DOES LYME DISEASE INCREASE RISK OF MISCARRIAGE?

The number of miscarriages among acutely lyme infected mothers, according to the study below, is fairly significant. WHY are we not hearing about this in the news? Why are more studies not being done and the information made available to the public? Instead we are being flooded with swine flu propaganda for the purpose of selling vaccines...and who knows for what other purposes. Some in the medical profession fear that there could be antifertility agents in the flu vaccines and in the Gardasil vaccine http://home.snafu.de/usp/antifert.htm

Abstract
Lyme disease is an inflammatory syndrome caused by infection with Borrelia burgdorferi. Although this syndrome has important implications for human pregnancy, little is known about gestational infection with B. burgdorferi. Fetal death occurred in 33 of 280 gestational sacs (12%) in 39 C3H/HeN female mice infected by intradermal injection of B. burgdorferi 4 days after mating (acute infection), compared with 0 of 191 sacs in 25 control mice (P = 0.0001).

Forty-six percent of acutely infected mice suffered at least one fetal death, compared with none of the control animals (P = 0.0002). There were no fetal deaths in 18 C3H/HeN mice infected 3 weeks prior to mating (chronic infection).

A sensitive PCR technique detected B. burgdorferi DNA in the uteri of acutely infected mice but did not detect DNA in the uteri of controls or chronically infected mice. Spirochete DNA was only rarely detected in fetal tissues, and its presence was not required for fetal death. The inclusion of an internal competitive PCR target indicated that the lack of B. burgdorferi sequences in fetal DNA was not due to the presence of a PCR inhibitor. Histologic analysis of gestational tissues from infected animals demonstrated nonspecific pathology consistent with fetal death. These findings indicate an association between murine fetal death and acute infection with B. burgdorferi early in gestation but not with chronic infection. Our data suggest that fetal death is due to a maternal response to infection rather than fetal infection. These findings could provide an explanation for observations in humans in which sporadic cases of fetal death in women infected with B. burgdorferi during pregnancy have been reported, while previous infection has not been associated with fetal death.

R M Silver, L Yang, R A Daynes, D W Branch, C M Salafia, and J J Weis Fetal outcome in murine Lyme disease. Infect Immun. 1995 January; 63(1): 66-72.
The Full Text of this article is available as a PDF

Lyme Disease and Still Births

O30 - Stillbirth and infection

Robert L GoldenbergDepartment of Obstetrics & Gynecology, Drexel University College of Medicine, Philadelphia,

USAStillbirths (SB) account for more than half the perinatal mortality in most settings world-wide with rates ranging from 3-5/1000 births in developed countries to 20 to nearly 100/1000 births in some developing countries. Infection likely accounts for about 15% of SB in developed countries to 50% in developing countries. Infection is more strongly associated with early gestational age SB than with late preterm or term SB. There are many mechanisms by which infection may cause SB ranging from 1) severe systemic infection of the mother without fetal involvement, to 2) placental infection, to 3) infections of the fetus causing congenital anomalies, to 4) infections of the fetus causing organ failure and death.*

Specific infections that are causally associated with SB include malaria, syphilis, Lyme disease, African tick- bourne gestational relapsing fever, listeria, tularemia and typhoid.* *More important numerically, are the intrauterine infections causing chorioamnionitis, such as placental membrane infections with group B streptococcus, E coli, and the mycoplasmas. Maternal viral infections associated with SB include parvovirus, coxsackie B, varicella, rubella and CMV.* The reasons for the high level of infection - related SB in developing countries likely include environmental pressure from large quantities of urogenital organisms plus poor host defenses likely associated with malnutrition.

http://www.isa2007.org/ISA_2007_Conference_Handbook_-_Scientific_Track.pdfpage