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Tuesday
Jul082008

PubMed Says: GBS infection in pregnancy

PubMed is a database of original journal articles in basic biological sciences and medicine maintained by the National Institutes of Health (NIH). I am, by virtue of my education as well as my temperament, a PubMed addict. That is to say, in researching my medical care, I like to go straight to the horse's mouth. So today, in the spirit of sharing what I learn in my digging and in hopes of said digging benefiting others, I am inaugurating a new periodic series at Glow in the Woods-- PubMed Says. For the first installment of the series, I am discussing an issue of interest in managing a subsequent pregnancy-- intrauterine infections with group B streptococcus (GBS).

Our immune systems are really a wonder of efficiency and adaptability. In fact, they are essentially mini-evolution machines, running in real time.  You see, with the number of pathogens we have the potential to encounter in our environment, encoding even a single fighter molecule for each of these would require more genes than we have in our entire genomes. Not to mention that pathogens evolve just like everything else (think new strains of flu every year), and so having static defenses is only marginally better than having no defenses at all. Ok, let me qualify that-- we have static immune systems too (skin being the biggest organ and biggest participant in that system), and we would not be able to hold off the assault of all the pathogens we encounter in our daily lives without that innate immune system. But neither could we do without the adaptive one-- the one we hear the most about, the one that has those famed antibodies as major players.

Antibodies are molecules made by the cells of our adaptive immune system that can recognize specific portions of specific pathogens. They are generated randomly, but according to rules-- one component of each specified type is picked randomly, and components are assembled in specified order. Sometimes the joining of the components is a bit off, which provides for even more variability.

Everything in biology happens via interaction of surfaces, tiny, microscopic shape fitting. Molecules are themselves signals, and their interaction is the passing of that signal. That, combined with the vast number of antibodies we generate, means two important things: 1) we can (and do) generate antibodies to pathogens we have never encountered before, to pathogens no-one has encountered before; and 2) we can and do generate antibodies that recognize our own molecules, molecules that are working hard to keep us chugging along. That last possibility is a problem, and the basis of autoimmune disorders.

So the reason autoimmune disorders are actually rare is that we also have a great way of "teaching" our immune system about self vs. non-self. We need it to know not to generate antibodies to self, only to the things that we would encounter from the outside, the non-self, the potential pathogens.

And this is finally where this little discussion becomes relevant to pregnancy-- the self vs. non-self education thing? It happens perinatally. Very loosely speaking, while the baby is cooking, the immune system is set to assume that everything it encounters is self, and so it kills off all the cells that would produce antibodies that can interact with these self molecules. At birth, the switch gets flipped, and the system gets reset to assume that everything new it encounters from then on is non-self, pathogen, signal for search and destroy. Pretty cool, right?

Well, there is one teensy-weensy problem. The problem, of course, is that baby in utero effectively has no functioning immune system. Ooops. But the good news is, the baby is in the sac that is in the uterus, and no pathogens are supposed to be able to get into the intact sac. And for most women, that is exactly how it goes. The bad news is that for some women some infections can get in, with fatal consequences.

This question is of special interest to me because my son A was infected with one of these infections, Group B Strep (GBS), and the pathologist ruled that to be a contributing factor in his death. Beyond the "what happened?" question, history of infections in the intact sac also have serious implications for any subsequent pregnancy, and that is why I chose this topic today.

A paper* (A 30-Year-Old Pregnant Woman with Intrauterine Fetal Death) was published last summer in the New England Journal of Medicine (NEJM), that both describes a particular case of a fatal GBS infection, and does a nice job reviewing in brief the general state of knowledge about causes of stillbirth in general, and infections in particular.

The case described in the paper is sad and tragic, and all too familiar to many of us here-- normal pregnancy with some minor causes for concern throughout, resulting in fetal death and stillbirth in the 40th week of gestation.  Although the text uses medical jargon, the upshot is that upon delivery the baby looked fine, with only the skin changes as a sign of having been dead for about a day being notable. In other words, without an autopsy there would have been no explanation for this tragedy, and no information to guide the family in making decisions about a subsequent pregnancy.

Multiple causes of stillbirth were considered, including fetal anomalies (ruled out by autopsy), maternal disease (discussed and found unlikely due to medical history), unexplained (always popular, no?), and fetal infection. According to the literature, infections account for approximately 10-25% of stillbirths, with significantly higher rates in economically depressed areas and in developing countries.

In light of what I said above, it should be pretty clear that any infection that can breach the sac is likely to lead to unfortunate consequences. Infections can be caused by bacteria, viruses, fungus, or protozoa. In addition to direct fetal infection, infections may also cause stillbirth via placental damage or severe maternal illness. There are very few pharmaceutical agents available to treat viral infections even in adults, and as far as I know there is not much that can be done for a fetus infected with a virus.  Yeast (a fungus) and various protozoa have been reported as causes of stillbirth, but extremely rare causes. What I want to do here is focus on bacterial infections, and GBS infections in particular, and then discuss management of a subsequent pregnancy if a diagnosis of infection as a primary or secondary cause of stillbirth was made or suspected.

