Lyme Disease Survival Manual References



Lyme on The Brain - Lecture Note - ReferencesReference Categories: August 30, 2010 General Lyme Disease ………………….2Lyme Tests …………………………………….9Lyme Arthritis/Myalgia/Lupus ……… 19Dermatological Lyme, EM, ACA ……23Ophthalmic Lyme ………………………….26Persistent Infection ……………………….27Cardiovascular ……………………………….32Antibiotic Therapy …………………………34Alternative Therapies ……………………41Neurological Lyme …………………………44Borrelia burgdorferi-seropositive Chronic encephalomyelopathy: Lyme neuroborreliosis? An Autopsied report…..………………………..54Epidemiology and Prevention………..56Microbiology …………………………………..67Veterinary Lyme …………………………….76Other Tick-Borne Illnesses ……………78Books………………………………………………79 Coping With Chronic Illness…………...80Non-Lyme References …………………..82Pregnancy and Lyme …………………….88Multiple Sclerosis & Neurological invasion by Borrelia. …………………….100Further Reading on neuroborreliosis/MS..105Antimyelin antibodies in Lyme………105Ceftriaxone Compared with Doxycycline for the Treatment of Acute Disseminated Lyme Disease 106General Lyme Disease TopicsAbstracts too numerous to list (2-3 thousand) most recently are the abstracts from the 1996, VII International Congress on Lyme Borreliosis, June 16-21, held in San Francisco, and the 1996 LDF International Lyme Borreliosis, and Tick-Borne Disease Conference held in Boston, Massachusetts.Asch ES, Bujak DI, Weiss M. Lyme disease: An infectious and post infectious syndrome. J Rheumatol 1994;21:454-61Baltimore RS, Shapiro ED. Lyme Disease. Pediatrics in Review. May 1994;15(5):167-174Bleiweiss John D. M.D. When to suspect Lyme disease. Lecture handout LDF Conference 1993Bryerson AD. Clinical pathology of the Jarisch-Herxheimer reaction. J of Infect Dis 1976;133:696-705Burgdorfer W. First decade of Lyme Borreliosis. Infection, July/August 1991;19(4)Burgdorfer W, Barbour AG, Hayes SF, Benach JL, Grunvaldt E, Davis JP. Lyme Disease - a tick borne spirochetosis ? Science 1982;216:1317-1319Burgdorfer W. Discovery of the Lyme disease spirochete: A historical review. Inter J Microbiol Hyg, Series A, 1986;7-9Burrascano JJ. Diagnostic Hints and Treatment Guidelines for Lyme Disease. 1995; 10th Edition handout from the 9th LDF Scientific Lyme Disease Conference. Held in Boston April 21-22 1996. Burrascano JJ. Diagnostic Hints and Treatment Guidelines for Lyme Disease. 1995; 11th Edition handout, from the 10th LDF Scientific Lyme Disease Conference. Held in Bethesda, MD/ NIH April 1997. Burrascano JJ. Diagnostic Hints and Treatment Guidelines for Lyme Disease. 1997; Conn’s Current Therapy . Cavert, Kathy. Psychosocial Issues of Lyme disease. Lyme Disease Update 1995Cimmino MA, Azzolini A, Tobia F, Pesce CM. Spirochetes in the spleen of a patient with chronic Lyme disease. American J Clin Pathol 1989;91(1):95-97Clark JR, Carlson RD, Sasaki CT. Facial Paralysis in Lyme disease. Laryngoscope 1985;95:1341-1345 *Coyle BS, Et al. The Public Health Impact of Lyme Disease in Maryland. J Infect Dis, 1996;173:1260-1262Dattwyler RJ. Lyme borreliosis: An Overview of the Clinical Manifestations. Laboratory Medicine 1990;21:290-292Dattwyler RJ, Luft BJ. Immunodiagnosis of Lyme Borreliosis. Rheumatic Disease Clinics of North America, November 1989;15(4):727-734Dinerman H, Steere AC. Lyme Disease associated with fibromyalgia. Ann Intern Med 1992;117:281-285Duffy J, Schoen RT, Sigal LH,. 1991 Update on Lyme Disease. Patient Care. 1991;June 15):24-51Eppes SC, Klein JD, Caputo GM, Rose CD. Physician beliefs, attitudes, and approaches toward Lyme disease in an endemic area. Clinical Pediatrics, March 1994:130-134Fallon BA, Nields JA, Burrascano JJ, et al. The Neuropsychiatric Manifestations of Lyme Borreliosis. American J of Psych, November 1994 and Psychiatric Quarterly, Spring 1992;63(1):95-117Feder HM, Gerber MA, Krause PJ, Ryan R. Early Lyme Disease: A Flu-Like Illness Without Erythema Migrans. Pediatrics, February 1993;91(2):456-459Feder HM, Hunt MS. Pitfalls in the Diagnosis and Treatment of Lyme Disease. JAMA 1995;274(1):66-68Felsenfeld Oscar MS M.D. , Borrelia-strains, Vectors, Human and Animal Diseases, 1971 Warren Green Inc. 10 South Brentwood Blvd, St. Louis MO 63105, Library of Congress # 72-127355Friedland JG, Warrell DA. The Jarisch-Herxheimer reaction in Leptospirosis: a possible pathogenesis and review. REV Infect Dis. 1991; 13:207-210Gerber MA, Shapiro ED. Diagnosis of Lyme disease in children. J Pediatrics 1992;121(1):157-62Goellner MH, Agger WA, Burgess JH, Durray PH. Hepatitis due to recurrent Lyme Disease. Ann Intern Med 1988;108:707-708Golightly MG. Laboratory considerations in the diagnosis and management of Lyme Borreliosis. [Review Article with 51 references] Amer J Clin Pathol 1993;99(2):168-74Hahlberg P, Granlund H, Nyman D. Panelius J, and Sapp?l? I. Treatment of Late Lyme Borreliosis. Infection 1994;29:255-261Hamilton DR. Lyme disease the hidden pandemic. Post Graduate Medicine 1989;85:303-314Herxheimer K, Krause E. Vebereine bei syphitischen Vorkommende Quecksilberreaktion. Deutch Med Wochenschr. 1902;28:895-897 *How to diagnose and treat Lyme disease in children. Infectious Diseases and Immunization committee, Canada Pediatric Society-Review Article 12 references. Canada Med Assoc J 1992;147(2):169-78Kindree Diane. How to diagnose and treat Lyme disease in children [Letter and Commentary] Canada Med Assoc J. January 15, 1993;148(2):132Huppertz H-I. Childhood Lyme Borreliosis. Neurology 1988;38:863-867Johnson RC, Schmid GP, Hyde AG, Steigerwalt AG, Brenner DJ. Borrelia burgdorferi species the etiologic agent of Lyme Disease. Int J Sys Bacteriology 34:496;97Kantor FS. Disarming Lyme Disease. Scientific American. September 1994:34-39Kaslow RA. Current Perspectives on Lyme Borreliosis. JAMA, March 11, 1992;267(10):1364-1367 and 1381-1383Kirsch M, Ruben FL, Steere AC, Durray PH et al. Fatal Adult respiratory Distress Syndrome in a patient with Lyme disease. JAMA 1988;259:2737-2739Leff Robert D, Akre Steven P. Late Stage Lyme Borreliosis in Children. Southern Med Journal 1989;82(8):954-956Lissman BA, et al. Spirochete-associated Lyme Arthritis in a Dog. J Amer Vet Assc 1984;185:219-20MacDonald, Alan B. Gestational Lyme Borreliosis. Rheum Dis Clin North America 1989;15(4(:657-672MacDonald, Alan B, Gestational Lyme Borreliosis and a Rationale for a Prospective study of Sudden Infant Death Syndrome (SIDS). 1989; Rheumatic Disease Clinic of North America 1989;15(4):657-677MacDonald AB, Benach JL, Burgdorfer W. Stillbirth Following Maternal Lyme Disease. New York State Journal of Med 1987MacDonald AB, Berger BW, Schwan TG. Clinical implications of delayed growth of the Lyme disease spirochete, Borrelia burgdorferi. Acta Tropica 1991;48:89-94Massarotti EM, Luger SW, Rahn DW et al. Treatment of Early Lyme Disease. American J Med 1992;92:396-403Masters EJ, Donnell D, Fobbs M. Missouri Lyme disease: 1989-1992. J Spiro and Tick-borne Dis 1994;1(1):12-17Michigan Department of Health Letters and response to correspondence. Mitchell Paul D. Ph.D. Lyme Borreliosis: A persisting diagnostic dilemma. Clin Microbiol Newsletter, April 15, 1993;15(8):57-64Moulton Chris. Lyme Disease: New facts only add to diagnostic frustrations. Adv for Med Lab Professionals July 29, 1991:18-19Mulberg AK, Linz C, et al. Identification of nonsteroidal drug induced gastrodoudenal injury in children with juvenile rheumatoid arthritis. Journal of Pediatrics 1993;122:647-649Nadleman RB et al. The clinical spectrum of early Lyme borreliosis in patients with culture-confirmed erythema migrans. Amer J Med, May 1996;100:502-508NIH State of the Art Conference. Diagnosis and Treatment of Lyme Disease. Cin Courier August, 1991;9:1-8NIH Gears up to test a hotly disputed theory. Science, October 1995;270(13):228-229Nields JA, Kveton JF. Tullio Phenomena and Seronegative Lyme Disease. Lancet. 