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Introduction
Lyme disease is not just spread from a tick. It can spread transplacentally from the mother to the organs of the fetus. Mothers can spread Lyme disease to their unborn baby. Congenital Lyme disease is associated with birth defects, miscarriage, and infant deaths.
In Congenital Lyme disease ...
- Autopsy evidence has established that spirochetes are in fetal or placental tissue.
- It is associated with birth defects, fetal death in utero, fetal death at term, or infant death after birth.
- Maternal blood is seronegative for specific antibodies against B. burgdorferi in cases where the spirochete can be demonstrated in the fetus or placenta so you can not rely on antibody testing.
- There was no inflammation in the tissues which contained the Lyme disease spirochetes.
The Enlarging Spectrum of Tick-Borne Spirochetoses: R. R. Parker Memorial Address 1
Willy Burgdorfer discovered the Lyme disease spirochete. He said the Lyme spirochete can infect the organs of the fetus from the mother causing congenital heart disease and even death of the infant.
... now we had found a spirochete capable of spreading transplacentally to the organs of the fetus, causing congenital heart disease and possible death of the infant [42] ;
— Willy BurgdorferREVIEWS OF INFECTIOUS DISEASES • VOL. 8, NO.6· NOVEMBER-DECEMBER 1986
Maternal-Fetal Transmission of the Lyme Disease Spirochete, Borrelia burgdorferi 2
We report the case of a woman who developed Lyme disease during the first trimester of pregnancy. She did not receive antibiotic therapy. Her infant born at 35 weeks gestational age, died of congenital heart disease during the first week of life. Histologic examination of autopsy material showed the Lyme disease spirochete in the spleen, kidneys, and bone marrow.
Ann Intern Med 1985;103:67-8
A Lyme infection was found in tissue where there was no inflammation. That's important because officially you cannot have an infection with no inflammation. These studies show that that is not true.
An autopsy of the infant showed widespread congenital cardiovascular abnormalities. ... There was no evidence of inflammation ...
Ann Intern Med 1985;103:67-8
Figure 1. ... autopsy spleen sample showing a single spirochete (arrow) near a fibrous trabeculum (B); proximal convoluted renal tubules showing B. burgdorferi (C, D) (note the absence of inflammatory cells); and spirochetes in sections of bone marrow (arrows), with the top micrograph showing a particularly long spirochete (E). All sections stained by a modified Dieterle silver impregnation method (original magnification, X 1250).
Human Fetal Borreliosis, Toxemia of Pregnancy, and Fetal Death 3
Clinical Case Summaries
Case 1:
A 24 year old woman (G 1, P 0, Ab 0) delivered a 2500 gram stillborn male fetus at term. Her prenatal care record was negative for factors associated with high risk pregnancy. No infections were diagnosed during the prenatal period.
Fig. 9. Borrelia burgdorferi in fetal myocardium, case one (magnification 1000 x, IFA, polycional human serum)
Fig. 10. Borrelia burgdorferi in arachnoid space of fetal midbrain, case one (magnification 1000 x, Warthin-Starry stain)
Case 2:
A 22 year old woman (G 1, PO, Ab 0) delivered a 514 gram stillborn macerated female fetus at nineteen weeks gestation. Her antepartum course was complicated by toxemia of pregnancy which had its onset during the seventeenth week of pregnancy and was manifest by hypertension, albuminuria, facial edema, and peripheral edema. No infections wer diagnosed during the prenatal period.
Fig. 13. Borrelia species in placental villus, case 2 (magnification 1000 x, IFA, polyclonal human serum)
Case 3:
A 37 year old woman (G 3, P 0, Ab 2) delivered a 490 gram stillborn male fetus showing mild maceration at twenty three weeks gestation. She had a chronic collagen disease in clinical remission during the pregnancy. The collagen disease was marked by episodes of fever, thrombocytopenia, anemia, arthritis, and lymphadenopathy and had been controlled with low dose oral prednisone. The patient was not receiving prednisone during the antepartum period. Amniocentesis was performed at the twentieth week of gestation and revealed a normal fetal karyotype. Toxemia of pregnancy had its onset during the twenty second week of gestation and was manifest as hypertension, and proteinuria. No infections were diagnosed during the prenatal period.
Fig. 15. Borrelia species in fetal liver, case 3 (magnification 1000 x, IFA, polyclonal human serum)
Case 4:
A 32 year old woman (G 2, P 0, Ab 1) delivered an 85 gram female fetus showing mild maceration at 15 weeks gestation. Her antepartum clinical record revealed no factors for a high risk pregnancy. No infections were diagnosed during the antepartum period.
