Fact 1: Bites of Ticks and Other Arthropods
Lyme disease can be transmitted to humans by the bite of an infected tick. It can also be transmitted via sand fleas, mosquitoes, fleas and other arthropods. A complete list of arthropods can be found here. In clinical cases of Lyme Disease, biting flies, mosquito’s and mites are suggested to have been responsible for the infection. Borrelia has been found in: numerous species of mites, fleas, biting flies, ie: bot flies, deer flies, horse flies and mosquito’s, indicating that these insects are capable of maintaining the bacteria within the environment and are potential vectors.
Fact 2: Contact Transmission
Borrelia spirochetes have been found in the urine of infected dogs, horses, cattle and mice. Studies on mice have found that the spirochetes in urine remained viable for 18-24 hours and concluded that “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” Evidence for direct contact transmission has been demonstrated in mice. These findings suggest that further research is needed to ascertain whether, like the spirochete that causes Leptospirosis, the borrelia spirochete is able to spread by the urine of infected animals to humans.
Fact 3: Human to Human Transmission
Sexual transmission: there is no direct evidence for sexual transmission, although spirochetes have been found in semen, suggesting that it is a possibility. Lyme disease has also been likened to another spirochetal disease, syphilis, which is a sexually transmittable infection.
Mother to baby: The possibility of placental transmission is acknowledged, although there are mixed reports regarding exactly what health risk congenital Lyme disease poses to the foetus/newborn. A brief dialogue regarding some examples and the quoted passages below: Allan MacDonald 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 International Disease Society of America (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 Centre for Disease Control (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”.
Blood Transfusions & Organ Transplantation
Fairly self explanatory.........
Because there is no widely used screening test for babesiosis (coinfection of Lyme), its spread poses a particular threat to the blood supply, scientists said. “We are very worried about it and are doing everything in our power to address this,” said Sanjai Kumar, chief of the laboratory of emerging pathogens at the Food and Drug Administration.
Researchers at the University of Wisconsin have reported that dairy cattle can be infected with Bb, hence milk could be contaminated. Bb can also be transmitted to lab animals by oral intake such as food.
So, in a nutshell, UNLESS you are a virgin, born of a virgin, living in Antarctica (and have never left), never had a blood transfusion or organ transplant and have never had raw milk, you COULD have Lyme!
Luger SW (1990) Lyme Disease Transmitted by a Biting Fly. N Engl J Med; 322(24):175 http://www.ncbi.nlm.nih.gov/pubmed/2342543
Herzer P, Wilske B, Preac-Mursic V, Schierz G, Schattenkirchner M and Zollner N (1986) Lyme arthritis: clinical features, serological, and radiographic findings of cases in Germany. Klin Wochenschr ; 64(5):206-15 http://www.ncbi.nlm.nih.gov/pubmed/3702279
Doby JM, Chastel C, Couatarmanac'h A, Cousanca C, Chevrant-Breton J, Martin A, Legay B and Guiguen C (1985) Etiologic and epidemiologic questions posed by erythema chronicum migrans and Lyme disease. Apropos of 4 cases at the Regional HospitalCenter, Rennes. Bull Soc Pathol Exot Filiales; 78(4):512-25 http://www.ncbi.nlm.nih.gov/pubmed/4075471
Hard S (1966) Erythema chronicum migrans (Afzelii) associated with mosquito bite. Acta Dermato-Venereol;46:473-476 www.ncbi.nlm.nih.gov/pubmed/4163724
Badalian LO, Kravchuk LN, Sergovskaia VD, Belousova VS and Minina AP (1994) The neurological syndromes in Lyme disease in children. Zh Nevrol Psikhiatr Im S S Korsakova; 94(3):3-6 http://www.ncbi.nlm.nih.gov/pubmed/7975984
Pokorny P (1989) Incidence of the spirochete Borrelia burgdorferi in arthropods (Arthropoda) and antibodies in vertebrates (Vertebrata). Cesk Epidemiol Mikrobiol Imunol; 38 (1): 52-60 http://www.ncbi.nlm.nih.gov/pubmed/2646031
Anderson JF and Magnarelli LA (1984) Avian and mammalian hosts for spirochete-infected ticks and insects in a Lyme disease focus in Connecticut. Yale J Biol Med ;57(4):627-41. http://www.ncbi.nlm.nih.gov/pubmed/6516460
Hubalek Z, Halouzka J and Juricova Z (1998) Investigation of haematophagous arthropods for borreliae--summarized data, 1988-1996. Folia Parasitol (Praha);45(1):67-72.http://www.ncbi.nlm.nih.gov/pubmed/9516997
Magnarelli LA, Anderson JF and Barbour AG (1986) The etiologic agent of Lyme disease in deer flies, horse flies, and mosquitoes. J Infect Dis 1986;154 (2) :355-8 http://www.ncbi.nlm.nih.gov/pubmed/2873190
Stanek G, Flamm H, Groh V, Hirschl A, Kristoferitsch W, Neumann R, Schmutzhard E and Wewalka G (1987) Zentralbl Bakteriol Mikrobiol Hyg (A) ;263(3):442-9 http://www.ncbi.nlm.nih.gov/pubmed/3591096