1991;338:128-129Norcross Karen. Injustice Based on Misunderstanding. September 6, 1994 Masters Thesis TreatmentOstrov BE, Athreya DJ. Lyme Disease-difficulties in diagnosis and management. Pediatric Clinics of North America, June 1991;38(3):535-553Pfister HW, Einhapl K, Preac-Mursi V, Wilske B, Schierz G. The spirochetal etiology of lymphocytic meningoradiculitis of Bannwarth’s Syndrome. J Neurol 1984;231:141-144Pfister HW, Wilske B, Weber K. Lyme Borreliosis: Basic science and clinical aspects. Lancet, April 23, 1994;343(8904):1013-1016Pfluger K-H, Reimers et al. Lyme-borreliosis and possible association with HLA antigens. Tissue Antigens. 1989;33:375-381 *Pietrucha, Dorothy M. Many Difficult Problems for Children with Lyme. Lyme Times, Newsletter of the Lyme Disease Resource Center – Summer 1992Pietrucha, Dorothy M. M.D. Neurologic Manifestations of Lyme Disease in Children. Lecture Handout 1-908-922-0337 FAX 908-922-1631 Pediatric Neurology, 3318 Route 33, Neptune New Jersey, 07753Pietrucha, D. IV Treatment and follow-up for children with neurologic Lyme disease. Lyme Times-Lyme Disease Resource Center 1991; 2(2):30-31Plotkin SA, Georges P. Treatment of Lyme Borreliosis in children. Pediatrics July 1991; 88:176-79Putkonen T, Salo OP, Mustakaillio KK. Febrile Jarisch-Herxheimer reaction in different phases of primary and secondary syphilis. British Journal of Venereal Diseases 1966; 42:181-184Rahn DW. Lyme Disease: Clinical manifestations, diagnosis, and treatment. Sem Arthritis and Rheum 1991;20(4):201-218Rahn DW, Malawista SE. Lyme disease: Recommendations for diagnosis and treatment. Annals of Internal Med 1991;114:472-482Rahn DW. Lyme Disease: Where’s the bug? [Letter} New Engl J Med, 1994;330(4):282-3Scrimenti RJ et al. Lyme disease redux: The legacy of Sven Hellerstrom. Wis Med J January 1993;92(1):20-21Scott JD. How to diagnose Lyme disease in children. [Letter] Canada Med Assoc J, January 15, 1993;148(2)132Shadick NA M.D. MPH, Phillips CB, Logigian EL, Steere AC, Kaplan RF, Beradi VP, Durray PH, Larson MG, Wright EA, Ginsburg KS, Katz JN, Liang MW. The Long Term Outcomes of Lyme Disease (A population based retrospective cohort study) American College of Physicians 1994: Ann Intern Med 1994;121:560-567Shrestha M, Grodzicki RL, Steere AC. Diagnosing Early Lyme Disease. American J Med 1985;78:235-240Sigal Leonard H. Editorial: Lyme disease: Primum Non Nocere. J Infect Dis 1995;171:423-424 Address responses to: Leonard H. Sigal MD, 1 Robert Wood Johnson Place, MEB 484, New Brunswick, NJ 08903-0019Sigal LH. Lyme disease: don’t let disguises fool you. Intern Med, June 1992;13:24-33Sigal LH. Lyme disease: Immunologic manifestations and possible immunologic mechanisms. Seminars in Arthritis and Rheum 1989;18:151-67Sigal LH, Lyme disease in New Jersey: A practical guide for clinicians. Princeton NJ: Academy of Med New Jersey 1993Sigal LH. Severe complications of Lyme disease; recognition and management. Management of the critically ill patient with rheumatic or immunologic illness. In Mandell BF. Edition New York: Marcel Decker;1993Sigal LH. Summary of the first 100 patients seen at a Lyme disease referral center. American J Med 1990;88:577-581Sigal LH, Schutzer S. Possible autoimmune mechanisms in Lyme disease. Molecular and Immunologic approaches to Lyme disease. Cold Spring Harbor Press, Plainview, NYSigal Leonard H. MD. The Lyme Disease Ccontroversy. Arch Internal Med, July 26,1996;156:1493-1500Steere AC. Seronegative Lyme Disease JAMA 1993;270(11):1369Steere AC, Levin RE, Molloy PJ et al. Treatment of Lyme Arthritis. Arthritis and Rheum 1994;37(6):878-888Steere AC, Bartenhagen NH, Craft JE et al. The Early Clinical Manifestations of Lyme Disease. Ann Intern Med 1983;99:76-82Steere AC, Grodzicki RL, Kornblatt AN et al. The spirochetal etiology of Lyme disease. New Eng J Med 1983;308:733-744Steere AC. Distinguishing Lyme Disease from Its Look-A likes. Emergency Medicine, August 1992;15:28-44Steere AC, Malawista AC. Cases of Lyme Disease in the United States: locations correlated to the distribution of Ixodes dammini. Ann Internal Med 1979;91:730-733Steere AC. Lyme Disease. New England J Med 1989;321:586-596.Steere AC, Taylor E, McHugh GL, Logigian EL. The Overdiagnosis of Lyme Disease. JAMA, April 14, 1993;269(14):1812-1816Sullivan, David Ph.D President of American Lifeline Inc. Makers of Florajen-acidophilus/bifida capsules. 1-800-257-5433 (Supplied various peer review studies and unpublished data on acidophilus and bifida supplementation. NIH, Diagnosis and Treatment of Lyme Disease. NIH State of the Art Conference, August 1991;9(5) Wisconsin Department of Health. “A Clinician’s Guide to Lyme Disease”. January 1989Ziska MH, Donta ST, Demarest FC. Physician Preferences in the Diagnosis and Treatment of Lyme Disease in the United States. Infection, 1996;24(2):182-186Lyme/Laboratory Tests (ELISA: Enzyme-Linked Immunosorbent Serum Assay)Bakken LL, Callister SM, Wand PJ, Schell RF. Interlaboratory Comparison of Test Results for the Detection of Lyme Disease by 516 Participants in the Wisconsin State Lab of Hygiene/College of American Pathologists Proficiency Testing Progrm. J Clin Microbiol 1997; Vol 35, No 3:537-543Bakken LL, Case KL, Callister SM et al. Performance of 45 Laboratories participating in a proficiency testing program for Lyme disease serology. JAMA 1992;268:891-895Barbour AG. Laboratory Aspects of Lyme borreliosis. Clin Microbiol Rev 1988;1:399-414Cameron DJ. False Positive. [Letter/Commentary on Arch Internal Med 1991;151(9):1837-40] Arch Internal Med 1992;152(6):1331Coyle PK. Borrelia burgdorferi specific antigen-antibody complexes in the CSF of 78 % of seronegative Lyme patients with early EM rashes. Fifth International Conference on Lyme Borreliosis, Arlington, VA, June 1992 and LDF Conference Atlantic City 1993.