Lecture Notes of Tom Grier: Tom Grier (Microbiologist from Minnesota) spoke at Lac Court Oreilles Convention Center in Hayward, WI. Tom’s life work is to do further research and bring awareness of this illness to everyone. For more info about Tom and his work checkout http://www.mibdec.com
Lyme disease was first recognized in Old Lyme CT in 1973 by two concerned mothers. Judy Mensch and Polly Murray felt there were too many diagnosed cases of Juvenile Rheumatoid Arthritis in their neighborhood children. Judy and Polly Murray who had backgrounds in public health collected over 200 local case histories and presented them to the CDC and CT health department.
Dr. Alan Steere M.D. investigated the local cases of JRA and coined the misnomer “Lyme Arthritis” in his 1975 publication that first described Lyme Borreliosis as an arthritic disorder.
Although the actual cause of Lyme Arthritis that was sometimes associated with a bull’s-eye rash was not yet known, a treatment protocol of two weeks of tetracycline was already being recommended.
The infectious etiology of Lyme disease was not known until 1981 when Dr. Willy Burgdorfer PhD from Rocky Mt Labs isolated the new species of Borrelia bacteria from a tick from Shelter Island. The fact that “Lyme Disease” was caused by a spirochete should have been a real concern and everything we thought we knew about Lyme disease should have been reevaluated at that time.
Borrelia was a family of bacteria not only associated with relapses and antibiotic treatment failures, but also is part of the same family of bacteria that causes Tick-Bourne- Relapsing Fevers, a group of over 300 variant diseases that can be deadly within months (Borrelia duttonii and Borrelia crocidurai of Northeast Africa), or considered mild and often mislabeled as “self-limiting” such as Borrelia recurrentis found in the Southwest USA. (Ron Ferris of Canada was diagnosed with Borrelia recurrentis and was sick for years despite treatment right up until the day he died).
In 1982 the Lyme bacteria was isolated from the “Lyme Bull’s-Eye rash” from patients from New England. With this new discovery causing so much excitement and demanding large sums of monies to investigate, no one wanted to admit that “Lyme” was just a new subclass of a larger world-wide disease spread by ticks that was well known for a century as tick-born-relapsing fevers.
We need to stop calling this disease Lyme disease and recognize that it is part of a worldwide problem called Borreliosis.
If we don’t recognize Lyme disease as a larger worldwide health problem caused by bacteria that have a built in mechanism for variation, our health departments will define the disease out of existence.
Technically the MS/Lyme patient that recently died in Australia (a high ranking tennis player) may not have had Lyme disease even though he tested positive on two serology tests.
Because if he had Borrelia in the brain that causes relapsing fever and that variant borrelia lacks the OSP-A DNA sequence and we use a PCR osp-A test to test his brain tissues: he may test negative for osp-A, but still have Neuroborreliosis that is an osp-A deficient variant. The report would say it is not “Lyme Disease” but is any Borrelia in the brain acceptable? Ask his widow who had to fight this case to the Supreme Court just to get an autopsy. But what good is an autopsy if they look for a species unlikely to be in Australia? If a murderer kills you with a 44 caliber or a 38 caliber your still just as dead. But our CSI people looking at Lyme need to be doing a better job if all they are going to look for is Borrelia burgdorferi (stricto sensu)
Despite documented case histories of Lyme patients still being in the rash stage and yet progressing on to serious late stage complications while on tetracycline- class antibiotics, the use of cyclines for 2 weeks is still the recommended Lyme treatment. This has to change.
When Lyme was found to be caused by a spirochete, no serious reevaluation of treatment protocols ever took place. Instead major medical institutions and universities made a mad rush to register patents for Lyme tests, Lyme vaccines, and patents on the bacteria’s DNA sequences for PCR testing.
But what no one did including the CDC and NIH, they didn’t do pathology studies to see if treatments were successful.
“Today when Lyme patients are told that they are cured, and that their continuing symptoms must be caused by something else: I would like to know what is out there in nature that defies antibiotic treatment better than a spirochete? Also if we keep discovering new infectious disease causing organisms like anaplasmosis, why do we assume that a patient with continuing symptoms that still responds to antibiotics is “cured”? Are we so arrogant to think we have to keep our options limited only to diseases that only appear on a hospital lab-order test check-list?
Are we so sure Lyme is so easily curable?
Just one brain-autopsy that finds spirochetes post antibiotic treatment, can disprove the misguided position that a few weeks of antibiotics is sufficient to “cure” Lyme disease, and that work has already begun.
But my question is:
Who do we hold accountable? The answer has to be who ever it is that is withholding or restricting antibiotic treatment from symptomatic patients.
Who has signed their guidelines in the blood of dying Lyme patients?”
Tom Grier Lyme Lecture Amery WI
Early on doctors and scientists seemed to want to talk about Lyme disease in absolutes.
Absolutes that changed:
Lyme was absolutely transmitted by a new tick species called Ixodes dammini, then it was discovered that this new species was the same as Ixodes scapularis ticks which had been around centuries and had a wider range than we first thought that Ixodes dammini had. But in California three major mountain ranges away from New England, Lyme was transmitted by Ixodes pacificus. In Missouri the Lone Star Dog Tick had a new Borrelia that caused Bull’s-eye rashes and Lyme, in Europe it was the Sheep Tick, or the Sea Bird Tick that transmitted Lyme, and their host reservoirs were different from America’s white footed mouse thought at one time the only reservoir of Borrelia burgdorferi and now just one of many rodents and possibly bird species.
