Congenital Lyme Disease
Maternal-Fetal transmission of Lyme Disease

 

O

What is this page about?

Lyme disease is not just spread from a tick. It can spread transplacentally from the mother to the organs of the fetus. Infants can be and are born with Lyme disease if they survive.


 

  • 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.
  • There was no inflammation in the tissues which contained the Lyme disease spirochetes.
 
  O Willy Burgdorfer

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 possible death of the infant.

 

The Enlarging Spectrum of Tick-Borne Spirochetoses:
R. R. Parker Memorial Address

This was printed in the IDSA's own Journal, Reviews of Infectious Diseases in 1986.

http://www.researchfraud.com/fetal-lyme-borreliosis/#burgdorfer1986

http://www.researchfraud.com/studies/fetal-lyme-borreliosis/burgdorfer1986.pdf
Syphilis Lyme disease
  O Ann Intern Med 1985;103:67-8

Maternal-Fetal Transmission of the Lyme Disease Spirochete, Borrelia burgdorferi

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.
An autopsy of the infant showed widespread congenital cardiovascular abnormalities. ... There was no evidence of inflammation ...

— Schlesinger PA et al.
  Ann Intern Med 1985;103:67-8

Borrelia burgdorferi
Borrelia burgdorferi

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).


Maternal-Fetal Transmission of the Lyme Disease Spirochete, Borrelia burgdorferi

Page 67
Page 67

http://www.researchfraud.com/fetal-lyme-borreliosis/#schlesinger1985
Lyme disease
 
  O Zentralbl Bakteriol Mikrobiol Hyg [A] 1986;263:189-200

Human Fetal Borreliosis, Toxemia of Pregnancy, and Fetal Death


This report describes four cases of fetal borreliosis which were encountered in a prospective study of abortuses.

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

Fig. 9. Borrelia burgdorferi in fetal myocardium, case one (magnification 1000 x, IFA, polycional human serum)

Fig. 10. Borrelia burgdorferi

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

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

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.
7c

Fig. 17. Borrelia species in fetal liver, case four (magnification 1000 x, IFA, polyclonal human serum)



Results
Culture of Fetal Tissues:

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. ...

image
— Dr. Alan B. Macdonald Southampton Hospital, Long Island, New York, U.S.A.



http://www.researchfraud.com/fetal-lyme-borreliosis/#macdonald1986
Lyme disease
  O Arthritis Rheum 3(Suppl):S50, 1987

Culture positive seronegative transplacental Lyme borreliosis Infant Mortality.

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.

http://www.researchfraud.com/fetal-lyme-borreliosis/#lavoie1987
Lyme disease
 
  O PMID: 3130607

Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy

Twenty-three hours after birth the child suddenly developed difficulty breathing and succumbed within half an hour.
— Weber et al.

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.
— Weber et al.

Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy
Page 286 1 of 3 Page 287 2 of 3 Page 288 3 of 3

http://www.researchfraud.com/fetal-lyme-borreliosis/#weber1988
Lyme disease
 
  O Dr. Alan Macdonald 1989

Gestational Lyme Borreliosis
Implications for the Fetus

 

The first 4 cases are described in a previous study. click here to go to that study.
This entry provides more information on case 1 of a previous study.
Case 1:Fetal Lyme Borreliosis with Ventriculosseptal Defect
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).

Points to emphasize from this case are:
  1. (1) lack of tissue inflammation in infected tissues;
  2. (2) discrepancy in serology testing;
  3. (3) positive cultures of spirochetes from fetal liver;
  4. (4) concurrence of first trimester infection with events of cardiac organogenesis and subsequent identification of ventriculoseptal defect;
  5. (5) intrauterine fetal growth retardation; and
  6. (6) acquisition of infection in a "nonendemic area" and identification of infection by entirely retrospective analysis.
Gestational Lyme Borreliosis case 1.
Gestational Lyme Borreliosis case 1

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.

Case 5: Fetal Lyme Borreliosis in Term Delivery and Postnatal Death After 4 Hours
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. 
Case 6:Fetal Borreliosis, Term pregnancy, With Postnatal Death at 30 Minutes
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.
Case 7:Fetal Lyme Borreliosis with Miscarriage at 17 Weeks Gestation
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.
Gestational Lyme Borreliosis case 7.
Gestational Lyme Borreliosis

Comments in red by the Author.

