Streptococcus agalactiae

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Streptococcus agalactiae
Scientific classification
Kingdom: 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 cocci with a tendency to form chains, streptococcus, beta-hemolytic, catalase-negative, and facultative anaerobe.[1][2] Streptococcus agalactiae is the species designation for streptococci belonging to the group B of the Rebecca Lancefield classification. GBS is encapsulated by a capsular exopolysacharide rich in sialic acid. GBS are subclassified into ten serotypes (Ia, Ib, II–IX) depending on the immunologic reactivity of their polysaccharide capsule.[1][3][4] 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.

Identification[edit]

β-hemolytic colonies of Streptococcus agalactiae, blood agar 18h at 36°C
Positim, ,ve 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] Hemolytic GBS strains produce an orange-brick-red polyenic pigment (granadaene) when cultivated on granada agar that allows its straightforward identification.[6]

Granadaene

Clinical significance[edit]

GBS is an asymptomatic (presenting no symptoms of disease) colonizer of the gastrointestinal human tract in otherwise healthy adults. Nevertheless, this opportunistic harmless bacteria can, in some circumstances, cause severe invasive infections. As other virulent bacteria GBS harbours an important number of virulence factors, the most important are the capsular polysaccharide (rich in sialic acid) and a pore forming toxin, β-hemolysin.[3][7][8]

Although GBS colonization usually does not cause problems in healthy women during pregnancy, it can sometimes cause serious illness for the mother and baby during gestation and after delivery. 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 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 bacterial septicemia of the newborn, which can lead to death or long-term sequelae.[3]

GBS infections in newborns are separated into 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][9] The most common clinical syndromes of EOD are sepsis without apparent focus, pneumonia, and less frequently meningitis. EOD is acquired vertically through exposure to GBS from the vagina of a colonized woman, vertical transmission, either intrautero or during birth after rupture of membranes. Infants can be infected during passage through the birth canal, nevertheless newborns who 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.[10] 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.[11] 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.[12]

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, young maternal age, and low levels of GBS anticapsular polysaccharide antibodies in the mother.[3][9] Nevertheless most babies who develop EOD are born to GBS colonized mothers without any additional risk factor.[9] 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. 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][9][13]

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][14] In contrast with EOD, the incidence of LOD has remained unchanged at 0.26 per 1000 live births in the US.[15] 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 late diagnosis.[2] GBS is also an important infectious agent able to cause life-threatening invasive infections in the elderly and in adults with predisposing diseases such as diabetes and cancer.[16]

Prevention[edit]

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 and EOD.[3][9] Cefazolin, clindamycin, and vancomycin are used to prevent EOD in infants born to penicillin-allergic mothers.[9]

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 administerd 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][17]

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, who are born to mothers without risk factors.[11]

The culture-based screening approach is followed in most developed countries such as the United States, France, Spain, Belgium, Canada, Argentina, Australia etc. The risk-based strategy is followed in the United Kingdom, and the Netherlands.[11]

Vaccination, Inmunoprophylaxis[edit]

Though IAP for EOD prevention is associated with a large decline in the incidence of the disease, there are not any effective strategies for preventing LOD.[18]

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 polysacharide of GBS is not only an important GBS virulence factor but it is also an excellent candidate for the development of an effective vaccine.[11][19][20]

Screening for GBS colonization[edit]

Though the GBS colonization status of women can change during pregnancy, cultures to detect GBS carried out ≤5 weeks before delivery predict quite accuratly 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 accuratly the GBS carrier status at delivery.[9][21] 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. Swabs should be placed into a non-nutritive transport medium and later inoculated into a selective enrichment broth (enrichment culture).[9][22] 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 subcultivated to granada agar[6][22] where GBS grows as pink-red colonies or to chromogenic agars.[9][22]

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)

Rapid nucleic acid amplification tests such as polymerase chain reaction (PCR) and DNA hybridization probes for identifying GBS directly have been developed, but they still can not replace antenatal culture for detection of GBS carriers.[9]

Non-human infections[edit]

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.[23]

GBS also causes severe epidemics in fish farmers causing septicemia and external and internal hemorragies, having been reported from wild and captive fish involved in epizootics in many countries.[24][25]

GBS has also been found in many other animals such as camels, dogs, cats, crocodiles, seals and dolphins.[26]

See also[edit]

References[edit]

  1. ^ a b 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. ^ a b Ryan KJ, Ray CG, et al, ed. (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 286–8. ISBN 0-8385-8529-9. 
  3. ^ a b c d e f g h i j k 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. 
  5. ^ a b Tille P. (2014). Bailey & Scott's Diagnostic Microbiology (13th ed.). Elsevier. ISBN 978-0-323-08330-0. 
  6. ^ a b 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. ^ 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. 
  8. ^ Rajagopal L (2009). "Understanding the regulation of Group B Streptococcal virulence factors" (PDF). Future Microbiol 4: 201–221. 
  9. ^ a b c d e f g h i j 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. 
  10. ^ Boyer KM, Gotoff SP. (1985). "Strategies for chemoprophylaxis of GBS early-onset infections". Antibiot Chemother. 267-280: 267–280. 
  11. ^ a b c d 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. 
  12. ^ CDC. [url=http://www.cdc.gov/groupbstrep/clinicians/clinical-overview.html "Group B Strep (GBS)-Clinical Overview"]. Retrieved 4 May 2015. 
  13. ^ 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 279: 547–556. 
  14. ^ 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. 
  15. ^ Baker CJ. (2013). "The spectrum of perinatal group B streptococcal disease". Vaccine 31s. doi:10.1016/j.vaccine.2013.02.030. 
  16. ^ Edwards MS,. Baker CJ. (2005). "Group B streptococcal infections in elderly adults" (PDF). Clin Infect Dis. 41: 839–847. 
  17. ^ 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. 
  18. ^ 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. 
  19. ^ 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. 
  20. ^ 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. 
  21. ^ 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. 
  22. ^ a b c Carey RB. [url=http://www.scacm.org/free/2010SpringMeetingPresentations/Carey%20GBS%20guidelines.pdf "Group B Streptococci: Chains & Changes New Guidelines for the Prevention of Early-Onset GBS"] (PDF). Retrieved 4 May 2015. 
  23. ^ Keefe GP (1997). "Streptococcus agalactiae mastitis: a review" (PDF). Can Vet J. 38: 199–204. 
  24. ^ 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. 
  25. ^ Liu G, Zhang W, Lu C (2013). "Comparative genomics analysis of Streptococcus" (PDF) 14. p. 775. 
  26. ^ 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. 

External links[edit]