Journal articles: 'Group B streptococcus'

1

MacLean, A. B. "Group B streptococcus." Journal of Obstetrics and Gynaecology 31, no. 3 (March 18, 2011): 203. http://dx.doi.org/10.3109/01443615.2011.556760.

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2

GREENSPOON, JEFFREY S., JOHN GORDEN WILCOX, and THOMAS H. KIRSCHBAUM. "Group B Streptococcus." Obstetrical & Gynecological Survey 46, no. 8 (August 1991): 499–508. http://dx.doi.org/10.1097/00006254-199108000-00001.

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Davies, Hannah G., Clara Carreras-Abad, Kirsty Le Doare, and Paul T. Heath. "Group B Streptococcus." Pediatric Infectious Disease Journal 38 (June 2019): S72—S76. http://dx.doi.org/10.1097/inf.0000000000002328.

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Leclair, Catherine M., Ashley E. Hart, Martha F. Goetsch, Heather Carpentier, and Jeffrey T. Jensen. "Group B Streptococcus." Journal of Lower Genital Tract Disease 14, no. 3 (July 2010): 162–66. http://dx.doi.org/10.1097/lgt.0b013e3181d3d40f.

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5

Schuchat, Anne. "Group B streptococcus." Lancet 353, no. 9146 (January 1999): 51–56. http://dx.doi.org/10.1016/s0140-6736(98)07128-1.

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6

Simpson, A. J. H., S. R. Heard, and B. Keith English. "Group B streptococcus." Lancet 346, no. 8976 (September 1995): 700. http://dx.doi.org/10.1016/s0140-6736(95)92308-x.

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Dangor, Ziyaad, Sanjay G. Lala, Gaurav Kwatra, and Shabir A. Madhi. "Group B Streptococcus." Current Opinion in Infectious Diseases 29, no. 3 (June 2016): 262–67. http://dx.doi.org/10.1097/qco.0000000000000266.

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8

Easmon, Charles S. F. "Group B Streptococcus." Infection Control & Hospital Epidemiology 7, S2 (February 1986): 135–37. http://dx.doi.org/10.1017/s0195941700065681.

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Over the past 25 years group B streptococci have become established as one of the main bacterial pathogens of the neonate in Western Europe and the United States. The attack rate of 0.25/1,000 live births found by Mayon White in Great Britain1 appears typical of many European countries. However, in some centers in the United States attack rates can be over 10 times higher.Two types of neonatal group B streptococcus (GBS) diseases exist, “early” and “late” onset. Early onset disease usually presents within the first few days of life. Often the most serious infections are present at birth or seen within a few hours. Early onset disease presents with pneumonia, respiratory distress and shock. Bacteremia is normally present and meningitis may occur. Mortality is high (50% to 75%). The portal of entry is probably the respiratory tract. Infants normally acquire the infecting organism from their mothers. Heavy maternal and infant colonization, prolonged rupture of membranes, prematurity, and obstetric complications are all risk factors.Delayed onset disease, as its name suggests, presents after the first week of life, primarily with bacteremia and meningitis. Mortality is much lower than for the early onset form, but still appreciable for a bacterial infection (14% to 18%). Its epidemiology is uncertain.

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Woo, Patrick CY, Jade LL Teng, Kit-wah Leung, Susanna KP Lau, Herman Tse, Beatrice HL Wong, and Kwok-yung Yuen. "Streptococcus sinensis may react with Lancefield group F antiserum." Journal of Medical Microbiology 53, no. 11 (November 1, 2004): 1083–88. http://dx.doi.org/10.1099/jmm.0.45745-0.

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Lancefield group F streptococci have been found almost exclusively as members of the ‘Streptococcus milleri’ group, although they have been reported very occasionally in some other streptococcal species. Among 302 patients with bacteraemia caused by viridans streptococci over a 6-year period, three cases were caused by Streptococcus sinensis (type strain HKU4T, HKU5 and HKU6). All three patients had infective endocarditis complicating their underlying chronic rheumatic heart diseases. Gene sequencing showed no base differences between the 16S rRNA gene sequences of HKU5 and HKU6 and that of HKU4T. All three strains were Gram-positive, non-spore-forming cocci arranged in chains. All grew on sheep blood agar as α-haemolytic, grey colonies of 0.5–1 mm in diameter after 24 h incubation at 37 °C in ambient air. Lancefield grouping revealed that HKU5 and HKU6 were Lancefield group F, but HKU4T was non-groupable with Lancefield groups A, B, C, D, F or G antisera. HKU4T was identified by the Vitek system (GPI), API system (20 STREP) and ATB system (ID32 STREP) as 99 % Streptococcus intermedius, 51.3 % S. intermedius and 99.9 % Streptococcus anginosus, respectively. Using the same tests, HKU5 was identified as 87 % Streptococcus sanguinis/Streptococcus gordonii, 59 % Streptococcus salivarius and 99.6 % S. anginosus, respectively, and HKU6 as 87 % S. sanguinis/S. gordonii, 77 % Streptococcus pneumoniae and 98.3 % S. anginosus, respectively. The present data revealed that a proportion of Lancefield group F streptococci could be S. sinensis. Lancefield group F streptococci should not be automatically reported as ‘S. milleri'.