Case 8:Fetal Lyme Borreliosis with Miscarriage at 16 Weeks Gestation
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.
Gestational Lyme Borreliosis case 8.
Gestational Lyme Borreliosis

Comments in red by the Author.

Case 9:Fetal Lyme Borreliosis with Miscarriage at 12 Weeks Gestation
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.
Gestational Lyme Borreliosis case 9.
Gestational Lyme Borreliosis

Case 10:Fetal Lyme Borreliosis with Intrauterine Death at 25 Weeks Gestation
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.
Case 11:Fetal Lyme Borreliosis Presenting as Neonatal Sepsis at term Pregnancy
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.

  Gestational Lyme Borreliosis case 11.

Gestational Lyme Borreliosis

Comments in red by the Author.


CASES 12, 13, 14 ended up healthy after less severe issues.
 

ANALYSIS - HISTOPATHOLOGY STUDIES OF GESTATIONAL LB
Macdonald AB. Gestational Lyme borreliosis. Implications for the fetus.
 Autopsy evidence for gestational LB establish that spirochetes are in fetal or placental tissue. Such cases show thatserological 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. 

CONTINUED in the next entry - Sudden Infant Death Syndrome ...



http://www.researchfraud.com/fetal-lyme-borreliosis/#macdonald1989
Lyme disease
  O Dr. Alan Macdonald 1989
Dr Macdonald continues with a study on Sudden infant death syndrome and Lyme disease. ...
Macdonald AB. Gestational Lyme borreliosis. Implications for the fetus.

RATIONALE FOR A PROSPECTIVE STUDY OF SUDDEN INFANT DEATH SYNDROME (SIDS)

Three observations which accrue from the cases of fetal borreliosis are:
  1. Tissue inflammation is absent in fetuses with transplacentally aquired B. burgdorferi infection.

  2. Gestational Lyme borreliosis may be associated with fetal death in utero, fetal death at term, or infant death after birth.

  3. Maternal blood is seronegative for specific antibodies against B. burgdorferi in cases where the spirochete can be demonstrated in the fetus or placenta.

...

 

Two of the 10 cases showed spirochetes morphologically consistent with B. burgdorferi in the infant brain; one of the cases was a male infant who had died suddenly at 4 months of age (Fig. 11); and the second was a female infant dead at 4 months of age.
...
No inflammation was identified in the microscopic fields which contained the spirochetes.

Gestational Lyme Borreliosis and SIDS deaths.
Gestational Lyme Borreliosis and SIDS deaths.

Comments in red by the Author.

CONTINUED in the next entry - Two bad studies on Lyme disease in pregnancy. One from CDC-Yale, the other from Williams et al....



http://www.researchfraud.com/fetal-lyme-borreliosis/#macdonald1989sids
Lyme disease S I D S

Gestational Lyme Borreliosis
Implications for the Fetus

RATIONALE FOR A PROSPECTIVE STUDY OF SUDDEN INFANT DEATH SYNDROME (SIDS)

Clinical and pathologic study of fetuses and infants with fetal borreliosis acquired in utero indicate that the expectations do not always correspond with the observations in the cohort.
Three observations which accrue from the cases of fetal borreliosis are:
  1. Tissue inflammation is absent in fetuses with transplacentally aquired B. burgdorferi infection.

  2. Gestational Lyme borreliosis may be associated with fetal death in utero, fetal death at term, or infant death after birth.

  3. Maternal blood is seronegative for specific antibodies against B. burgdorferi in cases where the spirochete can be demonstrated in the fetus or placenta.


Syphilis acquired in utero could in some cases present with death of the infant in the first year of life.8 Some of the infants with prenatal syphilis who died showed no clinical evidence of the infection when they were delivered. These observations from the clinical experience with syphilis led the author to test the following hypothesis. Some cases of sudden infant death syndrome (SIDS) might be circumstantially associated with subclinical persistent B. burgdorferi infections which were aquired in utero.

