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Charles Ray Jones, M.D.
Madison Towers
111 Park St., Suite F
New Haven, CT 06511
Tel. 203-772-1123-Fax 203-772-0682
UNDERSTANDING LYME WESTERN BLOT
There are nine known Borrelia burgdorferi genus specie specific KDA Western Blot
antibodies (bands): 1823301134373983 and 93. Only one of these Borrelia burgdorferi
genus specie specific bands is needed to confirm that there is serological evidence of exposure
to the Borrelia burgdorferi spirochete and can confirm a clinical diagnosis of Lyme disease.
CDC Western Blot IgM surveillance criteria includes only two Borrelia burgdorferi genus
specie specific antibodies for IgM 23 and 39 and excludes the other seven Borrelia
burgdorferi genus specie specific antibodies. CDC Western Blot IgG surveillance criteria
includes 18 23 30 37 39 and 93 and excludes bands H 34 and 83. It does not make sense to
exclude any Borrelia burgdorferi genus specie specific antibodies in a Lyme Western Blot
IgG and to include only two of these antibodies in IgM because all the antibodies in IgG were
once IgM. IgM converts to IgG in about two months unless there is a persisting infection
driving a persisting IgM reaction. This is the case with any infection including the Borrelia
burgdorferi induced Lyme disease. CDC wrongfully includes five non-specific cross-reacting
antibodies in its Western Blot surveillance criteria: 28 41 45 58 and 66. This leads to the
possibility of false positive Lyme Western Blots. There can be no false positives if only
Borrelia burgdorferi genus specie specific antibodies are considered. One can have a CDC
surveillance positive IgG Lyme Western Blot with the five non-specific antibodies without
having any Borrelia burgdorferi genus specie specific antibodies. This does not make sense.
CDC recommends that the Lyme Western Blot be performed only if there is a positive or
equivocal Lyme ELISA. In my practice of over 10,000 children with Lyme disease, 30% with
a CDC positive Lyme Western Blot have negative ELISA's. The Lyme ELISA is a poor
screening test. An adequate screening test should have false positives not false negatives.
Thank you for giving me this opportunity to present my experience in pediatric and
adolescent Lyme disease as well as other tick-borne diseases. I have been in the practice of
pediatric and adolescent medicine for 42 years. I have evaluated over 10,000 young people
with Lyme disease and other tick-borne diseases between the ages of 1 day to 18 years of age
on entering into my practice who come from every state in America and from every continent
abroad. All of these children live in or visit areas endemic for deer, field mice, chipmunks,
birds, Ixodes scapularis ticks and Lyme disease as well as other tick-borne diseases. The
Ixodes scapularis tick transmits the Borrelia burgdorferi spirochete which is the organism
that causes Lyme disease. The Ixodes scapularis tick also transmits the Babesia parasite, the
Ehrlichia (Anaplasma) organisms, the Bartonella henselae bacterium as well as Mycoplasma
fermentans. Forty percent of the children in my practice are co-infected with one or more of
these organisms. Fewer than 7% have had a history of primary or secondary erythema
migrans (EM) rashes. The EM rash is caused by the Lyme spirochete multiplying in the skin.
