Streptococcus agalactiae

Streptococcus agalactiae
Scientific classification
Domain: Bacteria
Phylum: Firmicutes
Class: Coccus
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Species: S. agalactiae
Binomial name
Streptococcus agalactiae
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.[1][2] 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).

Streptococcus agalactiae is the species designation for streptococci belonging to group B of the Lancefield classification. GBS is surrounded by a bacterial capsule composed of polysaccharides (exopolysacharide). The species is subclassified into ten serotypes (Ia, Ib, II–IX) depending on the immunologic reactivity of their polysaccharide capsule.[1][3][4] This is why 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 encountered.

Lab identification

β-hemolytic colonies of Streptococcus agalactiae, blood agar 18h at 36°C
Positive CAMP test indicated by the formation of an arrowhead where Streptococcus agalactiae meets the Staphylococcus aureus (white middle streak)

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.[5] 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.[5] GBS is also able to hydrolyze hippurate and this test can also be used to identify presumptively GBS.[5] Hemolytic GBS strains produce an orange-brick-red non-isoprenoid polyene pigment (granadaene) when cultivated on granada medium that allows its straightforward identification.[6]

Granadaene

Virulence

GBS is an asymptomatic (presenting no symptoms of disease) colonizer of the gastrointestinal human tract in up to 30% of otherwise healthy adults, including pregnant woman.[3][7] Nevertheless, this opportunistic harmless bacterium can, in some circumstances, cause severe invasive infections. As other virulent bacteria, GBS harbors an important number of virulence factors, the most important are the capsular polysaccharide (rich in sialic acid) [3][8] and a pore-forming toxin, β-hemolysin, that today is considered identical to the GBS pigment.[9][10][11]

GBS colonization

In different studies, GBS vaginal colonization rate ranges from 0% to 36%, most studies reporting colonization rates in sexually active women over 20%. These variations in the reported prevalence of asymptomatic GBS colonization could be related to the detection methods used, and differences in populations sampled.[7][12] Although GBS colonization usually does not cause problems in healthy women during pregnancy, it can sometimes cause serious illness for the mother and 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 and postpartum infections (after birth). GBS urinary tract infections (UTI) may induce labor and cause premature delivery.[3] In the western world, GBS (in the absence of effective prevention measures) is the major cause of several bacterial infections of the newborn, septicemia, pneumonia, and meningitis, which can lead to death or long-term sequelae.[3]

GBS infections in newborns are separated into two clinical syndromes, early-onset disease (EOD) and late-onset disease (LOD). EOD manifests from 0 to 7 living days in the newborn, most of the cases of EOD being apparent within 24h of birth.[3][13] 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.[14] In the past, the incidence of EOD ranged from 0.7 to 3.7 per thousand live births in the US[3] and from 0.2 to 3.25 per thousand in Europe.[12] In 2008, after widespread use of antenatal screening and intrapartum antibiotic prophylaxis, the CDC reported an incidence of 0.28 cases of EOD per thousand live births in the US.[15]

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.[3][13] Nevertheless, most babies who develop EOD are born to GBS colonized mothers without any additional risk factor.[13] 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.[13] 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.[3][13][16]

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.[3][17] In contrast with EOD, the incidence of LOD has remained unchanged at 0.26 per 1000 live births in the US.[18] 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.[2]

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 ≥4 hours before delivery to GBS colonized women are very effective at preventing vertical transmission of GBS from mother to baby and EOD.[3][13] Cefazolin, clindamycin, and vancomycin are used to prevent EOD in infants born to penicillin-allergic mothers.[13]

There are two ways to identifying 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 35 and 37 week’s gestation, 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.[3][19]

Additionally 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.

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.[12]

The culture-based screening approach is followed in most developed countries such as the United States, France, Spain, Belgium, Canada, Argentina, and Australia. The risk-based strategy is followed in the United Kingdom, and the Netherlands.[12]

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. In contrast, if the prenatal culture is performed more than 5 weeks before delivery it is unreliable for predicting accurately the GBS carrier status at delivery.[13][20] The clinical specimens recommended for culture of GBS at 35–37 weeks’ gestation are swabs collected from lower vagina and rectum through the anal sphincter. 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).[13][21] 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 agar[6][21] where GBS grows as pink-red colonies or to chromogenic agars, where GBS grows as colored colonies.[13][21]

Red colonies of S.agalactiae in granada agar. Vagino-rectal culture 18h incubation 36°C anaerobiosis
Streptococcus agalactiae colonies in chromogenic medium (ChromID CPS chromogenic agar)

Nucleic acid amplification tests (NAAT) such as polymerase chain reaction (PCR) and DNA hybridization probes for identifying GBS directly have been developed, but they still cannot replace antenatal culture for the most accurate detection of GBS carriers.[13]

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. GBS infections in adults include urinary tract infection, skin and soft-tissue infection (skin and skin structure infection) bacteremia, osteomyelitis, meningitis and endocarditis. 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.[22][23]

GBS infection in newborns

GBS is the most common pathogen causing neonatal infection. It is often fatal and typically originates in the lower reproductive tract of infected mothers.