GBS is known to be common in genital tract, and a large percentage of healthy adult women are colonized, i.e. have GBS in their vagina or lower intestine (This meta-study from Europe shows rates of colonization of 6.5-36% with great geographic variability) .  Recognition of GBS as a human pathogen did not occur until 1960s. In the 1970 it was recognized as a leading cause of neonatal infection and an important cause of maternal uterine infection. Since then, screening protocols have been put in place to identify women colonized with GBS, and antibiotic treatment during labor is recommended for women found to be colonized. These treatments are aimed at reducing the rate of neonatal infection, and establishing these guidelines has led to a marked decrease in early neonatal GBS infections.

In addition, and more relevant to our discussion here, 4-10% of stillbirths in United States and Europe are thought to be caused by GBS infections. Thus it is known that GBS can cross intact membranes and cause infection of amniotic fluid and/or fetus. In addition, GBS is associated with some cases of PPROM, and in at least one study, for at least one population, has been shown to be the leading cause of PPROM.

GBS, like other bacterial infections known to cross the intact membranes and cause stillbirth and other adverse perinatal outcomes, is an ascending infection, meaning that it rises up from mother's vagina, anus, or rectum, to the uterus. In most cases, infection occurs after the rupture of membranes, and that is why the guidelines for treatment of colonized mothers call for treatment with antibiotics while in labor.

As I mentioned above, this is an adequate protocol for most mothers. However, for those of us who have had infection, particularly bacterial infection, ruled to be a cause of stillbirth or PPROM, it is wise to consider additional measures in a subsequent pregnancy. I would, in abundance of caution, also suggest that families where the cause of stillbirth was unexplained, particularly those who did not have an autopsy performed, or whose autopsy did not include a report on possible infections, consider these additions to their subsequent pregnancy care protocol.

The NEJM paper, after providing fairly conclusive evidence for GBS being the cause of the stillbirth in the particular patient, includes the following possible interventions (beyond the general guidelines referenced above) aimed at attempting to prevent a recurrence of stillbirth caused by GBS:

  • Screen for GBS rectovaginally early in pregnancy and suppress or eradicate detected colonization with antibiotics. (It is worth noting that colonization with GBS can be intermittent, that treatment is not always successful at completely eradicating colonization, and that re-colonization occurs in up to 40% of subjects within 4 weeks.)
  • Screen for GBS in patient's sexual partners and suppress or eradicate detected colonization with antibiotics. (Same caveats as above.)
  • Advise abstinence or condom use.  (Evidence that GBS is sexually transmitted is weak. In the words of the article authors, "Both interventions are relatively harmless, but compliance may be poor.")
  • Vaccinate the mother. (No vaccine is currently available.  If it does become available in the future, it will not protect fetuses before 32 weeks of gestation because IgG antibodies that would be the actual mechanism of the protection are transferred across the placenta only poorly before that gestational age.)

My own protocol for my ongoing pregnancy includes early and frequent urine screenings for GBS and other bacteria. If and when any are found, I am treated with antibiotics in hopes of preventing an intrauterine infection.  This intervention was proposed by my OB, with the caveat that there have not yet been studies to show the effectiveness of this prevention method. I was more than happy to agree to this protocol, as this is pretty much the only thing we can actually do to try to prevent a recurrence.

Obviously this protocol is most useful for tracking GBS and other bacterial pathogens. I have not done enough research to comment on what measures might be able to prevent a recurrence of other types of infection. However, in the abundance of caution category, I would suggest that it might be wise to treat the ability of any type of previous ascending infection to cross the membranes as a red flag for the possibility of other ascending infections being able to do the same in subsequent pregnancies, i.e. that it might be useful to apply the protocol for attempted prevention of bacterial infection in cases where other infections were implicated in a previous pregnancy. This is a conjecture on my part. I do not know of any studies that quantify risks of different infections following a previous case of any given infection. However, each one of us, in each of our subsequent pregnancies, is concerned with the sample size of exactly one, and therefore, we, in consultation with our health care providers, can and should decide which protocols would give us peace of mind in addition to which are incontrovertibly scientifically justified.

 

I hope you found this useful, or, at least, interesting. If you have ideas for future installments of this series, please let me know.

 

*I can not place a pdf of the paper in public domain here. But I do have it (as well as the pdfs of the other papers mentioned in this entry) , and if you are interested, please email me through our contacts page, and I will be happy to send it to you. 

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Reader Comments (31)

great post Julia. I am so glad your OB was willing to do this for you. I have too many friends whose doctors are not willing to take unproven but potentially helpful measures.

July 8, 2008 | Unregistered Commenterlisa b

so glad we've got a resident scientist here. thanks for the very informative post. I'm so glad you have a good doctor, and I think the advice you gave STE was right on too.

I think my PPROM was due to fibroids, but infection is really one of the only other known causes. so good to know there is something you can do as prevention, as PPROM makes you feel so very helpless in a subsequent pregnancy -- not that I'd know firsthand, but I've had plenty of time to think about it...

thanks again.

