Back in 1986, a US patent was filed for a vaccine against Lyme disease by Dr. Russell Johnson (PhD), Department of Microbiology and Immunology from University of Minnesota.
In his patent application, several important points were highlighted when describing Lyme disease.
1: the spirochete could persist causing chronic forms of the disease
2: once infection has occurred, antibiotic therapy might not 'purge the host of the spirochete but only act to control the chronic forms of the disease' (thus once infection established, antibiotics control but do not eradicate the infection)
3: maternal-fetal transmission of Borrelia burgdorferi has resulted in neonatal death
4: for every symptomatic infection, there is at least one asymptomatic infection.
This is indeed troubling and highlights that persistence of this organism and maternal-fetal transmission are both well acknowledged entities.
As an FYI: There have been cases in the peer reviewed literature of asymptomatic mothers with NO HISTORY of tick bite or EM rash - transmitting Bb in utero to their baby - thus remarkably resembling congenital syphilis which is also a spirochete infection. (Lampert, 1986; MacDonald, 1989; Dattwyler et al, 1989; Trevisan etal, 1997; Maraspin et al, 1999; Horst, 2003; Onk, 2005).
There has been a report of confirmation of Bb spirochetes identified in three placentas by silver stain. 2 of these placentas were further tested using PCR and B. burgdorferi confirmed. All of these mothers were asymptomatic and would be considered seronegative (they had borderline ELISA's and negative or equivocal WB). Authors identified no relationship between placental spirochetes and results of the ELISA and WB and authors suggested long-term follow-up of infants born to mothers w placental spirochetes. (Figueroa et al, 1996)
There have also been cases of seronegative mothers also transmitting Bb to their baby in utero (Lavoie et al 1987), (Weber et al, 1988*), (Macdonald, 1989), (Dattwyler, 1989).
Excerpt from patent below:
"The chronic forms of the disease such as arthritis (joint involvement), acrodermatitis chronica atrophicans (skin involvement), and Bannwarth's syndrome (neurological involvement) may last for months to years and are associated with the persistence of the spirochete.
A case of maternal-fetal transmission of B. burgdorferi resulting in neonatal death has been reported. Domestic animals such as the dog also develop arthritis and lameness to this tick-borne infection. For every symptomatic infection, there is at least one asymptomatic infection. Lyme disease is presently the most commonly reported tick-borne disease in the United States.
The infection may be treated at any time with antibiotics such as penicillin, erythromycin, tetracycline, and ceftriaxone. Once infection has occurred, however, the drugs may not purge the host of the spirochete but may only act to control the chronic forms of the disease. Complications such as arthritis and fatigue may continue for several years after diagnosis and treatment. "
Lampert, R. Infantile multisystem inflammatory disease: another case of a new syndrome. Eur J Pediatr (1986) 144:593-596
Macdonald, AB. Human fetal borreliosis, toxemia of pregnancy and fetal death. Zentralbl Bakteriol Mikorbiol Hyg (A). 1986;263(1-2):189-200.
Burgdorfer, W. The Enlarging Spectrum of Tick-Borne Spirochetosis: R. R. Parker Memorial Address. Reviews of the Infectious Diseases, Vol 8, No. 6. Nov/Dec 1986
Lavoie PE, Lattner BP, Duray P. H et al. Culture positive, seronegative, transplacental Lyme borreliosis infant mortality. Arthritis Rheum; 1987. p. S50.
MacDonald A, Benach J, Burgdorfer W. Stillbirth following Maternal Lyme Disease. New York State Journal of Medicine vol 87, November 1987.
Weber K, Bratzke H, Neubert UWE et al. Borrelia Burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy. Pediatric Infectious Disease Journal Vol 7, No 4, 286-289, 1988 *(initially mother's sera was negative for Bb antibodies by IFA - so she would have been considered seronegative. A few years later, storied sera was re-examined and tested w ELISA IgM and positive).
Macdonald, AB. Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am. 1989;15(4):657-77.
Dattwyler R, Volkman D and Luft B. Immunologic aspects of Lyme borreliosis. Review of Infectious Diseases Vol 11(6) 1989.
Horst, H. (abstract no W/TH-P-20). In: Abstracts (book 1) of the 4th International Conference on Lyme borreliosis. Stockholm, Sweden, p 56.
Trevison G, Stinco G, Cinco M. Neonatal skin lesions due to a spirochetal infection: a case of congenital Lyme borreliosis? Journal of Dermatology, 1997, 36, 677.
Maraspin V, Cimperman J, Lotric-Furlan, S et al. Erythema migrans in pregnancy. Wein Klin Wochenschr (1999) 111/22-23:933-940.
Gardner, T. Lyme disease. In: Remington JK, J. editor. Infectious Diseases of the Fetus and Newborn, 5th ed: Saunders; 2001.
Horst, H. Borrelieninfektion in der Schwangerscharft und durch Bluttransfusionen. In H. Horst (ed.) Zeckenborreliose Lyme-Krankheit bei Mensch und Tier (4th ed., pp. 132-137). Balingn, Germany: Spitta Vergag GmbH & Co., KG. **translated from German
Onk G, Acun C, Kalayci M et al. Gestational Lyme Disease as a rare cause of congenital hydrocephalus. J Turkish German Gynecol Assoc, Vol 6(2); 2005-156-157.
Figueroa R, Bracero LA, Augero-Rosenfeld, M et al. Confirmation of Borrelia Burgdorferi spirochetes by polymerase chain reaction in placentas of women with reactive serology for Lyme antibodies. Gynecol Obstet Invest. 1996;41(4):240-3.
** this is not meant to be a discussion of the Lyme vaccine, rather highlighting how this organism had been described in 1989.
This was written by Sue Burke Faber who kindly gave permission for me to post on my blog.
For over 30 years our Government Health Authorities have been blindsided about Lyme Disease leaving thousands of patients suffering without appropriate treatment, based on opinions, when science was readily available that showed it to be a persistent infection, chronic and capable of maternal transmission.
Every day doctors tell sick patients that their short course of antibiotics has eradicated their infection and their remaining symptoms are now magically something else but not Lyme Disease.
How many sick patients will it take before doctors wake up to what is going on?
How many sick Doctors have to be infected with Lyme Disease before they convince their colleagues to use their brains and medical training to understand this disease?