*Coyle PK, Schutzer SE, Belman AL, Krupp LB, Golightly MG. Cerebrospinal fluid immune complexes in patients exposed to Borrelia burgdorferi: Detection of Borrelia-specific and non-specific complexes. Annal of Neurology, 1990;28:6:739-744Coyle PK, Deng Z, Schutzer SE, Belman AL, Benach J, Krupp LB, Luft B. Detection of Borrelia burgdorferi antigens in the cerebrospinal fluid. Neurology 1993;43:1093-1097Craft JE, Grodzicki RL, Steere AC. Antibody response in Lyme Disease: an evaluation of diagnostic tests. J Infect Dis 1988 158:754-60Craft JE, Fisher DK, et al. Antigens of Borrelia burgdorferi recognized during Lyme disease, Appearance of a new immunoglobulin M response and expansion of the IgG response late in the illness. J Clin Invest 1986;78:934-939Dattwyler RJ, Volkman DJ et al. Seronegative Lyme Disease. New Eng J of Med 1988;319:1441-1446Fawcett PT, Gibney KM et al. Adsorption with a soluble E. coli antigen fraction improves the specificity of ELISA tests for Lyme Disease. J Rheumatology 1991;18(5):705-708Fawcett PT, O’Brien AE, Doughty RA. An Adsorption Procedure to Increase the Specificity of Enzyme-Linked Immunosorbent Assays for Lyme disease without Decreasing Sensitivity. Arthritis and Rheum 1989;32(0):1-6 Feaga, Wendy P. D.V.M. Self dosing of the Borrelia dog Vaccine by Veterinarians. Poster Presentation LDF Lyme Research Symposia, Stamford CT, 1993*Fung BP, McHugh GL, Leong JM et al. Humoral Immune Response to Outer Surface Protein C in Lyme Disease: Role of the Immunoglobulin M Response in the Serodiagnosis of Early Infection. Infection and Immunity, August 1994;62(8):3213-3221Golightly MG. Laboratory considerations in the diagnosis and management of Lyme Borreliosis. [Review Article with 51 references] Amer J Clin Pathol 1993;99(2):168-74Hansen K, Hinderson P, Pederson NS. Measurement of antibodies to Borrelia burgdorferi flagellum improves serodiagnosis in Lyme disease. J Clin Microbiol 1988;26:338-346Karch H, Huppertz H-I, Bohme M, et al. Demonstration of Borrelia burgdorferi DNA in Urine Samples from healthy humans whose sera contain B. burgdorferi-specific antibodies. J Clin Microbiol September 1994;32(9):2312-2314Hansen, Klaus. Serodiagnosis of erythema Migrans and Acrodermatitis Chronica Atrophicans by Borrelia burgdorferi flagellum ELISA. J Clin Microbiol, March 1989;27(3):545-551Harris, Nick S. Ph.D. Overview of the Lyme Urine Antigen Test (LUAT). IgX 1-800-832-3200 Palo Alto, CA, IGenix Newsletter 1992;2(1) Harris Nick S. Ph.D., Kalberg G, Leung SS, Scott JS, Meier K. Detection of Borrelia burgdorferi antigen in urine from Lyme Disease patients. Abstract V International Conference on Lyme Borreliosis. Arlington VA, May 1992Hedberg CW, Osterholm MT, MacDonald KL, White KE. An inter-laboratory study of antibody to Borrelia burgdorferi. J Infect Dis 1987;155:1325-27Johnson BJB, Robbins KE, Bailey RE, et al. Serodiagnosis of Lyme Disease: Accuracy of a Two-Step Approach Using a Flagella-Based ELISA and Immunoblotting. J Infect Dis 1996;174:346-53Kaiser R, Lucking CH. Intrathecal Synthesis of Specific Antibodies in Neuroborreliosis. J Neurological Sciences, 1993;118:64-72Lane RS, Lennette ET, Madigan JE. Interlaboratory and Intralaboratory Comparisons of Indirect Immunofluorescence Assays for Serodiagnosis of Lyme Disease. J Clin Microbiol 1990;28(8):1774-1779Magnarelli LA. Quality of Lyme disease tests. JAMA 1989;262:3464-3465Magnarelli LA, Anderson JF. Enzyme-Linked Immunosorbent Assays for the Detection of Class-Specific Immunoglobulins to Borrelia burgdorferi. American J of Epidemiology, April 1988;127(4)818-825Magnarelli LA, Anderson JF, Johnson RC et al. Comparison of Different Strains of Borrelia burgdorferi Sensu Lato Used as Antigens in ELISA. J Clin Micro, May 1994;32(5):1154-1158Magnarelli LA. Serologic Diagnosis of Lyme Disease. Annals New York Academy of Sciences, 1988;539:154-161Magnarelli LA, Anderson JF, Johnson RC. Cross Reactivity in Serological Tests for Lyme Disease and other Spirochetal Infections. J Infectious Diseases, July 1987;156(1):133-138Magnarelli LA, Meegan JM, Anderson JF, Chappell JF et al. Comparison of indirect fluorescent antibody test with an ELISA for serological studies of Lyme disease. *Mitchell PD, Reed KD, et al. Comparison of four immunoserologic assays for detection of antibodies to Borrelia burgdorferi in patients with culture positive erythema migrans. J Clin Microbiol 1994;32(8):1958-1962Russell H, Sampson JS, Schmid GP, Wilkonson HW, Plikaytis B. Enzyme-linked immunosorbent assay for Lyme disease. J Infect Dis 1984;149:465-470Schwartz BS, Goldstein MD, Rebeiro JMC, Schulze TL. Antibody testing in Lyme disease: A comparison of results in four different laboratories. JAMA. 1989;262:3431-3434Sczepanski A, Benach JL. Lyme Borreliosis: Host response to Borrelia burgdorferi. Microbiol Review 1991;55:21 Telford SR, Kantor FS, Lobet Y, Barthold SW, Spielman A, Flavell RA, Fikrig E. Efficacy of Human Lyme disease Vaccine formulations in a Mouse Model. J Infect Dis 1995;171:1368-1370Weiss NL, Phillips MR, Sadock VA, Sigal LH, et al. False positive seroactivity to Borrelia burgdorferi in Rheumatic disease: The value of immunoblotting. Autoimmunity 1994 *Weyand CM, Gorozny JJ. Immune responses to Borellia burgdorferi in patients with reactive Lyme arthritis. Arthritis Rheum. 1989;32:1057-1064Williams CL, et al. Lyme disease: Pregnancy and congenital malformations: A cord blood serosurvey. Abstract IV International Conference on Lyme Borreliosis, Stockholm, Sweden 1990 * Zalneraitis EL Gerber MA. Prevalence of clinically significant neurological disorders attributable to congenital Lyme Borreliosis. Abstract IV International Conference on Lyme Borreliosis, Stockholm Sweden,1990*Zoller L, Haude M, Hassler D et al. Spontaneous and post-treatment antibody kinetics in late Lyme Borreliosis. Serodiagnosis Immunother Infect Dis 1989;3:345-353Zoschke DC. Is it Lyme disease? How to interpret results of laboratory testing. Postgrad Med, 1992;91(7):46-55(Western Blot)Craft JE, Fischer DK, Shimamoto GT et al. Antigens of Borrelia burgdorferi recognized during Lyme Disease. J Clinical Investigation. October 1986;78(4):934-939Dattwyler RJ, Luft BJ. Immunodiagnosis of Lyme Borreliosis. Rheumatic Disease Clinics of North America, November 1989;15(4):727-734Dressler F, Whalen JA, Reinhardt BN. Western Blotting in the Serodiagnosis of Lyme Disease. J Infect Dis. February 1993;167:392-400Dressler F. Lyme Borreliosis in European Children and Adolescents. Clinical and Experimental Rheumatology. September-October 1994;12(supplement 10):S49-S54Engstrom SM, Sshoop E, Johnson RC. Immunoblot Interpretation Criteria for the Serodiagnosis of Early Lyme Disease. J of Clin Micro, 1995 Minnesota Dept of Health Diagnosis Committee Handout.Hilton E, Tramontano A, DeVoti J, Sood SK. Temporal Study of Immunoglobulin M Seroreactivity to Borrelia burgdorferi in Patients Treated for Lyme Borreliosis.J Clin Microbiol 1997; Vol35, No 3:774-776Jain VK, Hilton E, et al. Immunoglobulin M Immunoblot for Diagnosis of Borrelia burgdorferi Infection in Patients with Acute Facial Palsy. J Clin Micro Biol, August,1996;34(8):2033-35Karlsson M. Western Immunoblot and Flagellum Enzyme-Linked Immunosorbent Assay for Serodiagnosis of Lyme Borreliosis. J Clin Micro, Sept 1990;28(9):2148-2150Ma B, Christen B, Leung D et al. Serodiagnosis of Lyme Borreliosis by Western Immunoblot: Reactivity of various significant antibodies against Borrelia burgdorferi. J Clin Micro. 