July 8, 2008 | Unregistered Commenterluna

woman + brains = super!
woman + brains + watching my back = best thing ever.


Thank you for your informative and approachable post. I'm looking forward to the sometimes-series!

Cheers

July 9, 2008 | Unregistered Commentersarah

Great, informative post. My son died from getting MRSA from me and the extent of the colonization (in me) has made future bio-children an impossiblity.

July 9, 2008 | Unregistered Commentercharmingdriver

(I'm not taking back what I wrote about fear on the 6x6, but I will say this: 8 years ago, this article would've made me freeze in my tracks, and stay up all night chewing my fingers. Now? I can only sigh, wish I knew this information before, and ponder how it is we continue to reproduce as a species.)

I also have GBS, knew it at the start of Maddy's pregnancy, and in fact, had a UTI circa 8w where it was present in the culture. I have asked the experts in every possible way I can think of how, whether this in ANY WAY had ANYTHING to do with her death: did it infect her? The placenta? Cause an abruption? ANYTHING? And they patiently tell me, no, no, no, a thousand times no. There are signs they say, things to look for, patterns that appear, and there does not seem to be any connection whatsoever between my fucking colony and her death.

But believe me you, if there is a next time, I'm marching in with this information and demanding frequent testing and abx. Thanks for this Julia, and I'm also looking forward to future installments.

July 9, 2008 | Unregistered Commentertash

Would this have been tested for automatically during the autopsy? I was trying to read my autopsy report again last night and I couldn't find anything about this. But I do remember my OB testing me a couple of weeks before I delivered for Strep and it came back negative. Is this part of the same test? And I did give weekly urine cultures, but I was so naive, I never bothered to ask what they were testing for. They just put a stip in the cup and it never showed anything negative. Any further insight you have would be appreciated. Thanks for the info.

July 9, 2008 | Unregistered CommenterCLC

CLC, the weakly urine cultures are for things that show up on these strips-- ketones (can be an indication of diabetes or a diet that is somewhat off) and protein (indication of pre-eclampsia). To take urine for bacterial culture, you would have to do a "clean catch"-- that's the one with three wetnaps and a screw-top container (the idea is to get the culture from inside and to keep it free from any air-born contaminants).
If your doctor tested you for GBS (as is the protocol for everyone except those who are already known to be carriers) between 35-37 weeks, that test is considered good for 5 weeks. So presumably there would not have been an infection with GBS that would've been advanced enough to impact Hannah by the time of the delivery. But it is still something they should've cultured for during an autopsy. There should be at least a line somewhere about it, but it is a bit hard to predict exactly where in the report to look for it. I can try to read the report for you, if you send it to me at some point. Please let me know if you want me to do that.

July 9, 2008 | Registered Commenterjulia

It's funny. I have an extensive list of things that I worry about. But infection isn't on it. Completely irrational, I know.

July 9, 2008 | Unregistered Commenterniobe

thank you so much for doing this, Julia... so insightful. Can't wait to see more.

July 9, 2008 | Unregistered Commenterkate

Thanks a million for this, Julia. Great stuff, and I am sure appreciated by many. You rock.

July 9, 2008 | Registered Commenterjanis

That is hugely helpful and I will definitely be asking about it. We have no information regarding what sort of infection may have caused the PPROM. We did not do an autopsy on Lennox because his cause of death at 3 days was a collapsed lung + extreme prematurity. I remember being catheterized the first day I was in the hospital so they could get a urine sample to culture and I was put on antibiotics as a matter of course. I'll have to track down the results of that urine culture and see if anything came up on it. Since I never made it to anything close to 35 weeks, I'll also have to see if a GBS test was done.

I would like to get a copy of the study when you have a chance. I don't think I'd get too much pushback from my doctors if I requested some extra testing, but you never know.

July 9, 2008 | Unregistered CommenterA.M.S.

Maybe you addressed this and I completely missed it, but what are your thoughts on limiting internal exams throughout the pregnancy? When I was pregnant the first time and GBS+, the support group I was involved in was adamant about no internals unless a very, very, very good reason.

July 9, 2008 | Unregistered CommenterJozet at Halushki

Jozet, I don't want to nitpick, but I think the answer here hinges on what one considers a very good reason. I, for example, have had rather a few internals this time around already. This is because I keep having contractions, and there really is no way to know whether they are productive unless a cervix check is performed. But I also have been doing frequent urine cultures (more frequent now than before as a result of these contractions-related visits), and when something tiny showed up on the last culture, I had been given antibiotics. Long way around to what I think my answer is, which is that internals are an important tool in certain situations, but that yes, they are a reason to become more watchful about the possibility of infection, and to consider a course of antibiotics.