Fig. 17. Borrelia species in fetal liver, case four (magnification 1000 x, IFA, polyclonal human serum)
Results in all four cases ...
Spirochetes were cultured from fetal liver tissue in each of the four cases. The time varied for a positive culture to be detected from 10 days to 6 months. Spirochetes were cultured from the fetal heart in case one. ...
— Dr. Alan B. MacdonaldSouthampton Hospital, Long Island, New York, U.S.A.
Culture positive seronegative transplacental Lyme borreliosis Infant Mortality. 4
In the section under "PATHOLOGY STUDIES" Dr. Macdonald describes a case from Lavoie PE. et al.: Culture positive seronegative transplacental Lyme borreliosis Infant Mortality. Arthritis Rheum 3(Suppl):S50, 1987 Where Dr. Macdonald states on page 659 regarding the Lavoie study;
Lavoie and colleages reported a full-term neonatal death due to aortic thrombosis in which BB was cultured from the infant's brain.
Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy 5
Twenty-three hours after birth the child suddenly developed difficulty breathing and succumbed within half an hour.
Pediatr Infect Dis J, 7:286-289, 1988
A Lyme infection was found in tissue where there was no inflammation. That's important because officially you cannot have an infection with no inflammation. These studies show that that is not true.
B. burgdorferi was identified in rare paraffin sections of the brain when the monoclonal antibody II 5332 directed against outer surface protein of this organism.
...
In our case and in two other cases of congenital LB [4,5] there was no significant inflammation in any organ examined.
Ann Intern Med 1985;103:67-8
Gestational Lyme Borreliosis Implications for the Fetus 6
Fetal Lyme Borreliosis with Ventriculosseptal Defect
Case 1:
(This entry provides more information on case 1 of a previous study.)
A 24 year old white woman was admitted in February 1985 in labor at term of her pregnancy. Ultrasound examination showed that the fetus was dead when she arrived at the hospital. Following the delivery of her stillborn infant and completion of the fetal autopsy, a retrospective interview established that she had aquired Lyme borreliosis in the first trimester of her pregnancy outside of Salt Lake City, Utah. Postpartum serologic studies yielded conflicting results because the Centers for Disease Control found strongly reactive results by IFA and ELISA, as did the New York State Department of Health; however, the Yale University laboratory of Dr. Allen Steere could detect no evidence of specific antibodies for B. burgdorferi. Fetal viscera showed B. burgdorferi in the liver, adrenal, brain, heart, and placenta. Spirochetes were seen by dark-field examination of fetal liver and these bound specific monoclonal antibody H5332. No microscopic inflammation was identified in tissue sections which contained the spirochete (Fig. 2).
Figure 2. A, B. burgdorferi in fetal autopsy myocardiam (Case 1). Indirect immunofluorescence. 1000X original magnification. B. B. burgdorferi in fetal autopsy adrenal gland(Case 1). Indirect immunofluorescence. 1500X original magnification
Points to emphasize from this case are:
- Lack of tissue inflammation in infected tissues;
- Discrepancy in serology testing;
- Positive cultures of spirochetes from fetal liver;
- Concurrence of first trimester infection with events of cardiac organogenesis and subsequent identification of ventriculoseptal defect;
- Intrauterine fetal growth retardation; and
- Acquisition of infection in a "nonendemic area" and identification of infection by entirely retrospective analysis.
Fetal Lyme Borreliosis in Term Delivery and Postnatal Death After 4 Hours
Case 5:
A 25 year-old black woman presented in September 1978 in labor in week 39 of pregnancy. Her antepartum course was remarkable only for a brief episode of vaginal bleeding in her second month of pregnancy. A 2250 gm female infant showed multiple anomalies at delivery including hydrocephalus, omphalocoele, clubfoot, spina bifida, and meningomyelocoele. Respiratory distress developed in the newborn nursery and 4 hours later the infant died. Autopsy disclosed a large ventriculoseptal defect as an additional malformation. Spirochetes were identified by immunohistochemistry in a retrospective examination of fetal autopsy tissue.
