ENCAPSULATED PLACENTA: THE GBS MYTH
In June of 2017 there was a case study released by the CDC that expressed a concern about transmission of GBS through the mother's use of placental pills postpartum. The baby was diagnosed with late onset GBS (group beta strep) attributed to high maternal colonization secondary to consumption of GBS-infected placental tissue. This has lead to many women questioning their choice to encapsulate or consume their placenta, raising questions directed towards the safety and efficacy of use. To throughly address these concerns, a full understanding of this one situational case study by the CDC needs to be discussed.
According to this case, my conclusion states:
1. GBS testing of the mother vaginal/rectal was not done, thus no conformation could be given.
2. Despite placenta testing positive, it could have been positive prior to delivery, at which time the baby would have already been infected.
3. GBS is normal in the stomach, it most likely would not have passed into breastmilk through consumption. Also, breastmilk tested negative.
4. There is no evidence that suggests that the GBS resulted from consumption of the encapsulated placenta.
Below are the studies and facts to support my conclusion (all in medical lingo) :)
Let's examine the information in the case study. The case study states:
1."The infant was born at term following an uncomplicated pregnancy; maternal GBS vaginal/rectal screening culture at 37 weeks’ gestation was negative." [1]
-Mother was assumed to have a normal healthy birth and pregnancy. There is no information about health care provider or birth setting. This is pertinent information, as GBS nosocomial infections (infections acquired by either the environment and/or staff working in the environment) occur in hospital birthing settings.
There was an article written addressing this particular issue in Korea. The article stated:
"Besides vertical transmission, other sources of GBS colonization in neonates have been established. Horizontal transmission from hospital (12-16) or community (15, 16) sources to neonates is one of the predominant modes for the transmission of infection. Cross-contamination from maternally infected to uninfected neonates can occur from the hands of nursery personnel. An epidemic report (17) of late-onset sepsis due to type Ib/c GBS sepsis in a neonatal intensive care unit revealed that none of the index cases had been colonized at birth, establishing that nosocomial acquisition was responsible. Their epidemiologic analysis suggested infant-to-infant spread via the hands of medical/healthcare personnel, but acquisition from two nurses who had been colonized by the same serotype Ib/c GBS strain was not excluded. This and other reports (18-20) have indicated that, during an outbreak, cohorting of culture-positive infants and enforced hand washing and gloving before any infant contact significantly diminish the rates of nosocomial acquisition."[2].
Despite this article in a different country, the same concerns remain in hospitals across the United States. Many mother/baby nurses attend more than one infant and more than one mother at a time. Many hospital protocols require nursing staff to wash their hands after three uses of the hand sanitizer. This is not always observed and nosocomial infections are possible.
2. "Shortly after birth, the infant developed signs of respiratory distress and was transferred to the neonatal intensive care unit where blood and cerebrospinal fluid (CSF) were obtained for culture; antibiotics were initiated for presumed sepsis. The blood culture was positive for penicillin-sensitive, clindamycin-intermediate GBS. CSF culture was negative. The infant was discharged and went home after completing an 11-day course of ampicillin (200 mg/kg/day). [1]
-"One in three women carry group B streptococci vaginally, which can infect the amniotic fluid even if the membranes are intact, or can infect the baby during delivery, causing sepsis, pneumonia, or meningitis...Early-onset neonatal sepsis usually occurs within the first 7 days of life, and is typically caused by infection with group B streptococcus. About 90% of cases present within 24 hours of birth. One in three women carry group B streptococcus, which exists as part of the normal bacterial flora in the vaginal and anal areas." [3] Despite the screening that is a part of routine OB care, GBS is not a certainty at the time of birth. GBS is a transient bacteria, which means it can move from one area to another. So women who are positive may be negative at birth and women who are negative may be positive. Routine testing of the mother is not done when a baby is found to be positive for GBS acquired infection. The assumption is that GBS was present. This is problematic, screening would confirm maternal transmission verses an assumption. Secondly, antibiotics do not always eliminate bacteria and remission is a possibility. "Group B Streptococcus is highly susceptible to most classes of antibiotics including penicillins. Group B Streptococcus grows more rapidly and requires a longer period of time for killing by antibiotics...The relatively slow bactericidal action of ampicillin on this organism may explain the difficulty in treating immunosuppressed hosts...Dosages in neonates of penicillin G as high as 500,000 units/kg/day or ampicillin at 300-400 mg/ kg/ day are recommended by some experts (4). While other treatment resources concur with higher dosages in neonates they also suggest adjusting the dosage based on age." Goup B Strep can be difficult to kill especially in immunocopmromised patients, such as newborns, and dosage recommendations make a relapse plausable in this this case study. [3]