July 9, 2008 | Registered Commenterjulia

Oh yes, I agree on the nitpicking, and your example is of course, one of medically necessary reasons to have an internal. I was just remembering as a first time pregnant mom, I wasn't well informed or knowledgeable on when an internal was necessary (subjective to some extent) or just a particular doctor's being...curious. I also remember that after my water broke and I still wasn't in active labor, a nurse was insisting on giving me an internal for a "look see"...maybe I just ran into my unfair share of medical personnel who wanted to poke around inside just because. I haven't been as current on my GBS reading lately, and I was mostly wondering to what extent any information about internals was added to or changed as part of any agreed upon protocols.

July 10, 2008 | Unregistered CommenterJozet at Halushki

I hope I was being respectful in my wondering and not using clumsy language. I hope I didn't make anyone feel defensive in their choices. I was just wondering out loud and you did answer my question. Thank you.

July 10, 2008 | Unregistered CommenterJozet at Halushki

The thing that is annoying me..is that while told it was an 'infection' of my plancenta that killed Scott..we have not EVER heard what the infection was or where it came from....

they have promised ALL sorts of tests if I am pregnant again..but I would really like to know what I had and where I got it from.

July 11, 2008 | Unregistered CommenterCrunchy Carpets

I was Strep B positive during both of my pregnancies. I was in the care of midwives(BC Canada) and took a test at about 36 weeks to see if I had Strep. The tests came back positive but nothing was done until labour as I was told that the stats of babies dying was so small and not to worry etc.. I was put on intravenous antibiotics during labour/delivery, which I was told was enough to deal with the Strep. Both my boys were not infected but there wasn't any follow up after the birth, to see if the Strep somehow infected the boys...I am not sure if this was standard procedure or not. Your story is the first I have heard of a baby dying from Strep(or complications from it) and I just wanted to say my heart goes out to you.

July 11, 2008 | Unregistered CommenterJenn

i was positive for gbs with my second pregnancy and was induced for fear of not getting the 2 abx doses in time as i have very fast labors. i'm on my 3rd pregnancy now and was just put on 7 day abx b/c they found gbs in my urine last week. as much as i would like to have a spontaneous labor (the first was also induced due to pre-e and one of the twins was thought to be very small,) i also want to err on the side of caution since the gbs was found in my urine and that means a higher concentration. if my water broke at home, i don't even know if i'd make the 30 minute drive to the hospital to have a baby, much less get abx. i go back this week for my first internal exam and will talk about induction this week.

July 12, 2008 | Unregistered Commentermommymae

I can completely understand your willingness to take antibiotics to keep your GBS infection at bay and protect your baby, however without knowing whether or not this is going to be effective, I think it would be prudent to consider the possible side effects of repeat antibiotic courses. In my estimation this may actually exacerbate the GBS infection. You will be killing off ALL bacteria in your body even the good stuff that keeps GBS in check and at the same time expose the GBS bacteria to antibiotics possibly making it resistant to antibiotic therapy later. What might happen if even with all the courses to kill of the GBS your baby is born alive, but with a GBS infection. Would the GBS be resistant to treatment? That could end badly, too. Have you asked the doc if you are likely to have another intrauterine infection because you have had one before? Antibiotics are one of the best gifts medicine has given us but we need to be careful with them. Consider daily doses of PRObiotics that will encourage the growth of beneficial bacteria and yeasts and discourage the growth of GBS, candida and a myriad of other harmful pathogens. You can eat them in the form of yogurt, kefir, cultured vegetables, and fermented coconut water (sounds weird but it works). Probiotics are also available in capsule preparations. Jarrow is a great one. If you can keep yourself from having GBS in the first place, you won't have to worry about antibiotic side effects. I hope this helps.

July 17, 2008 | Unregistered CommenterStephanie

Stephanie, I appreciate your concern. However, I am afraid you are mistaken in multiple ways.

First, and this is a common misconception, antibiotic use does not create antibiotic resistance. What it does is select for bacteria that are already antibiotic resistant. In other words, because bacteria replicate often, and every replication is a chance to make a mistake in copying DNA, some bacteria in the population may end up with random changes that allow it to be resistant to a particular antibiotic or class of antibiotics. Then, if, by chance, you happen to take that type of antibiotic at the time when these particular resistant bacteria are present, antibiotic will kill off the non-resistant ones, leaving more room and nutrients for the resistant ones to use. However, this is a very rare scenario, and certainly exceptionally rare on the level of an individual patient.

Overuse of antibiotics in populations allows for selection of antibiotic-resistant bacteria and for spread of those in vulnerable populations, such as hospital patients, prison populations, and other people in tight living quarters. Taking a chance that at the time of my antibiotics course (of which I have had the grand total of two in this pregnancy so far, one of them for a bronchial infection) there will be bacteria resistant to that particular antibiotic in my system vs. the chance that an untreated infection can breach the sac again? Yeah, this is the chance I am willing to take.

Note that I am not advocating for indiscriminate use of antibiotics on every pregnant woman or every patient with sniffles. THAT might indeed cause effects observable at the level of populations. As it stands, however, this is a question of assessing risk and reward based on a patient's medical history and various sub-populations to which she belongs.