Fifty percent have a history of Ixodes scapularis tick attachments and 50% have no history of
Ixodes scapularis tick attachments but they all have some history of decreased activity level,
fatigue unrelieved by rest, fevers, joint pain, with and without arthritis, headaches, irritability,
involuntary movements, light sensitivity, noise sensitivity, abdominal pain, impaired
memory, difficulty sustaining attention and focus, and impaired processing speed (i.e. it takes
them longer to do school related work than in the past), a word selectivity problem or verbal
fluency, and difficulty sleeping. All of the children with Lyme disease or other tick-borne
diseases have some of the clinical signs compatible with tick-borne diseases and have
laboratory evidence that supports their having exposure to Borrelia burgdorferi by Western
Blot or a PCR for the DNA of the organisms. Children in a Lyme endemic area treated with
oral antibiotics for 30 days at the time of an Ixodes scapularis attachment are given the best
opportunity to prevent them from developing Lyme disease. The duration of Ixodes
scapularis attachment should not be a factor because it does not take long for a small Ixodes
scapularis tick or nymph to attach, feed and inoculate organisms in the soft, thin, very
vascular skin of a child. It does not take long for Borrelia burgdorferi spirochetes to
disseminate from the skin, circulate briefly in the blood and lymphatics then become
intracellular throughout the body but especially the joints, heart, eyes, muscles, lungs,
bladder, GI tract and the nervous system especially the brain. A careful history must be taken
to determine if a child has low-grade fever, headaches and mild stiff neck at the time of an
EM rash or Ixodes scapularis tick attachment because these are early signs of CNS seeding
indicating early-disseminated Lyme disease with brain involvement. Children with Ixodes
scapularis tick attachments in the head-neck area, under the arms and in the belly button in
very young children seem to have a more rapid dissemination of Borrelia burgdorferi
spirochetes from the skin to the brain than those with Ixodes scapularis tick attachments
elsewhere. [CNS symptoms occur very early.]
The diagnosis of Lyme disease begins with a history of exposure to Ixodes scapularis
ticks, tick attachments and an EM rash. 50% of the over 10,000 children in my practice have a
history of Ixodes scapularis tick attachments, 50% have no history of Ixodes scapularis tick
attachments, 7% have a history of an EM rash and/or secondary EM rashes. The primary EM
rash occurs at the site of the inoculation of the Borrelia burgdorferi spirochete and the
expansion of the rash is due to the Lyme bacterium multiplying in the skin. The transient
secondary EM rash occurs as a result of the Borrelia burgdorferi spirochete internally
penetrating the skin from within while being briefly disseminated from a tick attachment site
by way of blood vessels and lymphatics to intracellular foci throughout the body (muscles,
lungs, thyroid, joints, peripheral nerves, spinal cord, brain, eyes, etc.).
Since there is no readily available gold standard culture to determine the presence of a
Borrelia burgdorferi infection, one has to rely on other lab tests to support the diagnosis of
Lyme disease as well as other tick-borne diseases: Ehrlichia (Anaplasma), Babesia microti,
Mycoplasma fermentans, and Bartonella henselae.
The CDC recommends the ELISA as a screening test. If the ELISA is positive, the
CDC recommends that a more definitive test, the Lyme Western blot be performed. The
ELISA is not a valid screening test because it lacks specificity and sensitivity. In my practice
1/3 of the children with a CDC positive Lyme Western blot have a negative ELISA. A valid
screening test should have false positives not false negatives. I have found that the Lyme C6
Peptide ELISA results in fewer false negatives as well.
The Lyme Western blot depends on the adequacy of the patient's immune mechanism
at the time of exposure to the Borrelia burgdorferi spirochete. Immune paralysis can occur if
one is inoculated with a large spirochetal load. By the time the immune mechanism recovers
the Borrelia burgdorferi spirochetes are intracellular. This is one mechanism for seronegative
Lyme. The Lyme Western blot has many other potential flaws. If the referent strain(s) of
Borrelia burgdorferi used in the Western blot are different from the patient's exposure strain
of Borrelia burgdorferi, the Western blot can be falsely negative. Igenex Laboratory uses two
reference strains of Borrelia burgdorferi in performing the Lyme Western blot thereby
increasing the probability of a match between the test Borrelia burgdorferi antigen and the
patient's antibody. Another flaw in the Lyme Western blot involves the CDC requirements
for positive IgM and IgG Western blots. The CDC includes 5 cross-reacting non-specific
antibodies in the Western blot; 28 41 45 58 66. These cross-reacting antibodies should have
no place in defining a positive Lyme Western blot. One can have these 5 non-specific
antibodies in an IgG Western blot and have a CDC positive Western blot. This is absurd!!!