Magnarelli LA and Anderson JF (1988)Ticks and Biting Insects Infected with the Etiologic Agent of Lyme Disease, Borrelia burgdorferi. J Clin Microbiol: 26 (8): 1482-6 http://www.ncbi.nlm.nih.gov/pubmed/3170711
Halouzka J, Wilske B, Stunzner D, Sanogo YO Hubalek (1999) Isolation of Borrelia afzelli from Overwintering Culex pipiens Biotype molestus Mosquitoes. 1999 Infection;27(4-5):275-7 http://www.ncbi.nlm.nih.gov/pubmed/10885843
Zakovska A, Capkova L, Sery O, Halouzka J and Dendis M (2006) Isolation of Borrelia afzelli from overwintering Culex pipiens biotype molestus mosquitoes. Ann Agric Environ Med; 13 (2): 345-348 http://www.ncbi.nlm.nih.gov/pubmed/17199258
Kosik-Bogacka DI, Juzna-Grygiel W and Jaborowska M (2007) Ticks and mosquitoes as vectors of Borrelia burgdorferi sl
in the forested areas of Szczecin. Folia Biol (Krakow): 55(3-4): 143-6 http://www.ncbi.nlm.nih.gov/pubmed/18274258
Tick-borne babesiosis threatens blood supply
Grauer GF, Burgess FC, Cooley AJ and Hagee JH (1998) Renal lesions associated with Borrelia burgdorferi infection in a dog. J Am Vet Med Assoc; 193 (2) 237-239 http://www.ncbi.nlm.nih.gov/pubmed/3403355
Cerri D, Farina R, Andreani E, Nuvoloni R, Pedrini A and Cardini G (1994) Experimental infection of dogs with Borrelia burgdorferi. Res Vet Sci; 57(2):256-8 http://www.ncbi.nlm.nih.gov/pubmed/7817018
Burgess EC (1988) Borrelia burgdorferi infection in Wisconsin horses and cows. Ann N Y Acad Sci; ;539:235-43 http://www.ncbi.nlm.nih.gov/pubmed/3190095
Manion TB, Khan, MI, Dinger J and Bushmich SL (1998) Viable Borrelia burgdorferi in the urine of two clinically normal horses. J Vet Diagn Invest 10 (2):196–199 http://www.ncbi.nlm.nih.gov/pubmed/9576355
Bosler EM and Schultze TL (1986) The prevalence and significance of Borrelia burgdorferi in the urine of feral reservoir hosts. Zentralbl Bakteriol Mikrobiol Hyg A; 263(1-2):40–44 http://www.ncbi.nlm.nih.gov/pubmed/3577491
Burgess EC, Amundson TE, Davis JP, Kaslow RA and Edelman R (1986) Experimental inoculation of Peromyscus spp. with Borrelia burgdorferi: evidence of contact transmission. Am J Trop Med Hyg; 35(2):355-359 http://www.ncbi.nlm.nih.gov/pubmed/3513648
And More Evidence:
Recovery of Lyme Spirochetes by PCR in Semen Samples of Previously Diagnosed Lyme Disease Patients. Presented by Dr. Gregory Bach, at the International Scientific Conference on Lyme Disease, April, 2001 http://www.samento.com.ec/sciencelib/4lyme/recoveryoflyme.html
Virginia Lyme site: https://sites.google.com/site/virginialyme/sexual
MacDonald AB (1989) Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am; 15(4):657-77
The International Disease Society of America (IDSA) guidelines: The Clinical Assessment, Treatment, and Prevention of Lyme Disease, Human Granulocytic Anaplasmosis, and Babesiosis: Clinical Practice Guidelines by the Infectious Diseases Society of America. (Clinical Infectious Diseases 2006; 43:1089–134) http://cid.oxfordjournals.org/content/43/9/1089.full
Centre for Disease Control: Lyme Disease; Pregnant Woman Fact Sheet : Accessed: February 2012 http://www.cdc.gov/lyme/resources/toolkit/factsheets/10_508_Lyme%20disease_PregnantWoman_FACTSheet.pdf
Centre for Disease Control: Lyme Disease; Resource Brochure : Accessed: February 2012 http://www.cdc.gov/lyme/resources/brochure/508_LD_Brochure.pdf
Weber K, Bratzke HJ, Neubert U, Wilske B and Duray PH (1988) Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy. Pediatr Infect Dis J; 7(4):286-9 http://www.ncbi.nlm.nih.gov/pubmed/3130607
Only the details of the journal article available at pubmed website (unless you have access): though J. Drulle writes about Weber et al’s findings
(1986) that were published (1988) in this article.
John Drulle MD Lyme Website: http://www.johndrullelymefund.org/pregnancy_and_lyme_disease.htm
Schlesinger PA, Duray PH, Burke BA, Steere AC and Stillman MT (1985) Maternal-fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi. Ann Intern Med; 103(1):67-8. http://www.ncbi.nlm.nih.gov/pubmed/4003991
Only the details of the journal article available at pubmed website: this article can be read in full via the
Canadian Lyme disease website : http://www.canlyme.com/Schlesinger_1985.pdf
National Institutes of Health, U.S. Department of Health and Human Services (2008). Lyme Disease: The Facts, the Challenge (NIH Publication No. 08-7041).
This Publication appears to have been removed from the National Institute of Health Website: http://www.niaid.nih.gov/topics/lymeDisease/Documents/lymedisease.pdf
The full publication can still be viewed (correct as at June 2012) at the Town of Boxborough, Massachusetts website:
Maternal-foetal transmission of Lyme disease
Brief Reports | 1 July 1985
Maternal-Fetal Transmission of the Lyme Disease Spirochete, Borrelia burgdorferi
PETER A. SCHLESINGER, M.D.; PAUL H. DURAY, M.D.; BARBARA A. BURKE, M.D.; ALLEN C. STEERE, M.D.; and M. THOMAS STILLMAN, M.D.
Ann Intern Med. 1985;103(1):67-68. doi:10.7326/0003-4819-103-1-67
This excerpt has been provided in the absence of an abstract.
