Immunity from maternal antibodies protects the majority of newborns, but 1-2% of colonized newborns will develop symptomatic disease. A woman can have a GBS infected baby without any risk factors (GBS in urine or previously GBS infant).
GBS was first identified with cows with udder infections, and recognized as a cause of neonatal septicemia in 1933, and in 1965 was recognized as the leading cause of infection and death in newborns. Its frequency has been increasing, and is also the cause of toxic shock syndrome. It is found in 10-30% of pregnant women, and is the number one killer of newborns. It goes unnoticed in the healthy population, as it causes no symptoms. GBS infections in infants occur at two different times and are differentiated by the time of onset. Early onset illness develops within 6-12 hours of birth. Late- onset happens a week or more after birth. It is thought that late-onset is not related to an infection passed from mother to baby but is acquired from hospital nurseries, and therefore is not a concern of homebirth. More than half of the babies with early-onset illness present within 6 hours of birth, and 45% have apgars of less than 5, and mostly present with respiratory distress. Additional signs are: abdominal distention, vomiting, bloody stool, non-physiological jaundice, and meconium- stained fluid, thereby suggesting that infection was present before birth. Other clinical symptoms are: apnea, seizures, lethargy, hypothermia, hyperthermia, impaired cardiac output, poor feeding, hepatosplenomegaly, pneumonitis, petechia or purpura, meningoencephalitis. Many GBS infected babies will develop neurological disorders, vision or hearing loss, Cerebral palsy, developmental delays and other permanent disabilities. 5-22% with early-onset disease will die. GBS congenital pneumonia was found in 91% of infants who died when onset occurred within the first 48 hours of life.
Mothers with heavy colonization in multiple sites have a very high likelihood (87.8%) of infecting their baby. The rate of infant colonization for lightly colonized women is 30%. Of colonized infants, 1-2% will develop disease. GBS in the urine is evidence of heavy colonization in the vagina.
GBS can be misdiagnosed as a yeast infection as it can cause burning, redness and discharge, but does not respond to yeast treatments.
GBS thrives in the genitourinary and especially in the lower gastrointestinal tracts of adults. It can be sexually transmitted. The bacteria can dissolve the mucous between the vagina and cervix and make toxins that can damage the baby and placenta before birth. Most adults show no signs or symptoms, but a GBS carrier can develop serious complications in pregnancy, such as UTI, pyelonephritis, spontaneous abortion, chorioamnionitis, and IUGR, and fetal malformations. It can cause premature labor and PROM, and is a cause of stillbirth. GBS postpartum complications include: endometritis, pelvic thrombophlebitis, and endocarditis.
The infection can be intermittent (50%), chronic (40%), or transient (10%), making it difficult to detect and treat. Most cases of early onset disease are a result of infection during labor and birth, but some babies become infected in utero before labor and are already septic at birth., and can cause pregnancy loss early in gestation. In one research paper, GBS was the most common cause of stillbirth., as the bacteria can penetrate intact placentas, usually via the bloodstream. Fetal infection can occur with intact membranes. Early-onset disease has been seen in infants born by Cesarian. Signs of intrauterine infection are not detected until the birth, although the pathological process has been progressing in utero. Research disagrees about the amniotic fluid’s ability to prevent growth of GBS within the fluid, despite many studies citing the bacteriostatic properties of amniotic fluid in inhibiting growth of E.coli, Staph aureus, listeria, and beta-hemolytic strep. Maternal antibody transfer protects the fetus. The pregnant woman who is most likely to colonize her infant is also the most likely to provide her baby with passive immunity if she is producing the necessary type- specific antibodies. Other researchers claim that GBS will grow rapidly in amniotic fluid. With prolonged PROM, a small amount of bacteria from the maternal genitalia will quickly infect the amniotic fluid, and challenge the babies immune system, especially if the mother is deficient in the needed immunological response. Uterine contractions and vaginal exams can move bacteria , including GBS, up into the uterus.
