The war had been long...casualties high. At last the people developed a secret weapon so powerful that the tide of the war would finally turn...and turn it did! The weapon was deployed against the great beast and it fell, presumed dead. The people rejoiced. Meanwhile, the not- quite-dead-after-all enemy lay brooding silently, mulling the powerful energy of the weapon through its body...embracing the changes it wrought. Then he rose from the earth infinitely more terrible than before, and very angry.
In 1928 humanity's secret weapon was deployed: Alexander Fleming discovered penicillin. The medical profession was giddy with the prospect of using this powerful weapon against bacterial pathogens. However, by 1929 this same researcher-hero predicted the eventual outcome of medicine’s war on the bacterial world: a dismal defeat. Within one year of his discovery, Fleming was aware of bacterial resistance to antibiotics. He sounded a voice of warning, but was drown out by the euphoric cheering of the medical community (Buhner, 2012). Without a doubt our arsenal of antibiotics has saved many lives, but with very limited understanding of our declared enemy, which is the vast pool of microbiotic life. Are we creating a terrible and dangerous beast?
Our bodies are complex ecosystems that include trillions of bacteria inhabiting our skin, mouth, respiratory tract, genital areas, and particularly the intestines. Thousands of species of microbes inhabit our gut alone (Ackerman, 2012). In fact, most cells in our bodies are microbial, not human; the ratio of microbes to human cells is ten to one (Blaser, 2006). Microbes have evolved with us for millennia, and in their natural form they are genetically programmed to be our symbiotic partners. Our death or illness means their death, so it is not in their best interest to become pathogenic. Symbiotic microbes generally increase the fitness of their human host. For example, they help the body utilize nutrients more efficiently; they help regulate the production of stomach acid and help us digest our food; they help regulate and develop the immune system; they protect us against pathogenic outsiders; they aid in organ development and metabolism. Without their presence within us, our human bodies would sicken and die.
The antibiotic war we have been waging against bacteria in our bodies has changed our microbiota in a number of ways. Bacteria are capable of creating strands of DNA called plasmids that they extrude outside of themselves. When a bacterium comes in contact with another bacterium of its own variety or another, the second bacterium copies the filament of DNA in the plasmid, takes the genetic information, and incorporates it into its own DNA. In this way a resistant strains of bacteria can pass along the genetic information for antibiotic resistance. Bacteria can also release strands of their DNA, some containing resistance information. Other bacteria encounter those pieces of DNA, ingest them, and incorporate the new information into their own DNA. So, whenever pathogenic bacteria exist in an environment where they are regularly exposed to antibiotics, they inevitably adapt and become resistant (Bennett, 2008). Bacteria also release substances similar to pheromones when they are confronted by stressors such as antibiotics. These pheromone-like substances then attract other bacteria to the “battleground” thus exposing exponentially more bacteria to the possibility of becoming resistant (Buhner, 2012).
In regards to birth protocols, the fact that bacteria can and do adapt to environmental stressors, especially to antibiotics, is important because Group B Streptococcus (GBS) is also becoming resistant to antibiotics, particularly Erythromycin and Clindamycin (Borchardt, 2006; Verani, 2010). One study found that erythromycin resistance was present in 22% of GBS isolates (Heelan, 2004). We are just beginning to see evidence of resistance to penicillin, which is our first line of defense against pathogenic GBS (Kimura, 2008; Verani, 2010).
Resistance is not the only way antibiotic use can change bacterial flora in our bodies. Research is also beginning to prove that resistance and virulence are linked. In other words, as a pathogen becomes resistant to antibiotics, it also tends to become more virulent and more likely to cause illness (Coburn, 2007; Buhner, 2012). Current CDC protocols advise that all women who have tested positive for Group B Strep in their intestinal and urogenital tracts be give antibiotics during labor. In the case of GBS, could the constant exposure to antibiotics when they are administered to 30% of laboring women make the bacteria not only resistant to our antibiotic tools but also create aggressive strains that make babies more ill if they do succumb to infection? Is GBS becoming more pathogenic?
Group B Streptococcus is a gram-positive bacterium that is very common in the human intestinal tract. Vaginal or rectal colonization occurs in 15% to 30% of women. The colonization can be intermittent, transient, or chronic, meaning that these colonies of bacteria can come and go in the intestinal or genital tracts rather quickly, or they can be permanent residents there.