1992;30(2):370-376Norman GL, et al. Serodiagnosis of Lyme Borreliosis by Borrelia burgdorferi sensu stricto, and B Garinii, and B. afzelii Western Blots (Immunoblots). J Clin Microbiol, 1996;34(7):1732-1738Simpson, WJ, Schrumpf ME, Schwan TG. Reactivity of Human Lyme Borreliosis Sera with a 39-Kilodalton Antigen Specific to Borrelia burgdorferi. J Clin Microbiol 1990;28(6):1329-1331Technical Report: ImmunoWell Borrelia burgdorferi Test, ImmunoWell P39 Test, and ImmunuDOT Borrelia (Lyme) Test Lecture Handout LDF Conference Atlantic City NJ, 1993, pp. 1-49 ABSTRACT # 1254Western Blot and False Negatives in Children:1995 Rheumatology Symposia Abstract #1254 Dr. Paul Fawcett et al. These data show that under the old Western Blot reporting criteria used by our lab, all of 66 pediatric patients with a history of a tick bite and bull’s-eye rash who were symptomatic, were accepted as positive under the old Western Blot interpretation. Under the newly proposed Dearborne, Michigan, criteria only 20 were now considered positive. That means 46 children of the 66 total who originally presented with a known tick bite and bull's-eye rash and were all symptomatic, would probably be considered NEGATIVE by the newly proposed Western Blot reporting criteria.That’s a diagnostic success rate of only 31% even in cases of clearly defined tick-bite and rash. Undertaking a new Reporting Criteria before it was tested in human field trials, should be reconsidered. 66 Children with bull’s-eye rash Old W. Blot Criteria 100 % positive New NIH Criteria 31 % positive The verbatim conclusion of the researchers was: The proposed Western Blot Reporting Criteria are grossly inadequate, because it excluded 69% of the infected children.? (Reprinted from "Complexities of Lyme Disease: A microbiology Primer: by Tom Grier, Pedagogue Press 1995 ) (Antigen Detection)Baranton G, Postic D, Saint-Girons I, et al. Delineation of Borrelia burgdorferi Sensu Stricto, Borrelia garinii sp. nov., and Group VS461 Associated with Lyme Borreliosis. International J Sys Bacteriology. July 1992;42(3):378-383Coyle PK, Deng Z, Schutzer SE, Belman AL, Benach J, Krupp LB, Luft B. Detection of Borrelia burgdorferi antigens in cerebrospinal fluid. Neurology. June 1993;43(6):1093-8Dattwyler RJ, Volkman DJ, Luft BJ, Halperin JJ et al. Seronegative Lyme disease: dissociation of the specific T- and B-lymphocyte response to Borrelia burgdorferi. New Engl J Med. 1988;319:1441-1446Dressler F, Yoshinari NH, Steere AC. The T-cell proliferation assay in the diagnosis of Lyme disease. Ann Intern Med. 1991;115:533-539Dorward DW, Schwan TG, Garon CF. Immune Capture and Detection of Borrelia burgdorferi Antigens in Urine, blood, or tissues from Infected Ticks, Mice, Dogs, and Humans. J Clin Micro. June 1991;29(6):1162-1170Dressler F, Yoshinari NH, Steere AC. The T-cell proliferation assay in the diagnosis of Lyme disease. Ann Intern Med. 1991;115:533-539Klempner MS, Noring R, Steere AC, Schwan TG. Antibodies to a 39 kDa antigen of Borrelia burgdorferi are a specific marker of late but not early Lyme disease. Abstract Fifth International Conference on Lyme Borreliosis, Arlington, VA, May 30-June 2, 1992*Rasiah C et al Use of hybrid protein consisting of the variable region of the Borrelia burgdorferi flagellin and part of the 83-kDa protein as antigen for serodiagnosis of Lyme Disease. J Clin Microbiol 1994;32(4):1011-1017Schutzer SE, Coyle PK, Belman AL, Golightly MG, Drulle J. Sequestration of antibody to Borrelia burgdorferi in immune complexes in seronegative Lyme disease. Lancet. 1990;335:312-315Simpson WJ, Burgdorfer W, et al. Antibody to 39-kilodalton Borrelia burgdorferi Antigen (P39) as a marker for infection in experimentally and naturally infected animals. J Clin Microbiol 1991;29(2):236Simpson WJ, Schrumpt ME, Schwan TG. Reactivity of Human Lyme Borreliosis Sera with a 39 - Kilodalton antigen specific to Borrelia burgdorferi. J Clin Micro Biol 1990;28:1329-1331(Culture)Asbrink E, Hovmark A. Successful cultivation of spirochetes from the skin lesions of patients with erythema migrans, Afzelius and Acrodermatitis Chronica Atrophicans. Acta Pathol Microbiol Immunol Scand, 1985;sect B, 93:161-163 *Barbour AG. Isolation and cultivation of Lyme disease spirochetes. Yale J Biol Med 1984;57:521-525Benach JL, Bosler EM, Hanrahan JP, Coleman JL, Habicht GS, Bast TF et al. Spirochetes isolated from the blood of two Lyme disease patients. New Eng J Med. 1983;308:740-742Berger BW, Johnson RC, Kodner C, et al. Cultivation of Borrelia burgdorferi from the blood of two patients with erythema migrans lesions lacking extracutaneous signs and symptoms of Lyme Disease. J American Acad Derm. January 1994;30(1):48-51*Berger BW, Johnson RC, Kodner C et al. Cultivation of Borrelia burgdorferi from erythema migrans lesions, and perilesional skin. J Clin Microbiol, February 1992;30(2):359-361Callister SM, Schell RF, Case KL, et al. Characterization of the Borreliacidal Antibody Response to Borrelia burgdorferi in Humans: A serodiagnostic test.[The Gunderson Lyme Test] J Infect Dis 1993;167:158-164Cogswell FB, Bantar C, et al. Host DNA Can Interfere with the Detection of Borrelia burgdorferi in Skin Biopsy Specimens by PCR. J Clin Microbiol, April 1996;34(4):980-982Gunderson Lyme Test: The Most Frequently asked Questions. LaCosta Clinical Laboratory 5919 Farnsworth CT. Carlsbad, CA, 92008, 1-800-522-5070, Newsletter 1 volume 1 1993Petney TN, et al. Comparison of urinary bladder and ear biopsy samples for determining prevalence of Borrelia burgdorferi in rodents in central Europe. J Clin Microbiol, 1996;34(5):1310-1312 Pfister HW, Preac-Mursic V, Wilske B, et al. Latent Lyme Neuroborrelliosis: Presence of B. burgdorferi in the CSF without concurrent inflammatory signs. Neurology 1989;39:1118-1120Nadleman et al. Isolation of Borrelia burgdorferi from the blood of seven patients with Lyme disease. 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J Infect Dis, 1996;173:1027-30Feder HM Jr., et al. The persistence of serum antibodies to Borrelia burgdorferi in patients treated for Lyme disease. Clin Infect Dis 1992;15(5):788-93Fried Martin D, Durray P. Gastrointestinal Disease in Children with Persistent Lyme Disease: Spirochetes isolated from the G.I. tract despite antibiotic therapy. 1996 LDF Lyme Conference Boston, MA, Abstract*Fraser DD, Kong LI, & Miller FW. Molecular detection of persistent Borrelia burgdorferi in a man with dermatomyosistis. Clin and Exp Rheum 1992;10:387-390Georgilis K, Peacocke M, and Klempner MS. Fibroblasts protect the Lyme Disease spirochete, Borrelia burgdorferi from ceftriaxone in vitro. J. Infect Dis 1992;166:440-444Hassler D, Riedel K, Zorn J, and Preac-Mursic V. Pulsed high dosed cefotaxime therapy in refractory Lyme Borreliosis (Letter to Editor) Lancet 1991;338:193Haupl TH, Krause A, Bittig M. 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An autopsied report.Kobayashi K, Mizukoshi C, Aoki T, Muramori F, Hayashi M, Miyazu K, Koshino Y, Ohta M, Nakanishi I, Yamaguchi N.Department of Neuropsychiatry, Kanazawa University School of Medicine, Japan.AbstractA 36-year-old Japanese woman presented with progressive cerebellar signs and mental deterioration of subacute course after her return from the USA. Her serum antibody to spirochete Borrelia burgdorferi was significantly elevated. A necropsy 4 years after her initial neurological signs revealed multifocal inflammatory change in the cerebral cortex, thalamus, superior colliculus, dentate nucleus, inferior olivary nucleus and spinal cord.The lesions showed spongiform change, neuronal cell loss, astrocytosis and proliferation of activated microglial cells. The internal capsule was partially vacuolated and the spinal cord, notably at the thoracic level, was demyelinated and cavitated in the lateral funiculus. Microglial cells aggregated within and around the spongiform lesions and microglial nodules were present in the medulla oblongata. Use of Warthin-Starry stain demonstrated silver, impregnated organisms strongly suggesting B. burgdorferi in the central nervous tissues. The dentate nucleus and inferior olivary nucleus showed the most advanced lesions with profound fibrillary gliosis. Occlusive vascular change was relatively mild, and fibrous thickening of the leptomeninges with lymphocyte infiltrates was localized in the basal midbrain. The ataxic symptoms were due to the dentate and olivary nucleus lesions and mental deterioration was attributable to the cortical and thalamic lesions. Spongiform change, neuronal cell loss, and microglial activation are characteristic pathological features in the present case. The cerebellar ataxia and subsequent mental deterioration are unusual clinical features of Lyme neuroborreliosis. 