Yes, the Lyme can be passed through breast milk. Here are some links to studies:
(sorry - this is a long post, I'll share other thoughts in response to your questions in a separate post)
Here is more specific info about
congenital transmission and I highlighted specific info about
· Alan MacDonald (notable lyme researcher) notes that adverse reactions, such as fetal death and cortical blindness, have been associated with gestational Lyme disease and suggests the need for further research in order to ascertain whether the associations are co-incidental or related to the infection.
· The IDSA guidelines typically downplays any risk, associated with Lyme, and in this regard notes that “there is little evidence that a congenital Lyme disease syndrome occurs”.
· The CDC notes that while “Lyme disease can be dangerous for your unborn child”, and “may lead to infection of the placenta and may possibly lead to stillbirth”, it follows the IDSA guidelines that “favorable outcomes can be expected when pregnant women with Lyme disease are treated with standard antibiotic regimen”.
· Contrary to this statement, there are reports of adverse outcomes, including the death of newborns, with or without antibiotic treatment of the mother. The National Institutes of Health, puts it short and sweet: “If you are pregnant, be especially careful to avoid ticks in Lyme disease areas because you can pass on the infection to your unborn child”.
· One physician has cared for 5000 children with LD: 240 of these children were born with the disease. Dr. Charles Ray Jones, the leading pediatric specialist on Lyme Disease, has found 12 breastfed children who have developed LD. Miscarriage, premature births, stillbirths, birth defects, and transplacental infection of the fetus have all been reported. Studies at the University of Vienna have found Bb in urine and breast milk of LD mothers. www.samento.com.ec/sciencelib/4lyme/Townsendhowens.html
The following are lists of studies - I grabbed these from my online investigation and I don't have a summary of what the studies say but they might reveal more info if you are interested in investigating further:
28 Peer-reviewed studies on congenital transmission of lyme:
o MacDonald A. Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am. 1989 Nov;15(4):657-77.
o MacDonald AB, Benach JL, Burgdorfer W. Stillbirth following maternal Lyme disease. N Y State J Med. 1987 Nov;87(11):615-6.
o MacDonald A. Human fetal borreliosis, toxemia of pregnancy, and fetal death. Zentralbl Bakteriol Mikrobiol Hyg A. 1986 Dec;263(1-2):189-200.
o Schlesinger PA, Duray PH, Burke BA, Steere AC, Stillman MT. Maternal-fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi. (1985) Ann Intern Med, 103, 67-8.
o Markowitz LE, Steere AC, Benach JL, et al. Lyme disease during pregnancy. JAMA.(1986); 255(24), 3394-6.
o Lavoie PE, Lattner BP, Duray PH, Barbour AG, Johnson HC. Culture positive seronegative transplacental Lyme borreliosis infant mortality. (1987) Arthritis Rheum, 30(4), 3(Suppl):S50.
o Mikkelsen AL, Palle C. Lyme disease during pregnancy. (1987) Acta Obstet Gynecol Scand 66(5), 477-8.
o Weber K; Bratzke HJ, Neubert U, Wilske B, Duray PH. (1988) Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy. Pediatr Infect Dis J, 7:286-9.
o Carlomagno G, Luksa V, Candussi G, et al. (1988) Lyme Borrelia positive serology associated with spontaneous abortion in an endemic Italian area. Acta Eur Fertil 19(5), 279-81. Abstract
o Weber K, Bratzke HJ, Neubert U, et al. (1988) Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy. Pediatr Infect Dis J 7(4), 286-9. Full Citation
o Nadal D, Hunziker UA, Bucher HU, et al. (1989) Infants born to mothers with antibodies against Borrelia burgdorferi at delivery. Eur J Pediatr 148(5), 426-7. Abstract
o Schutzer SE, Janniger CK, Schwartz RA (1991) Lyme disease during pregnancy. Cutis 47(4), 267-8. Abstract
o Strobino BA, Williams CL, Abid S, et al. (1993) Lyme disease and pregnancy outcome: a prospective study of two thousand prenatal patients. Am J Obstet Gynecol 169(2 Pt 1), 367-74.
o Jovanovi R, Hajri A, Cirkovi A, et al. (1993) [Lyme disease and pregnancy]. Glas Srp Akad Nauka Med (43), 169-72.
o Kumi D J, Harris O.(1995) Viability of Borrelia burgdorferi in stored semen. Br Vet J Mar-Apr;151(2): 221-4 PMID: 8920118
o Williams CL, Strobino B, Weinstein A, et al. (1995) Maternal Lyme disease and congenital malformations: a cord blood serosurvey in endemic and control areas. Paediatr Perinat Epidemiol 9(3), 320-30.