Second, as I explained in the post above, GBS is an ascending infection. That means that it starts out in the vagina, rectum, or anus, and moves upwards towards the cervix and the uterus. On the other hand, when you take probiotics, they enter your system from the opposite end, through the stomach and onto intestinal tract. It's a great way to replenish your intestinal flora following a treatment with antibiotics. It is, however, of dubious helpfulness with vaginal flora.

Finally, as I clearly stated above, the course of my care was in fact proposed by my doctor. I assure you that not only do I have full trust in this particular doctor (and his rather long and impressive list of peer-reviewed publications), but I have discussed with him both the NEJM paper I refer to above, and the logic of this particular treatment plan in light of my own medical history and information available in the literature.

As to the likelihood of a having another intrauterine infection, basic biology says that the likelihood is indeed increased for those with a history of one getting through the intact sac. As I mentioned in the post, all processes in biology happen via interaction of surfaces. Bacteria did not magically get into my son's sac-- some interaction of molecules on the surface of a bacterium and the surface of the sac allowed for the transport of the bacterium through the sac and the subsequent infection. Knowing that it happened once does in fact suggest that it can happen again. The reason it happened to me and not to a majority of women out there is most likely some minor difference in the structure of some molecule on that sac, a difference that likely impacted nothing else about the process of implantation and development, but did allow for the infection to occur. And yes, the same difference may occur in a subsequent pregnancy, and is more likely to occur in someone to whom it happened before than in someone to whom it had not.

I hope this clarifies these issues for you.

July 17, 2008 | Registered Commenterjulia

Good luck, Julia. I hope for a safe delivery for you and your baby.

July 19, 2008 | Unregistered CommenterStephanie

Julia-I found this article in Pubmed. I thought it was interesting. I'm sure you may have come across it in all of your research but just in case you missed it. Here is the text and there will be a link underneath the text.

Zárate G, Nader-Macias ME.
Centro de Referencia para Lactobacilos (CERELA)-CONICET, San Miguel de Tucuman, Argentina.

AIMS: Lactobacilli, the predominant micro-organisms of the vaginal microbiota, play a major role in the maintenance of a healthy urogenital tract by preventing the colonization of pathogenic bacteria. The aim of the present study was to assess the ability of four vaginal Lactobacillus strains, previously selected for their probiotic features, to block in vitro the adherence of three human urogenital pathogens to vaginal epithelial cells (VEC). METHODS AND RESULTS: Three types of assays were performed in order to determine the inhibitory effect of lactobacilli on adhesion of urogenital pathogens to VEC: blockage by exclusion (lactobacilli and VEC followed by pathogens), competition (lactobacilli, VEC and pathogens together) and displacement (pathogens and VEC followed by the addition of lactobacilli). Bacterial adhesion to VEC was quantified by microscopy (x1000) after Gram's stain. All the strains were able to inhibit by exclusion and competition the adhesion of Staphylococcus aureus to VEC but none was able to decrease the attachment of Escherichia coli by neither of the mechanisms assayed. Only Lactobacillus acidophillus CRL 1259 and Lactobacillus paracasei CRL 1289 inhibited the attachment of Group B streptococci (GBS) to VEC by exclusion and competition respectively. CONCLUSIONS: Lactobacillus of vaginal origin were able to inhibit the attachment of genitouropathogenic Staph. aureus and GBS to the vaginal epithelium. SIGNIFICANCE AND IMPACT OF THE STUDY: The results support the probiotic potential of these Lactobacillus strains as anti-infective agents in the vagina and encourage further studies about their capacity to prevent and manage urogenital tract infections in females.

PMID: 16869901 [PubMed - indexed for MEDLINE]


I have had good luck taking probiotics orally to help support vaginal flora, regardless of the science behind ascending infections versus descending infections. Bacteria emerging from the anus does have a way of making it into the vagina and urethra. According to this study, though, you could put the probiotics right where you want them and they are effective.

http://www.ncbi.nlm.nih.gov/sites/entrez

July 20, 2008 | Unregistered CommenterStephanie

Stephanie, I admire your persistence. Nevertheless, this paper (even from the abstract, and more so from the full text that I just pulled up via my electronic journal access) does not in any way say that "you could put the probiotics right where you want them and they are effective." What it says is that vaginal epithelial cells collected from 5 patients who are not prone to UTIs can, under certain in-vitro conditions (that means not in living organisms) be inhibited from attachment by particular strains of pathogens by particular strains of beneficial bacteria.

I can spend a couple of paragraphs critiquing their methods (the biggest question to me being that experiments were performed with rare epithelial cells rather than an epithelial layer), or talking about the complete absence of molecular work or controls where epithelial cells are drawn from patients susceptible to UTIs in the paper, and, thus, inability of the authors to say how widely applicable these results are. But I think I will just stick with the author's own concluding paragraph, which conveys what I believe is the most charitable possible interpretation and implication of their results:

"In conclusion, the data suggest a probiotic potential of these Lactobacillus strains as anti-infective agents in the vagina and encourage further in vivo studies, such as clinical trials designed to test their capacity to prevent and manage urogenital tract infections in females."

