Other Modes of Transmission
Comments from three Lyme treating doctors...
1.) "Many years ago, I followed four women who contracted Lyme during pregnancy (all had EM and all tested positive for Lyme). They were not treated during pregnancy, and after delivery, all four had their milk tested by Alan MacDonald. Two were tested by PCR and two were tested by culture. In every case, Bb was demonstrated in breast milk. Thus my recommendation not to breast feed if Lyme is present.
Yes, these patients were untreated and therefore probably had a higher spirochete load, but consider that Bb can survive treatment, be present during treatment, and that Bb has a preference for skin and skin structures, which breast tissue actually is. Even if the risk is very low, who would be willing to risk their newborn's health? Finally, Willi Burgdorfer flatly states that Bb may enter through mucous membranes and even through intact skin."
2.) "Many years ago, while I was working with MacDonald, there were four cases in which a pregnant woman presented with an EM rash. In all four cases the milk was tested- two by his culture, and two by his PCR. The result? All four were positive."
3.) "I believe it can transferred in breast milk. I commonly use amoxicillin in pregnancy and so far have not seen problems in newborns whose mothers were treated the ENTIRE time from diagnosis through delivery. I discourage breast feeding due to the Lyme and prefer to change antibiotics once they deliver. But.. most of my patients insist on breastfeeding anyway and I continue them on amox as long as breastfeeding. I watch the babies for any failure to gain weight or developmental delays."
Thanks to Dr. Marie Kroun for compiling and
providing the following information.
Transmission by Contact via Feces, urine or Tick-excretes
Unusual features in the epidemiology of Lyme borreliosis.
In this study two cases of Lyme borreliosis are presented. First, the author describes how he contracted Lyme borreliosis 24 hours after he visited an endemic area.
The second case described is that of a woman who developed Lyme borreliosis symptoms, when intestinal content of an infected tick came into contact with her conjunctiva. In both cases the diagnosis is based on clinical picture and positive serological tests.
The first case shows the probability of contracting Lyme borreliosis when the duration of the tick's attachment to the skin is less than 24 hours. The second case, described demonstrates transmission of B. burgdorferi by contact.
Experimental inoculation of dogs with Borrelia burgdorferi.
Zentralbl Bakteriol Mikrobiol Hyg A 1986 Dec; 263(1-2): 49-54 PMID: 3554844
To determine if dogs could serve as a reservoir for Borrelia burgdorferi, three beagles were inoculated subcutaneously (SQ) with 200 laboratory cultured spirochetes which were originally isolated from blood of a Peromyscus leucopus from Ft. McCoy, Wisc.
One four month old beagle was inoculated SQ with 5 ground Ixodes dammini from Shelter Island, N.Y. which came from an area with a 50% B. burgdorferi tick infection rate; and another uninfected four month old beagle was housed loose on the floor with the tick inoculated dog.
All three spirochete inoculated beagles developed IFA antibody titers to B. burgdorferi of (7 log2) to (8 log2) by day 28 post inoculation. All were apparently healthy and no spirochetes were cultured from the blood.
In an attempt to exacerbate the disease two of the dogs were given 3 mg of dexamethasone on day 68 post inoculation. B. burgdorferi was isolated from blood of all these dogs on days 4 and 97 days post inoculation.
The tick inoculated dog developed a B. burgdorferi IFA antibody titer of (10 log2) by day 14 post inoculation. The contact exposed dog also developed a B. burgdorferi IFA antibody titer of (7 log2) on post contact day 21 indicating contact infection. B. burgdorferi was not isolated from either of these dogs. These results indicate that, contact transmission of B. burgdorferi may occur between dogs, dogs can be subclinically infected with B. burgdorferi and have persistent infections.
Clinical and serologic evaluations of induced Borrelia burgdorferi infection in dogs.
Feeding infected ticks on 4 dogs (group 1) failed to cause seroconversion, and SC inoculation with 500 organisms caused minimal seroconversion in 2 of 4 dogs (group 2). At 56 days, approximately 3.01 X 10(8) B burgdorferi organisms were injected IV into group-1 dogs, and intraperitoneally into group-2 dogs.
A control group of 4 dogs (group 3) had noninfected ticks feed on them, and then were given IV injection of physiologic saline solution. Increases in immunoglobulin M (IgM) titers were detected in 2 of 4 group-2 dogs approximately 7 days after the initial exposure. These titers returned to negligible values 20 days later.
Immunoglobulin G titers increased approximately 10 days after the initial exposure and were mildly increased 56 days later, when dogs were exposed a second time. Both the IV and intraperitoneal injections (second exposures) resulted in increased IgM titers, which in both groups eventually returned to preexposure values after approximately 2 months.