3. "Five days later, the infant was taken to the emergency department because of irritability and was admitted to a second hospital. A blood culture yielded penicillin-sensitive, clindamycin-sensitive GBS. CSF was sterile, expressed breast milk did not yield GBS, and serial exams did not reveal a source." [1]
- I do find it interesting that the baby was admitted to a second hospital, I do wonder the reason for this as records would need to be sent and different staff would be putting together a different picture. There may be many different reasons for why this was done, but I do find it interesting to note. Blood cultures showed the same type of bacteria that was found previously when the first initial treatment of antibiotics was done. Expressed breastmilk showed no infection.
And this is the part everyone has been waiting for:
4."Three days into the infant’s admission to the second hospital, the treating physician was notified by a physician from the birth hospital that the mother had requested release of the placenta at the time of delivery. The mother confirmed that she had registered with Company A to pick up and encapsulate her placenta for ingestion. Three days after the infant’s birth, the mother had received the dehydrated, encapsulated placenta and began ingesting two capsules three times daily. The physician instructed the mother to stop consuming the capsules. A sample of the capsules was cultured, yielding penicillin-sensitive, clindamycin-sensitive GBS. The infant was treated with ampicillin (300 mg/kg/day) for 14 days and gentamicin (3 mg/kg/daily) for the first 6 days and discharged home.The three GBS isolates (one from each blood infection, and one from the placenta capsules) were indistinguishable by pulsed-field gel electrophoresis. Whole genome sequencing (WGS) performed at CDC revealed no single nucleotide polymorphisms between strains. WGS predicted serotype III, multilocus sequence type 17 (ST17), and tetM+ (tetracycline resistance). The strains had surface-anchored hypervirulent GBS adhesin Hvga, pilus island PI2b, and serine-rich repeat protein Srr2 (1); these virulence factors can facilitate adhesion and invasion from the infant’s intestine into the bloodstream and potentially across the blood brain barrier (2). Although transmission from other colonized household members could not be ruled out, the final diagnosis was late-onset GBS disease attributable to high maternal colonization secondary to consumption of GBS-infected placental tissue (3)." [1]
-There was a conformation that GBS was cultured on the placenta. Whole Genome Testing and pulsed-field gel electrophoresis were used to gather information about the GBS strains. Pulsed-field gel electrophoresis is the most commonly used method for typing of rapidly growing bacteria that causes disease. Whole genome sequencing reveals the complete DNA make-up of an organism, it helps to determine the differences in bacteria. These tests predicted that the GBS strain may have been a more aggressive strain. With that finding along with the diagnosis of having a late onset makes it difficult to determine the causative factors for the secondary GBS acquired infection. According to the library of medicine, "Newborns with early-onset GBS disease acquire the organism intrapartum from their mothers, who are colonized with GBS in the genital tract. Most early-onset disease results from ascending spread of the organism into the amniotic fluid, where aspiration of contaminated amniotic fluid leads to invasive disease in some infants. Perinatal transmission can occur across intact membranes...Although about 50% of mothers of infants with late-onset disease were found to carry the same GBS serotype as that causing infection in their infants, the source of infection in other infants is unclear (15, 53). Nosocomial and community sources are probably involved in some cases of late-onset disease (173), but the risk factors are not well understood. Even for infants with late-onset infections whose mothers have the same serotype, the precise mechanism of apparent mother-infant transmission has not been identified."[4]
My Thoughts:
Just by looking at the facts and what knowledge we have of GBS, I believe it is possible that the infant could have acquired the bacteria during labor, exhibiting the first symptoms several days after birth. As stated prior in early onset GBS, the placenta can be affected prior to labor. The first course of antibiotics may not have been affective or did not fully destroy the bacteria. If it was late onset, according to the library of medicine, the transmission may be unclear.