Fetal Borreliosis, Term pregnancy, With Postnatal Death at 30 Minutes
Case 6:
A 33 year-old white woman was admitted in February 1979 in week 40 of pregnancy. Her antepartum course was remarkable for uterine growth retardation as detected in serial obstetrical ultrasound examinations. A 1950-gm female infant showed poor color and poor respiratory activity at birth. The infant showed profound bradycardia with heart rates of less than 60 beats per minute, with progressive decline in cardiac output and death 30 minutes after birth dispite maximum support in the neonatal nursery. Autopsy disclosed a large (1 cm diameter) ventriculoseptal defect and showed an absence of the left hemidiaphragm with herniation of abdominal viscera into the left hemithorax. Spirochetal fragments were identified by indirect immunofluorescence in a retrospective examination of fetal autopsy tissue.
Fetal Lyme Borreliosis with Miscarriage at 17 Weeks Gestation
Case 7:
A 34-year-old black woman was admitted in March 1986 in week 17 of her third pregnancy. She delivered a 30 gm male fetus in the emergency room. In the 2 weeks prior to admission, she had experienced vaginal bleeding and abdiminal cramping. An obstetric ultrasound examination in week 12 of pregnancy had shown normal appearing fetus with no abnormalities in head circumference or femur length and suggested normal fetal development. An autopsy disclosed fetal hydrocephalus and spirochetes were identified in fetal brain by indirect immunofluorescence (Fig. 5). Postpartum maternal blood showed a nonreactive result in Lyme serology.
Fetal Lyme Borreliosis with Miscarriage at 16 Weeks Gestation
Case 8:
A 21-year-old black woman was admitted in July 1988 in active labor in week 16 of her third pregnancy. In the 2 weeks before admission, she experienced vaginal bleeding, abdominal cramps, low-grade fever, and on the day of admission noted a foul-smelling vaginal discharge. A 150-gm macerated male fetus showed no malformations at autopsy. Spirochetes were identified in fetal brain with immunohistochemistry using monoclonal antibodies (Fig. 6). Postpartum material blood was negative for antibodies to B. burgdorferi. No inflammation was found in fetal viscera at autopsy.
Fetal Lyme Borreliosis with Miscarriage at 12 Weeks Gestation
Case 9:
A 25-year-old white woman was admitted in active labor in November 1986 at week 12 of her third pregnancy. She delivered a nonmascerated 294-gm male fetus in the emergency room. An autopsy disclosed no external or internal anomalies. The patient's two previous pregnancies had ended at 8 weeks and 26 weeks gestation; neither fetus had been examined histologically. Routine sections showed no inflammatory infiltrates. Culture of fetal viscera in BSK medium yielded B. burgdorferi and other bacteria from fetal kidney (Fig. 7), although no spirochetes were found in cultures of fetal brain, liver, spleen, heart, ot thymus. No spirochetes were identified in fetal viscera using immunohistochemistry.
Fetal Lyme Borreliosis with Intrauterine Death at 25 Weeks Gestation
Case 10:
A 27-year-old black woman was admitted for induction of labor at 25 weeks gestation after a routine obstetric ultrasound examination confirmed that the fetus had died in utero. No high-risk factors were noted in the patient's prenatal care record and no infections were identified. The patient reported in retrospect that she had experienced myalgias, arthralgias, and episode of headache for which she did not seek medical attention. A macerated male fetus showed no external anomalies at delivery. An autopsy showed a large intraventricular septal defect without additional internal anomalies. Postpartum Lyme serology performed on maternal blood was nonreactive. B. burgdorferi was identified in tissue by indirect immunofluorescence.
Fetal Lyme Borreliosis Presenting as Neonatal Sepsis at term Pregnancy
Case 11:
A 19-year-old black woman was admitted in January 1986 in active labor. She delivered an 8 lb 5oz male infant who developed respiratory distress in the first hour of life and was transferred to a neonatal intensive care unit at a university hospital. Examination of the placenta revealed otherwise normal appearing villi which contained rare B. burgdorferi spirochetes (Fig. 8). The infant responded to intravenous antibiotic therapy.
ANALYSIS - HISTOPATHOLOGY STUDIES OF GESTATIONAL LB
Summary Of All Studies
Autopsy evidence for gestational LB establish that spirochetes are in fetal or placental tissue. Such cases show that serological evidence is often lacking when maternal blood is tested for antibodies to BB immediately after the delivery of a living or dead fetus. Routine tissue studies with ordinary microscopic techniques, namely hematoxylin and eosin stained sections, fail to provide clues that infection has reached the fetus because none of the autopsies to date has shown inflammation in the tissues which contained BB. In each of the previously published cases, a strong index of suspicion was the sole cause for the intricate and exhaustive medical investigation specifically directed toward the subtle clinical and histopathologic evidence of LB and its spirochetal agent BB. Patience and diligence are required if the histopathologist is to succeed in visualizing BB with oil immersion magnification. There are many potential pitfalls and there are many opportunities to fail when looking for the spirochete.