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Neurology 1993;43:403-407Pregnancy and LymeTITLE:?Lyme borreliosis as a cause of facial palsy during pregnancy. ?AUTHORS:?Grandsaerd MG; Meulenbroeks AA?AUTHOR AFFILIATION:?Department of Otorhinolaryngology, Rijnstate hospital Wagnerlaan 55 6815 AD, Arnhem, The Netherlands?ABSTRACT:?The medical history of a pregnant woman in whom the initial pattern of complaints suggested hyperemesis gravidarum is described. After about 18 days the patient developed left facial palsy. Repeated tests eventually confirmed the diagnosis of neuroborreliosis. The problems concerning diagnostics, therapy and the possible complications of Lyme borreliosis during gestation are described. ?NLM PUBMED CIT. ID: 10817889 NLM CIT. ID: No Cit. ID Assigned?SOURCE:?Eur J Obstet Gynecol Reprod Biol 2000 Jul 1;91(1):99-101TITLE:?Maternal Lyme disease and congenital malformations: a cord blood serosurvey in endemic and control areas. ?AUTHORS:?Williams CL; Strobino B; Weinstein A; Spierling P; Medici F?AUTHOR AFFILIATION:?Child Health Center, American Health Foundation, Valhalla, New York 10595, USA.?ABSTRACT:?This report describes a cohort study of over 5000 infants and their mothers who participated in a cord blood serosurvey designed to examine the relationship between maternal exposure to Lyme disease and adverse pregnancy outcome. Based on serology and reported clinical history, mothers of infants in an endemic hospital cohort are 5 to 20 times more likely to have been exposed to B. burgdorferi as compared with mothers of infants in a control hospital cohort. The incidence of total congenital malformations was not significantly different in the endemic cohort compared with the control cohort, but the rate of cardiac malformations was significantly higher in the endemic cohort [odds ratio (OR) 2.40; 95% confidence interval (CI) 1.25, 4.59] and the frequencies of certain minor malformations (haemangiomas, polydactyly, and hydrocele), were significantly increased in the control group. Demographic variations could only account for differences in the frequency of polydactyly. Within the endemic cohort, there were no differences in the rate of major or minor malformations or mean birthweight by category of possible maternal exposure to Lyme disease or cord blood serology. The disparity between observations at the population and individual levels requires further investigation. The absence of association at the individual level in the endemic area could be because of the small number of women who were actually exposed either in terms of serology or clinical history. The reason for the findings at the population level is not known but could be because of artifact or population differences.?NLM PUBMED CIT. ID: 7479280 NLM CIT. ID: 96061203?SOURCE:?Paediatr Perinat Epidemiol 1995 Jul;9(3):320-30TITLE:?[Manifestation of Lyme arthritis in the puerperal period]?VERNACULAR TITLE:?Manifestation einer Lyme-Arthritis im Wochenbett?AUTHORS:?Bussen S; Steck T?AUTHOR AFFILIATION:?Universitatsfrauenklinik Wurzburg.?ABSTRACT:?Lyme disease, a tick-transmitted spirochetal illness caused by Borrelia burgdorferi, usually begins with a characteristic erythema chronicum migrans accompanied by flu-like symptoms. This phase may later be followed by meningitis, neuritis, carditis or arthritis.Congenital abnormalities due to maternal infection during pregnancy have been described. We report on a case of a 36-year old V gravida III para. After a normal pregnancy and a Cesarean section the patient developed postpartal an acute Lyme arthritis.?NLM PUBMED CIT. ID: 7975802 NLM CIT. ID: 95066274?SOURCE:?Z Geburtshilfe Perinatol 1994 Aug;198(4):150-2TITLE:?Congenital infections and the nervous system. ?AUTHORS:?Bale JF Jr; Murph JR?AUTHOR AFFILIATION:?Department of Pediatrics, University of Iowa College of Medicine, Iowa City, Iowa.?ABSTRACT:?Despite vaccines, new antimicrobials, and improved hygienic practices, congenital infections remain an important cause of death and long-term neurologic morbidity among infants world-wide. Important agents include Toxoplasma gondii, cytomegalovirus, Treponema pallidum, herpes simplex virus types 1 and 2, and rubella virus. In addition, several other agents, such as the varicella zoster virus, human parvovirus B19, and Borrelia burgdorferi, can potentially infect the fetus and cause adverse fetal outcomes. This article provides an overview of these infectious disorders and outlines current strategies for acute treatment and long-term management.?NLM PUBMED CIT. ID: 1321971 NLM CIT. ID: 92342460?SOURCE:?Pediatr Clin North Am 1992 Aug;39(4):669-90TITLE:?[Borrelia infections from a dermatological viewpoint] ?VERNACULAR TITLE:?Borrelieninfektion aus dermatologischer Sicht.?AUTHORS:?Vocks E; Engst R; Borelli S?AUTHOR AFFILIATION:?Dermatologische Klinik und Poliklinik Technischen Universitat Munchen. ABSTRACT:?Erythema migrans (EM), Borrelia lymphocytoma (BL) and acrodermatitis chronica atrophicans (ACA) are the established dermatological manifestations of borrelia infection, a complex multiorganic disease. Analogous to syphilis Borrelia infection can be classified by three stages, at which stage I (localized infection) and II (disseminated infection) are manifestations of early infection and stage III (persistent infection) a symptom of late infection. At all stages skin manifestations can be present, the above mentioned as stage-marker as well as other non-specific polymorphous skin lesions which sometimes appear at stage II. Because of its frequent (60-80%) occurrence in all borrelia infections EM has a pathognomonic importance for borrelia infection. In diagnosis serology is currently the only practical laboratory aid. False negative and false positive results must be considered. Treatment of choice is ceftriaxone, penicillin G (or amoxycillin) or tetracycline. Prophylactic antibiotic therapy for tick bites is not recommended. Congenital borrelia infections seem to be unusual, but it is likely that they can occur and cause different adverse fetal outcome or abortion. ?NLM PUBMED CIT. ID: 1922122 NLM CIT. ID: 92017931?SOURCE:?Monatsschr Kinderheilkd 1991 Jul;139(7):425-8TITLE:?Lyme disease during pregnancy. ?AUTHORS:?Schutzer SE; Janniger CK; Schwartz RA?AUTHOR AFFILIATION:?Department of Allergy and Immunology, New Jersey Medical School, Newark 07103-2714.?ABSTRACT?Lyme disease, caused by infection with Borrelia burgdorferi, can affect those exposed to a vector tick. Pregnant women are no exception, and such infection places the fetus at risk. It is particularly important to recognize the disease early so that effective therapy may be instituted. Although the present patient had a favorable outcome, not all do. Clinical diagnosis is especially important since conventional laboratory tests may be inadequate or require lengthy periods of time before a positive result occurs. The dermatologic sign of Lyme disease, erythema migrans, although occurring in only 50 percent of cases, is likely to be the most important diagnostic sign.?NLM PUBMED CIT. ID: 2070648 NLM CIT. ID: 91300895?SOURCE:?Cutis 1991 Apr;47(4):267-8TITLE:?Gestational Lyme borreliosis. Implications for the fetus. ?AUTHORS:?MacDonald AB?AUTHOR AFFILIATION:?Southampton Hospital, New York.?