GBS- The truth
Top 10 things about GBS of the newborn for which there is a lack of research:
1. How many full term babies are permanently injured (not killed) from GBS disease of the newborn? How many experience each of the various types (deafness, learning disabilities, CP) of morbidity?
2. Do prophylactic antibiotics to GBS positive women prevent or decrease long term GBS morbidity in full term newborns (vs. mortality)?
3. The presence of GBS antibodies in the mother has been shown to be protective against Newborn GBS(10). Women with high titers of antibodies to GBS are thought to pass on immunity to GBS to their fetus and thereby have less GBS infected babies. Smokers, drug abusers, obese and immune suppressed women produce less antibodies. Are they more likely to have a baby with GBS disease? Is some/most/all GBS disease of the newborn associated with women with low titers of antibodies to GBS?
4. There is only one published study asking whether pregnant women who culture GBS positive in urine, also culture positive in rectovaginal culture. Of 1036 assymptomatic women who underwent routine urine culture in pregnancy, 10.7% had GBS in their urine, of those 70% of those had <10,000 CFU (colony forming units) and 30% had >10,000 CFU which is considered highly colonized. Of the 111 women who had GBS in their urine (bacteriuria), 40% cultured negative for GBS on rectovaginal swabs. Women who were heavily colonized in urine were no more likely than those lightly colonized in urine to have positive rectovaginal cultures. (16)
Approximately 11% of women colonized positive for GBS in urine and their healthy babies culture positive for GBS than other babies, however no one has ever documented higher rates of GBS DISEASE associated with maternal GBS bacteriuria. GBS in urine has been associated with chorioamnionitis- uterine infections in the mother- which is most closely associated with prolonged labors, as well as frequent vaginal exams, internal monitoring, prolonged ROM, cesareans, and teenage pregnancies, but to date not documented to be associated with GBS disease of the newborn.
There are many claims that antibiotics during pregnancy given to women wiht GBS bacteriuria can prevent preterm birth, but this data is confounded by studying high risk populations. A RCT study contradicts this claim, found that women with GBS bacteriuria, additional exposure to antibiotics is associated with an increased, not decreased, risk of preterm birth. In this study the rate of preterm birth for women with bacteriuria was 16% and without GBS bacteriuria was also 16% and 28% among women with GBS bacteriuria who received antibiotics. (17) All three rates reflect outcomes only seen in extremely high risk populations. Healthy, well fed populations, the preterm rate is 7%. Asymptomatic GBS bacteriuria may not have a role in preterm birth but rather may be a marker for low socioeconomic status which is associated with low birth weight. (18) The quality of even the best studies on asymptomatic bacteriuria in pregnancy is poor. (18)
The unanswered question is: Do heavily colonized full term women have more GBS newborn disease or perhaps less newborn GBS due to higher titers of antibodies against GBS that they pass to the fetus? Are women who heavily colonized with GBS, whether in urine or vagina, more likely or less likely to have babies with GBS disease? We dont know.
Does giving oral antibiotics to pregnant women with asymptomatic GBS bacteriuria decrease or increase the occurrence of GBS disease of newborn?
5. 50% of GBS disease of the newborn occurs to babies of women with the following risk factors: Premature, IUGR, LBW, ROM > 18 hours, and fever. The other 50% occurs to babies of women without those risk factors. Of those women, how many had ROM between 2 and 17.9 hours? Since prolonged ROM is known to increase the risk of GBS disease, how would eliminating AROM affect the occurrence of GBS disease of newborn?
Is there a difference in the GBS disease among women with impressive, flowing ROM which fills up pads quickly and women who have a high leak that is leaks 1 to 2 cc per hour? Is a high leak a risk of newborn GBS at all?
6. On page 11 of the 2002 CDC protocols appears one of several unqualified statement “GBS can cross intact amniotic membranes.” A study of 550 babies born to GBS positive women, by CS without ROM, and without prophylaxis, demonstrated not a single case of GBS disease, where one would expected 5 sick newborn if GBS crossed membranes, supporting the theory that GBS either never crosses membranes. In vitro study has not been able to demonstrate GBS crossing membranes, even at concentrations of 1,000,000,000 CFU. (20) Further investigation into how GBS could cross intact membranes demonstrated that GBS failed to invade amnion cells under a variety of assay conditions (21) and fetal membranes demonstrated an inhibitory effect on GBS. (22). Cases of colonized infants born by CS in the absence of ruptured membranes could be due to any number of other vectors other than the mother that come in contact with the baby.
7. Over 6 vaginal exams significantly increased rates of GBS disease(15). Scalp electrodes double the risk of GBS colonization of amniotic fluid (19)
In my practice, with restricted AROM and Vaginal exams and no scalp electrodes, 3% of births the baby’s head comes out in the sac and never makes direct contact with the uterus, cervix or vaginal walls at all. How would restricted AROM, Vaginal exams and scalp electrodes affect GBS disease rates?.among low risk women? Among high risk women?