Usually, the presence of these bacteria represents the natural, healthy flora of a woman’s body. On rare occasions, however, they can cause illnesses. Intrauterine infections and cystitis can be the result of the colonization ascending into the genital and urinary tract. During pregnancy GBS can also, on extremely rare occasions, cause chorioamnionitis, endometritis, wound infections, preterm labor, preterm delivery, premature rupture of membranes, miscarriage, and stillbirth. In newborns, the infection can cause sepsis, meningitis, and pneumonia, and it is a leading cause of neonatal morbidity and mortality. In the United States annually, approximately 1600 babies develop GBS illnesses, and there are 80 deaths among those babies who become sick (Schrag, 2002). Stated another way, in the United States there are around 4,000,000 births every year (Hamilton, 2011). One in every 2,500 babies born will become sick with GBS. One in every 50,000 babies born will die of GBS. One in 20 who get sick with this disease will die.
The Center for Disease Control and Prevention recommends that all pregnant women be screened at 35-37 weeks gestation for GBS, and those testing positive should be given IV antibiotics during their labor (Schrag, 2002). The CDC also recommends that if a woman develops a fever above 100.4 degrees F, if her membranes rupture more than 18 hours before the baby’s birth, if she has a premature labor or birth (before 37 weeks gestation), or if she has had a previous baby with GBS infection, she should also receive IV antibiotics during labor (CDC, 2010).
This means that around 30% of laboring women will receive prophylactic antibiotic treatment, and 30% of babies receive a dose of antibiotics at a critical time for the acquisition of essential bacterial cultures. What are the effects of disturbances in the development of robust bacterial flora in newborn’s body? We know that neonates need to be exposed to numerous genera, species and strains of bacteria that perform nutritive, metabolic, immunological and protective functions (Fanero, 2003). What damage is caused to possibly every system of the baby’s body when acquisition of bacterial cultures is interrupted? For example, newborns have low levels of vitamin K because it does not pass from mother to baby through the placenta, and before birth a baby’s intestines are not yet colonized with bacteria that synthesize vitamin K2 (Linus Pauling Institute, 2011). How does a bolus of antibiotic at birth affect the colonization of bacteria that create Vitamin K2? Science is only just beginning to understand the ramifications of bacterial colonization in infants and has barely begun to face possible consequences for a baby who is inundated with antibiotics at this critical time. We do not understand the long-term effects of antibiotic prophylaxis on the future health of babies.
Another possible complication of the prophylactic protocol for women who test positive to GBS and receive the antibiotic during labor is the risk of anaphylactic shock. One in ten people have an allergy to penicillin (ACAAI, 2010). Up to 4 in 10,000 women will have a serious, life-threatening anaphylactic reaction to penicillin (Chaudhuri, 2008; Shrag, 2002). The probability of a baby dying of GBS infection is 1 in 50,000. Thus, the risk of life-threatening anaphylactic shock in the mother is much higher than the risk of a baby dying of GBS infection.
Several years ago in Midwifery Today, midwife Helena Wu made this statement: “If a woman's Group B strep culture comes back positive, I have them do an herbal regimen similar to treating yeast or other vaginal infections along with dietary modifications (no sugar or carbs, and add probiotics) for one week. They really have to follow it. Re-test. So far, the tests have come back negative” (2010). I was intrigued with this statement and contacted Helena. This is still her protocol, and she still, after more than two years, has had no GBS test come back positive on the second test. Helena lives in Vermont where midwives are not authorized to give IV antibiotics. “The goal is not so much to kill GBS but to bring the body into a state of health where it will balance its microbes on its own. Herbs, flower essences and essential oils can interfere with the microbes in various ways and enhance the functioning of the body allowing it to regain a better balance in its ecosystem.” If the body is healthy, naturally healthy flora will be prevalent, thus minimizing the group B strep strains. If a mom is healthy, her baby will be healthy and will be less likely to succumb to an infection (H. Wu, personal communication, December 3, 2012). Herbs she recommends are goldenseal, echinacea, thyme, oregano, rosemary, and usnea. Helena also believes we need to carefully teach parents with neonates the signs and symptoms of GBS illness. We need to be scrupulous in our postpartum visits, always carefully observing the health and well being of each baby. It is important to note, however, that these practices may reduce quantity of GBS bacteria only as long as the regimen is followed. So, the woman needs to continue with the protocol until the baby is born.
Several studies have proven that water births have extremely low incidences of GBS infection. In one study, only one baby in 4432 births developed a GBS infection (Cohain, 2011).
Buhner recommends using these three types of herbs in an anti-bacterial herbal formulation:
1. Systematic antibacterial: herbs that are broadly systemic and are spread by the bloodstream throughout the body (for example, cryptolepis, sida, alchornea, bidens, and artemisia)
2. Localized antibacterial (for example, the berberines, juniper, honey, usnia)
3. Facilitative or synergistic herb (for example, licorice, ginger, and black pepper) (2012, p. 82)
An anti-streptococcal part of an herbal protocol for genital infections might look like this: 1. Echinacea augustifolia tincture: 1 tablespoon in minimal water, every hour
2. Cryptolepsis, sida, or alchornea tincture: 1 tablespoon every hour
3. Lomatium, thodiola, and eleuthero (equal parts) tincture: 1 teaspoon 4 times daily (2012, p. 52).
Note: not all of these herbs are considered completely safe for use during pregnancy, so they shouldn't be used without consulting with an experienced herbalist or holistic healthcare professional.
