective vaccine.<ref name="Rodriguez-Granger2012" /><ref name=Baker2014>{{cite journal|vauthors=Baker CJ, Carey VJ, Rench MA, Edwards MS, Hillier SH, Kasper DL, Platt R|title=Maternal Antibody at Delivery Protects Neonates From Early Onset Group B Streptococcal Disease|journal=J Infect Dis|date=2014|volume=209|issue=5|pages=781–788|url= |doi=10.1093/infdis/jit549|pmid=24133184|pmc=3923540}}</ref><ref name=Edwards-Gonik2013>{{cite journal|vauthors=Edwards MS, Gonik B|title=Preventing the broad spectrum of perinatal morbidity and mortality through group B streptococcal vaccination|journal=Vaccine|date=2013|volume=31S|pages=D66–71|doi=10.1016/j.vaccine.2012.11.046|pmid=23200934}}</ref><ref name="MadhiCutland2016">{{cite journal|last1=Madhi|first1=Shabir A|last2=Cutland|first2=Clare L|last3=Jose|first3=Lisa|last4=Koen|first4=Anthonet|last5=Govender|first5=Niresha|last6=Wittke|first6=Frederick|last7=Olugbosi|first7=Morounfolu|last8=Meulen|first8=Ajoke Sobanjo-ter|last9=Baker|first9=Sherryl|last10=Dull|first10=Peter M|last11=Narasimhan|first11=Vas|last12=Slobod|first12=Karen|title=Safety and immunogenicity of an investigational maternal trivalent group B streptococcus vaccine in healthy women and their infants: a randomised phase 1b/2 trial|journal=The Lancet Infectious Diseases|volume=16|issue=8|year=2016|pages=923–934|issn=1473-3099|doi=10.1016/S1473-3099(16)00152-3|pmid=27139805}}</ref> Protein-based vaccines are also in development.<ref name="Heath 2016">{{cite journal|author=Heath PT|title=Status of vaccine research and development of vaccines for GBS|journal=Vaccine|date=2016|volume=34|issue=26|pages=2876–2879|doi=10.1016/j.vaccine.2015.12.072|pmid=26988258|doi-access=free}}</ref><ref name="Song 2018 Vaccine">{{cite journal |vauthors=Song JY, Lim JH, Lim S, Yong Z, Seo HS |title=Progress toward a group B streptococcal vaccine |journal=Hum Vaccin Immunother |date=2018 |volume=14 |issue=11 |pages=2669–2681 |pmc=6314413 |pmid=29995578 |doi=10.1080/21645515.2018.1493326 }}</ref><ref name="Carreras-Abad 2020" /><ref name="Dominguez 2022">{{cite journal |last1=Dominguez K, Randis TM. |title=Toward the development of a protein-based group B Streptococcus vaccine. |journal=Cell Rep Med. |date=2022 |volume=3 |issue=2 |article-number=10.1016/j.xcrm.2022.100536 |doi=10.1016/j.xcrm.2022.100536 |pmid=35243427 |pmc=8861943 }}</ref>
== GBS infection in adults == GBS is also an important infectious agent able to cause invasive infections in adults. Serious life-threatening invasive GBS infections are increasingly recognized in the elderly and individuals compromised by underlying diseases such as diabetes, cirrhosis and cancer.<ref name="Graux 2020">{{cite journal |author=Elena Graux, Maya Hites, Delphine Martiny, Evelyne Maillart, Marc Delforge, Pierrette Melin, Nicolas Dauby. |title=Invasive group B Streptococcus among non-pregnant adults in Brussels-Capital Region, 2005-2019 |journal=Eur J Clin Microbiol Infect Dis |date=2021 |volume=40 |issue=3 |pages=515-523 |doi=10.1007/s10096-020-04041-0 |pmid=32944894 |pmc=7498195 |doi-access=free }}</ref> GBS infections in adults include urinary tract infection, skin and soft-tissue infection (skin and skin structure infection) bacteremia, osteomyelitis, meningitis and endocarditis.<ref name="Edwards-Baker-Mandell">{{cite book|vauthors=Edwards MS, Baker CJ |chapter=Streptococcus agalactiae (group B streptococcus) |veditors=Mandell GL, Bennett JE, Dolin R |title=Principles and practice of infectious diseases|date=2010|publisher=Elsevier|isbn=978-0-443-06839-3|pages=Cap. 202|edition=7th.}}</ref> GBS infection in adults can be serious and related with high mortality. In general penicillin is the antibiotic of choice for treatment of GBS infection.<ref name=Edwards-Baker2005>{{cite journal|author=Edwards MS|author2=. Baker CJ|title=Group B streptococcal infections in elderly adults|journal=Clin Infect Dis|date=2005|volume=41|issue=6|pages=839–847|doi=10.1086/432804|pmid=16107984|doi-access=free}}</ref><ref name="Farley 2001">{{cite journal|author=Farley MM|title=Group B Streptococcal Disease in Nonpregnant Adults|journal=Clinical Infectious Diseases|date=2001|volume=33|issue=4|pages=556–561|doi=10.1086/322696|pmid=11462195|doi-access=free}}</ref> Gentamicin (for synergy with penicillin G or ampicillin) can also be used in patients with life-threatening invasive GBS.<ref name="Edwards-Baker2005" />