There are 9 Borrelia burgdorferi genus specie specific antibodies: 18 23 30 31 34 37 39 83
93. All one needs is one of these Borrelia burgdorferi genus specie specific antibodies to
confirm serological evidence of exposure to the Borrelia burgdorferi spirochete and support
the clinical diagnosis of Lyme disease. CDC excludes all but two Borrelia burgdorferi genus
specie specific antibodies in Lyme Western blot IgM and includes only 6 Borrelia burgdorferi
specific antibodies in Lyme Western blot IgG. This is doubly absurd because no Borrelia
burgdorferi genus specie specific bands should be excluded from IgM or IgG because all
bands in IgG were once IgM.
DNA by PCR can be used to determine the presence of Borrelia burgdorferi and
tick-borne co-infections; however, PCR's are highly specific but highly insensitive in urine,
blood, serum, synovia! fluid, and spinal fluid. If the PCR's are positive one can assume that
the organism is present, however there are false negatives. The PCR's are more sensitive in
solid tissues obtained from endoscopy, colonoscopy, placenta! biopsy, umbilical cord section,
foreskin remnants, synovial membranes, and other solid tissue biopsies.
Thus the diagnosis of Lyme disease remains clinical as the CDC stipulates. The CDC
surveillance criteria are rigid and exclusive and include an EM rash, arthritis involving one
knee, facial paralysis, Lyme meningitis, and heart block. This CDC case definition excludes
99% of the patients who have Lyme disease.
The earlier antibiotic treatment is begun the easier it is to treat disseminated Lyme
disease. Two thirds of the 10,000 children with Lyme disease in my practice have been off
antibiotics for 2 months to years after they have received continuous uninterrupted oral, IM
and/or IV antibiotic treatment for 3 to 7 years. These children are clinically cured of their
Lyme disease. These children must be carefully monitored because they were born with
aromas (pheromones) that attract ticks. I have many children who have developed a second
and third bout of Lyme disease 1-4 years later from another well-documented tick attachment.
Since persisting Lyme symptoms indicate a persisting Borrelia burgdorferi infection,
antibiotics should be continued uninterrupted until two months after all Lyme symptoms
resolve, for two months after there is no longer a Jarisch-Herxheimer reaction to spirochetal
killing, for two months after there is no longer a Lyme flair-up triggered by a non-Borrelia
burgdorferi infection such as a common cold, influenza, tonsillitis, otitis, or menstruation,
etc., and, if the patient feels that all Lyme symptoms have resolved. When these criteria for
stopping antibiotic therapy in Lyme disease are met, there are no relapses and the child's
Lyme disease can be considered cured and all Borrelia burgdorferi spirochetes eradicated. If
antibiotic therapy is stopped before all Lyme symptoms resolve, the patient will relapse and
develop more Borrelia burgdorferi brain and body injury by a more resilient and more
difficult to treat Lyme organism. Children with Lyme disease should not become victims of
the invalid hypothesis that Lyme disease can be cured and all Borrelia burgdorferi spirochetes
can be eradicated with an arbitrary 3-6 weeks of antibiotic therapy. There has never been a
study in the history of Lyme disease that, even in the simplest way, proves that a short course
of 3-6 weeks of antibiotic therapy results in a bacteriological cure for all patients. There has
never been a double blind study to determine the optimal duration of antibiotic treatment for
Lyme disease that results in the eradication of all Borrelia burgdorferi spirochetes. There is
ample documentation in the peer-reviewed medical literature of the ability of the Borrelia
burgdorferi spirochete, the bacterium that causes Lyme disease, to survive intensive and
prolonged antibiotic treatment of six months or longer. [See the Handout: Stephen Phillips
Presentation to the Connecticut General Assembly on Lyme disease which documents these
facts.]
The duration of antibiotic therapy necessary to treat a child's Lyme disease is
illustrated as follows. Adam had multiple Ixodes scapularis tick attachments from 3 years of
age on. He had partially treated (2-6 wks) Lyme disease from the time he was 4 to 6 years old
with several courses of 2-6 antibiotics. Adam was referred to me when he was 6 years old
with late disseminated Lyme disease with joint and brain involvement. He had fatigue,
irritability, fevers, chills, headaches, arthritis, involving his fingers, wrists, knees and ankles,
generalized severe arthralgia, attention and cognitive problems characterized by impaired
memory, verbal fluency and processing speed decline in school grades and function. While
on antibiotics, he had another tick attachment which inoculated and disseminated Borrelia
burgdorferi spirochetes that were resistant to the antibioticsJie. was taking,. He .had a full
Lyme relapse. Adam subsequently developed optic neuritis with total loss of vision in his left
eye and 75% loss of vision in his right eye. He was treated with 2 years of oral antibiotics and
2 years of IV and oral antibiotics. He has been off antibiotics for 8 years and has 20/10 vision
in each eye and no stigma of Lyme disease. Aq^ftpi has had subsequent Ixodes scapularis tick
attachments, which have been successfully tuqa^ed with one month of oral antibiotics.