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. Further research is necessary to investigate possible teratogenic effects that might occur if the spirochete reaches the fetus during the period of organogenesis.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. It is my expectation that the spectrum of gestational Lyme borreliosis will expand into many of the clinical domains of prenatal syphilis. ?NLM PUBMED CIT. ID: 2685924 NLM CIT. ID: 90069113?SOURCE:?Rheum Dis Clin North Am 1989 Nov;15(4):657-77TITLE:?[Clinical aspects of Borrelia burgdorferi infections] ?VERNACULAR TITLE:?Klinische Aspekte der Borrelia-burgdorferi-Infektionen.?AUTHORS:?Neubert U?AUTHOR AFFILIATION:?Dermatologische Klinik der Ludwig-Maximilians-Universitat Munchen.?ABSTRACT:?Skin lesions due to Borrelia burgdorferi-like erythema migrans, lymphadenosis cutis benigna, and acrodermatitis chronica atrophicans - are hall-marks of a systemic infection, which tends to a chronically relapsing course. Even if the skin lesions are missing, or disappear spontaneously, the infection may persist and affect other organs. This presumption is supported by the outcome of a long-term follow-up study on seropositive forest workers. In association with meningopolyneuritis (Garin-Bujadoux-Bannwarth disease) and acrodermatitis chronica atrophicans - myositis and fasciitis have been recently reported as further possible manifestations of Borrelia burgdorferi infection. Borrelial infection during pregnancy should promptly be treated with antibiotics in high dosages, in order to prevent maternal-fetal transmission of borrelial organisms resulting in stillbirth or congenital defects of the newborn. ?NLM PUBMED CIT. ID: 2678790 NLM CIT. ID: 90021654?SOURCE:?Z Hautkr 1989 Aug 15;64(8):649-52, 655-6TITLE:?Infants born to mothers with antibodies against Borrelia burgdorferi at delivery. ?AUTHORS:?Nadal D; Hunziker UA; Bucher HU; Hitzig WH; Duc G?AUTHOR AFFILIATION:?Abteilungen fur Infektionskrankheiten und Immunologie der Universitat, Zurich, Switzerland.?ABSTRACT:?A serological survey over a 1-year period of 1416 mothers at delivery and their 1434 offspring for the presence of anti-Borrelia burgdorferi antibodies revealed a prevalence of 0.85%. Clinically active Lyme disease during pregnancy was found in 1 of these 12 women with elevated titres and the child was born with a ventricular septal defect.Of six affected children, two had hyperbilirubinaemia, one muscular hypotonia, one was underweight for gestational age, one was macrocephalic, and one had supraventricular extrasystoles. Anomalous findings could not be attributed to B. burgdorferi due to a lack of serological evidence of intrauterine infection. Our data do not imply the need for serological screening in pregnancy, however, the importance of recognition and treatment of Lyme disease in pregnancy is emphasized. ?NLM PUBMED CIT. ID: 2920747 NLM CIT. ID: 89153177?SOURCE:?Eur J Pediatr 1989 Feb;148(5):426-7TITLE:?Lyme Borrelia positive serology associated with spontaneous abortion in an endemic Italian area. ?AUTHORS:?Carlomagno G; Luksa V; Candussi G; Rizzi GM; Trevisan G?AUTHOR AFFILIATION:?Dept. of Obstetrics and Gynecology, University of Trieste School of Medicine.?ABSTRACT:?Lyme borreliosis acquired during pregnancy may be associated with stillbirth and fetal malformations. This paper reports preliminary results of a study intended to evaluate the frequency of Borrelia burgdorferi infection associated with spontaneous abortion in an endemic Italian area. ?NLM PUBMED CIT. ID: 3252658 NLM CIT. ID: 89300130?SOURCE:?Acta Eur Fertil 1988 Sep-Oct;19(5):279-81TITLE:?[Multiple neurologic manifestations of Borrelia burgdorferi infection] ?VERNACULAR TITLE:?Les multiples manifestations neurologiques des infections a Borrelia burgdorferi.?AUTHORS:?Dupuis MJ?AUTHOR AFFILIATION:?Clinique St-Pierre, Ottignies, Belgique.?ABSTRACT:?The neurological spectrum of Borrelia burgdorferi infections is still enlarging. We review epidemiological, pathological and serological data of Lyme disease. The course of the disease is divided in three stages: stage 1 during the first month is characterised by erythema chronicum migrans and associated manifestations; stage 2 includes not only the classical European meningoradiculitis but also less specific neurological symptoms:isolated lymphocytic meningitis with an acute or even relapsing course, apparently idiopathic facial palsy, neuritis of other cranial nerves, polyneuritis cranialis, Argyll-Robertson sign, peripheral nerve involvement, acute transverse myelitis, severe encephalitis, myositis. During stage 3, three to five months or longer after the onset of the disease, chronic arthritis, acrodermatitis chronica atrophicans and various neurological symptoms can be observed:chronic neuropathy with mainly sensory or motor signs, recurrent strokes due to cerebral angiopathy and progressive encephalomyelitis; this third stage the central nervous system involvement is characterised by slowly progressive or fluctuating course during months or years, ataxic or spastic gait disorder, bladder disturbances, cranial nerve dysfunction including optic atrophy and hypoacusia, dysarthria, focal and diffuse encephalopathy. This chronic central nervous system disease can mimic multiple sclerosis, anorexia nervosa, psychic disorders or subacute presenile dementia. It is often associated with pleiocytosis, abnormal EEG and evoked potentials, sometimes multifocal and mainly periventricular white matter lesions visualised by CT or MRI, and as a rule high antibody titers against Borrelia burgdorferi. High doses of penicillin can halt the disease, sometimes induce spectacular regression of symptoms or sometimes be inefficient; ceftriaxone could be a more powerful therapy. Similarities between syphilis and Borreliosis are multiple: both of these spirochetes contain plasmids, can be transmitted through the placenta and progress for many years through successive stages, with multiorgan symptoms, including parenchymatous and vascular lesions of the central nervous system. Borrelia burgdorferi is the new great imitator.?NLM PUBMED CIT. ID: 3070690 NLM CIT. ID: 89186273?SOURCE:?Rev Neurol (Paris) 1988;144(12):765-75TITLE:?Lyme disease during pregnancy. ?AUTHORS:?Markowitz LE; Steere AC; Benach JL; Slade JD; Broome CV?ABSTRACT:?Lyme disease is an increasingly recognized tick-borne illness caused by a spirochete, Borrelia burgdorferi. Because the etiologic agent of Lyme disease is a spirochete, there has been