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.[24]

Vaccination is considered an ideal solution to prevent not only EOD and LOD but also GBS infections in adults at risk. Nevertheless, though research and clinical trials for the development of an effective vaccine to prevent GBS infections are underway, no vaccine is currently available in 2015. 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.[12][25][26]

Non-human infections

In addition to humans infections, 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 "no milk"). Outbreaks in herds are common, and 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.[27]

GBS also causes severe epidemics in fish farmers causing septicemia and external and internal hemorrages, having been reported from wild and captive fish involved in epizootics in many countries.[28][29]

GBS has also been found in many other animals such as camels, dogs, cats, crocodiles, seals and dolphins.[30]

See also

References

  1. 1 2 Whiley RA, Hardie JM (2009). Genus I. Streptococcus Rosenbach 1884. Bergey's Manual of Systematic Bacteriology: Vol 3: The Firmicutes (2nd ed.). Springer. pp. 655–711. ISBN 978-0-387-95041-9.
  2. 1 2 Ryan KJ, Ray CG, et al, eds. (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 286–8. ISBN 0-8385-8529-9.
  3. 1 2 3 4 5 6 7 8 9 10 11 12 Edwards MS, Nizet V. (2011). Group B streptococcal infections. Infectious Diseases of the Fetus and Newborn Infant (7th ed.). Elsevier. pp. 419–469. ISBN 978-0-443-06839-3.
  4. ↑ Slotved HC, Kong F, Lambertsen L, Sauer S, Gilbert GL (2007). "Serotype IX, a proposed new Streptococcus agalactiae serotype" (PDF). J Clin Microbiol. 45: 2929–2936. doi:10.1128/jcm.00117-07.
  5. 1 2 3 Tille P. (2014). Bailey & Scott's Diagnostic Microbiology (13th ed.). Elsevier. ISBN 978-0-323-08330-0.
  6. 1 2 Rosa-Fraile M, Rodriguez-Granger J, Cueto-Lopez M, Sampedro A, Biel Gaye E, Haro M , Andreu A. (1999). "Use of Granada medium to detect group B streptococcal colonization in pregnant women". J Clin Microbiol. 37: 2674–2677.
  7. 1 2 Barcaite E, Bartusevicius A, Tameliene R, Kliucinskas M, Maleckiene L, Nadisauskiene R. (2008). "Prevalence of maternal group B streptococcal colonisation in European countries.". Acta Obstet Gynecol Scand. 87: 260–271. doi:10.1080/00016340801908759.
  8. ↑ Rajagopal L (2009). "Understanding the regulation of Group B Streptococcal virulence factors" (PDF). Future Microbiol 4: 201–221. doi:10.2217/17460913.4.2.201. PMC 2691590. PMID 19257847.
  9. ↑ Rosa-Fraile M, Dramsi S, Spellerberg B. (2014). "Group B streptococcal haemolysin and pigment, a tale of twins." (PDF). FEMS Microbiol Rev. 38: 932–946. doi:10.1111/1574-6976.12071.
  10. ↑ Whidbey C, Harrell MI, Burnside K, Ngo L, Becraft AK, Iyer LM, Aravind L, Hitti J, Waldorf KM, Rajagopal L. (2013). "A hemolytic pigment of Group B Streptococcus allows bacterial penetration of human placenta.". J Exp Med 210 210: 1265–1281. doi:10.1084/jem.20122753. PMC 3674703. PMID 23712433.
  11. ↑ 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. (2015). "A streptococcal lipid toxin induces membrane permeabilization and pyroptosis leading to fetal injury." (PDF). EMBO Mol Med. 7: 488–505. doi:10.15252/emmm.201404883. PMC 4403049. PMID 25750210.
  12. 1 2 3 4 5 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. (2012). "Prevention of group B streptococcal neonatal disease revisited. The DEVANI European project". Eur J Clin Microbiol Infect Dis 31: 2097–2114. doi:10.1007/s10096-012-1559-0.