Immunoglobulin G titers increased within a week after the second exposure, and in 3 dogs monitored for 8 months, returned to negligible values after the 8-month period. One control dog had a slightly increased IgG titer 24 days after the second inoculation. The possibility of urine transmission is suggested.
Clinical status, hemograms, serum biochemical profiles, ECG and results of urinalyses remained normal throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)
The prevalence and significance of Borrelia burgdorferi in the urine of feral reservoir hosts. Bosler EM, Schulze TL. Zentralbl Bakteriol Mikrobiol Hyg A 1986 Dec; 263(1-2): 40-4 PMID: 3577491
Live Borrelia burgdorferi were isolated from the blood and/or urine of white-footed mice (Peromyscus leucopus) collected on Shelter Island, New York, in 1984 and 1985. Prevalence of spirochetes in urine was consistently higher than in blood or both fluids simultaneously. Spirochetes remained viable for 18-24 hours in urine and were maintained in culture for one week. Mice removed from the field were spirocheturic for at least 13 months.
One spirocheturic mouse developed spirochetemia one month after field removal indicating the pathogen can return to the peripheral circulation. Twenty-one kidneys from 22 mice had spirochetes in the interstitial areas and bridging the tubules. A positive correlation between Babesia microti infection and spirocheturia was seen.
Although the mechanism of entry into the urine is unknown, B. microti infection may increase glomerular permeability. Babesia induced hematuria may provide possible nutrients to maintain spirochetes. Urine may provide a method for contact non-tick transmission of B. burgdorferi in natural rodent populations particularly during periods of nesting and/or breeding.
Transmission by MILK or food?
Most spirochetes (and other bacteria) ingested will probably be killed by the high acidic content in the stomach, but people with achlorhydria and newborns that have very low stomach acid production, does not have this protective barrier and might be at increased risk for getting infected by the oral route, if they ingest live spirochetes.
Experimental inoculation of Peromyscus spp. with Borrelia burgdorferi: evidence of contact transmission.
In order to determine if Peromyscus spp. could become infected with the Lyme disease spirochete (Borrelia burgdorferi) by direct inoculation and to determine the duration of spirochetemia, 4 P. leucopus and 5 P. maniculatus were inoculated by the intramuscular, intraperitoneal, and subcutaneous routes with an isolate of B. burgdorferi obtained from the blood of a trapped wild P. leucopus from Camp McCoy, Wisconsin.
All of the mice developed antibodies to B. burgdorferi which reached a peak indirect immunofluorescent (IFA) geometric mean antibody titer of 10 log2 21 days post-inoculation. B burgdorferi was recovered from the blood of 1 P. maniculatus 21 days post-inoculation.
One uninfected Peromyscus of each species was housed in the same cage with the infected Peromyscus as a contact control. Both of the contact controls developed IFA B. burgdorferi antibodies by day 14, indicating contact infection.
These findings show that B. burgdorferi can be transmitted by direct contact without an arthropod vector.
Borrelia burgdorferi infection in Wisconsin horses and cows.
Blood samples from Wisconsin horses and cows suspected of having clinical disease due to Borrelia burgdorferi infection were submitted by veterinary practitioners. All serum, milk, colostrum, and synovial samples were tested for B. burgdorferi antibodies by immunofluorescence.
Whole blood, milk, colostrum, and synovial fluid samples were cultured for B. burgdorferi. Records were kept on the clinical signs of antibody-positive animals, date of sample, and location of the animal by county. Of the samples tested for antibodies 282/430 cow sera, 118/190 horse sera, 5/10 cow synovial fluids, 3/6 horse synovial fluids, 2/3 cow colostrums, 0/44 cow milk samples and 1 aborted fetus serum were antibody positive at a titer of 1:128 or greater.
Of samples cultured 7/156 cow bloods, 2/35 horse bloods, 1/14 cow synovial fluids, 0/4 synovial fluids, 1/3 cow colostrums, 0/44 cow milk, and 2/10 cow urine samples were B. burgdorferi culture positive.
For both cows and horses October and May were the two peak months for the number of antibody-positive samples. The most frequent clinical signs in antibody-positive horses and cows were lameness and swollen joints, but many also had stiffness, laminitis, abortions, and fevers.
Not all antibody-positive animals showed clinical signs. These findings show that B. burgdorferi infection occurs in horses and cows and can cause clinical illness in some but not all animals. Infection in cows and horses occurs most frequently 1 month after the emergence of adult I. dammini.
Because spirochetes could be isolated from blood, synovial fluid, colostrum, and urine, these animals could be important in providing an infected blood meal for ticks and bringing B. burgdorferi in direct contact with humans.