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10

Verrall, Rosemary. "The Streptococcus milleri Group." Infection Control 7, no. 11 (November 1986): 558–60. http://dx.doi.org/10.1017/s0195941700065334.

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Microbiologists traditionally have relied on biochemical and serologic tests to identify only group A, group B, and group D streptococci isolated from patients with serious infections. Until recently there has been little interest in the further classification of other streptococci isolated from clinical specimens.In 1956, Guthof repeatedly isolated a particular streptococcus from dental abscesses and named the organism Streptococcus milleri in honor of the microbiologist, W.D. Miller. In 1976, Parker and Ball associated this microorganism with other pyogenic infections and later described the characteristics of 346 strains. The Streptococcus milleri group is now recognized as both virulent and invasive and some believe it is responsible for more suppurative infections than any other group of streptococci. Physicians need to consider the unique ability of these bacteria to form abscesses in a wide range of tissue. Microbiology laboratories, therefore, need to develop schemes to identify this important group of streptococci.

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11

Burianová, Iva, Magdalena Paulová, Pavel Čermák, and Jan Janota. "Group B Streptococcus Colonization of Breast Milk of Group B Streptococcus Positive Mothers." Journal of Human Lactation 29, no. 4 (March 22, 2013): 586–90. http://dx.doi.org/10.1177/0890334413479448.

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12

Manning, Shannon D. "Molecular epidemiology of Streptococcus Agalactiae Group B Streptococcus." Frontiers in Bioscience 8, no. 6 (2003): s1–18. http://dx.doi.org/10.2741/985.

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13

TAPSALL, J. W. "Pigment production by Lancefield-group-B streptococci (Streptococcus agalactiae)." Journal of Medical Microbiology 21, no. 1 (February 1, 1986): 75–81. http://dx.doi.org/10.1099/00222615-21-1-75.

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14

Singh, Mary. "Group B streptococcus-an update." Morecambe Bay Medical Journal 4, no. 12 (September 1, 2005): 356–57. http://dx.doi.org/10.48037/mbmj.v4i12.916.

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Group B streptococcus (GBS) infection has long been recognised as an important cause of neonatal morbidity. It is now known to be the most common serious neonatal infection in the developed world. In the United Kingdom (UK), it is estimated that 1 in 1000 babies develops a GBS infection. A recent London study, however, estimated the incidence of culture-proven plus suspected cases of GBS infection to be significantly higher (approximately 3.6 per 1000 babies born). Despite this, there is no standard of practice in the UK for stopping GBS infections in newborn babies. Mary Singh, specialist registrar at the Royal Lancaster Infirmary, explains.

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15

Heath, Paul T., and Robert G. Feldman. "Vaccination against Group B streptococcus." Expert Review of Vaccines 4, no. 2 (April 2005): 207–18. http://dx.doi.org/10.1586/14760584.4.2.207.

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16

Beattie, Robert Bryan. "Guide to: Group B Streptococcus." British Journal of Midwifery 26, Sup7 (July 2018): 1–5. http://dx.doi.org/10.12968/bjom.2018.26.sup7.1.

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17

Vigneswaran, Rasiah, John A. O'Loughlin, and Helen M. McDonald. "Group B Streptococcus and Pregnancy." Australian and New Zealand Journal of Obstetrics and Gynaecology 35, no. 2 (May 1995): 117–19. http://dx.doi.org/10.1111/j.1479-828x.1995.tb01852.x.

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18

Turpin, Arielle, Ana Mendes, Diogo Ribeiro, Victor Fernandes, Duarte Garcao, Manuel Caneira, Hugo Freitas, Miguel Neves, and Fatima Xambre. "Emerging Group B Streptococcus Infection." Journal of Medical Cases 9, no. 1 (2018): 26–28. http://dx.doi.org/10.14740/jmc2910w.