 

Permission to study 10 cases of SIDS was obtained from the Chief Medical Examiner of Suffolk County, New York. All cases were certified as SIDS10 using the strict criteria of forensic pathology, all cases had been thoroughly examined with a detailed autopsy, routine histology, and toxicology studies. A condition of the study was that strict patient confidentiality be maintained. Sections of the heart, brain, kidney, and liver were prepared and Warthin starry silver impregnation was performed. Two of the 10 cases showed spirochetes morphologically consistent with B. burgdorferi in the infant brain; one of the cases was a male infant who had died suddenly at 4 months of age (Fig. 11); and the second was a female infant dead at 4 months of age. Spirochetes were not identified in the representative sections from kidney, liver, or heart. No inflammation was identified in the microscopic fields which contained the spirochetes.
Gestational Lyme Borreliosis and SIDS deaths.
Gestational Lyme Borreliosis and SIDS deaths.

Comments in red by the Author.

  O Dr. Alan Macdonald 1989

Gestational Lyme Borreliosis
Implications for the Fetus

Those were the good studies. Here is a description of two bad studies. One was from CDC-Yale.

SEROLOGY STUDIES

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.p. 658

 

SEROLOGY STUDIES continued

The author is referring to this study by Williams et al.
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.

This is like conducting a study to see if Ebola can cause death. Researchers could enroll patients who contracted Ebola and survived. After enrollment, the researchers could count how many of the enrolled patients died. The answer would be zero because they only enrolled patients who survived. The result is based on their selection method and not reality. According to their "evidence-based" "scientific" method they could conclude it is unlikely that Ebola causes death.

The error in the experimental design of the Ebola example is easy to identify. The problem is intellectually simple to see. The problem in Williams study is also easy to identify once you realize he excluded miscarriages, and stillborn.

How intelligent should we expect researchers to be? Some errors are simple and very obvious. Only enrolling Ebola survivors to test if Ebola can be deadly is intellectually equal to enrolling infant survivors in a study on infant malformations.

 


ResearchFraud.com would describe the Williams trial in stronger terms than the description above.

    The Williams trial was designed to deliberately create a result which does not match reality. The Williams trial and the CDC-Yale trial were designed to deny the existence of congenital Lyme disease. They are both good examples of junk science from the industry. We can not expect the industry to correct this kind of research. This was published in the Annals of the New York Academy of Sciences, a prestigious peer reviewed journal. This was deemed acceptable to the peer reviewers even though the researchers excluded miscarriages, stillbirths and neonatal deaths.


http://www.researchfraud.com/fetal-lyme-borreliosis/#macdonald1989more
 
  O Under Our Skin

Eugene Shapiro, a Lyme Disease Guidelines Author Lied About 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.
There have been many documented cases of congenital Lyme disease. Many are on this web page. First here is Schlesinger et al.
Maternal-Fetal Transmission of the Lyme Disease Spirochete, Borrelia burgdorferi
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

— Schlesinger PA et al.
  Ann Intern Med 1985;103:67-8


Image B is a Lyme spirochete in the infants spleen. Images C, D are Lyme spirochetes in the infants kidney, Image E are Lyme spirochetes in the infants bone marrow. This is transplacental transmission of the Lyme disease spirochete to the infants organs. This is congenital Lyme disease.
Borrelia burgdorferi
Borrelia burgdorferi

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).


 

Shapiro is clearly wrong, but can we show he knew it was wrong when he said it? It turns out he did know of the Schlesinger study.


  • References listed on the bottom of scientific publications are studies which have been read by the authors.
  • Shapiro was an author of the Lyme disease guidelines from 2006. The IDSA Lyme disease Guidelines
  • One of the references at the bottom of the guidelines is this.
     
    46. Schlesinger PA, Duray PH, Burke SA, Steere AC, Stillman MT. Maternal-fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi. Ann Intern Med 1985 ; 103:67–8.
  • That is the Schlesinger study described in this entry above.

 

We have,
 
  1. In the Under Our Skin interview Shapiro said "There has not been one documented case of congenital Lyme disease."
  2. The Schlesinger study described a case of congenital Lyme disease and was referenced in the Lyme disease guidelines.
  3. Shapiro was one of the guideline authors so he read it.

The conclusion?


Dr. Eugene Shapiro, a Lyme disease guidelines author knew of a documented case of congenital Lyme disease and lied when he said no cases existed.

 

    A Lyme disease guideline author can lie about the existence of a study documented in the guidelines itself, yet the guideline stands. Many good doctors who have treated their patients based on good science have lost their medical license due to the guide. It is power that rules the medical industry not science and it is power that keeps the lies in place.


http://www.researchfraud.com/fetal-lyme-borreliosis/#shapiro-lied
Lyme disease
 
O

Conclusion


  Congenital Lyme Disease is a fact, not a theory. It is associated with birth defects, miscarriage, fetal, and infant deaths.