concern about the effect of maternal Lyme disease on pregnancy outcome. We reviewed cases of Lyme disease in pregnant women who were identified before knowledge of the pregnancy outcomes. Nineteen cases were identified with onset between 1976 and 1984. Eight of the women were affected during the first trimester, seven during the second trimester, and two during the third trimester; in two, the trimester of onset was unknown. Thirteen received appropriate antibiotic therapy for Lyme disease.Of the 19 pregnancies, five had adverse outcomes, including syndactyly, cortical blindness, intrauterine fetal death, prematurity, and rash in the newborn. Adverse outcomes occurred in cases with infection during each of the trimesters. Although B burgdorferi could not be implicated directly in any of the adverse outcomes, the frequency of such outcomes warrants further surveillance and studies of pregnant women with Lyme disease.?NLM PUBMED CIT. ID: 2423719 NLM CIT. ID: 86227939?SOURCE:?JAMA 1986 Jun 27;255(24):3394-6Additional References pertaining to Multiple Sclerosis and Neurological invasion by Borrelia1. MRI Reveals Pathology in Neuro Lyme Disease. "Diagnostic Imaging-MRI Insights".2. "Biopsy-confirmed CNS Lyme Disease: MR Appearance at l.5T" American Journal of Neuroradiology-11:482-484.3. Allen Steere, MD. et al. "The Long Term Course of Lyme Arthritis in Children" The New England Journal of Medicine. Vo. 325No. 4, Jly 18, 1991.4. Stephen L. Schechter, MD. "Lyme Disease Associated with Optic Neuropathy" The American Journal of Medicine. July 1986. v. 81, 143-1455. H. Kohler, Dept. Clinical Neurology and Neurophysiology, University of Freiburg, West Germany. "Letter to the Editor". Borrelia encephalomyelitis." The Lancet. July 5, 1986, p35.6. "Kyke Award: GD-DTPA-Enhanced MR Imaging of Experimental Bacterial Meningitis: Evaluation and Comparison with CT. American Journal of Neuroradiology. 9:1045-1050; Nov./Dec. 1988.7. Derek Gay et al. "Multiple Sclerosis Associated with Sinusitis: Case-controlled study in General Practive. [Ed. note: Recent research in showing 99% Lyme patients have active sinusitis as presenting symptoms which often go undetected {unpublished results from personal research on symptomatology}]. The Lancet. Saturday 12 April 1986. 815-819.8. Eric L. Logigian, MD; Allen Steere, MS et al. "Chronic Neurologic Manifestations of Lyme Disease. "The New England Journal of Medicine" 323:21;1438-1444, 1990.9. Derek Gay , "Hypothesis" Is Mutiple Sclerosis caused by an Oral Spirochete? The Lancet. July 12. 1986. pp. 75-77.10. Fernandez et al. "Lyme Disease of the CNS: MR Imaging: Findings in 14 cases. American Journal of Neuroradiology. 11; May/Jyne, 1990.11. John Halpersin, MD et al. "Immunologic Reactivity Against Borrelia burgdorferi In Patients with Motor Neuron Disease." Archives of Neurology 47:586-594. May 1990.12. Will Kohlhepp. et al. "Extrapyramidal Features in Central Lyme Borreliosis." European Neurology. 29:150-155, 1989.13. Joh J. Halpersin, MD "Lyme Neuroborreliosis." Laborabory Medicine. 21:5; May 1990.14. Louis Reik, Jr., MD et al. "Demyelinating Encephalopathy in Lyme Disease. Neurology. 46:790-795, July, 1989.16. Presentation to Rocky Mountain Lab by Kenneth Liegner, MD from Armonk, New York, re: growing evidence for link between Lyme and MS. Missoulian Newspaper. Wed August 15, 1990. Gred Lakes. Hamilton, Montana, Rocky Mountain Lab; NIH facility where Dr. Willy Burgdorfer discovered the spirochetal etiology of Lyme disease.17. R. Ackerman, E. Gollmer and B. Rehse-Kupper. "Progressive Borrelial Encephalomyelitis": The Chronic Neurologic Manifestations of Erythema Chronicum Migrans (ECM) Disease." Lyme Times Newsletter. April, 1993, p. 48 Phyllis Mervine, Editor. Reprint of German publication called Deutsche Medizinische Wochenschrift 110. 1995. Translated by Ron Ferris, Calgary, Alberta, Canada. Reprinted with persmission. English title, "Untreated neuroborreliosis progresses over years to cause serious MS-like encephalomyelitis."18. J.H.J. Wokke, MD:,.van Gign, MD; A. Elderson, MD; and G. Stanek, MD. "Chronic Forms of Borrelia burgdorferi infection of the nervous system," Neurology 37:1031-1034: 1987.19. Michael B. chancellor, MD; David E. McGinnis. Patrick J. Shenot, MS et al. Dept. Urology, Jefferson Medical College. Thomas Jefferson University, PA 19107. "lette" The Lancet. Vol 339: May 16, 1992 p.1237-1238.20. Keffreu A. Nelson, MD; Mitchel, D. Wolf, MD; William T.c. Yuh, MD et al. "Cranial nerve involvement with Lyme borreliosis demonstrated by magnetic resonance imaging". Neurology. 42:671-673. March 1992.21. P.K. Coyle,MD; Z.Deng, MS; S.E. Schutzer, MD; A.L. Gelman,MD et al. "Detection of Borrelia buergdoferi antigens in cerebrospinal fluid." Neurology. 43:1093-1097, 1993.22. Saul Rosen, PhD, MD, Section Editor. "Current Perspectives on Lyme Borreliosis". Journal American medical Association. 276;10, March 11, 1992. "Gran Rounds at the Clinical Center of the National Institute of Health.".23 Ackerman, R, MD; Rehse-Kupper, B. MD, "Chronic Neurologic manifestations of erythema chronicum migrans borreliosis". Annals NY Academy of Science. 539-16-23.24. Matuschka, Fr. and Spielman, A. The emergence of Lyme disease in a changing encironment in North American and Central Europe". Experimental and Applied Acarology. 2: 1986; 1337-1353.25. JJ Halpersin, MD; Raymond Dattwyler, MD et al. "Lyme Disease: Cause of a Treatable Peripheral Neuropathy." Neurology. 37; No 11; 1700-06; 1987.26. Belman, A.L.; Coyle, Patricia K.; Nachman, S. and Roche, C. "Brain MRI abnormalities in children infected by Borrelia burgdorferi." Neurology. 41 (Suppl 1) Item 73 P: March 1991.27. Vincent Marshal, DVM, "Multiple Sclerosis is a chronic central nervous system infection by a spirochetal agent." Medical Hypothesis. 25:89-92, 1988.28 A. Kirk E. winward, MD; J. Lawton Smith, MD et al. "Ocular Lyme Borreliosis."[Ed. note: eye diseases found in MS patients called "pars planitis" and uveitis, scotomas, disk edema, optic neuritis and neuropathy, blurred vision etc. are implicated in this article as Lyme disease eye phenomenon as well]. "A similar association with pars planitis has been reported in multiple sclerosis [18] because a demyelinating syndrome nearly indistinguishable from multiple sclerosis may also occur in Lyme disease, it is possible that Lyme borreliosis, pars planitis, and demyelinating disease may, in some cases, share a common pathogenic mechanism." p. 656. American Journal of Ophthalmology 108:651-657, 1989.30. A. Berger, B.C., and Leopold, I.H. "The incidence of uveitis in mutiple sclerosis." American Journal of Ophthalmology. 