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Group B Strep Article

Posted by fullerbirthsupport on January 10, 2011 at 12:13 PM

Group B Strep is a bacterial infection that women are tested for usually in their 36th week of pregnancy. Although it is harmless to us, there is a small risk of the infection being transferred to the baby during delivery, and so it is procedure in hospitals to administer antiobiotics to the mother during labour if she has tested positive for GBS, or if her GBS status is unknown.

 

Here is a great article that every pregnant woman should read about Group B Strep:

 

Newborn Group B Strep Infection: Top 10 Reasons to Not Culture at 36 Weeks

by Judy Slome Cohain

Copyright: Midwifery Today 2010

 

 

1. Culturing at 36 weeks and treating GBS-positive women prophylactically in labor has never been shown to decrease newborn GBS disease more than not culturing and only treating women who go into labor prematurely, have ruptured membranes for more than 18 hours, or have a fever and is far more costly. Culturing at 36 weeks and treating GBS-positive women prophylactically in labor has never been shown to decrease newborn GBS disease by randomized controlled trials.

 

 

2. The premise that GBS cultures are accurate for five weeks is based on a single study of 116 women. Larger studies failed to reproduce these results and have shown GBS cultures are not reliable for even 24 hours.

 

 

3. Penicillin-resistant GBS has been documented since 2007 and in one study already makes up 10% of GBS cultured from women. Based on history, 25-45 years from now, 50% of GBS is likely to be resistant to penicillin. It is plausible, that giving mega doses of penicillin to a million women in labor each year will speed the selection for penicillin resistant strains. No new antibiotic families have been discovered since 1960 so there is little hope for discovery of more effective antibiotics.

 

 

4. About 50% of GBS is already “resistant” to the antibiotics (clindamycin and erythromycin) used by the 7-10% of women who are allergic to penicillin. When the GBS is resistant, the alternative antibiotic, vancomycin, has been causing strong side effects such as hypotension and “Red Man syndrome” (i.e. hives, histamine reaction and feeling lousy).

 

 

5. The US Centers for Disease Control (2002) declared antibiotics a “temporary solution” because of the known risk of penicillin-resistant GBS, though failed to define temporary.

 

 

6. A GBS vaccine is never going to happen, because the surface antigens of GBS mutate too quickly to give the vaccine before pregnancy, and the legal liability of giving pregnant women vaccines is too great. The last 30 years of efforts to find an effective vaccine have failed.

 

7. One in 10,000 women have serious anaphylactic reactions to penicillin.

 

 

8. Vaginal GBS is twice as prevalent in states and countries that overuse antibiotics.

 

 

9. If the noses of newborns who have no GBS disease, are cultured, many will culture positive for GBS even if the mother was given Penicillin in labor. But the newborns who culture positive for GBS who’s mother’s received Penicillin in labor had three times more newborn respiratory distress (nasal flaring, grunting, retraction or tachypnea i.e.respiration rate >60 breaths/minute, within 48 hours after birth compared with GBS colonized newborns of untreated mothers. Antibiotics given during pregnancy also seem to be associated with increased allergies and asthma in children.

 

 

10. Telling women they have a bacteria that may kill their newborn is terrifying to most pregnant women.

 

 

Top 10 Things We Don’t Yet Know About GBS of the Newborn

 

1. How many full-term babies are injured (not killed) from GBS disease of the newborn? What morbidity do they experience?

 

 

2. Do prophylactic antibiotics to GBS-positive women prevent GBS morbidity in full-term newborns (vs. mortality)?

 

 

3. What is the effect of giving antibiotics to pregnant women with asymptomatic GBS bacteriuria on the occurrence of GBS disease of newborn?

 

 

4. Since prolonged ROM is known to increase the risk of GBS disease, how would eliminating AROM as well as scalp internal electrodes affect the occurrence of GBS disease of newborn?

 

 

5. Since frequent vaginal exams (more than six) have been shown to increase the risk of GBS disease, how would eliminating vaginal exams affect the occurrence of GBS disease of newborn?

 

6. We know that 99% of babies colonized with GBS don’t get GBS disease. Why? We know that 99.999% of women colonized with GBS don’t get GBS vaginitis. Why? Why does GBS sometimes cause infection and sometimes live in ecological balance?

 

 

7. Why is GBS present in two to three times as many women in the US than in Ireland, Cambodia, Taiwan, Philippines or Africa?

 

 

8. How does GBS inhibit the growth of lactobacillus in the vagina?

 

 

9. Since many have tried and no one has ever demonstrated that GBS crosses intact fetal membranes, why is it still believed that that happens? If so, how?

 

 

10. How many newborns will die of GBS disease in 10 years? 20 years? 40 years?

 

 

 

Judy Slome Cohain, CNM, is devoted to illuminating the field of women’s health with objective evidence.

 

1. Ohlsson A, Shah VS. Intrapartum antibiotics for known maternal Group B streptococcal colonization. Cochrane Database of Systematic Reviews 2009, Issue 3. Art. No.: CD007467

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.S4. 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.

13. Lin FY, Troendle JF. Hypothesis: Neonatal respiratory distress may be related to asymptomatic colonization with group B streptococci. Pediatr Infect Dis J. 2006 Oct;25(10):884-8.

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.

17. Anderson BL, Simhan HN, Simons K, Wiesenfeld HC. Additional antibiotic use and preterm birth among bacteriuric and nonbacteriuric pregnant women. Int J Gynaecol Obstet.2008;102(2):141-5.

18 . Smaill F, Vazquez JC. Antibiotics for asymptomatic bacteriuria in pregnancy. Cochrane Database Syst Rev. 2007; 18;(2):CD000490.

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.

21. Winram SB, Jonas M, Chi E, Rubens CE. Characterization of group B streptococcal invasion of human chorion and amnion epithelial cells In vitro. Infect Immun. 1998 Oct;66(10):4932-41.

22. Kjaergaard N, Hein M, Hyttel L, Helmig RB, Schønheyder HC, Uldbjerg N, Madsen H. Antibacterial properties of human amnion and chorion in vitro. Eur J Obstet Gynecol Reprod Biol.2001;94(2):224-9.

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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1 Comment

Reply Sean
11:12 AM on June 20, 2011 
So what is your hypothesis? Should we not treat mother with antibiotic based on the lack of clinical evidence to show improvement. Are risk factor associated with antibiotic treatment a greater risk when they have not been able to show improvement in the mortality of newborns.