The problems parents face in getting proper treatment for their children's Lyme
disease is illustrated as follows: 3-year-old Jane lives in an area in Connecticut where Lyme
disease is epidemic. After a nap and a bath Jane played in her yard for an hour and a half on a
sunny spring afternoon. When she came indoors at 4:00 p.m. her mother noticed what looked
like a speck of dirt on her bouncy, happy 3-year-old daughter's left lower eyelid. This speck
"of dirt" had not been on Jane's lower eyelid before she went out to play.
On closer inspection, the speck of "of dirt" had legs and turned out to be an attached Ixodes
scapularis nymph. The tick was removed intact with tweezers and sent for PCR testing to
determine if it were infected with Borrelia burgdorferi spirochetes. Jane's mother called her
pediatrician before 5:00 p.m. on the same day and asked if her daughter could be placed on a
prophylactic antibiotic because she lived in a community where 60% of the ticks were
infected with Borrelia burgdorferi spirochetes and every 5th household had at least one
occupant with Lyme disease. The request for prophylactic antibiotics was denied because the
Ixodes scapularis tick had not been attached for 48 hours and she was told that the
prophylactic use of antibiotics to prevent Lyme disease was not cost-effective and was not
advised by "authorities" on Lyme disease. Jane awakened crying at 6:00 a.m. the next day, 14
hours after the Ixodes scapularis nymph had been removed from her lower left eyelid. She
had a temperature of 103 F°, headache, mild stiff neck, light sensitive, joint pain and arthritis,
involving her fingers, wrists, hips, knees and ankles, total left facial paralysis and a large
12cm EM (bull's eye) rash extended over the left side of her face, ear, and upper neck with her
left eye being the center of the bull's eye (EM) rash.
She called her pediatrician and made an appointment for Jane to be seen that same
morning. On seeing Jane, at 10 a.m., the pediatrician told her mother that Jane could not have
Lyme disease because the tick had not been attached long enough (48 hours) and if she had
had a significant attachment it takes more than 14 hours for Lyme disease symptoms to
develop. The pediatrician concluded that the rash around her eye could not be a bull's eye rash
because it had no center. Her mother then pointed out that her eyeball was the center!! Jane
was diagnosed as having idiopathic Bell's palsy. "The Lyme Dream Team" in nearby tertiary
medical center concurred. Jane's mother insisted that Jane had Lyme disease. Amoxicillin
125mg PO TID x 10 days was finally prescribed to assuage her mother's Lyme hysteria and
get Jane and her mother out of the office. A follow-up appointment was not deemed
necessary. Jane's mother was not satisfied with the diagnosis and treatment and got my name
from the local neighborhood Lyme network.
I saw Jane the same day and confirmed the diagnosis of early disseminated Lyme
disease with facial paralysis, an EM rash and brain and joint involvement. The amoxicillin
was increased to 375mg PO TID and Zithromax (azithromycin) lOOmg PO BID was added to
her antibiotic regimen. Both antibiotics were continued for 3 months. Jane had a
Jarisch-Herxheimer reaction to spirochetal killing two days after starting the
amoxicillin/Zithromax antibiotic combination. Jane's headache, fever, stiff neck,
photophobia, arthritis and EM rash had resolved by the 7th day. Her left facial paralysis
improved rapidly and had completely resolved one month after antibiotic therapy was
initiated and about the same time a report arrived indicating that the Ixodes scapularis tick
removed from Jane's left lower eyelid was PCR positive for Borrelia burgdorferi spirochetes.