 

One more time from the IDSA's own journal, Reviews of Infectious Diseases here is a quote from the discoverer of the Lyme disease spirochete Willy Burgdorferer

 

 ... 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.1 

ResearchFraud.com ResearchFraud.com Action Points...

"Lyme disease can spread by ticks and from mother to infant during pregnancy."
Always include the second part "and from mother to infant during pregnancy".

 

Every congenital Lyme baby needs to be acknowledged. Do not let powerful organizations such as the CDC and IDSA keep their existence in the dark where infants continue to die.
 
— www.ResearchFraud.com/fetal-lyme-borreliosis/  
O

Definitions

  1. the presence of albumin in the urine, a common sign of renal or chronic disease.
    See also proteinuria.
    albuminuria. (n.d.) Mosby's Medical Dictionary, 8th edition. (2009). Retrieved May 21 2016 from albuminuria
  2. antepartum
    an·te·par·tum (an'tē-pahr'tŭm)

    Before labor or childbirth.
    Compare: intrapartum, postpartum

    [ante- + L. pario, pp. partus, to bring forth]

    antepartum. (n.d.) Medical Dictionary for the Health Professions and Nursing. (2012). Retrieved May 21 2016 from antepartum
  3. The delicate middle layer of the three MENINGES covering the spinal cord and brain, lying between the pia mater and dura mater. Unlike the pia mater, the arachnoid bridges over the grooves (sulci) on the surface of the brain and covers many large blood vessels lying in the sulci. Bleeding from any of these vessels causes a subarachnoid haemorrhage.

     

    From the Greek arachne, a spider.
    arachnoid. (n.d.) Collins Dictionary of Biology, 3rd ed.. (2005). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/arachnoid
  4. arthralgia
    ar·thral·gi·a (ahr-thral'jē-ă)
    Pain in a joint, especially noninflammatory.
    arthralgia. (n.d.) Medical Dictionary for the Health Professions and Nursing. (2012). Retrieved June 1 2016 from http://medical-dictionary.thefreedictionary.com/arthralgia
    pain in a joint, especially if the absence of inflammation makes the term arthritis inappropriate.
    intermittent or periodic arthralgia joint pain at intervals, usually accompanied by swelling (e.g. of the knee).
    arthralgia. (n.d.) Dictionary of Sport and Exercise Science and Medicine by Churchill Livingstone. (2008). Retrieved June 1 2016 from http://medical-dictionary.thefreedictionary.com/arthralgia
  5. borreliosis
    [bo-rel″e-o´sis]

    infection with spirochetes of the genus Borrelia.

    Lyme borreliosis a general term encompassing several different diseases that are caused by Borrelia burgdorferi and have similar manifestations, including Lyme disease, acrodermatitis chronica atrophicans, and erythema chronicum migrans.

    borreliosis. (n.d.) Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. (2003). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/borreliosis
  6. Slow heart rate, commonly defined as a rate of < 60 bpm or a rate which is too slow to be physiologically appropriate for the person and/or activity (generally recognised as < 45 beats/minute in men, < 50 beats/minute in women). A notable exception is aerobic athletes, whose resting heart rates are significantly lower than those of non-athletes.

    Clinical findings
    Symptoms may be specific (syncope) or nonspecific (dizziness, fatigue, weakness, heart failure).

    Management
    Beta blockers (pindolol), pacemaker.

    bradycardia. (n.d.) Segen's Medical Dictionary. (2011). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/bradycardia
  7. adjective Referring to a condition present at birth, regardless of cause.
    congenital. (n.d.) Segen's Medical Dictionary. (2011). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/Congenital
  8. A laboratory procedure in which a sample from a wound, the blood or other body fluid is taken from an infected person. The sample is placed in conditions under which bacteria can grow. If bacteria grow, identification tests are done to determine the bacteria species causing the infection.
    culture. (n.d.) Gale Encyclopedia of Medicine. (2008). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/culture
  9. edema
    e·de·ma (e-dē'mă),
    1. An accumulation of an excessive amount of watery fluid in cells or intercellular tissues.
    2. At the gross level, used to describe the physical sign commonly likened to swelling or increased girth that often accompanies the accumulation of fluid in a body part, most often a limb.