== Non-human infections == ''Streptococcus agalactiae'' was historically studied as a disease of cattle that harmed milk production, leading to its name "agalactiae" which means "absence of milk". Strains of bovine and human bacteria are generally interchangeable, with evidence of transmission from animals to humans and vice versa.<ref name=":0">{{cite journal | doi=10.1099/mgen.0.000648 | title=The fall and rise of group B Streptococcus in dairy cattle: Reintroduction due to human-to-cattle host jumps? | date=2021 | last1=Crestani | first1=Chiara | last2=Forde | first2=Taya L. | last3=Lycett | first3=Samantha J. | last4=Holmes | first4=Mark A. | last5=Fasth | first5=Charlotta | last6=Persson-Waller | first6=Karin | last7=Zadoks | first7=Ruth N. | journal=Microbial Genomics | volume=7 | issue=9 | doi-access=free | pmid=34486971 | pmc=8715428 }}</ref>
=== Cattle === GBS is a major cause of mastitis (an infection of the udder) in dairy cattle and an important source of economic loss for the industry. GBS in cows can either produce an acute febrile disease or a subacute more chronic condition. Both lead to diminishing milk production (hence its name: agalactiae meaning "of no milk").<ref name="Ruegg Mastitis">{{cite journal |last1=Ruegg PL. |title=A 100-Year Review: Mastitis detection, management, and prevention |journal=J. Dairy Sci. |date=2017 |volume=100 |issue=10381–10397 |pages=10381–10397 |doi=10.3168/jds.2017-13023 |pmid=29153171 |url=https://www.journalofdairyscience.org/article/S0022-0302(17)31032-9/pdf |access-date=22 November 2019|doi-access=free }}</ref> Outbreaks in herds are common, so this is of major importance for the dairy industry, and programs to reduce the impact of ''S. agalactiae'' disease have been enforced in many countries over the last 40 years.<ref name="Keefe1997">{{cite journal|author=Keefe GP|title=Streptococcus agalactiae mastitis: a review|journal=Can Vet J|date=1997|volume=38|issue=7|pages=199–204|pmc=1576741|pmid=9220132}}</ref><ref name=":0" />
=== Other animals === GBS also causes severe epidemics in farmed fish, causing sepsis and external and internal hemorrhages, having been reported from wild and captive fish involved in epizootics in many countries.<ref name=Evans2009>{{cite journal|vauthors=Evans JJ, Klesius PH, Pasnik DJ, Bohnsack JF|title=Human Streptococcus agalactiae isolate in Nile tilapia (Oreochromis niloticus)|journal=Emerg Infect Dis|date=2009|volume=15|issue=5|pages=774–776|doi=10.3201/eid1505.080222|pmid=19402966|pmc=2687030}}</ref><ref name=LiuG2013>{{cite journal|vauthors=Liu G, Zhang W, Lu C|title=Comparative genomics analysis of Streptococcus|date=2013|volume=14|page=775|pmc=3831827|pmid=24215651|doi=10.1186/1471-2164-14-775|journal=BMC Genomics |doi-access=free }}</ref> Vaccination is an effective method to prevent pathogenic diseases in aquaculture and different kinds vaccines to prevent GBS infections have been developed recently.<ref name="Liu 2016">{{cite journal|vauthors=Liu G, Zhu J, Chen K, Gao T, Yao H, Liu Y, Zhang W, Lu C |title=Development of Streptococcus agalactiae vaccines for tilapia|journal=Dis Aquat Org|date=2016|volume=122|issue=2|pages=163–170|doi=10.3354/dao03084|pmid=28000606|doi-access=free}}</ref>
GBS has also been found in many other animals, such as camels, dogs, cats, crocodiles, seals, elephants and dolphins.<ref name=Delannoy2013>{{cite journal|vauthors=((Delannoy CMJ)), Crumlish M, Fontaine MC, Pollock J, Foster G, Dagleish MP, Turnbull JF, Zadoks RN|title=Human Streptococcus agalactiae strains in aquatic mammal and fish|journal=BMC Microbiology|date=2013|volume=13|page=41|doi=10.1186/1471-2180-13-41|pmid=23419028|pmc=3585737 |doi-access=free }}</ref><ref name="Eisemberg 2017">{{cite journal|vauthors=Eisenberg T, Rau J, Westerhüs U, Knauf-Witzens T, Fawzy A, Schlez K, Zschöck M, Prenger-Berninghoff E, Heydel C, Sting R, Glaeser SP, Pulami D, van der Linden M, Ewers C |title=Streptococcus agalactiae in elephants. A comparative study with isolates from human and zoo animal and livestock origin|journal=Vet. Microbiol.|date=2017|volume=204|pages=141–150|doi=10.1016/j.vetmic.2017.04.018|pmid=28532793}}</ref>
== References == {{Reflist|30em}}
==External links== * [https://www.cdc.gov/groupbstrep/index.html CDC—Group B Strep (GBS)] * [http://www.gbss.org.uk/ Group B Strep Support UK] *[http://bacdive.dsmz.de/index.php?search=14712&submit=Search Type strain of ''Streptococcus agalactiae'' at Bac''Dive'' - the Bacterial Diversity Metadatabase]
{{Gram-positive bacterial diseases}}
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{{DEFAULTSORT:Streptococcus Agalactiae}} agalactiae Category:Obstetrics Category:Gram-positive bacteria Category:Health issues in pregnancy Category:Polysaccharide encapsulated bacteria Category:Bacteria described in 1896 Category:Pathogenic bacteria