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19

Mercer, Brian M., and Rodney G. Briggs. "Group B Streptococcus and Pregnancy." Pediatric Annals 25, no. 4 (April 1, 1996): 206–14. http://dx.doi.org/10.3928/0090-4481-19960401-08.

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20

Creti, Roberta, Monica Imperi, Alberto Berardi, Marco Pataracchia, Simona Recchia, Giovanna Alfarone, and Lucilla Baldassarri. "Neonatal Group B Streptococcus Infections." Pediatric Infectious Disease Journal 36, no. 3 (March 2017): 256–62. http://dx.doi.org/10.1097/inf.0000000000001414.

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21

Furfaro, Lucy, Barbara Chang, and Matthew Payne. "Maternal Group B Streptococcus colonisation." Microbiology Australia 38, no. 3 (2017): 134. http://dx.doi.org/10.1071/ma17049.

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Streptococcus agalactiae, commonly known as Group B Streptococcus (GBS), is an important neonatal pathogen known to cause sepsis, meningitis and pneumonia. Australian pregnant women undergo screening during pregnancy in an effort to eradicate GBS before delivery where transmission to the neonate can occur. Preventative treatment includes intrapartum antibiotic prophylaxis and results in widespread treatment of the 10–40% of pregnant women colonised. GBS are separated into ten different capsular polysaccharide serotypes and previous studies have suggested associations between specific serotypes and disease. At present, however, minimal data exist on serotype distribution within Western Australian-pregnant women, information that may play an important role in future prophylactic treatment regimens. Our preliminary data, obtained from GBS isolated from vaginal swabs from 191 pregnant women, suggests that GBS serotype distributions in Western Australia are different to other parts of Australasia. In particular, compared to the eastern Australian states and New Zealand, in our cohort, serotype Ib prevalence was 7–17 times lower, II was 2–6 times greater and VI was 2–12 times greater. In addition, serotype IX represented 6.3% of all serotypes. Understanding which serotypes are present in our population will provide valuable data for future targeted treatment regimens such as vaccination and bacteriophage therapy.

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22

Coley, Maive. "Spotlight on: Group B Streptococcus." British Journal of Healthcare Assistants 10, no. 5 (May 2, 2016): 214. http://dx.doi.org/10.12968/bjha.2016.10.5.214.

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23

Greenberg, David N., David P. Ascher, Bradley A. Yoder, Donna M. Hensley, Howard S. Heiman, and Julian F. Keith. "Group B streptococcus serotype V." Journal of Pediatrics 123, no. 3 (September 1993): 494–95. http://dx.doi.org/10.1016/s0022-3476(05)81778-0.

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24

BEARDSALL, K. "Guidelines for Group B streptococcus." Archives of Disease in Childhood - Fetal and Neonatal Edition 84, no. 1 (January 1, 2001): 77Fb—77. http://dx.doi.org/10.1136/fn.84.1.f77b.

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25

Morosky, Christopher M. "Group B Streptococcus: Current Concepts." Postgraduate Obstetrics & Gynecology 31, no. 13 (July 2011): 1–7. http://dx.doi.org/10.1097/01.pgo.0000398945.25127.7e.

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26

&NA;. "Group B Streptococcus: Current Concepts." Postgraduate Obstetrics & Gynecology 31, no. 13 (July 2011): 8. http://dx.doi.org/10.1097/01.pgo.0000398946.32751.19.

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27

Lee, Shu-Yen, and Soon-Phaik Chee. "Group B Streptococcus endogenous endophthalmitis." Ophthalmology 109, no. 10 (October 2002): 1879–86. http://dx.doi.org/10.1016/s0161-6420(02)01225-3.

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28

Calubiran, Ofelia V., Ephraim Zackson, and Burke A. Cunha. "Group B Streptococcus hemorrhagic tonsillopharyngitis." Annals of Emergency Medicine 19, no. 8 (August 1990): 951–52. http://dx.doi.org/10.1016/s0196-0644(05)81592-6.

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29

Levy, Nancy J., and Dennis L. Kasper. "Immunity to group B Streptococcus." Clinical Immunology Newsletter 7, no. 2 (February 1986): 27–31. http://dx.doi.org/10.1016/s0197-1859(86)80008-5.

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30

RATHORE, MOBEEN H., and LESLIE L. BARTON. "Group B streptococcus occult bacteremia." Pediatric Emergency Care 8, no. 1 (February 1992): 36–37. http://dx.doi.org/10.1097/00006565-199202000-00011.