CDC Guidelines recommend the use of one of two preventative strategies:
1. Culture all women at 35-37 weeks, then offer intrapartum antibiotics to all women testing positive cultures. Intrapartum prophylactic antibiotics are also offered for preterm labor or PROM less than 37 weeks and for those in labor without culture results. This means that 26.7% women will receive antibiotics during labor, and 86% of GBS early-onset will be prevented.
As GBS is difficult to grow and culture, proper culture collection technique and lab procedure is important. 2 swabs should be used, both from the vaginal introitus and rectum. Women who self collected got higher yields of GBS when compared to physician collection. It is necessary to use a selective broth medium containing antimicrobials to suppress competing organisms, which increases the GBS yield by 50%. Cultures late in the third trimester correlate with intrapartum results 75-90% , but will not catch the colonized women who develop premature labor. Screening at onset of labor with a rapid diagnostic technique has a poor sensitivity and not reliable.
2. Intrapartum antibiotics to all patients with risk factors: Maternal fever over 38
, PROM more than 18 hours, PROM at less than 37 weeks, Preterm birth, Birth weight less than 2.5 kilo, Maternal GBS UTI, Internal fetal monitoring for over 12 hours, Multiple births, Previous baby with active GBS infection,
For women with any of these risk factors the transmission rate is near 40%. Preterm babies are at greatest risk, but over half of the cases of sepsis occur in term babies.
This risk factor approach means that 18.3% of women will get antibiotics, and 68% early onset GBS will be prevented.
The CDC sites 4 studies that show intrapartum antibiotics decrease neonatal colonization in premies or with PROM more than 12 hours. Other research conflicts this, and shows no improvement in preventing early-onset GBS in term babies. The main concern is that widespread use of penicillin will lead to resistant organisms. The CDC estimates that 26.7% of pregnant women could get antibiotics in labor when only 1 in 870 newborns has suspected GBS infection.
There is also a potentially fatal risk of anaphylactic shock.
HOLISTIC HEALTH OPTIONS
500-1000 mg. Vit. C with bioflavinoids
Cranberry capsules and garlic pearls 3 times a day
Acidophilus capsules or live culture yogurt each day
Bee propolus tincture
Echinacea agustifolia, astragalus and Usnea lichen
Herbal vaginal suppositories for 2 wks followed by 1 wk inserting multiple strain acidophilus capsules that produce hydrogen peroxide.
Hydrogen peroxide internal vaginal rinse
Use peri-rinse after toilet: equal parts of thyme, calendula, rosemary and yarrow. 4-6
Tbs per liter boiling water. Infuse for 4 hours, and strain. Add ¼ cup sea salt,
10 drops lavender oil, and 30 cc. Echinacea tincture.
Caution with goldenseal ( stresses liver and kidneys, raises WBC, and can cause contractions.
CHLORHEXADINE (common antiseptic and mouthwash over the counter)
Summary from internet correspondence
Use of chlorhexadine gel in the vagina during labor can reduce GBS disease in newborn, according to study of 17 women in Holland in 1989.
A single vaginal washing by squeeze bottle with 2g/L chlorhexidine before ARM in l9 carrier women proved effective.
In Sweden 4483 GBS carriers received either placebo saline or 60 cc chlorhexadine by vaginal flushing every 6 hours. Chlorhexadine reduced the rate of admission to NICU, 1998
In Norway, vaginal douching with chlorhexadine reduced transmission rate from 35% to 18%., and significantly reduced early onset disease. Maternal fever in the postpartum was also reduced. .
2002, Italy, 244 GBS positive mothers at term, randomized to get either 140 g. chlorhexadine by vaginal flushings every 6 hrs or 2 g. ampicillin IV . Similar apgars and rates of neonatal colonization with 2 cases of early- onset GBS disease (1 from each group). Conclusion: chlorhexadine rinsing and IV ampicillin has same efficacy.