Very, very far from "you could put the probiotics right where you want them and they are effective." But I am certainly glad that you have had such great success, regardless of the science. I am just, forgive me, not inclined to stake my child's life on your great success. Or on a single in-vitro study in what isn't, by any stretch of the imagination, a first-tier journal.

July 20, 2008 | Registered Commenterjulia

Julia-This is the last post I will make and I would like to clarify that in no way was I proposing that I think it would be better to use probiotics INSTEAD of antibiotics (which is what I must assume you believe when you say "I am just, forgive me, not inclined to stake my child's life on your great success."). I was suggesting it as a way to prevent being infected in the first place. Then, if you still became colonized with GBS, of course take the antibiotics. There are other articles in Pubmed from different countries citing the success of different probiotic cultures that have proved successful in supressing the growth of GBS and other harmful pathogens in the urogenital tract. I'd also like to clarify that my persistence in writing about this isn't to try and persuade YOU to eat yogurt and cultured foods (not sure how this puts any lives at stake). It is so others that have posted here that have been GBS positive could possibly benefit from probiotic use. I wouldn't want to put yogurt in my vagina either, but you were so absolutely sure that probiotics taken orally would be of no help to you. Again, I will reiterate that I DON'T BELIEVE TAKING PROBIOTICS SHOULD TAKE THE PLACE OF ANTIBIOTIC USE IN THE CASE OF GBS COLONIZATION. I believe the two could be used to produce the best outcome. Who wouldn't want that? Hopefully using probiotics early in pregnancy and consistently would keep GBS colonization supressed so that antibiotics and the resulting side effects from their use could be avoided. If a GBS infection did occur, by all means take the antibiotics. I have tried to express myself in a friendly manner, but both of your posts back to me have had a very condescending tone. I'm not sure why you are so threatened by someone suggesting pregnant women eat yogurt, cultured foods and take probiotic supplements to HELP control GBS infections. I also do not understand how that would be staking your new little baby's life. Here are some other articles related to this subject from pubmed. You will probably have a myriad of problems with them, too, however maybe someone else is interested. I meant what I said about hoping for a safe delivery for you and your baby. That is all I ever hope for any pregnant mommie. Good luck.

Açikgöz ZC, Gamberzade S, Göçer S, Ceylan P.
Fatih Universitesi Tip Fakültesi, Mikrobiyoloji ve Klinik Mikrobiyoloji Anabilim Dali, Ankara.

Neonatal group B streptococcal (GBS) infections are one of the important health problems because of their high mortality and morbidity rates in certain countries. There are some preventive approaches, including perinatal antibiotic therapy against these infections. Recently, vaccination with conjugated GBS polysaccharides has also been practised. In this study, the in vitro inhibitory effects of 51 lactobacilli (of them 50 were purified from vaginal swabs, 1 from a commercial vaginal tablet) on five GBS (4 clinical isolates and 1 standard strain) were investigated by sandwich plate technique and deferred antagonism well technique. Ten clinical isolates (20%) and the drug-purified Lactobacilli expressed pronounced inhibitory effects on growth of GBS. All of the inhibitory isolates and 10 randomly selected non-inhibitory isolates were identified by API 50CHL kit (BioMeriéx, France). Seven (70%) of the inhibitory clinical isolates were Lactobacillus rhamnosus. The inhibitory isolates had higher acid production than the non-inhibitory ones (p < 0.05), and pH-adjustment destroyed their inhibitory effects entirely. If these results could be applied in vivo, it could be postulated that administration of certain lactobacilli as probiotics via an appropriate regimen may be a safe, physiological and cheaper alternative for prevention of neonatal GBS infections.

PMID: 15900833 [PubMed - indexed for MEDLINE]

and another
about probiotic use to prevent recurring bacterial vaginosis after antibiotic treatment

McLean NW, Rosenstein IJ.
Imperial College of Science, Technology and Medicine, Department of GenitoUrinary Medicine, London.

This paper reports the results of characterising and selecting a strain of Lactobacillus for potential use as a probiotic in regenerating the vaginal flora of women with recurrent episodes of bacterial vaginosis (BV). BV is a condition characterised by a depletion of vaginal lactobacilli accompanied by an overgrowth of a mixed vaginal flora of aerobic, anaerobic and micro-aerophilic species in very large numbers. BV has been associated with various gynaecological and obstetric complications and has an extremely high recurrence rate, due in part to the failure to establish a normal vaginal flora after antimicrobial therapy. A total of 60 vaginal isolates of lactobacilli was assessed for characteristics considered important for vaginal re-colonisation. The characteristics studied were the in-vitro inhibitory activity of the lactobacilli against bacterial species isolated from women with recurrent BV, acid production after growth of the lactobacilli in liquid culture, production of hydrogen peroxide (H2O2) and adhesiveness of the lactobacilli to exfoliated vaginal epithelial cells (VEC). Four strains of lactobacilli, L. acidophilus (61701 and 61880), L. crispatus (55730) and L. delbrueckii subsp. delbrueckii (65407), demonstrated the greatest inhibitory activity against the BV-associated bacterial species. Two of these isolates (55730 and 61880) produced H2O2. All four isolates produced a highly acidic environment after growth in liquid medium (pH <4). Only one of these (strain 61701) was strongly adherent to VEC (>100 bacteria/VEC). A further isolate (L. acidophilus 48101) did not demonstrate maximum inhibitory activity against BV-associated bacteria, but was found to be a strong producer of H2O2 and was also highly adherent to VEC. Isolates 61701 and 48101 could be candidates for use as probiotics for vaginal re-colonisation.