Length of Tick Attachment: A tick must be attached for at least 36-48 hours. WOW! How could you ever make that conclusion on the sparse veterinary and human data we have? In fact the data suggests this is not true. Studies that looked at improper removal of a tick showed much shorter attachments are possible.
What child removes a tick properly?
Dr Elizabeth Burgess DMV Madison: her work has been overlooked for decades. Her preliminary work showed that the Borrelia species of spirochete possessed some mechanism and ability to penetrate mucous membranes suggesting transmission in cattle could be through urine –to- mouth contact putting cattle at a risk besides just ticks. Dr Burgess’s work veternary was harshly and unjustly criticized without investigation or inspection. A decade later we see that Borrelia is a champion at penetrating mammalian blood vessels and endothelial cells that line the blood vessels. How hard is it to imagine mucosa capillaries in cattle are exposed targets for Borrelia to penetrate on contact? Since the introduction of the veternary Lyme vaccines, we here little about entire herds of cattle and horses being infected.
Two weeks of doxycycline is adequate despite persisting symptoms: I am curious: Has two weeks of tetracycline ever cured a case of acne???
Let YALE defend their own position:
A synopsis of this view point can be found in the Yale Medicine
Report, May 15, 1996 in an article by Marc Woortman states that:
(Excerpts from page 11, Yale Medicine, May 15th, 1996)
· If you suspect the tick was attached for at least 36 hours,
observe the site of the bite for development of the characteristic
skin rash, erythema chronica migrans (sic), usually a circular red
patch, or expanding “bull’s eye,” that appears between three days and
one month after the bite. Not all rashes at the site of the bite are
due to Lyme disease. Allergic reactions to tick saliva are common.
Preventative antibiotic treatment is not necessary, is costly, and
may cause side effects.
· If symptoms of later-stage Lyme disease develop, such as
arthritic swelling of a joint, most often the knee, or facial nerve
palsy, have a test done. If the test is positive, have a more precise
test done. Only if this test proves positive should a course of
antibiotic therapy begin. Expect some symptoms to linger up to three
months. No further antibiotic treatment is necessary.
This article suggests that treating a symptomatic patient with a
negative Lyme test with antibiotics, may be more harmful than
treating Lyme disease based on a single positive test and late stage
symptoms. It is clear that the Yale perspective on diagnosing Lyme
disease is that late stage Lyme symptoms, including a swollen knee
and Bell’s Palsy, do not warrant antibiotic treatment despite a
positive ELISA test! It is suggested that delaying treatment in a
symptomatic Lyme patient with these late stage symptoms is better
than risking antibiotics.
The statement from the second paragraph tells us the
intentions, “Only if this [second] test proves positive should a
course of antibiotic therapy begin.”
This statement tells us that Yale puts more faith in serology tests
than in a patient’s symptoms, Even symptoms that include an expanding
EM rash after a known tick bite, a swollen knee, Bell’s Palsy, and a
positive blood test must all be ignored because antibiotics are
costly and could cause side effects! (Apparently no one told this to
dermatologists who often prescribe tetracycline for acne for years at
a time at a cost of about $10 a month.) I have to ask; What motivates
these doctors to deny treatment to a symptomatic patient who has a
rash and a positive ELISA serology?
(For full article and reference see canlyme.com)
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What happens when a tick attaches?
This is the essence of the pathogenisis of Lyme disease: if you understand this concept of infection, you begin to understand why the conservative viewpoint of Lyme is causing latent morbidity and mortality.
In several mammal studies in the late 1980s, it was shown in many species including dogs that within hours of tick attachment that the Lyme organism is with every beat of the heart circulating through the entire body. The spirochete’s motility allows it to position itself into the cracks and folds of a blood vessel wall.
Borrelia burgdorferi has a tropism or an attraction to attach to the endothelial cells lining blood vessels. Once the bacteria has attached it traps tissue plasminogen that converts to plasmin and this begins the process of inflammation. This irritation causes the endothelial cells to release digestive enzymes such as basement membrane laminase, hyaluronidase, lipases, proteases. White blood cells join in at the site releasing Metalo-Matrix- Protease that facilitates cell penetration, and Tumor Necrosis Factor Alpha, and Il-1, Il-6 and TGF beta, all which play a role in cell communications and begin inflammatory cascades to begin.
The net result is within 24-48 hours we can measure the breakdown of the blood-brain- barrier in dogs that peaks at 48 hours and lasts for up to 14 days! So are we really going to say that a tick has to be attached 48 hours? This animal model suggests that the infection is potentially already established within the brain. This study was done by tagging normal blood albumin with radioactive Iodine and tracking it into the CSF of the dogs. (1989 Immunological Methods of Borreliosis Cold Spring Harbor)
If the Borrelia bacteria which as a family has been known to be neurogenic and deadly since 1910 can penetrate blood vessels, then why do physicians who should know better still make public statements in the media that Lyme disease is not transmitted transplacentally to the fetus during pregnancy. Nine published fetal autopsies since 1987 suggest otherwise, so what is their agenda for pretending to be ignorant of the facts?
END of Part 1
Lyme Lecture Notes From
Lyme On The Brain by Tom Grier