Lyme disease usually begins with a characteristic skin lesion, erythema chronicum migrans, accompanied by "influenza-like" or "meningitis-like" symptoms (1). Some patients later develop cardiac abnormalities such as atrioventricular heart block or myopericarditis, neurologic complications, or intermittent attacks of arthritis (1). The causative agent, the Lyme disease spirochete Borrelia burgdorferi (2), is transmitted by Ixodes dammini or related ixodid ticks (3). Antibiotic treatment with tetracycline or penicillin is usually curative (4).
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 fist week of life. Histological examination of autopsy material showed the Lyme disease spirochete in the spleen kidneys and bone marrow.
The International Disease Society of America (IDSA):
“Some practitioners prescribe a 10–14-day course of prophylactic amoxicillin for pregnant women after I.Scapularis tick bites, because case reports have suggested that Lyme disease during pregnancy may be associated with adverse outcomes for the fetus. However, a large body of data from clinical and epidemiologic studies suggest that favorable outcomes can be expected when pregnant women with Lyme disease are treated with standard antibiotic regimens. Indeed, there is little evidence that a congenital Lyme disease syndrome occurs” (Pg 10).
MacDonald AB (1989) Gestational Lyme borreliosis. Implications for the fetus:
Abstract: “Great diversity of clinical expression of signs and symptoms of gestational Lyme borreliosis parallels the diversity of prenatal syphilis. It is documented that transplacental transmission of the spirochete from mother to fetus is possible... Autopsy and clinical studies have associated gestational Lyme borreliosis with various medical problems including fetal death, hydrocephalus, cardiovascular anomalies, neonatal respiratory distress, hyperbilirubinemia, intrauterine growth retardation, cortical blindness, sudden infant death syndrome, and maternal toxemia of pregnancy. Whether any or all of these associations are coincidentally or causally related remains to be clarified by further investigation”.
National Institutes of Health (NIH): (2008). Lyme Disease: The Facts, the Challenge (NIH Publication No. 08-7041)
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” (Pg 15).
The Centre for Disease Control (CDC):
Pregnancy Fact Sheet: “Untreated, Lyme disease can be dangerous to your unborn child. Lyme disease that goes untreated can also cause you to have brain, nerve, spinal cord, and heart problems”.
Lyme Disease Resource Brochure: “Prevention and early diagnosis of Lyme disease are important during pregnancy. Rarely, Lyme disease acquired during pregnancy may lead to infection of the placenta and may possibly lead to stillbirth. Studies of women infected during pregnancy have found that there are no negative effects on the fetus when the mother receives appropriate antibiotic treatment for her Lyme disease ".
This is Google's cache of http://www.samento.com.ec/sciencelib/4lyme/recoveryoflyme.html. It is a snapshot of the page as it appeared on 16 Sep 2013 12:40:20 GMT. The current page could have changed.....??
RECOVERY OF LYME SPIROCHETES BY
PCR IN SEMEN SAMPLES OF PREVIOUSLY
DIAGNOSED LYME DISEASE PATIENTS
Presented by Dr. Gregory Bach, at the International
Scientific Conference on Lyme Disease, April, 2001.
Lyme disease, being a spirochete with pathology similar to syphilis, is often found difficult to treat due to the spirochete invading sanctuary sites and displaying pleomorphic characteristics such as a cyst (L-form). Because a significant portion of sexually active couples present to my office with Lyme disease, with only one partner having a history of tick exposure, the question of possible secondary (sexual)vector of transmission for the spirochete warrents inquiriy.
Additionally, sexually active couples seem to have a marked propensity for antibiotic failure raising the question of sexually active couples re-infecting themselves through intimate contact.
Lyme spirochetes/DNA have been recovered from stored animal semen. Recovery of spirochete DNA from nursing mother's breast milk and unbilical cord blood by PCR (confirmed by culture/microscopy), have been found in samples provided to my office.
Suprisingly, initial laboratory testing of semen samples provided by male Lyme patients (positive by western blot/PCR in blood) and the male sexual partner of a Lyme infected female patient were positive approximately 40% of the time. PCR recovery of Lyme DNA nucleotide sequences with microscopic confirmation of semen samples yielded positive results in 14/32 Lyme patients (13 male semen samples and 1 vaginal pap).
ALL positive semen/vaginal samples in patients with known sexual partners resulted in positive Lyme titers/PCR in their sexual partners. 3/4 positive semen patients had no or unknown sexual partners to be tested. These preliminary findings warrent futher study. Current a statistical design study to evaluate the possibility of sexual transition of the spirochete is being undertaken.
Our laboratory studies confirm the existence of Lyme spirochetes in semen/vaginal secretions. Whether or not further clinical studies with a larger statistical group will support the hypothesis of sexual transmission remains to be seen. A retrospective clinical study is also underway.
We are reviewing the medical records, collecting semen samples of patients who were previously diagnosed with current and previously treated Lyme disease are bing asked to provide semen,pap and blood samples for extensive laboratory testing.
With the initially impressive data, we feel the subsequent statistical sudy on the sexual transmission of the Lyme spirochete will illuminate a much broader sectrum of public health concerns associated with the disease than the originally accepted tick borne vector.
Sexual transmission. See Military on Lyme Disease section..
Or go directly to link:
Spring Brings Tick Threat to Peace Enforcers JAMA, May15,1996, Medical News & Perspective
Comments from Website author: JAMA writes here of a caution for troops in Bosnia-Herzegovina (which I believe also extends to the Mid-East region) that tick-borne disease is a danger. They caution that the same risks are additionally associated with mosquitoes, sand flies, fleas, mites, biting flies, and lice. "Desert Storm Syndrome" parallels one characteristic of Lyme in that this spirochetal infection also can be sexually transmitted to spouse.