o Silver H. (1997) Lyme Disease During Pregnancy. Inf Dis Clinics of N. Amer. Vol 11, No 1,
o van Holten J, Tiems J, Jongen VH (1997) Neonatal Borrelia duttoni infection: a report of three cases. Trop Doct 27(2), 115-6.
o Harvey WT, Salvato P. (2003) ‘Lyme disease’: ancient engine of an unrecognized borreliosis pandemic? Med Hypotheses. 60(5), 742-59.
o Stricker, R.B., D.H. Moore, and E.E. Winger. (2004). Clinical and immunologic evidence of transmission of Lyme disease through intimate human contact. J. Invest. Med. 52, S15
o Onk G, Acun C, Kalayci M, Cagavi F, et al. (2005) Gestational Lyme disease as a rare cause of congenital hydrocephalus. J Turkish German Gynecology Association Artemis, 6(2), 156-157.
o Jones CR, Smith H, Gibb E, Johnson L (2005) Gestational Lyme Disease: Case Studies of 102 Live Births. Lyme Times. Gestational Lyme Studies 34-36
o Hercogova J, Vanousova D (2008) Syphilis and borreliosis during pregnancy. Dermatol Ther 21(3), 205-9.
o Lakos A, Solymosi N (2010) Maternal Lyme borreliosis and pregnancy outcome. Int J Infect Dis 14(6), e494-8.
o Mylonas I (2011) Borreliosis During Pregnancy: A Risk for the Unborn Child? Vector Borne Zoonotic Dis. 11:891-8.
o Gardner T. Infectious Diseases of the Fetus and Newborn, 5th edition, (1995) Chapter 11, page 447 – 528.
o Gardner T. Lyme disease. 66 Pregnancies complicates by Lyme Borreliosis. Infec Dis Fetus and Newborn Infant. Saunders, 2000.
o Kumi-Diaka J, Harris O. Br Vet J. Viability of Borrelia burgdorferi in stored semen. 1995 Mar-Apr;151(2):221-4.
o MEDLINE results for: borrelia pregnancy AND human. 88 journal articles in the PubMed database BDH, July 2012, Latest Revision November 2012, www.Huismans.de.vu
Mothers with active Lyme Disease, Treated: 14.6% of the pregnancies with sequelae, Untreated: 66.7% of the pregnancies with sequelae, Unknown as to treatment: 30.3% with sequelae.
Specific adverse outcomes included: cardiac 22.7%, neurologic 15.2%, orthopedic 12.1%, opthalmic 4.5%, genitourinary 10.6%, miscellaneous anomalies 12.1%, 2nd trimester demise 12.1%.
Highest rate of adverse outcome (72.7%) in women with infection acquired prior to or during first trimester. [Gardner T]
These are found on the NIH U.S. Natl Library of Medicine site.
NIH & CDC(idsa)
Neonatal relapsing fever due to transplacental transmission of Borrelia.
Transplacental transmission of relapsing fever occured; spirochetes of the genus Borrelia were demonstrated in the blood of the mother and infant and in the cerebrospinal fluid (CSF) of the infant. Autopsy of the baby, who died 39 hours after birth, showed meningitis and typical splenic lesions with numerous spirochetes. Some unusual aspects of this case are the transplacental transmission, fatal outcome in the infant, and the demonstration of spirochetes in the CSF on direct smear.jama.jamanetwork.com/article.aspx?articleid=345386www.ncbi.nlm.nih.gov/pubmed/5818572
Tick-borne relapsing fever in the Pacific Northwest: an underdiagnosed illness?
Some 30 cases of tick-borne relapsing fever due to Borrelia are known to have occurred between 1965 and 1978 in the Pacific Northwest. This disease was found more frequently in young men with a history of wilderness exposure during the summer months. Recurrent fever was the most common symptom with temperatures reaching higher than 39.5 degrees C (103.1 degrees F) in all cases, and many patients had three or more febrile episodes. Splenomegaly was the second most common finding reported. Diagnosis of relapsing fever was made in 20 cases by identifying spirochetes on peripheral blood smears. In ten remaining cases the diagnosis was made on clinical and epidemiologic grounds. Information regarding therapy was available in 21 cases. Ten patients received a tetracycline drug and all had a prompt response without relapse. Two of the patients died, a 68-year-old woman with possible myocardial involvement and a newborn infant with infection acquired in utero and meningeal involvement. The diagnosis was often delayed in spite of outpatient evaluation and admittance to hospital, probably because borreliosis was not considered in the differential diagnosis.