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31

Yancey, M. "Screening for Group B Streptococcus." ACOG Clinical Review 2, no. 2 (March 4, 1997): 5. http://dx.doi.org/10.1016/s1085-6862(97)81008-4.

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32

El Beitune, Patrícia, Silvana Maria Quintana, Geraldo Duarte, and Cláudia Maria Leite Maffei. "Group B Streptococcus and pregnancy." American Journal of Obstetrics and Gynecology 199, no. 6 (December 2008): e14. http://dx.doi.org/10.1016/j.ajog.2008.06.003.

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33

Madhi, S. "Group B Streptococcus (GBS) vaccine." International Journal of Infectious Diseases 73 (August 2018): 31. http://dx.doi.org/10.1016/j.ijid.2018.04.3493.

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34

Nikonov, A. P., N. S. Naumenko, O. R. Astsaturova, A. V. Belova, and L. S. Aleksandrov. "Prevention of neonatal infection caused by group B streptococci." Voprosy ginekologii, akušerstva i perinatologii 19, no. 6 (2020): 12–16. http://dx.doi.org/10.20953/1726-1678-2020-6-12-16.

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Objective. To evaluate the prevalence of vaginal carriage of Streptococcus agalactiae among pregnant women at 35–37 weeks of gestation and assess the efficacy of intrapartum antibiotic prophylaxis (IAP) for group B streptococcus (GBS) infection in newborns. Patients and methods. We examined 800 pregnant women at 35–37 weeks of gestation (bacteriological examination of vaginal microbiota with biomaterial collected from the posterior vaginal fornix). Identified carriers of S. agalactiae who had vaginal delivery (n = 50) received antibiotic prophylaxis to prevent infection in newborns. We also evaluated the frequency of vertical transmission of streptococci in all infants during the first hour of life (bacteriological examination of pharyngeal swabs and meconium). Identification of microorganisms was performed by direct protein profiling using MALDI-TOF mass spectrometry (FLEX series, Bruker Daltonic GmbH, Germany). Results. Maternal vaginal colonization with S. agalactiae in the third trimester was observed in 13.5% of patients tested (n = 108). Fifty women had vaginal delivery and received antibiotic prophylaxis to prevent infection in newborns. Postpartum samples of only 1 newborn gave scanty growth of S. agalactiae at bacteriological examination (1 × 101 CFU/mL in meconium and 1 × 103 CFU/mL in the pharyngeal sample), while the remaining 49 newborns had sterile samples. Thus, the frequency of S. agalactiae vertical transmission with intrapartum antibiotic prophylaxis was 2% (n = 1). Of note, infection in the newborn caused no inflammation. Conclusion. Relatively low prevalence of vaginal carriage of S. agalactiae among pregnant women gives no sufficient grounds for the inclusion of such bacteriological examination into compulsory screening for infections in pregnant women in the Russian Federation. However, intrapartum antibiotic prophylaxis is an effective method to prevent streptococcal infection in newborns; it should be used in women at risk of GBS infections. Kew words: vaginal carriage of bacteria, intrapartum antibiotic prophylaxis, neonatal sepsis, Streptococcus agalactiae, intrauterine infection, screening for infections

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35

Oganyan, Kristina Al’bertovna, Ol’ga Nikolaevna Arzhanova, Alevtina Mikhaylovna Savicheva, and Svetlana L’vovna Zatsiorskaya. "Prophylactic antimicrobial drugs to pregnant women colonized with group B streptococcus." Journal of obstetrics and women's diseases 64, no. 2 (June 15, 2015): 59–63. http://dx.doi.org/10.17816/jowd64259-63.

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Group B streptococcus (GBS), Streptococcus agalactiae, are the causative agents of severe infection of the fetus and newborn child. The aim of the study was to evaluate the efficacy of antibacterial drugs in women in the III trimester of pregnancy for the prevention of B streptococcal infection. Studied during childbirth and the postpartum period, 70 women colonized by group B streptococcus, treated and not treated with antibacterial perparaty in the III trimester of pregnancy. Evaluated as a new-born children of these women. In pregnant women who received antibiotics in the III trimester of pregnancy, significantly fewer were delayed rupture of membranes, preterm labor, subinvolution uterus. Less common was marked asphyxia. Group B streptococcus significantly more frequently (in 43.5 % of cases) were identified in children born to mothers who did not receive antibiotics during pregnancy. In 26.1 % of these children diagnosed with intrauterine infection. Thus, the use of antimicrobials in the III trimester of pregnancy in detecting GBS in the urine in any quantity, simultaneous detection of these microorganisms in urine and vaginal discharge of a concentration of greater than 104 CFU/ml reduces the rate of preterm birth, postpartum complications, and neonatal asphyxia and intrauterine infection B streptococcal etiology.