AS THE HALFWAY point approaches in the year-long North Atlantic Treaty Organization (NATO) peace-enforcement effort in Bosnia-Herzegovina, military are putting more physicians emphasis than ever on keeping US troops healthy. US Army, Air Force, Navy, and Marine Corps personnel in the former Yugoslavia are carrying laminated plastic cards reminding them of the diseases that can be transmitted via various vectors there, particularly ticks (JAMA. 1994;272:337-340 and p 1470 in this issue). With the arrival of warmer weather, ticks are expected to be a problem until as late as November.
Although there is talk of a few troops staying longer, November and early December are when US forces are supposed to withdraw (JAMA. 1996;275:24). President Clinton made a public pledge to extract US troops within a year of the December 20, 1995, date when NATO assumed peace-enforcement duties from the United Nations, meaning that pull-out planning could begin as early as next month.
In the meantime, US Military physicians are concerned about tick-born encephalitis and Lyme Disease, for which Ixodes ricinus is the primary vector; Crimean-Congo hemorrhagic fever, for which Hyalomma marginatum marginatum is the primary vector, and perhaps boutonneuse fever rickettsiosis or Bhanja virus fever, also transmitted by the bite of an infective tick.
Troops are being urged to tuck their trousers in their boots and otherwise cover their skin when in tick-infested areas, use tick repellent, check frequently for the presence of ticks on clothing or skin, and to remove ticks carefully, seeking medical assistance if possible and applying an antiseptic to the bite site.
What?s more, US troops are reminded that mosquitoes, sand flies, fleas, mites, biting flies and lice may also present a disease threat in specific locations. Use of repellents and "maintaining good personal hygiene" are urged.
In addition, there is the potential for hantavirus (Bunyaviridae family) infection, a cause of hemorrhagic fever or respiratory problems, and thought to result from direct contact with, or inhaling, dust contaminated by infected rodents' excretions. Thus, rats, mice, squirrels, voles, and other rodents also are a concern for the military in the Balkans (JAMA. 1996;275:422 and Lancet. 1996;347:30), and troops are being cautioned to "mist" or lightly spray previously unoccupied areas to avoid dust inhalation before mopping or sweeping preparatory to moving in. Removing trash and sources of water, sealing tiny wall openings, and using repellents can reduce the chance of disease transmission from rodents, the troops are advised. They are told to seek immediate medical assistance if bitten or scratched by a rodent.
The US Army Center for Health Promotion and Preventive Medicine, Aberdeen (Md) Proving Ground, has been working on these and other health-precaution efforts. As always, American GIs have their own name for the laminated materials, calling them "tick cards."
So far, there has been no major increase in illness or injury among US troops participating in the peace-enforcement effort. John G. Jernigan, MD, the US Air Force brigadier general-designee who is command surgeon, Air Mobility Command, Scott Air Force Base, Ill, says that, to date, there has been no increase in demand for aeromedical evacuation above that normally required to support US troop activity in Europe other than Bosnia-Herzegovina.
--by Phil Gunby
All the other clinicians with whom the authors spoke agreed that Lyme has reached epidemic proportions. How is this possible? Obviously 25% of Americans haven't been bitten by one of a select few species of ticks. The answer is that Lyme is not transmitted just by ticks.
"Of the more than 5,000 children I've treated, 240 have been born with the disease," says Dr. Jones, who specializes in Pediatric and Adolescent Medicine. "Twelve children who've been breast-fed have subsequently developed Lyme. Bb can be transmitted transplacentally, even with in vitro fertilization; I've seen eight children infected in this way.
People from Asia who come to me with the classic Lyme rash have been infected by fleas and gnats."
Gregory Bach, D.O., presented a study on transmission via semen at the American Psychiatric Association meeting in November 2000. He confirmed Bb DNA in semen using the PCR test (Polymerase Chain Reaction). Dr. Bach calls Bb "a brother" to the syphilis spirochete because of their genetic similarities. For that reason, when he treats a Lyme patient in a relationship, he often treats the spouse; otherwise, he says, they can just pass the Bb back and forth, reinfecting each other.
Dr. Tang adds other avenues of infection: "Transmission may also occur via blood transfusion and through the bite of mosquitoes or other insects." Dr. Cowden contends that unpasteurized goat or cow milk can infect a person with Bb.
Synthesis of the Work of Enderlein, Bechamps and other Pleomorphic Researchers
For some 'strange' reason - this ENTIRE site has been removed! Luckily, I PDF'd ALL of it !!
This is Google's cache of http://www.samento.com.ec/sciencelib/4lyme/Townsendhowens.html. It is a snapshot of the page as it appeared on 11 Sep 2013 17:43:16 GMT. The current page could have changed in the meantime.
New Ideas About the Cause, Spread
and Therapy of Lyme Disease
by Dr. James Howenstine
Townsend Letter for Doctors and Patients, July 2004
Lyme Disease was initially regarded as an uncommon illness caused by the spirochete Borrelia burgdorferi (Bb). The disease transmission was thought to be solely by the bite from a tick infected with this spirochete. The Bb spirochete is able to burrow into tendons, muscle cells, ligaments, and directly into organs. A classic bulls-eye rash is often visible in the early stage of the illness. Later in the illness the disease can afflict the heart, nervous system, joints and other organs. It is now realized that the disease can mimic amyotrophic lateral sclerosis, Parkinson’s disease, multiple sclerosis, Bell’s Palsy, reflex sympathetic dystrophy, neuritis, psychiatric illnesses such as schizophrenia, chronic fatigue, heart failure, angina, irregular heart rhythms, fibromyalgia, dermatitis, autoimmune diseases such as scleroderma and lupus, eye inflammatory reactions, sudden deafness, SIDS, ADD and hyperactivity, chronic pain and many other conditions.