Jane remained on antibiotics for 3 months. She made a complete recovery and has no
residual left facial weakness and no signs of Lyme disease 9 years later. I concluded that the
Borrelia burgdorferi spirochetes causing her Lyme disease had been eradicated.
Conclusion:
1. It does not take long, certainly less than 24-48 hours, for a small Ixodes scapularis tick
or nymph to attach, feed and disseminate organisms in a young child with soft, thin,
very vascular skin.
2. Children with Ixodes scapuiaris tick attachments in the head/neck area, under the arms
or under the collar bones and in the belly button seem to result in Borrelia burgdorferi
spirochetes disseminating rapidly to the brain causing early CNS symptoms
presumably because spirochetes are picked up by arteries going to the brain via the
circle of Willis.
4.
5.
6.
7.
3. In order to eradicate all Borrelia burgdorferi spirochetes, antibiotics should be
continued for 2 months after all symptoms of Lyme disease resolve, for 2 months after
they no longer have a Jarisch-Herxheimer reaction, for 2 months after they no longer
have a Lyme flair-up induced by a non-Lyme infection such as common cold,
chicken pox, influenza and tonsillitis or menstruation. If these criteria are met then
the child's Lyme disease appears cured and all Borrelia burgdorferi spirochetes can be
considered eradicated. If antibiotic therapy is stopped prematurely, before all Lyme
symptoms resolve, these children will have a Lyme relapse and have more brain and
body injury by a more resilient, more difficult to treat Lyme organism. The concept
that 3-6 weeks of antibiotic therapy can eradicate all Borrelia burgdorferi spirochetes
and cure Lyme disease has no bearing in fact and evolved from an arbitrary
pontiilcation in a tertiary medical center 20 years ago. This concept is perpetuated in
the medical community by academia, specialty boards, the real estate lobby, and by
medical insurance companies. There has never been a study in the history of Lyme
disease that indicates the duration of antibiotic therapy needed to eradicate all Borrelia
burgdorferi spirochetes. There is, however, ample evidence in the peer-reviewed
medical literature that the Borrelia burgdorferi spirochete can persist after prolonged
IV antibiotic therapy of Imonth to 1 year or longer.
Persisting Lyme symptoms indicate a persisting Borrelia burgdorferi infection in need
of continuous antibiotic therapy until all symptoms resolve.
In children, persisting Lyme symptoms indicate a persisting Borrelia burgdorferi
infection and not "Post-Lyme-syndrome", not fibromyalgia, not MS, not CFS (chronic
fatigue syndrome), not a psychiatric disorder and not another diagnosis.
Withholding needed antibiotic therapy can result in the children of Lyme disease
having unnecessary permanently injured lives.
I have treated and evaluated over 10,000 children with Lyme disease, % of these
children are well and without signs of Lyme disease 1-15 years after receiving 3
months to 7 years of continuous antibiotic therapy. One third of these 10,000 children
are newly diagnosed or have a persisting deeply entrenched, more difficult to treat
Borrelia burgdorferi infection as a result of a delay in diagnosing their Lyme disease
and/or inadequate initial antibiotic therapy.
8. Forty percent of these children have Bartonella henselae, Babesia microti,
Ehrlichia (Anaplasma), and/or Mycoplasma fermentans co-infections.
The effect Lyme disease has on children is depicted in a video by Dolly Curtis and
Dan Peck titled The Children of Lvme Disease. Before seeing a portion of the video
demonstrating the problems children can face with Lyme disease, I would like to briefly
mention some of the different patterns of pediatric and adolescent Lyme disease observed in
my practice; i.e., children presenting with FDD and autistic-like behavior, [children with
severe destructive arthritis], children with gestational or breast milk Lyme disease, and
children with profound rage reactions with loss of time due to Borrelia burgdorferi brain
involvement.
I have 40 Lyme disease children in my practice who have profound behavior changes;
hypotonia and developmental delay following an Ixodes scapularis tick attachment or breast
milk exposure to Borrelia burgdorferi spirochetes before two years of age. They have
impaired cognitive function on neuropsychological testing which improved after 10-24
months or more of antibiotic therapy.