  13. 1 2 3 4 5 6 7 8 9 10 11 Verani JR, McGee L, Schrag SJ. (2010). "Prevention of perinatal group B streptococcal disease: revised guidelines from CDC, 2010" (PDF). MMWR Recomm Rep. 59(RR-10): 1–32.
  14. ↑ Boyer KM, Gotoff SP. (1985). "Strategies for chemoprophylaxis of GBS early-onset infections". Antibiot Chemother. 35: 267–280.
  15. ↑ CDC. "Group B Strep (GBS)-Clinical Overview". Retrieved 27 Oct 2015.
  16. ↑ Edmond KM, Kortsalioudaki C, Scott S, Schrag SJ, Zaidi AK, Cousens S, Heath PT. (2012). "Group B streptococcal disease in infants aged younger than 3 months: systematic review and meta-analysis" (PDF). Lancet 379: 547–556. doi:10.1016/s0140-6736(11)61651-6.
  17. ↑ Libster R, Edwards KM, Levent F, Edwards MS, Rench MA, Castagnini LA, Cooper T, Sparks RC, Baker CJ, Shah PE. (2012). "Long-term outcomes of group B streptococcal meningitis". Pediatrics 2012: e815.
  18. ↑ Baker CJ. (2013). "The spectrum of perinatal group B streptococcal disease". Vaccine 31s: D3–D6. doi:10.1016/j.vaccine.2013.02.030.
  19. ↑ Clifford V, Garland SM, Grimwood K. (2011). "Prevention of neonatal group B streptococcus disease in the 21st century.". J Paediatr Child Health 48: 808–815. doi:10.1111/j.1440-1754.2011.02203.
  20. ↑ Valkenburg-van den Berg AW, Houtman-Roelofsen RL, Oostvogel PM, Dekker FW, Dorr PJ, Sprij AJ. (2010). "Timing of group B streptococcus screening in pregnancy: a systematic review". Gynecol Obstet 69: 174–183. doi:10.1159/000265942.
  21. 1 2 3 Carey RB. "Group B Streptococci: Chains & Changes New Guidelines for the Prevention of Early-Onset GBS" (PDF). Retrieved 27 Oct 2015.
  22. ↑ Edwards MS,. Baker CJ. (2005). "Group B streptococcal infections in elderly adults" (PDF). Clin Infect Dis. 41: 839–847. doi:10.1086/432804.
  23. ↑ Farley MM. (2001). "Group B Streptococcal Disease in Nonpregnant Adults" (PDF). Clinical Infectious Diseases 33: 556–561. doi:10.1086/322696.
  24. ↑ 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; Active Bacterial Core Surveillance (ABCs)/Emerging Infections Program Network, CDC (2008). "Revisiting the need for vaccine prevention of late-onset neonatal group B streptococcal disease: a multistate, population-based analysis". Pediatr Infect Dis J. 27: 1057–1064. doi:10.1097/inf.0b013e318180b3b9.
  25. ↑ Baker CJ, Carey VJ, Rench MA, Edwards MS, Hillier SH, Kasper DL, Platt R. (2014). "Maternal Antibody at Delivery Protects Neonates From Early Onset Group B Streptococcal Disease" (PDF). J Infect Dis. 209: 781–788. doi:10.1093/infdis/jit549.
  26. ↑ Edwards MS, Gonik B (2013). "Preventing the broad spectrum of perinatal morbidity and mortality throughgh group B streptococcal vaccination". Vaccine 31S: D66–71. doi:10.1016/j.vaccine.2012.11.046.
  27. ↑ Keefe GP (1997). "Streptococcus agalactiae mastitis: a review" (PDF). Can Vet J. 38: 199–204. PMC 1576741. PMID 9220132.
  28. ↑ Evans JJ, Klesius PH, Pasnik DJ, Bohnsack JF. (2009). "Human Streptococcus agalactiae isolate in Nile tilapia (Oreochromis niloticus)" (PDF). Emerg Infect Dis 15: 774–776. doi:10.3201/eid1505.080222. PMC 2687030. PMID 19402966.
  29. ↑ Liu G, Zhang W, Lu C (2013). "Comparative genomics analysis of Streptococcus" (PDF). BMC Genomics 14: 775. doi:10.1186/1471-2164-14-775. PMC 3831827. PMID 24215651.
  30. ↑ Delannoy CMJ, Crumlish M, Fontaine MC, Pollock J, Foster G, Dagleish MP, Turnbull JF, Zadoks RN. (2013). "Human Streptococcus agalactiae strains in aquatic mammal and fish" (PDF). BMC Microbiology 13: 41. doi:10.1186/1471-2180-13-41. PMC 3585737. PMID 23419028.

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