Borrelia burgdorferi: another cause of foodborne illness?
Borrelia burgdorferi was identified as the etiological agent of Lyme disease in 1982. This Gram-negative spirochete is classified in the order Spirochaetales and the family Spirochaetaceae.
The pathogen is fastidious, microaerophilic, mesophilic and metabolises glucose through the Embden-Meyerhof pathway. A generation time of 11 to 12 h at 37 degrees C in Barbour-Stoenner-Kelly medium has been reported.
Lyme disease, named after Lyme in Connecticut, is distributed globally. It is the most commonly reported vector-borne disease in the United States, where the incidence is highest in the eastern and midwestern states.
Since establishment of national surveillance in 1982, there has been a nine-fold increase in the number of cases reported to the U.S. Centers for Disease Control. The deer tick of the genus Ixodes is the primary vector of Lyme borreliosis.
The tick may become infected with B. burgdorferi, by feeding on an infected host, at any point in its 2-year life cycle which involves larval, nymphal and adult stages. The infection rate in deer ticks may be as high as 40% in endemic areas. The primary vertebrate reservoirs for Ixodes are the white-footed mouse (Peromyscus leucopus) and the white-tailed deer (Odocopileus virginianus).
Dairy cattle and other food animals can be infected with B. burgdorferi and hence some raw foods of animal origin might be contaminated with the pathogen. Recent findings indicate that the pathogen may be transmitted orally to laboratory animals, without an arthropod vector.
Thus, the possibility exists that Lyme disease can be a food infection. In humans, the symptoms of Lyme disease, which manifest themselves days to years after the onset of infection, may involve the skin, cardiac, nervous and/or muscular systems, and so misdiagnosis can occur.
Evidence for in utero Transmission of Borrelia burgdorferi from Naturally Infected Cows
(excerpts from the abstract: Five of 15 adult cows were spirochetemic at parturition; 4 of the calves from these cows were also spirochetemic at birth (PCR). Spirochetes were cultured from the placentas in 2 of 10 cows and from the uterine fluid in 1 of 8 cows.
Borrelia burgdorferi DNA was detected in the colostrum in 4 of 12 cows.
Three of 15 calves were stillborn; Borrelia burgdorferi DNA was detected by PCR in 3 of 3 and spirochetes cultured from 2 of 3 stillborn calves. Fetal tissues from which Borrelia burgdorferi DNA was detected include blood, spleen, bladder, kidney, synovial fluid and tissue, heart, cerebrum, and aqueous humor.
Borrelia burgdorferi was cultured from the spleen of one stillborn calf and the kidney of another. Detection of Borrelia burgdorferi DNA from the tissues of stillborn calves, as well as spirochetemia in neonatal liveborn and stillborn calves, gives evidence for in utero transmission of Borrelia burgdorferi in naturally infected dairy cattle.)
Last, a splenectomized mice study, yet unpublished, but Sousan Altaie very kindly provided me with her draft text, and she has allowed me to refer to her data, as stated to me in a mail per 28-03-00:
Transmission of Borrelia burgdorferi from Experimentally Infected Mating Pairs to Offsprings in a Murine Model.
Splenectomized 6-8 week-old mice were divided into 4 groups. Groups A, B, and C had 23, 24, and 26 mating pairs respectively.
Immediately prior to mating, in group A only females, in group B only males, and in group C both females and males were infected subcutaneously with 106-107 B. burgdorferi in 250 ml SKB II media.
The control group D had 12 mating pairs in which both male and females received sterile SKB II as placebo.
The resulting pups were sacrificed at 1, 7, 14, and 21 days of age. The milk content of the stomach, sections from ear, skin, heart, liver, spleen, brain, bladder, and kidney of the 1, 7, and 14 day-old pups were cultured for B. burgdorferi. The cultures were read at 3, 6, and 9 weeks post incubation. The above mentioned tissues except milk were also cultured from sacrificed 21 day-old weanlings.
Transmission to offsprings was indicated when B. burgdorferi was isolated from any tissue from a given pup.
From the experimentally infected females in which the milk was cultured (total 25 females in groups A and C), 2 (8%) transmitted B. burgdorferi to their pups on day one via their milk: 2 pups from a litter of 4 in group C, 1 pup from a litter of 8 in group A.
No transmission was detected via milk on days 7 or 14. Among 49 infected females from groups A and C,5 (10.2%) transmitted B. burgdorferi to their pups either in utero or intrapartum.
Two of the transmissions were detected on day 1 (litter one, 2/6; litter two, 1/7), two on day 7 (litter three, 1/7; litter four, 2/6), and one on day 14 (litter five, 2). Interestingly, four of the litters from the mating pairs in group B [in which only MALE MICE were infected!] had infected pups (litter one, 3/5; litter two, 1/8; litter three, 3/6; and litter four, 2/4).