So, with deepest concern for the moms and babies, how should women be counseled in regard to prophylactic antibiotic treatments during labor? The midwifery model of care teaches the important principle of informed consent. It is a midwife's responsibility to educate and share these principles, and then support each mother’s intuitive and educated decision. Antibiotic prophylaxis has risks, dangers, and ethical shortcomings. Perhaps in the long run we can learn to manage the microbiota within us in a way that will reserve the power of antibiotics for life-threatening illness and not use it as a prophylaxis. And finally, may we look forward to the time when managing our microbiota isn’t a battle but an act of nurturing and supporting the microflora that are essential to our own health and well being.
Ackerman, J. (2012). The ultimate social network. Scientific American, 306:6.
American College of Allergy, Asthma & Immunology. (2010). Penicillin allergy. Retrieved from http://www.acaai.org/allergist/allergies/Types/drug-allergy/Pages/penicillin-allergy.aspx
Bennett, P.M. (2008). Plasmid encoded antibiotic resistance: acquisition and transfer of antibiotic resistance genes in bacteria. British Journal of Pharmacology, 153, S347- S357.
Blaser, M.J. (2006). Who are we? Indigenous microbes and the ecology of human diseases. EMBO reports, 7(10): 956-960. (European Molecular Biology Organization)
Borchardt, S.M., DeBusscher, J.H., Tallman, P.A., Manning, S.D., Marrs, C.F., Kurzynski, T.A., & Foxman, B. (2006). Frequency of antimicrobial resistance among invasive and colonizing Group B Streptococcal isolates. BMC Infectious Diseases, 6:57.
Buhner, S.H. (2012). Herbal antibiotics: natural alternatives for treating drug-resistant bacteria. North Adams, MA: Storey Publishing.
Center for Disease Control and Prevention. (2010). Group B Strep (GBS). Retrieved from http://www.cdc.gov/groupbstrep/guidelines/new-differences.html
Chaudhuri K., Gonzales, J., Jesurun C.A., Ambat, M.T., & Mandal-Chaudhuri S. (2008). Anaphylactic shock in pregnancy: a case study and review of the literature. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/18691872
Coburn, P.S., Baghdayan, A.S., & Shanker, N. (2007). Horizontal transfer of virulence genes encoded on the enterococcus faecalis pathogenicity island. Molecular Microbiology 63(2): 530-544.
Cohain, J.S., (2011). Waterbirth and GBS. Midwifery Today Int. Midwife. Winter; (96): 9-10.
Fanaro, S., Chierici, R., Guenini, P., & Vigi, V. (2003). Intestinal microflora in early infancy: composition and development. Acta Paediatrica, 92(s441):48.
Hamilton, B.E., Martin, J.A., Ventura, S.J. (2011). Births: Preliminary Data for 2010. National Vital Statistics Report, 60:2.
Heelan, J.S., Hasenbien, M.E., & McAdam, A.J. (2004). Resistance of Group B Streptococcus to selected antibiotics, including erythromycin and clindamycin. Journal of Clinical Microbiology 42(3):1263-4.
Kimura, K., Suzuki, S., Wachin, J., Kurokawa, H., Yamane, K., Shibata, N, & et al. (2008) First molecular characterization of Group B Streptococci with reduced penicillin susceptibility. antimicrobial Agents and Chemotherapy. 52:8.
Linus Pauling Institute. (2011). Micronutrient information center: Vitamin K. Retrieved from http://lpi.oregonstate.edu/infocenter/vitamins/vitaminK/
Schrag, S.J., Zell, E. R., Lynfield, R., Roome, A., Arnold, K.E., Craig, A.S., et al. (2002). A population-based comparison of strategies to prevent early-onset group B streptococcal disease in neonates. New England Journal of Medicine, 347:233-239.
Schrag, S.J., Gorwitz, R., FultzpButts, K., & Schuchat, A. (2002). Prevention of perinatal Group B Streptococcal disease. MMWR 51(RR11); 1-22.
Verani, J.R., McGee, L, & Schrag, S.J. (2010). Prevention of perinatal Group B streptococcal Disease: Revised guidelines from CDC, 2010. Recommendations and Reports, 59(RR10);1-32.
Wu, H. (2010). Tricks of the trade. Midwifery Today, Summer 2010.