Thirty children with autism spectrum disorder who have developed Lyme disease are
improving with continuous oral, IV, and/or IM antibiotic therapy. Eight of these children
have no stigma of autism or Lyme disease following antibiotic treatment.
Sixty children between the ages of 2-16 years with a history of Ixodes scapularis tick
attachments or EM rashes developed episodes of severe blind rage reactions with a loss of
time as the most significant manifestation of their Lyme disease. They all had fatigue,
arthritis and arthralgia, low-grade fevers, light and noise sensitivity, however their behavior
change was the most evident problem. All sixty had positive Lyme serologies and 10 of these
children had Borrelia burgdorferi tests that were PCR positive as well. Brain SPECTs
typically revealed hypoperfusion. MRls were normal. LPs were normal. A 5-year-old and a
7-year-old boy had an abnormal EEG with a temporal lobe focus. None responded to
psychopharmacologicals or anticonvulsants. Their rage reactions resolved on oral and or IV
antibiotics. One 11-year-old boy, Robin Miller, whose rage reactions from Lyme disease and
Babesiosis began when he was 2 years old was not treated or diagnosed until he was 8. Robin
responded to IV Rocephin, oral Mepron for Babesiosis, and HBO therapy. Robin is in the
video The Children of Lvme Disease and was featured on a channel 12 TV documentary. A
Child with Lvme Disease: One Family's Story.
Although the Borrelia burgdorferi spirochete, the bacterium that causes Lyme disease,
is usually transmitted by Ixodes scapularis ticks, over 300 of the over 10,000 children in my
practice have Lyme disease as a result of trans-placental or breast milk Borrelia burgdorferi
exposure. These children have gestational or early neonatal Lyme disease from their mother's
undiagnosed, untreated, or inadequately treated Lyme disease. Among all of these over 300
children, maternal symptoms of Lyme disease occurred prior to the child's conception, during
gestation or while breast-feeding. These children with gestational and early neonatal Lyme
disease had a myriad of problems, which improved or resolved with prolonged oral or IV
antibiotics. Several have been off antibiotics and are doing well so far.
Mothers of gestational Lyme disease children have frequent miscarriages. Most of
theu pregnancies are difficult and most of the children have manifestations of disease at, or
shortly after birth. 40% have gastroesophageal reflux with vomiting and coughing. 80%
irritability. 60% low-grade fevers, pallor and dark circles under their eyes—they look ill.
72% fatigue and lack of stamina, 23% have secondary EM rashes and 45% had other rashes.
30% had eye problems: posterior cataracts, myopia, astigmatism, conjunctiva! erythema
(Lyme eyes), optic nerve atrophy and optic neuritis and/or uveitis. 40% have a history of
frequent upper respiratory tract infections and otitis, starting in infancy. 20% have abdominal
pain. 40% have history of noise, light, and skin sensitivity. 50% have arthritis and painful
joints. 18% have developmental delay, including language and speech problems and
hypotonia. 80% have cognitive problems, learning disabilities and mood swings. 30%
cavernous hemagiomas.
Tests:
50% have positive Lyme Western Blots
20% were PCR Positive
21% had positive LUATS
37% had positive Borrelia burgdorferi blood cultures
11 % had a positive Brain SPECT
80% had cognitive problems on neuropsychological evaluation
There is a reprint of Gestational Lyme Disease Case Studies from 102 Live Births in
the syllabus. [Charles Ray Jones, M.D., Edina Gibb & Harold Smith]
New data from my practice involves the treatment of 160 mothers with Lyme
disease with antibiotics prior to conception and during the entire pregnancy. All of
them have normal healthy infants. However, 8 of these pregnancies have resulted in
Borrelia burgdorferi and Bartonella henselae positive placentas, umbilical cords,
and/or foreskin remnants. Those with positive PCRs were treated with 6 months of
oral antibiotics and are without symptoms 3 months to 8 years later. There seems to be
an increased incidence of multiple cavernous hemagiomas in children exposed to,
Borrelia burgdorferi during gestation.