Biology professor, Lida Mattman, author of Cell Wall Deficient Forms: Stealth Pathogens, has been able to recover live spirochetes of Bb from mosquitos, fleas, mites, semen, urine, blood, and spinal fluid. A factor contributing to making Bb so dangerous is that it can survive and spread without having a cell wall (cell wall-deficient CWD). Many valuable antibiotics kill bacteria by breaking down the cell wall. These antibiotics often prove ineffective against Bb.
Lyme Disease is now thought to be the fastest growing infectious disease in the world. There are believed to be at least 200,000 new cases each year in the US and some experts think that as many as one in every 15 Americans is currently infected (20 million persons). Dr. Robert Rowen knows a family where the mother’s infection spread to 5 of her 6 children1 all of whom recovered with appropriate therapy. It is difficult to believe that these children were all bitten by ticks and seems more plausible that person to person spread within the family caused this problem. Dr. Mattman states “I’m convinced Lyme disease is transmissible from person to person.” In 1995 Dr. Mattman obtained positive cultures for Bb from 43 of 47 persons with chronic illness. Only 1 of 23 control patients had a positive Bb culture. Dr. Mattman has subsequently recovered Bb spirochetes form 8 out of 8 cases of Parkinson’s Disease, 41 cases of multiple sclerosis, 21 cases of amyotrophic lateral sclerosis and all tested cases of Alzheimer’s Disease. The complete recovery of several patients with terminal amyotrophic lateral sclerosis after appropriate therapy shows the great importance of establishing the diagnosis of Lyme Disease.
Some very important information has recently become available about the spread and magnitude of the problem with Lyme Disease. The severity of the Lyme illness is related to the spirochete load in the patient. Few spirochetes produce mild and asymptomatic infection. A study from Switzerland in 1998 pointed out that only 12.5% of patients testing positive for Bb had developed symptoms. A German boy developed Lyme arthritis 5 years after his tick bite. Often mycoplasmal infections remain without symptoms until the victim suffers a traumatic event (stress, injury, accident, etc.). These stressing events enable the mycoplasma to begin consumption of cholesterol and symptoms may begin to present. The mechanism of this deterioration is thought to be suppression of the immune system secondary to stress.
Many patients with LD have concomitant infections with other parasites (Ehrlichia in white blood cells and Babesia in red blood cells). Some patients have all 3 parasites. Each requires a different therapy with Babesia being particularly difficult to eradicate. Recently, Artemisinin appears effective in Babesia infections. All co-infections must be eliminated to obtain a successful result.
Dr. Joanne Whitaker relates that nearly every patient with Parkinson’s Disease (PD) has tested positive for Bb. Dr. Luis Romero reports that 3 patients with PD are 99% better after TOA-free cat’s claw (Uncaria tomentosa) therapy. When Dr. Mattman cultures 25 patients with fibromyalgia all subjects had positive cultures of the CWD Bb, which causes LD. She relates that Bb can be found in tears and could thus easily appear on the hands where touching could spread LD. Several families are now documented where nearly every family member is infected. How sick the individual patient becomes probably relates to their initial spirochete dose, immune system, detoxification capability and stress levels.
Transmission of the disease has been clearly documented after bites by fleas, mites, mosquitos and ticks. There is compelling evidence that Lyme disease (LD) can be spread by sexual and congenital transfer. 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.
Researchers at the University of Wisconsin have reported that dairy cattle can be infected with Bb, hence milk could be contaminated. Bb can also be transmitted to lab animals by oral intake such as food.
The Sacramento, California blood bank thinks that LD can be spread by blood transfusions. The CDC (Center of Disease Control) in Atlanta, Georgia states that their data indicates that Bb can survive the blood processing techniques used for transfusions in the US.
Lyme Disease is the fastest growing epidemic in the world. LD is grossly under-reported so there may be far more than the 200,000 cases reported annually in the US. Drs. Harvey and Salvato estimate that 1 billion persons in the world may be infected with LD. LD is thought to be a contributing factor in 50% of patients who have chronic illness.
Dr. Joanne Whitaker, a Lyme disease victim from childhood, has developed a reliable test for the presence of Lyme disease. This test looks for the Bb organism, not antibodies, and is able to identify the cell wall deficient (CWD) form of the spirochete as well as the actual Bb organism. The test is called Q-RIBb which stands for quantitative rapid identification of Bb. Dr. Lida Mattman has confirmed that Dr. Whitaker’s test is sensitive because there has been a 100% correlation between a positive culture of Bb by Dr. Mattman’s lab and a positive Q-RIBb test from Dr. Whitaker’s Laboratory.
Case Reports Illustrating the Critical Importance of
Establishing the Diagnosis of Lyme Disease.
Case 1: Larry Powers, a former Mr. America in 1962, became ill with the symptoms of Parkinson’s Disease in 1990. Sinemet therapy was taken for eight years but he gradually became worse. He became confined to a wheel chair and required help with eating. After learning that Lyme Disease might be causing his symptoms of PD he started taking TOA-free cat’s claw (Uncaria tomentosa). Within three weeks he was out of his wheelchair and fishing for 100 pound tarpon.