     

    [G. oidēma, a swelling]
    edema. (n.d.) Medical Dictionary. (2009). Retrieved May 22 2016 from http://medical-dictionary.thefreedictionary.com/edema
  10. And others.

    [L. et alii]

    et al. (n.d.) Medical Dictionary for the Health Professions and Nursing. (2012). Retrieved May 24 2016 from http://medical-dictionary.thefreedictionary.com/et+al
  11. The study of a tissue specimen by staining it and examining it by LM. See Light microscopy.
    histologic examination. (n.d.) McGraw-Hill Concise Dictionary of Modern Medicine. (2002). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/histologic+examination
  12. histopathology The microscopic study of disease processes in tissues.
    histopathology. (n.d.) Collins Dictionary of Medicine. (2004, 2005). Retrieved June 7 2016 from http://medical-dictionary.thefreedictionary.com/histopathology
  13. [IMAGE] n abnormal condition in which cerebrospinal fluid collects in the cranium, thus causing the ventricles to dilate. May be present at birth or may manifest in early adulthood. Caused by brain tumors, infection, trauma, or developmental anomalies. Also called hydrocephaly.
    hydrocephalus. (n.d.) Jonas: Mosby's Dictionary of Complementary and Alternative Medicine. (2005). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/hydrocephalus
  14. immunohistochemistry
    im·mu·no·his·to·chem·is·try (im'yū-nō-his'tō-kem'is-trē),
    Demonstration of specific antigens in tissues by the use of markers that are either fluorescent dyes or enzymes such as horseradish peroxidase.
    immunohistochemistry. (n.d.) Farlex Partner Medical Dictionary. (2012). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/immunohistochemistry
  15. karyotype
    [ker′ē·ətīp′]
    image Etymology: Gk, karyon + typos , mark
    1 the number, form, size, and arrangement within the nucleus of the somatic chromosomes of an individual or species, as determined by a microphotograph taken during metaphase of mitosis.
    2 a diagrammatic representation of the chromosome complement of an individual or species, in which the chromosomes are arranged in pairs in descending order of size and according to the position of the centromere.

     

    See also chromosome, Denver classification, idiogram. karyotypic, adj
    karyotype. (n.d.) Mosby's Medical Dictionary, 8th edition. (2009). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/karyotype
  16. lymphadenopathy
    [limfad′inop′əthē]
    any disorder characterized by a localized or generalized enlargement of the lymph nodes or lymph vessels.
    lymphadenopathy. (n.d.) Mosby's Medical Dictionary, 8th edition. (2009). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/lymphadenopathy
  17. macerated adjective Referring to a tissue—especially skin—that is moist, soft and in a state of deterioration (usually for a prolonged period of time).
    macerated. (n.d.) Segen's Medical Dictionary. (2011). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/macerated
  18. meningomyelocoele
    [mi″ĕ-lo-mĕ-ning´go-sēl]
    hernial protrusion of the spinal cord and its meninges through a defect in the vertebral arch (spina bifida); see also neural tube defect. Called also meningomyelocele.
     
    imageChild with a large thoraco-lumbar myelomeningocele consisting of protruding spinal cord covered by meninges. From Mueller and Young, 2001.
    meningomyelocele. (n.d.) Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. (2003). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/meningomyelocele
  19. Muscular pain or tenderness, typically of a diffuse and/or nonspecific nature.
    Mentioned in: Chronic Fatigue Syndrome, Ross River Virus
    myalgia. (n.d.) Gale Encyclopedia of Medicine. (2008). Retrieved May 22 2016 from http://medical-dictionary.thefreedictionary.com/myalgia
  20. myocardium
    mi″o-kar´de-um]
    the middle and thickest layer of the heart wall, composed of cardiac muscle. adj.,

     

    adj myocar´dial.
    myocardium. (n.d.) Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. (2003). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/myocardium
  21. omphalocele
    [om´fah-lo-sēl″]
    protrusion, at birth, of part of the intestine through a defect in the abdominal wall at the umbilicus; see also umbilical hernia. image
    A large omphalocele with structure and contents of the hernial sac. From Betz et al., 1994.
    interventricular. (n.d.) Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. (2003). Retrieved May 22 2016 from http://medical-dictionary.thefreedictionary.com/interventricular
  22. organogenesis
    [-jen′əsis]
    Etymology: Gk, organon + genesis, origin (in embryology) the formation and differentiation of organs and organ systems during embryonic development. In humans the period extends from approximately the end of the second week through the eighth week of gestation. During this time the embryo undergoes rapid growth and differentiation and is extremely vulnerable to environmental hazards and toxic substances. Any interference with the sequential processes involved with organogenesis causes an arrest in development and results in one or more congenital anomalies. Also called organogeny. See also embryological development, prenatal development.

