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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).