Case 2: Tom Coffey at age 34 developed diplopia, severe hypertension uncontrolled by drugs, and impaired balance. A diagnosis of amyotrophic lateral sclerosis was made. Surgery was performed to correct the diplopia. By June 2001 he was unable to swallow saliva and feeding tube nutrition was begun. His weight had fallen by 100 pounds. Nutritional support from the tube feedings produced slow resolution of the swallowing problem. Consultation with a Lyme expert uncovered the history of a bulls-eye rash after a tick bite. Therapy with Rocephin led to complete recovery.
Case 3: A young male college student developed such sever cognitive difficulties he was forced to drop out of school. A Q-RIBb test was positive for LD and he resumed a normal life after receiving 4 months of antibiotic therapy.
What Causes Neurone Death in Amyotrophic Lateral Sclerosis (ALS)?
One of the most insidious mimics for Lyme Disease is ALS. The neurotoxins released by the Bb organism are capable of causing neurologic dysfunction in the central nervous system that produces symptoms typical of amyotrophic lateral sclerosis. The pathological hallmark of ALS is motor neurone degeneration and death.
Research performed by Dr. Harold Clark and Dr. Garth Nicholson and coordinated by Donald W. Scott2 has resulted in a breakthrough in our understanding of amyotrophic lateral sclerosis.
Mycoplasma was discovered in 1898. These are living particles of bacterial nucleic acid which do not have a cell wall. In 1971 Rottem et al.3 learned that most species of mycoplasma were absolutely dependent for their growth on the consumption of pre-formed sterols including cholesterol obtained from animal and human host cells. These mycoplasmas live harmlessly in host cells until they are stimulated to activity by a stressing traumatic event (bullet wound, bad fall, injury from accident etc.). The growth of the mycoplasma consumes the cell’s cholesterol resulting in death of the affected cell. Mycoplasmas have been identified in ALS using high resolution blood morphology. In the November 9, 2001 issue of Science Dr. Daniel Mauch4 et al. revealed that the glial cells surrounding the motor neurone sully the extra cholesterol needed to repair and replace aging synapses. If the repair does not properly occur, the motor neurone cells proceed to die form overwork. Glial cells are also heavily involved in gathering, processing and storing glutamate. Elevations in glutamate have been found in brain tissue in ALS.
A mycoplasma species, probably fermentans, which was harmlessly sequestered in a glial cell, becomes aroused by some traumatic stressful event. This mycoplasma then consumes the glial cholesterol which makes up 40% of the glial cell membrane, causing rupture and death of the glial dell. The death of these glial cells releases large amounts of glutamate which becomes elevated in brain tissue. Within the neurone some of the excess glutamate accesses a urea molecule. The urea molecule gives up an ammonia ion which converts a glutamate molecule into less dangerous glutamine. This leaves the former urea molecule as a cyanate ion which damages the motor neurone’s mitochondria. One of the consequences of the damaged mitochondria is a decrease in the energy output available to the neurone. This produces the severe weakness and fatigue seen in patients with chronic fatigue syndrome. If the mitochondrial injury is severe the neurone dies. The death of motor neurone stops message delivery to muscle tissue – a universal finding in ALS.
This avid consumption of cholesterol may also contribute to the endocrine dysfunction seen in ALS because it decreases the amount of cholesterol available to produce estrogen, testosterone, progesterone, hydrocortisone, and aldosterone. Patients with ALS, fibromyalgia, and chronic fatigue syndrome often have hypothalamic dysfunction which may result in adrenal insufficiency, hypothyroidism, and gonadal failure.
Lyme disease frequently exhibits neurologic abnormalities because the Bb neurotoxins are drawn to the fatty tissue found in the brain and peripheral nerves. As a consequence sudden deafness, Bells palsy, Parkinson’s Disease, Multiple Sclerosis, reflex sympathetic dystrophy, peripheral neuritis, and chronic pain may appear.
The Influence of Toxins from Bb on the Symptoms and Course of Lyme Disease
Autopsy examinations of young persons (30s) dying from what appeared to be Parkinson’s disease (PD) have frequently failed to confirm the basal ganglion damage that would be expected in classic PD seen in the elderly. Some patients with illnesses of many years’ duration misdiagnosed as Amyotrophic Lateral Sclerosis, Multiple Scleroris, and Parkinson’s Disease have made incredible recoveries within periods as short as 24 to 72 hours when placed on TOA-free Uncaria tomentosa (cat’s claw) for LD. This rapid response could not rationally be attributed to improved immune function or bacteriocidal effects on spirochetes. Bb is known to produce a group of neurotoxins. The most sensible explanation for this recovery lies in turning off or blocking the neurotoxins effects of Bb on the lipid containing structures that the Bb neurotoxins are attracted to (central nervous system, peripheral nerves, muscles, joints, etc.). This sudden improvement appears to be the result of blockage and inhibition of the neurotoxins.5 The most important example of a “Biotoxin Illness” appears to be Lyme Disease.6 Patients with symptoms of Parkinson’s Disease at a young age caused by neurotoxins would not be expected to show permanent structural destruction in the basal ganglia. These neurotoxins probably act at specific sites such as neuro-transmitters-pre and post synaptic membranes, altering dopamine, serotonin, GABA, and acetylcholine molecules, thereby blocking surface membrane receptors of various kinds which would interfere with the proper action of enzymes, coenzymes and hormones. This is only one of the damaging mechanisms of action of the neurotoxins.
The Uncaria tomentosa may have three direct beneficial effects in humans with LD:
Immune modulation (correcting immune dysfunction).
Direct broad spectrum anti-microbial effect on spirochetes. Quinovic acid glycosides found in TOA-free cat’s claw are similar to the quinilones widely used as antibiotics.