Two Bad Studies
7
Described By Macdonald
Those were the good studies. Here is a description of two bad studies.
This one was from CDC-Yale.
The CDC-Yale study of Lyme disease in pregnancy did not have serology data for each of the patients. Patients were diagnosed with Lyme disease based on the erythema migrans lesion. Seroconversion is expected in only 40 to 60 percent of patients after the EM lesion is identified. Examination of umbilical cord blood specemins from five clinically normal infants showed no evidence of detectable antibodies to BB. The authors concluded, based on the seronegative status of the five infants, that "there was no evidence of occult infection." (A single negative serologic result from umbilical cord blood certainly does not exclude LB, especially in light of the recent documentation of a seronegative state in certain patients with chronic disease[2] and in light of the observation of Stokes in prenatal syphilis. A sixth infant's umbilical cord blood speciman was positive for antibodies to BB, but 7 months later the infant was sseronegative. The authors did not indicate whether this infant's antibodies were of the IgM class (indicating intrauterine infection) and did not state whether they believe that this infant had an occult infection which might have reverted to a seronegative state as a result of antibiotic therapy.
The other refers to a study by Williams et al. The experimental design incorporated a logic error called survivorship bias. By only including infants that were born, the researchers were able to completely ignore fetal deaths from Congenital Lyme disease. Multiple studies before this showed fetal deaths from Lyme disease. It is curious that the researchers chose a clearly inadequate experimental design.
A conspicuous absence of fetal deaths or miscarriages in the Williams patient study group is an inevitable consequence of the selection process in this study. Only live born infants were included. The opportunity to observe congenital anomalies associated with miscarriages, still-birth, or perinatal infant death was not permitted due to the design of the study. Therefore, the author's conclusion that no association can be supported between gestational LB and congenital malformation should be a highly qualified statement with multiple disclaimers.
Eugene Shapiro, a Lyme Disease Guidelines Author Lied When Denying Documented Cases Of Congenital Lyme Disease.
Dr. Eugene Shapiro, a Yale pediatrician said this in the Lyme disease Documentary Under Our Skin which came out in 2008.
Transmission of Lyme disease to a fetus has been of concern to patients. There has not been one documented case of congenital Lyme disease.
— Eugene ShapiroDocumentary Under Our Skin
- In the Under Our Skin interview Shapiro said "There has not been one documented case of congenital Lyme disease."
- The Schlesinger study described a case of congenital Lyme disease and was referenced in the Lyme disease guidelines itself.
- Shapiro was one of the guideline authors.
A Lyme disease guideline author can lie about the existence of a study documented in the Lyme disease guideline itself. Officially transplacental Lyme disease doesn't happen yet there are many proven cases in the peer reviewed medical literature. There are many more cases than are presented here. Every case listed on this page occured years before 2008. The year Under Our Skin was released. Many good doctors who have treated their patients based on good science have lost their medical license due to the lies in the guide. If science ruled the medical industry then lies like his would be impossible. It is power that rules the medical industry not science and it is power that keeps the lies in place.
Conclusion
There are dozens of cases of Congenital Lyme disease described in medical literature. The medical authorities are willfully denying it's validity. Mothers can spread Lyme disease to their unborn baby. It is associated with birth defects, miscarriage, and infant deaths.
References
- Burgdorfer W. The enlarging spectrum of tick-borne spirochetoses: R. R. Parker Memorial Address. Rev Infect Dis. 1986;8(6):932-40.
- Schlesinger PA, Duray PH, Burke BA, Steere AC, Stillman MT. Maternal-fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi. Ann Intern Med 1985;103:67-8
- Macdonald AB. Human fetal borreliosis, toxemia of pregnancy, and fetal death. Zentralbl Bakteriol Mikrobiol Hyg A. 1986;263(1-2):189-200.
- Lavoie PE. et al: Culture positive seronegative transplacental Lyme borreliosis Infant Mortality. Arthritis Rheum 3(Suppl):S50, 1987
- Weber K, Bratzke HJ, Neubert U, Wilske B, Duray PH. Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy. Pediatr Infect Dis J. 1988;7(4):286-9.
- Macdonald AB. Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am. 1989;15(4):657-77.
- Macdonald AB. Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am. 1989;15(4):657-77.
- Williams, CL, Benach, JL, Curran, AS et al, Lyme disease during pregnancy: a cord blood serosurvey. Ann NY Acad Sci. 1988;539:504–506.
- Under Our Skin