PMID: 10847208 [PubMed - indexed for MEDLINE]

and another

Rönnqvist PD, Forsgren-Brusk UB, Grahn-Håkansson EE.
Department of Clinical Bacteriology, Umeå University, Sweden. daniel.ronnqvist@essum.se

BACKGROUND: The relationship between lactobacilli and other microbes and the association with vaginal pH in the female genital tract were examined. The study also included evaluation of the possibility of supplying probiotics to the genital tract by using panty liners impregnated with the probiotic strain Lactobacillus plantarum LB931. METHODS: This was a randomized, placebo-controlled, double-blind, multicenter study involving 191 healthy fertile women. Specified microbes were counted and vaginal pH was measured once a month for five consecutive months. RESULTS: Major individual variations in the genital microflora composition and the vaginal pH were found among the women. The number of lactobacilli was significantly related to vaginal pH (p<0.001) and approximately 70% of the women were permanent carriers of individual lactobacilli strains. Women with high numbers of lactobacilli were less prevalent with Group B streptococci than women with low numbers (p=0.036), and these women had a lower mean vaginal pH. The number of lactobacilli also correlated with the prevalence of yeast. LB931 could be found in 86% of the labial samples and 54% of the vaginal samples. CONCLUSIONS: High numbers of lactobacilli may contribute to a low vaginal pH and seem to have a negative influence on Group B streptococci. LB931 could be transferred from the panty liners to both the vagina and the labial fold.

PMID: 16752267 [PubMed - indexed for MEDLINE]

July 20, 2008 | Unregistered CommenterStephanie

Stephanie, the tone of my replies was due entirely to the misinformation, misstatements, and the tone in your posts. Starting with "...I think it would be prudent to consider the possible side effects of repeat antibiotic courses. In my estimation this may actually exacerbate the GBS infection" and continuing with misconceptions on what causes and propagates antibiotic resistance, just for starters, is not a good way to convince me that you know what you are talking about. It is, however, an excellent way to not so much imply as state that you think the course of action designed by my OB and myself is inferior to your estimation. And yes, that statement also implies that things you suggest should be done instead of the course we mapped out (not to mention that not until your last post did you ever say that you didn't mean your helpful suggestions to be used instead of antibiotics). That there is what could potentially put my baby's life at risk. I didn't even address all the things that were factually wrong in your original comment-- I was simply too tired and my reply was getting too long.

But since we are talking honestly here, what the hell was this: "Have you asked the doc if you are likely to have another intrauterine infection because you have had one before?" Did you think I didn't ask him? Did you think his answer was "your chances are no greater than anyone else, but we will treat you aggressively just for the hell of it"? Or did you, maybe, not catch on to the fact that I understand enough basic biology to be able to answer that question myself?

Having access to information is one thing. Using that information carefully is another. Overstating what can be concluded based on the work you reference is not insignificant. When done in academic settings, it is, to say mildly, frowned upon. When done in public debates, it can be downright dangerous since it has a possibility to influence people's behavior.

Go back and reread the entry. Note how carefully I qualify the information that can be gleaned from every paper I link to. Note how I phrase my conclusions to carefully state what is known, what can be supported by existing studies, and what is my suggestion. It's not just good academic hygiene or, you know, intellectual integrity. It's no less than is owed to this audience, or any audience for that matter. That you do not understand and do not practice this level of scruples is a big red flag for me.

I am not in any way threatened by your suggestions. I am annoyed to all hell by the flimsy foundations of the same, and your attempts to pretend otherwise. All the papers you list are miles and years away from proving anything about therapeutic properties of various beneficial bacteria preparations in the vaginal flora. Notice that the authors of these papers do not make the claims you feel entitled to make. That you do feel entitled to make these claims is not just dishonest, it is extremely inappropriate, and I will not tolerate you spreading this level of disinformation in the post that is meant to help people make informed decisions about their care in what is sure to be stressful and scary time in their lives.

As the last abstract you quote refers to, the content of individual women's flora is, shock, individual. Years and years and studies and studies are needed before we know whether some of us simply lack the receptors on our epithelial cells that allow or encourage beneficial bacteria to stick, i.e. whether some of us are genetically predisposed to have problematic flora. It will be years and years more before we figure out whether a hell of a lot can be done about it.

I have problems with you quoting these papers in the way that you are not because I am getting paid by big pharma to hawk antibiotics on every street corner (I am not). I have problems with it because you use these, whether maliciously or because you don't know better, in a way that is directly counter to the purpose of this post-- to provide good valid information. I have no problem with debate. I don't even have a problem with being wrong. That is how science is done. What I do have a big huge problem with is dishonesty and flimsy arguments. And as long as you traffic in those, I will be here to push back.