Cluster of Observations from a
Practice of Pediatric and Adolescent
Lyme Disease
1. Borrelia burgdorferi can be transmitted in utero.
2. Borrelia burgdorferi can be transmitted through breast milk.
3. Since there are multiple strains of Borrelia burgdorferi it is not uncommon to
have geographic variability in symptoms, presumably reflecting Borrelia
burgdorferi strain differences.
• Abdominal Pain
•
Dysuria
• Frequent Enuresis
• Diarrhea
• CNS eye/ear
• Dribbling urine All strains of Borrelia burgdorferi target nerve tissue,
brain and PNS (peripheral NS).
4. Many have skin/hair sensitivity to touch or clothing.
5. The longer Lyme disease exists due to untreated or inadequate treatment,
the more difficult it is to treat—requiring longer courses of antibiotics to
resolve symptoms/signs and eradicate Borrelia burgdorferi spirochetes,
6. Borrelia burgdorferi infection will amplify pre-existing
problems.
• ADD/ADHD
•
OCD
•
PPD
• Autism
• Aspergers Disorder
• Sensory defensiveness
• Dyslexia
•
Tic disorder
• Anxiety
• Depression
7. Young children more rapidly become symptomatic after a Borrelia burgdorferi
infection.
8. There is a more rapid occurrence of CNS symptoms associated with anatomical
location of Ixodes scapularis tick attachment head/neck, axilla, and belly button
(umbilicus).
9. Fewer than 7% have EM rashes in my practice.
10. About 50% have no history of tick attachments. All have history of high risk for
geographical exposure to Ixodes scapularis ticks where they live or vacation.
11.18% have endocrine involvement associated mostly with the thyroid gland,
12. The best way to prevent Lyme disease is to treat Ixodes scapularis tick
attachments in a Lyme endemic area with 30 days of oral antibiotics.
13. Persisting .oral, IM or TV antibiotic therapy has no permanent adverse effect on the
child's immune system, liver function, kidney function or bone marrow, but, a
persisting Borrelia burgdorferi infection has an adverse effect on the child's entire
body and immune system.
14. The CDC recommendation to only perform a Western blot if there is a positive or
equivocal ELISA is not valid because 20-30% with negative ELISA's have a CDC
positive Western blot.
15. According to the CDC, the rigid Western blot requirement for
surveillance purposes should not be used to diagnose Lyme disease. All that
is needed is one Borrelia burgdorferi genus specie specific band to indicate a
serological reaction to Borrelia burgdorferi spirochetes and give laboratory
support to the clinical diagnosis of Lyme disease. There are 9 such bands: j_8,
23, 30, 31, 34, 37, 39, 83., and 93. See the enclosed Understanding Lyme
Western Blot in the syllabus.
Excerpts from the video Children of Lvme disease depict problems children with
Lyme disease live with due to a delay in diagnosis and inadequate treatment.
Matthew (6 years old)
• Gestational and acquired Lyme disease.
• Arthritis, right facial paralysis.
•
HLA DR4 positive
Sebastian Osborn (10 years old)
• Spinal cord proprioceptive
problem. » Arthritis. Cognitively
impaired.
• Day after video could not stand or walk for two years.
• Lyme WB bands 31 & 34 positive
Robin Miller (10 years old)
• Disseminated Lyme disease with joint and brain involvement.
• Blind rage reactions.
• Robin is so much better today as evident by Channel 12 video.
Erin Morrissey (14 years old)
•
Basal ganglia involvement.
• An over zealous immune system with increased Myelin basil protein
antibodies.
• Narcolepsy, cataplexy-post sleep paralysis.
• Erin has responded to hyperbaric oxygen therapy, IV gamma globulin and oral
and IV antibiotics.
• She is HLA DR4 and DR2 positive and therefore predisposed to the
development of a Lyme induced autoimmune reaction.
• Lyme WB bands 31 & 34 positive
Andrea Sinclair (18 years old)
• Inadequate treatment of Lyme disease resulting in fatigue and cognitive
problems and affecting her left knee when she was 10 years old (arthritis).