Because tick-borne relapsing fever is eventually a self-limited disease in most patients, it is probably not recognized often enough. Awareness of this disease and examination of the peripheral blood smear for spirochetes will lead to earlier diagnosis. Prompt initiation of tetracycline therapy should reduce morbidity associated with borreliosis.www.ncbi.nlm.nih.gov/pubmed/7415171
Maternal-fetal transmission of the Lyme disease spirochete, Borrelia burgdorferiwww.ncbi.nlm.nih.gov/pubmed/4003991
Tick-borne relapsing fever in a premature infantwww.ncbi.nlm.nih.gov/pubmed/2415056
Human fetal borreliosis, toxemia of pregnancy, and fetal death.www.ncbi.nlm.nih.gov/pubmed/?term=3554838www.sciencedirect.com/science/article/pii/S0176672486801225/part/first-page-pdf
Two cases of neonatal Borrelia infection occurred. www.ncbi.nlm.nih.gov/pubmed/3969988
Borrelia infections in children in Central Europewww.ncbi.nlm.nih.gov/pubmed/3487761
Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancywww.ncbi.nlm.nih.gov/pubmed/3130607
Epidemiological studies of Lyme borreliosis and tick-borne encephalitis.
The hard tick Ixodes ricinus, vector of Borrelia burgdorferi and TBE virus (TBEV), is most abundant in the southern and central parts of Sweden. about
2000 cases of Lyme borreliosis (LB) and 50-80 cases of tick-borne encephalitis (TBE) are estimated to occur in Sweden annually. Five populations, including 903 individuals living in five different areas close to Stockholm where LB and TBE are endemic, were studied with regard to the clinical manifestations and antibody prevalence of LB and TBE.www.ncbi.nlm.nih.gov/pubmed/8047853
Neurologic manifestations in children with Lyme disease.
Of 69 children who met criteria for LD, 32% (22) had new neurologic signs, 73% (16) of which were accounted for by facial palsy and aseptic meningitis. Five of those with neurologic findings also had erythema migrans (EM), and one had both EM and arthritis. Among those with neurologic involvement, boys outnumbered girls two to one. Neurologic abnormalities resolved spontaneously in five children before their serologic results were known.
In our series, only 27% of children with neurologic abnormalities due to LD had a history of EM or arthritis. Seropositivity commonly constituted the primary basis for diagnosis of LD. Despite its nonspecificity, seropositivity for LD in children with neurologic symptoms usually signifies active neuroborreliosis.
Treatment of borrelial lymphocytoma.
results in 65 patients with borrelial lymphocytoma (22 on the ear lobe and 43 on the breast), registered at the Department of Infectious Diseases, University Medical Centre Ljubljana, from January 1986 to March 1995...www.ncbi.nlm.nih.gov/pubmed/8852477
Cerebrospinal fluid findings in children with Lyme disease-associated facial nerve palsy.
To determine the relative frequency of abnormal cerebrospinal fluid (CSF) findings in children with Lyme disease-associated facial nerve palsy.
A clinical series. A prospective evaluation was undertaken of the condition of children seen between 1988 and 1996 at a single medical center in a Lyme disease endemic area.
Forty children (24 boys and 16 girls, aged 3-19 years) with new onset facial nerve palsy who met the Centers for Disease Control and Prevention case definition of Lyme disease.
Neurologic examinations. Cerebrospinal fluid analysis.
Cerebrospinal fluid white blood cell count, protein level, or both were abnormal in 27 (68%) of the children. Thirty-six (90%) of the 40 children had a CSF abnormality consistent with central nervous system infection or immune involvement by B burgdorferi. Of the 22 children with CSF pleocytosis, only 7 (32%) had headache and none had meningeal signs.www.ncbi.nlm.nih.gov/pubmed/9412598
Neonatal Borrelia duttoni infection: a report of three cases.www.ncbi.nlm.nih.gov/pubmed/9133806
Lyme borreliosis in Slovenia.
Lyme borreliosis has been mandatory reportable in Slovenia for the last 11 years. It is the most common tick-borne disease and is present all over the country. The incidence has been increasing. In 1997 155/100,000 cases were recorded; in some regions the incidence was even substantially higher. The disease affects both sexes (as a rule more often women than men) and all age groups. The incidence is the highest in persons 30-50 years of age, followed by children aged 6-15 years. Erythema migrans is by far the most common recorded manifestation.www.ncbi.nlm.nih.gov/pubmed/10652723
The outcome of Lyme borreliosis in children
Austria is an endemic area for Lyme borreliosis.www.ncbi.nlm.nih.gov/pubmed/10666805
CNS Lyme disease manifestation in children
The antibiotic treatment was successful in 7 patients and only partially effective in 2 children with facial nerve paralysis.