8. When does GBS cause disease? 99% of babies colonized with GBS, dont get GBS disease. 99.99% of women colonized with GBS, dont get GBS vaginitis. Why does GBS sometimes attack and sometimes live in ecological balance? Why is GBS present in 2-3 times as many women in the USA than in Ireland, Cambodia, Taiwan, Philippines or Africa? (11) Why is long term (over 6 months duration) Symptomatic GBS Vulvovaginitis becoming more common in the western world? (12)
9. How does GBS inhibit lactobacillus growth?
10. How many newborns will die of GBS disease in 10 years? 20 years? 40 years?
In the presence of so many unknowns, current protocols reflect an bias to take action in the presence of a lack of appreciation or humility for the complex habits of GBS and no consideration of the next generation of newborns.
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2. Yancey MK, Schuchat A, Brown LK, Ventura VL, Markenson GR.The accuracy of late antenatal screening cultures in predicting genital group B streptococcal colonization at delivery. Obstet Gynecol 1996;88:811–5.
3. Itakura A.Kurauchi O Morikawaa S, Matsuzawab K Mizutania S, Tomodaa Y. Variability of peripartum vaginal group B streptococcal colonization. International Journal of Gynecology & Obstetrics 55 (1996) 19-22.S
4. Tamerou Asrat, et.al.The accuracy of late third trimester antenatal screening for group B streptococcus in predicting GBS colonization at delivery American Journal of Obstetrics and Gynecology, Volume 195, Issue 6, Supplement 1, December 2006, Page S40
5. Chu YW, Tse C, Tsang GK, So DK, Fung JT, Lo JY. . Invasive group B Streptococcus isolates showing reduced susceptibility to penicillin in Hong Kong. Antimicrob Chemother. 2007 Dec;60(6):1407-9.
6. Joachim A, Matee MI, Massawe FA, Lyamuya EF. Maternal and neonatal colonisation of group B streptococcus at Muhimbili National Hospital in Dar es Salaam, Tanzania: prevalence, risk factors and antimicrobial resistance. BMC Public Health.;2009: 9:437.
7. Klevens RM, Morrison MA, Nadle J, et al.Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA. 2007 Oct 17;298(15):1763-71.
8. Appelbaum, P. C. 1992. Antimicrobial resistance in Streptococcus pneumoniae: an overview. Clin. Infect. Dis. 15:77-83.
9. Jacobs, M. R., S. Bajaksouzian, A. Zilles, G. Lin, et al. 1999. Susceptibilities of Streptococcus pneumoniae and Haemophilus influenzae to 10 oral antimicrobial agents based on pharmacodynamic parameters: 1997 U.S. Surveillance study. Antimicrob. Agents Chemother. 43:1901-1908.
10. Walsh CT Fischbach MA New ways to squash superbugs. Scientific American, 2009. 301:32.
11. Whitney CG. et.al.The International Infections in Pregnancy Study: group B streptococcal colonization in pregnant women. The Journal of Maternal–Fetal and Neonatal Medicine 2004;15:267–274.
12. Cohain, JS. Long term Symptomatic GBS Vulvovaginitis – 8 cases resolved with freshly cut garlic. European Journal of OBGYN Reprod Biology. 2009;146(1):110-1.
14. McKeever TM, Lewis SA, Smith C, Hubbard R. . The importance of prenatal exposures on the development of allergic disease: a birth cohort study using the West Midlands General Practice Database. Am J Respir Crit Care Med. 2002 Sep 15;166(6):827-32.
15. P T Heath,1 G F Balfour,1 H Tighe,1 N Q Verlander,2 T L Lamagni,3 A Efstratiou Group B streptococcal disease in infants: a case control study. Arch Dis Child 2009 94: 674-680.
16. Centelles-Serrano MJ, Pérez-Moreno MO, Llovet-Lombarte MI, Cortell-Ortolá M, Jardí-Baiges AM, Buj-González JI.Effectiveness of systematic investigation for Group B Streptococcus in urine samples to identify colonized pregnant women. Enferm Infecc Microbiol Clin. 2009 Aug-Sep;27(7):394-8.
19. Keski-Nisula L, Kirkinen P, Katila ML, Ollikainen M, Saarikoski S. Cesarean delivery. Microbial colonization in amniotic fluid.J Reprod Med. 1997;42(2):91-8.
20. Kjaergaard N, Helmig RB, Schønheyder HC, Uldbjerg N, Hansen ES, Madsen H. Chorioamniotic membranes constitute a competent barrier to group b streptococcus in vitro. Eur J Obstet Gynecol Reprod Biol. 1999 Apr;83(2):165-9.
23. Centers for Disease Control and Prevention (CDC). Trends in perinatal group B streptococcal disease – United States, 2000-2006. MMWR Morb Mortal Wkly Rep. 2009 Feb 13;58(5):109-12.
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