Ingestion of the bacteria is not necessarily a mode of transmission. According to the CDC, "Group B strep bacteria are common in the gastrointestinal tract (the part of your body that digests food, including the stomach and intestines) of men and women." [5] Despite a more aggressive strain, GBS is common and normal in the stomach. The breastmilk was tested and found to be negative of any GBS.
According to the American Academy of Pediatrics "A minority of infants with group B streptococcus (GBS) late-onset disease are born to GBS-colonized mothers. Intrapartum prophylaxis does not appear to prevent late-onset GBS disease, implicating infected breast milk and nosocomial or community sources in these cases...Most mothers of neonates with late-onset disease are identified at diagnosis with anogenital GBS infection. Even in the absence of mastitis, GBS-infected milk may be a source of late-onset disease. Intrapartum antibiotic prophylaxis is associated with both delayed and milder presentation of late-onset disease."[6] According to this article, antibiotics may delay or have a milder presentation of the disease. It also states most common sources are nosocomial, community sources, GBS infected milk, or mothers with anogenital (rectal) GBS. The mother in the case study was not anogentially tested for GBS once the baby was diagnosed with GBS acquired infection.
Unfortunately there is not enough information to find sure causative factors, this is even stated by the CDC case study "...Although transmission from other colonized household members could not be ruled out..." [1] However stating "the final diagnosis was late-onset GBS disease attributable to high maternal colonization secondary to consumption of GBS-infected placental tissue" [1] is lacking the scientific evidence to support this diagnosis. There is no direct correlation or causative factors to support a late onset GBS diagnosis by consumption of placental pills.
References:
[1] Buser GL, Mató S, Zhang AY, Metcalf BJ, Beall B, Thomas AR. Notes from the Field: Late-Onset Infant Group B Streptococcus Infection Associated with Maternal Consumption of Capsules Containing Dehydrated Placenta — Oregon, 2016. MMWR Morb Mortal Wkly Rep 2017;66:677–678. DOI: http://dx.doi.org/10.15585/mmwr.mm6625a4.
[2] Kim, H. J., Kim, S. Y., Seo, W. H., Choi, B. M., Yoo, Y., Lee, K. H., … Kim, H. J. (2006). Outbreak of Late-onset Group B Streptococcal Infections in Healthy Newborn Infants after Discharge from a Maternity Hospital: A Case Report. Journal of Korean Medical Science, 21(2), 347–350. http://doi.org/10.3346/jkms.2006.21.2.347
[3] BMJ Clin Evid. 2008; 2008: 0323. » Routine antibiotic prophylaxis versus monitoring and selective treatment for early-onset group B streptococcal infection
[4] Schuchat, A. (1998). Epidemiology of Group B Streptococcal Disease in the United States: Shifting Paradigms. Clinical Microbiology Reviews, 11(3), 497–513.
[5] https://www.cdc.gov/groupbstrep/about/adults.html
[6] Group B Streptococcus Late-Onset Disease: 2003−2010 Alberto Berardi, Cecilia Rossi, Licia Lugli, Roberta Creti, Maria Letizia Bacchi Reggiani, Marcello Lanari, Luigi Memo, Maria Federica Pedna, Claudia Venturelli, Enrica Perrone, Matilde Ciccia, Elisabetta Tridapalli, Marina Piepoli, Raffaella Contiero, Fabrizio Ferrari and on behalf of the GBS Prevention Working Group, Emilia-Romagna Pediatrics originally published online January 6, 2013