This study has also been presented on the following conferences, but I don't have the abstracts (I any of you readers have them, please send me a copy, will you?):
Marie Kroun’s comments:
Above papers at least document that there is already some evidence present for:
Borrelia burgdorferi can infect humans by direct contact VIA (INTACT or BROKEN?) MUCOUS MEMBRANES!
There is evidence found that Borrelia burgdorferi can be EXCRETED INTO SOME HUMAN SECRETIONS!
I think it is better to remember always that “Absence of proof is not proof of absence” and it’s “better to be safe than sorry”!
You should always take the necessary precautions to protect yourself and your partner and your offspring against transmission of infections via secretions (use condoms or avoid sex and other potentially risky close contacts) &
Many have over the years asked me questions about Borreliosis during pregnancy and after birth and what I would consider reasonable actions to take, in case.
I have unfortunately not yet had the time and energy to search ALL the published literature thoroughly for the subject of “pregnancy acquired Borrelia cases in mother and child” (PubMed search for borreli*+pregnan*”, but I am aware that there are a number of publications demonstrating probable and certain maternal to foetal transmission of Borrelia infectionvia Google search, Art Doherty’s review and not the least an extensive review by Gardner T in “Infectious Disease of the Fetus and Newborn Infant, Saunders Philadelphia 1995 4th ed.; Chapter 11: 447-528”: 81 pages; 428 references reviewed, which describes 5 previously unpublished cases of probable or proven maternal to foetal transmission of B. burgdorferi and a review of the literature of 46 adverse outcomes of pregnancies complicated by Lyme Borreliosis!
BUT when reading those articles please bear in mind, that there are many published papers on culture, PCR and/or microscopy proven Borrelia SERONEGATIVE cases, i.e. that absence of positive Borrelia titer in mother and/or child does NOT exclude neither an active nor a latent Borreliosis, that might not give the congenitally infected child any symptoms of Borreliosis until several months to years after birth!
Thus negative serology does unfortunately NOT safely exclude congenital infection; on the other hand the trypanosoma paper illustrates that via placenta transmitted maternal IgG antibodies may take up to 8 months after birth to clear from the child’s blood! – so a for months persistent positive IgG antibody reaction must not be taken as sign that the baby was congenitally infected either! – this is probably true for other infections also?!
The most famous and important - because his parents later co-founded the Lyme Disease Foundation (LDF) –congenitally acquired fatal Borreliosis case described is the son of a during pregnancy infected mother Karen Vanderhoof-Forschner and Thomas Forschner (read more here and here), Jamie Forschner (1985-1991), whose short life story is told by his mother here:
In 1990, NIH's new test that they had developed, which is not available to the public yet, photographed the bacteria in my son despite his repeated treatment, and not only him, but other people across the country,showing that short-term treatment, for a few people, may not ever work, and may not work at all. I was dismayed.When I showed this to the pediatricians, they said if we retreated our son, based on what they got from our local health department and our local people in the state, they would cancel us, and they canceled my son as a patient. We had no physician in the state, and we took our son to New Jersey.
Once he was retreated, all his speech came back again, and for the third time he learned how to speak. Muscle tone came back, vision came back, indeed they were able to show his intelligence was very high. He was mainstreamed into kindergarten. He developed girlfriends, went to birthday parties, and we finally found a little boy inside the diseased body. We waited over one year for NIH's tests to be released.
We were hoping we could use it to check on our son's progress so that he wouldn't have a relapse and die.
As my son started to relapse, I waited, and waited, and I waited too long. Our son's last relapse came on, and he started having seizures and brain infection. Within 24 hours he was dead. His brain had swelled up so much it had killed itself.
And at some point, his report, combined with other deaths due to Lyme, combined with other children with trans-placental information, may indeed, at some time in the future, have enough peer-reviewed publications that the CDC may indeed accept trans-placental transmission or death due to Lyme, in which case public health policy can be improved.
I warmly recommend all readers to buy and read Karen Vanderhoof-Forschners book: “Everything you need to know about Lyme disease” since it contains an extensive review of all times Borrelia literature!
There are good reasons NOT to PLAN to try to get pregnant, when you have a clinically ACTIVE chronic disease, especially one that could potentially be caused by a known or unknown microbial infection, and hence bear a potential risk of transmitting the disease to your child and partner!
If you are a new mother and show signs of ACTIVE Borreliosis you should probably avoid direct breastfeeding of your newborn baby; don’t rely on the baby’s low stomach acid level to be high enough to kill the ingested bacteria!