Blocking the adverse neurotoxic effects on cells, enzymes, and hormones.
Whether the serious lack of energy and fatigue seen in LD are similar to the cyanate7 induced damage to the mitochondria’s ability to produce energy in the motor neurone found in amyotrophic lateral sclerosis, or is due to failure of proper calcium channel function is not clear.
Favorable Therapeutic Results with TOA-Free Cat’s Claw in Lyme Disease
A pilot study treated 28 patients with Advanced Chronic Lyme Disease with TOA-Free Uncaria tomentosa. Conventional cat’s claw contains TOA alkaloids that interfere with the desired immune modulation. The 14 person control group was given antibiotic therapy. At the study’s termination 85% of those receiving the cat’s claw preparation no longer had positive blood tests for Bb. All 28 persons had experienced a dramatic improvement in their clinical condition. No significant changes were seen in the control group. The Prima Uña de Gato can be obtained from Allergy Research Group 800-545-9960, Nutramedix (product name Samento Plus) 561-745-2917, and from Farmacopia at 800-896-1484. Dr. Whitaker’s lab can be reached by Internet at www.Bowen.org or by calling 727-937-9077 to arrange blood Bb testing. Improving nutrition, detoxifying and improving mental health all contribute to good results. Removal of mercury amalgams and treatment of heavy metals may be needed.
Much of this information about LD was obtained from “Lyme disease: Nutraceutical Breakthrough Using TOA-Free Cat’s Claw” published in Focus by Allergy Research Group (October 2003) and from the November and December 2003 issues of Dr. Robert Rowen’s Second Opinion.
Why Are We Experiencing an Epidemic of Lyme Disease?
I do not have a certain answer to this question. There are some facts that may be relevant. Several US government scientists including Dr. Shuy-Ching Lo, of the American Institute of Pathology, hold a patent on a Pathogenic Mycoplasma (mycoplasma fermentans) which has been converted into a crystalline form. In the patent application the diseases AIDS, chronic fatigue syndrome, Wegener’s Granulomatosis, Sarcoidosis, lupus and Alzheimer’s Disease were mentioned as related to this patented form of mycoplasma fermentens. The crystalline form of mycoplasma fermentens contains the part of the brucella bacteria that causes disease in patients. In its crystalline form this mycoplasma can be transmitted into subjects by intravenous administration or injections, spread as an aerosol, implanted by the bite of an insect, or placed into food or water. There is no laboratory evidence for infection by brucella in subjects who have received the “crystalline pathogenic mycoplasma.”
When a nation is developing biologic warfare agents it is imperative that these agents be tested on humans to evaluate the results. If an infectious biologic warfare agent was able to produce person to person transfer it would have to be regarded as a gigantic success.
In the Faroe Islands in 1943 British biowar researchers ran tests to see if sheep could be infected by air-borne brucella. The brucella spread into sheep dogs as brucella canis and then appeared to cause several humans to develop multiple sclerosis.
In 1947 and 1948, approximately 1,100 school children in remote northern Icelandic villages (Akureyri) became ill with a new disease that caused severe burning pain in the limbs, profound muscle weakness, and severe fatigue. Of these 1,100 teenagers who became ill, 5 of the students developed an aggressive form of Parkinson’s disease and proceeded to die (unheard of in teenagers not using methedrine-like drugs). The United States had effective control of Iceland during these years and a research scientist trained in plant and animal virology at the Rockefeller Institute (oriented toward eugenics), Dr. Bjorn Sigurdson, was installed to start an Institute of Experimental Pathology at the University of Iceland with $200,000 in grant money from the Rockefeller Institute. In 1950 a group of American physicians, microbiologists, and biologic researchers sponsored by the Rockefeller Foundation arrived in Iceland to study the effects of the mystery illness that had struck Northern Iceland. The appearance of a new disease was of such great interest that Icelandic Disease was promptly reported in the New England Journal of Medicine.
The Canadian government set up the Dominion Parasite Laboratory in Belleville, Ontario in the 1950’s and 60’s to grow one hundred million mosquitos a month. In late August of 1984, 500 persons in the St. Lawrence Valley became ill with a mystery illness which had the profound weakness seen in brucellosis without any laboratory evidence of brucella infection. One woman was certain her illness came from a mosquito bite. She recalled being bitten by a mosquito and woke up the next day with a target skin lesion at the bite site (same skin lesion as seen in Lyme Disease) and such profound weakness she was unable to get out of bed. Another woman recalled a target lesion at the site of a mosquito bite. Both women remain ill 20 years later.
Citizens in Punta Gorda, Florida woke up one spring morning in 1956 with a cloud of mosquitos in their town. Calls to the Meteorological Service about the mosquito influx were answered with the information that there had been a forest fire thirty miles away in the Everglades and that these mosquitos had fled the fire. The truth is mosquitos will not move from one side of a barn to the other when a fire breaks out, let alone fly 30 miles. One week later 5 persons appeared in the local medical clinic with symptoms of chronic fatigue syndrome.
In 1984 mycoplasma may have been transmitted by aerosol into a high school in Incline Village, Nevada, where many persons suddenly developed chronic fatigue syndrome. Children became ill with a similar mysterious illness in 1984 after drinking goat’s milk in Lyndonville, New York. The cities of Adelaide, Australia 1949, West Otago, New Zealand 1984, and Royal Free Hospital London, England 1955 have all been visited by mini-epidemics of chronic fatigue syndrome.