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36

Teran, Carlos G., Ariel O. Antezana, Jerome Salvani, and Deborah Abaitey. "Group B streptococcus endocarditis associated with multiple pulmonary septic emboli." Clinics and Practice 1, no. 1 (April 4, 2011): 7. http://dx.doi.org/10.4081/cp.2011.e7.

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Endocarditis is a rare presentation of group B streptococcal infection. Its association with pulmonary septic embolism was only barely studied and limited data is available up to date. Multiple septic emboli is a common complication of bacterial endocarditis, but only a few cases have been documented in relation to group B streptococcus. We present the case of an 87-year-old female patient with multiple underlying conditions that predisposed the development of bacterial endocarditis secondary to group B streptococcus and subsequently multiple pulmonary septic emboli. The patient was treated with ceftriaxone and azythromycin with good response and complete recovery without any further complications. In the event of a diagnosed case of group B streptococcus endocarditis, there should be a low threshold for the suspicion of septic pulmonary emboli especially in cases with right valves involvement.

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37

Erdogan, Sezgin, Peter K. Fagan, Susanne R. Talay, Manfred Rohde, Patricia Ferrieri, Aurea E. Flores, Carlos A. Guzmán, Mark J. Walker, and Gursharan S. Chhatwal. "Molecular Analysis of Group B Protective Surface Protein, a New Cell Surface Protective Antigen of Group B Streptococci." Infection and Immunity 70, no. 2 (February 2002): 803–11. http://dx.doi.org/10.1128/iai.70.2.803-811.2002.

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ABSTRACT Group B streptococci (GBS) express various surface antigens designated c, R, and X antigens. A new R-like surface protein from Streptococcus agalactiae strain Compton R has been identified by using a polyclonal antiserum raised against the R protein fraction of this strain to screen a lambda Zap library. DNA sequence analysis of positive clones allowed the prediction of the primary structure of a 105-kDa protein designated BPS protein (group B protective surface protein) that exhibited typical features of streptococcal surface proteins such as a signal sequence and a membrane anchor region but did not show significant similarity with other known sequences. Immunogold electron microscopy using a BPS-specific antiserum confirmed the surface location of BPS protein on S. agalactiae strain Compton R. Anti-BPS antibodies did not cross-react with R1 and R4 proteins expressed by two variant type III GBS strains but reacted with the parental streptococcal strain in Western blot and immunoprecipitation analyses. Separate R3 and BPS immunoprecipitation bands were observed when a cell extract of strain Compton R was tested with an antiserum against Compton R previously cross-absorbed to remove R4 antibodies. Immunization of mice with recombinant BPS protein by the subcutaneous route produced an efficient antigen-specific response, and immunized animals survived challenge with a lethal dose of a virulent strain. Therefore, BPS protein represents a new R-like protective antigen of GBS.

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38

Patras, Kathryn A., Philip A. Wescombe, Berenice Rösler, John D. Hale, John R. Tagg, and Kelly S. Doran. "Streptococcus salivarius K12 Limits Group B Streptococcus Vaginal Colonization." Infection and Immunity 83, no. 9 (June 15, 2015): 3438–44. http://dx.doi.org/10.1128/iai.00409-15.

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Streptococcus agalactiae(group B streptococcus [GBS]) colonizes the rectovaginal tract in 20% to 30% of women and during pregnancy can be transmitted to the newborn, causing severe invasive disease. Current routine screening and antibiotic prophylaxis have fallen short of complete prevention of GBS transmission, and GBS remains a leading cause of neonatal infection. We have investigated the ability ofStreptococcus salivarius, a predominant member of the native human oral microbiota, to control GBS colonization. Comparison of the antibacterial activities of multipleS. salivariusstrains by use of a deferred-antagonism test showed thatS. salivariusstrain K12 exhibited the broadest spectrum of activity against GBS. K12 effectively inhibited all GBS strains tested, including disease-implicated isolates from newborns and colonizing isolates from the vaginal tract of pregnant women. Inhibition was dependent on the presence of megaplasmid pSsal-K12, which encodes the bacteriocins salivaricin A and salivaricin B; however, in coculture experiments, GBS growth was impeded by K12 independently of the megaplasmid. We also demonstrated that K12 adheres to and invades human vaginal epithelial cells at levels comparable to GBS. Inhibitory activity of K12 was examinedin vivousing a mouse model of GBS vaginal colonization. Mice colonized with GBS were treated vaginally with K12. K12 administration significantly reduced GBS vaginal colonization in comparison to nontreated controls, and this effect was partially dependent on the K12 megaplasmid. Our results suggest that K12 may have potential as a preventative therapy to control GBS vaginal colonization and thereby prevent its transmission to the neonate during pregnancy.