July 20, 2008 | Registered Commenterjulia

I appreciate your need to "push" back. I'm not trying to push you, though. I'm sorry that some of what I have said has seemed obtuse to you. When I asked if you had asked your doctor if you were more likely to have another intrauterine infection I should have worded it differently. I should have just asked "Are you more likely to have another intrauterine infection". I did not comment to try and get women who have had intrauterine infections or vaginal GBS infections to use probiotics in lieu of antibiotics. In fact I said in my first comment " If you can keep yourself from having GBS in the first place, you won't have to worry about antibiotic side effects." which is similar to what I said in my last post when I said "Hopefully using probiotics early in pregnancy and consistently would keep GBS colonization supressed so that antibiotics and the resulting side effects from their use could be avoided." I also asked as a question "Would the GBS be resistant to treatment?" in my first post. I did not tout it as fact. I find it very odd that you continue to say my suggestions are dangerous because they are not supported by scientific fact. Obviously there are studies being done all over the world on this subject and there are countless clinical trials being conducted and financed on the benefits of probiotics against GBS infections, intrauterine infection and many, many other applications. All of these clinical trials would not be financed if there was not a reason to form this hypothesis in the first place. By your own admission, you are willing to follow a protocol of prophylactic antibiotic use without a study proving its effectiveness against preventing GBS infection recurrence (I said in my first comment thatI completely understand your willingness to do this.). Why then, are you so against adding some yogurt, kefir, cultured veggies and probiotic preparations to your protocol that in some studies have shown to suppress GBS colonization? Doing both would be a conservative way to cover all your bases. Eating probiotics does not have negative side effects. They aren't dangerous. I wish you would stop trying to make me out to be some sort imbecile and slow down enough to read and absorb EVERYTHING in my comments. You didn't interpret everything I have said because you are so ready to wring my neck. I'm sorry to have upset you and I'm sorry that you feel I have just swept in here with disinformation. I said probiotics may help control GBS infection in the urogenital and intestinal tract and the papers have said that, yes, they may. I'm sorry I have horrible "academic hygiene" and "intellectual integrity". I posted the abstracts so that women may read them for themselves, do some more of their own research and form their own opinion. I never once said that probiotics should be used solely in lieu of antibiotics. You are putting words into my mouth.

July 20, 2008 | Unregistered CommenterStephanie

Stephanie, you don't need my help to make you out to be some sort of an imbecile-- you are doing a bang up job of it all by yourself.

No, none of the papers you listed show that eating probiotics, or even sticking them in your vagina is going to suppress or prevent GBS or E.coli infections. (And I spent considerable amount of time pulling up and reading full texts of these paper, just to make sure, which I am pretty sure you didn't bother to do.) That you are unable to stick to the claims in the actual papers, even after I pointed out to you how inappropriate that is pretty much tells me all I ever needed to know about your ability to draw conclusions supported by data.

And no, the protocol I am willing to follow and am following does not include prophylactic use of antibiotics. The protocol involves frequent testing, but treatment only when bacteria are found that could be dangerous to the baby. The difference is that for people who do not have a history of bacteria breaching the sac treatment is not necessary until the waters break or labor commences. For people with such history, however, killing off these dangerous bacteria before they have a chance to breach the sac again seems prudent. This is not prophylactic, this is a differential time course of treatment. (And I didn't say anything here I didn't say in the post. You being unable to get that information from the post is also telling.)

It may help you to appreciate just how out of line you are if I tell you that I do routinely use probiotic preparations to improve intestinal flora after antibiotic treatments. I even gave it to my infant daughter when she was having problems with intestinal yeast overgrowth. But there is a huge difference between that and what you are doing here. I am not against probiotics. I am against unsupported claims and very bad use of marginal scientific results.

I appreciate you thinking that you are being helpful. But you are not. Misstating science is not helpful. Overreaching is not helpful. Trying to pass a little for a lot is not helpful. Please stop.

July 21, 2008 | Registered Commenterjulia
Auto-immune diseases are not rare.
August 13, 2008 | Unregistered CommenterGSV
Is it true that Strep B and other bacteria are naturally occuring? If some individuals's chemistry offers the Strep B an environment where it can take over (increase it's colonization compared to other more friendly bacteria), wouldn't it serve to reason that the chemical environment the host is offering be considered ?.... We can influence the balance of bacteria that exist in our bodies, right ?
June 4, 2009 | Unregistered Commenterconcerned
Our immune systems are really a wonder of efficiency and adaptability
July 28, 2010 | Unregistered Commenterbaby carriers
I delivered at 22w 6/7, was found positive with GBS and placed on antibiotics while I labored. My doctors couldn't tell me what caused my PPROM. They suspect either GBS (highly unlikely, according to them) or that I have an incompetent cervix.

I love knowing that my body fucked up.
December 30, 2010 | Unregistered CommenterC

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