     

    organogenetic, adj.
    organogenesis. (n.d.) Mosby's Medical Dictionary, 8th edition. (2009). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/organogenesis
  23. The presence of protein in the urine exceeding normal levels.
    proteinuria. (n.d.) Gale Encyclopedia of Medicine. (2008). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/proteinuria
  24. seronegative Immunology The lack of antibodies or other immune markers in serum that would indicate exposure to a particular organism or antigen; in an immunocompetent person, exposure to an antigen results in a seroconversion and the subject is said to then be seropositive. Cf Seropositive.
    seronegative. (n.d.) McGraw-Hill Concise Dictionary of Modern Medicine. (2002). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/seronegative
  25. spinabifida
    spi·na bi·fi·da (spī'nă bī'fi-dă)
    Embryologic failure of fusion of one or more neural arches that will become vertebral arches; subtypes of spina bifida are based on degree and pattern of deformity associated with neuroectoderm involvement.
    (Added: neuroectoderm - Central region of the outer layer of cells in the embryo that eventually forms the brain and spinal cord.)
    spina bifida. (n.d.) Medical Dictionary for the Health Professions and Nursing. (2012). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/spina+bifida
  26. thrombocytopenia
    throm·bo·cy·to·pe·ni·a (throm'bō-sī'tō-pē'nē-ă),
    A condition in which an abnormally small number of platelets is present in the circulating blood.

     

    Synonym(s): thrombopenia
    [thrombocyte + G. penia, poverty]
    thrombocytopenia. (n.d.) Farlex Partner Medical Dictionary. (2012). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/thrombocytopenia
  27. toxemia
    [tok-se´me-ah]

    1. the condition resulting from the spread of bacterial products (toxins) by the bloodstream.
    2. a name formerly used to indicate a pregnancy-related syndrome typified by edema, proteinuria, and hypertension that was thought to be due to a toxin released by the mother in response to a foreign protein of the developing fetus.

    adj., adj toxe´mic.
    toxemia of pregnancy former name for preeclampsia-eclampsia syndrome.

    toxemia of Pregnancy. (n.d.) Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. (2003). Retrieved May 22 2016 from http://medical-dictionary.thefreedictionary.com/toxemia+of+pregnancy
  28. ventricular septal defect
    ven·tric·u·lar sep·tal de·fect (VSD) (ven-trik'yū-lăr sep'tăl dē'fekt)
    A congenital defect in the interventricular septum, usually resulting from failure of the spiral septum to close the interventricular foramen.
    ventricular septal defect. (n.d.) Medical Dictionary for the Health Professions and Nursing. (2012). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/ventricular+septal+defect
  29. viscera Organs within a body cavity, especially digestive organs. The singular form of the word is viscus.
    viscera. (n.d.) Collins Dictionary of Medicine. (2004, 2005). Retrieved May 21 2016 from http://medical-dictionary.thefreedictionary.com/viscera

References


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  2. 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
  3. Macdonald AB. Human fetal borreliosis, toxemia of pregnancy, and fetal death. Zentralbl Bakteriol Mikrobiol Hyg A. 1986;263(1-2):189-200.
  4. Lavoie PE. et al: Culture positive seronegative transplacental Lyme borreliosis Infant Mortality. Arthritis Rheum 3(Suppl):S50, 1987
  5. 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.
  6. Dattwyler RJ, Volkman DJ, Luft BJ. Immunologic aspects of Lyme borreliosis. Rev Infect Dis. 1989;11 Suppl 6:S1494-8.
  7. Macdonald AB. Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am. 1989;15(4):657-77.
  8. Macdonald AB. Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am. 1989;15(4):657-77.
  9. Macdonald AB. Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am. 1989;15(4):657-77.
  10. Williams, CL, Benach, JL, Curran, AS et al, Lyme disease during pregnancy: a cord blood serosurvey. Ann NY Acad Sci. 1988;539:504–506.
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Last modified: 8/9/2016 8:30pm