62-540., 1966.31.DuPuis, MJ , Multiple neurologic manifestations of Borrelia burgdorferi infection , Reviews in Neurology (Paris), 1988;144(12):765-775. [Article in French, English abstract available on Medline] ?Exerpt: The central nervous system involvement is characterised by slowly progressive or fluctuating course during month or years,ataxic or spastic gait disorder,bladder disturbances,cranial nerve sydrunction includingoptic atrophy andhypoacusia,dysarthria,focal and diffuse encephalopathy.This chronic central nervous system disease can mimic multiple sclerosis psychic disorders or subacute presentile dementia. It is often associated withpelocytosis,abnormal EEG andevoked potentials,sometimes multifocal and mainly periventricular white matter lesions visualized by CT or MRI......Similarities between syphilis and Borreliosis are multiple: both of these spirochetes contain plasmids, can be transmitted through the placenta and progress for many years through successive stages, with multiorgan symptoms, including parencymetous and vascular lesions of the central nervous system. Borrelia burgdorferi is the new great imitator...and can causeacute transverse myelitis,severe encephalitis,myositis,chronic neuropathy,recurrent strokes,meningoradiculitis,lyphocytic meningitis with an acute or even relapsing course,apparently idiopathic facial palsy,neuritis of other cranial nerves,polyneuritis cranialis,Argyll-Robertson sign, and so on.32. Baig S., Osson T, Hojeberg G, Link H., Dept. of Neurology, Karolinska Institute, Hugginge Unversity Hospital, Stockholm, Sweden, Cells secreting antibodies to myelin basic protein in cerebrospinal fluid of patients with Lyme neuroborreliosis. Neurology 1991; April, 41(4):581-587.33. Lyme borreliosis neuropathy. A Case report Am J. Phys. Medicine and Rehabilitation, 1996 Jul;75(4):314-316.34. Coyle, PK, Dept. of Neurology, School of Medicine, State University of New York, Stony Brook, Neurologic complications of Lyme disease. Rheumatologic Discussion Clinical North American, 1993, Nov;19(4)993-1009._____________________, Nervenarzt. 1990 Apr;61(4):248-9. German.Further Reading on Neuroborreliosis/MSLawrence C, Lipton RB, Lowy FD, Coyle PK, Seronegative chronicrelapsing neuroborreliosis. Eur Neurol 995;35(2):113-7.Garcia-Monco JC, Seidman RJ, Benach JL,? Experimental immunization with Borrelia burgdorferi induces development of antibodies to gangliosides.Infect Immun 1995 Oct;63(10):4130-7 (Full text)Mattman L, Spirochaeta Myelophthora in Multiple Sclerosis, in: Cell Wall Deficient Forms: Stealth Pathogens, 2nd Edition, CRC Press, Boca Raton, Boston, London, New York, Washington D.C., 1993Antimyelin antibodies in Lyme?Epidemiol Mikrobiol Imunol 2002 Apr;51(2):60-5 ????? [Article in Czech] ??Ryskova O, Vyslouzil L, Honegr K, Lesna J, Horacek J, Skrabkova Z.Ustav klinicke mikrobiologie, UK Praha, LF Hradec Kralove. ryskovao@lfhk.cuni.cz The method of enzyme immunoassay (ELISA) was used for detection of antibodies against the basic protein myelin (antimyelin antibodies) for a group of serum samples (n 36) with positive anti-borrelia immunoglobulins IgG and IgM (ELISA-Borrelia afzelii) and their immune complexes (ELISA-PEG).Antimyelin antibodies (ELISA-Doxa Kit-Myelin Basic Protein Antibodies) were assessed in 31% (n 11) of examined serum samples of patients with the working diagnosis of Lyme borreliosis.Statistical analysis (p 0.07) confirmed a more frequent incidence of antimyelin antibodies in younger female subjects (age 31 years) as compared with a group of sera (n 25) where the authors did not record the formation of immunoglobulins against the basic myelin protein (age 51 years).Neither the value of titres nor the frequency of detected anti-borrelia IgG and IgM and immune complexes differed significantly in the two groups. From the assembled results ensues that in the course of Lyme borreliosis, in chronic affection of organs an autoimmune reaction may develop where the basic myelin protein is damaged (demyelinizatio) and subsequently antimyelin antibodies are formed.PMID: 11987581 [PubMed - in process]The study that allowed insurance companies to substitute doxycycline for IV Rocephin. But choosing Lyme patients with no symptoms other than a rash, and then a follow up of patients for only two weeks hardly is good science. But on August 1, 1997, over two dozen Minnesota patients were cut off from IV meds despite a patient protection bill. Ceftriaxone Compared with Doxycycline for the Treatment of Acute Disseminated Lyme DiseaseRaymond J. Dattwyler, M.D., Benjamin J. Luft, M.D., Mark J. Kunkel, M.D., Michael F. Finkel, M.D., Gary P. Wormser, M.D., Thomas J. Rush, M.D., Edgar Grunwaldt, M.D., William A. Agger, M.D., Michael Franklin, M.D., Donald Oswald, Louise Cockey, and Dionigi Maladorno, M.D.N Engl J Med 1997; 337:289-295, July 31, 1997AbstractArticleReferencesCiting Articles (24)BACKGROUNDLocalized Lyme disease, manifested by erythema migrans, is usually treated with oral doxycycline or amoxicillin. Whether acute disseminated Borrelia burgdorferi infection should be treated differently from localized infection is unknown.Full Text of Background...METHODSWe conducted a prospective, open-label, randomized, multicenter study comparing parenteral ceftriaxone (2 g once daily for 14 days) with oral doxycycline (100 mg twice daily for 21 days) in patients with acute disseminated B. burgdorferi infection but without meningitis. The erythema migrans skin lesion was required for study entry, and disseminated disease had to be indicated by either multiple erythema migrans lesions or objective evidence of organ involvement.Full Text of Methods...RESULTSOf 140 patients enrolled, 133 had multiple erythema migrans lesions. Both treatments were highly effective. Rates of clinical cure at the last evaluation were similar among the patients treated with ceftriaxone (85 percent) and those treated with doxycycline (88 percent); treatment was considered to have failed in only one patient in each group. Among patients whose infections were cured, 18 of 67 patients in the ceftriaxone group (27 percent) reported one or more residual symptoms at the last follow-up visit, as did 10 of 71 patients in the doxycycline group (14 percent, P > 0.05). Mild arthralgia was the most common persistent symptom. Both regimens were well tolerated; only four patients (6 percent) in each group withdrew because of adverse events. Full Text of Results...CONCLUSIONSIn patients with acute disseminated Lyme disease but without meningitis, oral doxycycline and parenterally administered ceftriaxone were equally effective in preventing the late manifestations of disease.Full Text of Discussion...Read the Full Article...SOURCE INFORMATIONFrom the Department of Medicine, State University of New York, Stony Brook (R.J.D., B.J.L.); the Department of Infectious Diseases, Danbury Hospital, Danbury, Conn. (M.J.K.); the Middelfort Clinic, Eau Claire, Wis. (M.F.F.); New York Medical College, Valhalla (G.P.W.); Briarcliff Manor, N.Y. (T.J.R.);Greensport, N.Y. (E.G.); La Crosse, Wis. (W.A.A.); Willow Grove, Pa. (M.F.); and Hoffmann–La Roche, Nutley, N.J. (D.O., L.C., D.M.).Lecture DVD Available; details on next page.Lecture DVD AvailableA live lecture DVD is available from MIBDEC of Tom Grier giving the first of several lectures called “Lyme On The Brain”. It was recorded live in Superior, Wisconsin on September 14, 2009, and sponsored by the Wisconsin Public Health Nurses. Lyme On The Brain DVD 2 hours long with Questions and Answers and has special features including a preview of the Minnesota Lyme Patient Documentary and the presentation slides without narration. $ 19.95 + $ 2.99 P&S = $ 22.94 total Send to:MIBDEC 902 Grandview Ave Duluth MN 55812Checks payable to MIBDEC for tax deductible contribution. Bulk quantities, please e-mail tomgrier@ ................
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