These mycoplasmas, when activated by stress, are avid consumers of sterols including cholesterol. A series of chemical reactions ensues culminating in the creation of cyanate which causes failure of normal energy production by the mitochondria of the cells. This could produce the profound weakness and fatigue characteristics of chronic fatigue syndrome. A 2 to 3 month trial of 300 to 500 mg. of CoQ10 daily might be able to improve energy output by the mitochondria thus possibly alleviating the profound fatigue.
When the illness causes painful trigger points, it is best termed fibromyalgia. These painful sites are located where blood flow is stagnant. Chronic infections are known to produce high viscosity blood which tends to clot a flow more slowly than normal.
Profound dysfunction of the hypothalamus, pituitary, adrenal, thyroid glands and gonads is very common in mycoplasmal, fungal, and anerobic bacterial infections. The avid consumption of cholesterol by activated mycoplasma could be a contributing factor to these endocrine disorders because cholesterol is needed to create several important hormones (estrogen, testosterone, progesterone, hydrocortisone, aldosterone).
Bacteriologist Dr. Arthur Kendall was able to produce 16 distinct bacteria8 by simply using different culture media to culture the same bacteria. Dr. Royal Rife’s Universal Microscope could see organisms as small as viruses. By using Dr. Rife’s microscope Dr. Kendall could actually see living organisms change their characteristics as the culture media were changed. Dr. G.C. Gruner of McGill University used an asparagus media to grow a fungus found in the blood of patients with cancer. When this fungus was grown in Kendall’s medium it converted into the Bx virus which had been proven by Koch’s postulates to cause cancer. These experiments proved that the fungus that Dr. Gruner saw in the blood of cancer patients was actually the same organism as the Bx virus that Dr. Kendall had proven causes cancer. Obviously, biologic micro-organisms exhibit considerable pleomorphism which may explain why observers do not find the same organisms in patients with chronic fatigue syndrome, fibromyalgia, and Lyme Disease as those being found by other observers (HHN-G, CMV, EBV viruses, parasites Bb, ehrlichae, babesia, bartonella, mycoplasma, Chlamydia, anerobic bacteria, yeast and fungi have all been implicated).
There is considerable evidence that many patients with Chronic Fatigue Syndrome, Fibromyalgia, and Lyme disease have an infectious disease. Lyme disease needs to be considered in every patient with a chronic illness. LD can produce every disease found in the Diagnostic Symptoms Manual for psychiatric illness (attention deficit disorder ADD, antisocial personality, panic attacks, anorexia nervosa, autism, Aspergers syndrome, etc.). Skilled antimicrobial therapy should permit many of these unfortunate patients to regain their health. TOA-free cat’s claw will be valuable for many persons with Bb found by blood tests and culture. Sulfoxime and dioxychlor will relieve the pain found in fibromyalgia. Dietary changes, correction of pH, detoxification and stress reduction counseling can all be beneficial.
The United States maintains a biological warfare research laboratory on Plum Island directly across Long Island Sound from the sites where Lyme Disease and West Nile Disease were first encountered in Old Lyme and Madison, Connecticut. Massive deaths of birds are common at the sites where West Nile viral disease appears, suggesting that the illness may afflict birds before entering humans. Dr. Warren Levin of Wilton, Connecticut states that 56% of the families in Wilton have at least one family member with LD. Could seagulls containing crystalline mycoplasma fermentens and West Nile Virus have escaped or been released from Plum Island?
Much of this information about biowarfare agents and crystalline mycoplasma fermentens is from an article written by biochemist Donald W. Scott and published in the Winter 2003 edition of The Journal of Degenerative Diseases Volume 5 Number 1. The publisher is Common Cause Medical Research Foundation, Box 133, Station B, Sudbury, Ontario, Canada P3E 4NR Canada.
Dr. James Howenstine is a specialist in internal medicine. He is author of the book A Physician’s Guide to Natural Health Products that Work, 328 pg. $17.95. His book can be obtained from Amazon.com, naturalhealthteam.com and by calling 1-800-416-2806. Dr. Howenstine can be reached at firstname.lastname@example.org and by writing Dr. James Howenstine c/o Remarsa USA SB 37, P.O. Box 25292, Miami, Florida 33102-5292
Rowen, Robert. If you have any chronic debilitating disease, you could be the victim of a Monster Epidemic! Second Opinion Vol X111 No. 11 November 2003
Scott, D.W., Crusader P.O. Box 618205, Orlando, FL 32861-8205 October-November 2002 pg. 26-32. Also see Scott, D.W. and Scott, W.L.C. Amyotrophic LateralSclerosis: The Probable Cause; A Possible Cure 233 Government St., Suite 6E, Victoria, B.C. Canada V8T 4P4; 888-232-444,
Rottem, Pfend, Hayflick. Sterol Requirements of T-strain Mycoplasmas Journal of Bacteriology 1971
Daniel Daniel H., Nagler, Goritz, Muller, Otto, Pfrieger. CNS Synaptogenesis Promoted by Glia-Derived Cholesterol. Science Nov. 9, 2001
Romero, Luis M.D.,PhD, Neurotoxins Focus, Allergy Research Group Newsletter pg. 10 Oct. 2003
Shoemaker, C. M.D., Hudnall, Kenneth, PhD. Focus, Allergy Research Group Newsletter pg. 10 Oct. 2003
Scott, Donald W. Lou, Gehrig’s Disease is Not a Mistery Anymore Crusader pg. 31 Oct-November 2002
Montgomery, Shawn, The Rise and Fall of a Scientific Genius (video) Zero Zero Productions, 3 Baldoon Rd., Toronto, Ontario, Canada M1B 1Vd; www.zerozerotwo.org