The most common symptom of neuroborreliosis in children is motor dysfunction. Acute ataxia may be a clinical presentation of neuroborreliosis. It is probable that borreliosis_triggers seizures in children with EEG abnormalities.www.ncbi.nlm.nih.gov/pubmed/18431910
Acute ataxia in a 4-year-old boy: a case of Lyme disease neuroborreliosis
We present a case of a 4-year-old who presented to the emergency department with an unsteady gait for 2 days. Ataxia is a rare but known manifestation of cerebellar involvement in Lyme disease. A 4-year-old (17 kg) boy with no significant medical history presented to the emergency department (ED) with history of nonbloody emesis for 2 weeks and an unsteady gait for 2 days. Over the past 2 days, his gait had gotten progressively worse until he was unable to walk without assistance. The vomiting would usually occur 1 hour after eating meals. He had also complained of a single headache, which occurred approximately 10 days before admission. The headache did not occur in the early morning hours or wake him up from his sleep. His appetite for the weeks before admission had progressively decreased, and he had also become more irritable, especially when stimulated. He had increased fatigue for the week before presentation. His parents denied any fever, rhinorrhea, cough, diarrhea, rash, bruising, bleeding, or hematuria. The patient denied any abdominal pain or headache while in the ED.www.ncbi.nlm.nih.gov/pubmed/19091290
Clinical characteristics of childhood Lyme neuroborreliosis in an endemic area of northern Europe
Neuroborreliosis may be caused by different species of Borrelia burgdorferi (BB) and the clinical presentation of neuroborreliosis in children may differ between geographical areas due to occurrence of different BB genospecies. The aim of this study was to evaluate the clinical characteristics in children with neuroborreliosis in an endemic area of Scandinavia. During 1996-2006, children with suspected neuroborreliosis referred to Stavanger University Hospital were investigated by a standard procedure including a lumbar puncture. A total of 143 children were diagnosed with neuroborreliosis, and all cases were diagnosed from April to December. The most common clinical presentations were symptoms of mild meningitis (75%) and/or facial nerve palsy (69%). Radicular pain was present in only 10 children. In all but 5 children, laboratory signs of meningitis were present. Erythema migrans preceded the neurological symptoms in only 27% of the children. In conclusion, we have found that in an endemic area of northern Europe, meningitis is present in the majority of children with neuroborreliosis, and that symptoms of a mild meningitis or facial nerve palsy are the most common presentations.www.ncbi.nlm.nih.gov/pubmed/19065451
Lyme neuroborreliosis: manifestations of a rapidly emerging zoonosis.
Lyme disease has a worldwide distribution and is the most common vector-borne disease in the United States. Incidence, clinical manifestations, and presentations vary by geography, season, and recreational habits. Lyme neuroborreliosis (LNB) is neurologic involvement secondary to systemic infection by the spirochete Borrelia burgdorferi in the United States and by Borrelia garinii or Borrelia afzelii species in Europe. Enhanced awareness of the clinical presentation of Lyme disease allows inclusion of LNB in the imaging differential diagnosis of facial neuritis, multiple enhancing cranial nerves, enhancing noncompressive radiculitis, and pediatric leptomeningitis with white matter hyperintensities on MR imaging. The MR imaging white matter appearance of successfully treated LNB and multiple sclerosis display sufficient similarity to suggest a common autoimmune pathogenesis for both. This review highlights differences in the epidemiology, clinical manifestations, diagnosis, and management of Lyme disease in the United States, Europe, and Asia, with an emphasis on neurologic manifestations and neuroimaging.www.ncbi.nlm.nih.gov/pubmed/19346313
Uncommon manifestations of neuroborreliosis in children
Lyme borreliosis is a tick-borne spirochetal infection which affects the skin, joints, heart and nervous system. Children with a neuroborreliosis usually present with a facial nerve palsy or aseptic meningitis, but the spectrum also includes other rare manifestations. We report four unusual cases of childhood neuroborreliosis and show that seizures with regional leptomeningeal enhancement, acute transverse myelitis, meningoradiculitis with pain and paraesthesia and cranial nerve palsies other than facial nerve palsy can be the leading symptoms of children with neuroborreliosis. All children had serological evidence of an acute infection with Borrelia burgdorferi, a pleocytosis in the cerebrospinal fluid and a complete response to antibiotic treatment. An intrathecal synthesis of IgG antibodies was detected in three children. Thus, diagnostic work up in children with unusual neurological symptoms should include cerebrospinal fluid studies with determination of the white blood cell count and calculation of the antibody index against B. burgdorferi.www.ncbi.nlm.nih.gov/pubmed/19748808