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TERAO, Michinori, Yuuichi OKAO, and Shuzo OKETANI. "Mechanism of Chloramphenicol Resistance in Group B Streptococci (Streptococcus agalactiae)." Journal of the Japanese Association for Infectious Diseases 61, no. 4 (1987): 449–55. http://dx.doi.org/10.11150/kansenshogakuzasshi1970.61.449.

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40

Chihara, Shingo, and Eddie Siccion. "Group B Streptococcus Endocarditis With Endophthalmitis." Mayo Clinic Proceedings 80, no. 1 (January 2005): 74. http://dx.doi.org/10.4065/80.1.74.

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41

Kling, David E., Lawrence C. Madoff, and James L. Michel. "Subcellular Fractionation of Group B Streptococcus." BioTechniques 27, no. 1 (July 1999): 24–28. http://dx.doi.org/10.2144/99271bm03.

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42

Greene, Alexis Dyana, and Marjorie L. Pilkinton. "Group B Streptococcus Bacteremia After Hysterosalpingogram." Obstetrics & Gynecology 125 (May 2015): 93S. http://dx.doi.org/10.1097/01.aog.0000463191.28127.4c.

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43

Miller, Tiffany R., Catherine Gonsalves, Kendall Steadmon, and Stacy G. Beal. "Educational Case: Group B Streptococcus Meningitis." Academic Pathology 6 (January 1, 2019): 237428951989252. http://dx.doi.org/10.1177/2374289519892524.

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The following fictional case is intended as a learning tool within the Pathology Competencies for Medical Education (PCME), a set of national standards for teaching pathology. These are divided into three basic competencies: Disease Mechanisms and Processes, Organ System Pathology, and Diagnostic Medicine and Therapeutic Pathology. For additional information, and a full list of learning objectives for all three competencies, see http://journals.sagepub.com/doi/10.1177/2374289517715040 .1

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44

Atherton, Cathy. "Group B Streptococcus: silent but deadly." British Journal of Midwifery 10, no. 11 (November 8, 2002): 687–91. http://dx.doi.org/10.12968/bjom.2002.10.11.687.

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45

Read, Sue. "Group B Streptococcus: testing and treatment." British Journal of Midwifery 11, no. 3 (March 2003): 160–63. http://dx.doi.org/10.12968/bjom.2003.11.3.11126.

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46

Plumb, Oliver. "Group B streptococcus and legal liability." BJOG: An International Journal of Obstetrics & Gynaecology 126, no. 4 (January 2019): 512. http://dx.doi.org/10.1111/1471-0528.15531.

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47

Arora, Harbir Singh, Saurabh Shankar Chiwane, Nahed Abdel-Haq, Kevin Valentine, Paul Lephart, and Basim Isa Asmar. "Group B Streptococcus Sepsis in Twins." Pediatric Infectious Disease Journal 34, no. 5 (May 2015): 548–49. http://dx.doi.org/10.1097/inf.0000000000000611.

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48

Kaplan, Amber, Kathy Chung, Hande Kocak, Cristina Bertolotto, Andy Uh, Calvin J. Hobel, Charles F. Simmons, Kelly Doran, George Y. Liu, and Ozlem Equils. "Group B streptococcus induces trophoblast death." Microbial Pathogenesis 45, no. 3 (September 2008): 231–35. http://dx.doi.org/10.1016/j.micpath.2008.05.003.

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49

Chihara, Shingo, and Eddie Siccion. "Group B Streptococcus Endocarditis With Endophthalmitis." Mayo Clinic Proceedings 80, no. 1 (January 2005): 74. http://dx.doi.org/10.1016/s0025-6196(11)62961-3.

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50

Towers, CraigV. "Group B streptococcus: the US controversy." Lancet 346, no. 8969 (July 1995): 197–99. http://dx.doi.org/10.1016/s0140-6736(95)91262-2.

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Journal articles on the topic 'Group B streptococcus'

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