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Lyme on The Brain - Lecture Note - References
Reference Categories:
August 30, 2010
General Lyme Disease …………………. 2
Lyme Tests ……………………………………. 9
Lyme Arthritis/Myalgia/Lupus ……… 19
Dermatological Lyme, EM, ACA …… 23
Ophthalmic Lyme …………………………. 26
Persistent Infection ………………………. 27
Cardiovascular ………………………………. 32
Antibiotic Therapy ………………………… 34
Alternative Therapies …………………… 41
Neurological Lyme ………………………… 44
Borrelia burgdorferi-seropositive
Chronic encephalomyelopathy:
Lyme neuroborreliosis? An
Autopsied report…..………………………..54
Epidemiology and Prevention……….. 56
Microbiology …………………………………..67
Veterinary Lyme …………………………….76
Other Tick-Borne Illnesses …………… 78
Books……………………………………………… 79
Coping With Chronic Illness…………...80
Non-Lyme References ………………….. 82
Pregnancy and Lyme ……………………. 88
Multiple Sclerosis & Neurological
invasion by Borrelia. ……………………. 100
Further Reading on neuroborreliosis/MS..105
Antimyelin antibodies in Lyme………105
Ceftriaxone Compared with Doxycycline for the
Treatment of Acute Disseminated Lyme Disease 106
1
General Lyme Disease Topics
Abstracts 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;21:454-61
Baltimore RS, Shapiro ED. Lyme Disease. Pediatrics in Review. May
1994;15(5):167-174
Bleiweiss John D. M.D. When to suspect Lyme disease. Lecture handout
LDF Conference 1993
Bryerson AD. Clinical pathology of the Jarisch-Herxheimer reaction.
J of Infect Dis 1976;133:696-705
Burgdorfer 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:
1317-1319
Burgdorfer W. Discovery of the Lyme disease spirochete: A historical
review. Inter J Microbiol Hyg, Series A, 1986;7-9
Burrascano 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 1995
2
Cimmino 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):95-97
Clark 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;173:1260-1262
Dattwyler RJ. Lyme borreliosis: An Overview of the Clinical
Manifestations. Laboratory Medicine 1990;21:290-292
Dattwyler RJ, Luft BJ. Immunodiagnosis of Lyme Borreliosis. Rheumatic
Disease Clinics of North America, November 1989;15(4):727-734
Dinerman H, Steere AC. Lyme Disease associated with fibromyalgia.
Ann Intern Med 1992;117:281-285
Duffy J, Schoen RT, Sigal LH,. 1991 Update on Lyme Disease. Patient
Care. 1991;June 15):24-51
Eppes SC, Klein JD, Caputo GM, Rose CD. Physician beliefs, attitudes,
and approaches toward Lyme disease in an endemic area. Clinical
Pediatrics, March 1994:130-134
Fallon 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):95-117
Feder HM, Gerber MA, Krause PJ, Ryan R. Early Lyme Disease: A FluLike Illness Without Erythema Migrans. Pediatrics, February
1993;91(2):456-459
Feder HM, Hunt MS. Pitfalls in the Diagnosis and Treatment of Lyme
Disease. JAMA 1995;274(1):66-68
Felsenfeld 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 # 72-127355
Friedland JG, Warrell DA. The Jarisch-Herxheimer reaction in
Leptospirosis: a possible pathogenesis and review. REV Infect Dis. 1991;
13:207-210
3
Gerber MA, Shapiro ED. Diagnosis of Lyme disease in children.
J Pediatrics 1992;121(1):157-62
Goellner MH, Agger WA, Burgess JH, Durray PH. Hepatitis due to
recurrent Lyme Disease. Ann Intern Med 1988;108:707-708
Golightly MG. Laboratory considerations in the diagnosis and
management of Lyme Borreliosis. [Review Article with 51 references]
Amer J Clin Pathol 1993;99(2):168-74
Hahlberg P, Granlund H, Nyman D. Panelius J, and Sappälä I. Treatment
of Late Lyme Borreliosis. Infection 1994;29:255-261
Hamilton DR. Lyme disease the hidden pandemic. Post Graduate
Medicine 1989;85:303-314
Herxheimer 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):169-78
Kindree Diane. How to diagnose and treat Lyme disease in children
[Letter and Commentary] Canada Med Assoc J. January 15,
1993;148(2):132
Huppertz H-I. Childhood Lyme Borreliosis. Neurology 1988;38:863-867
Johnson RC, Schmid GP, Hyde AG, Steigerwalt AG, Brenner DJ. Borrelia
burgdorferi species the etiologic agent of Lyme Disease. Int J Sys
Bacteriology 34:496;97
Kantor FS. Disarming Lyme Disease. Scientific American. September
1994:34-39
Kaslow RA. Current Perspectives on Lyme Borreliosis.
JAMA, March 11, 1992;267(10):1364-1367 and 1381-1383
Kirsch M, Ruben FL, Steere AC, Durray PH et al. Fatal Adult respiratory
Distress Syndrome in a patient with Lyme disease. JAMA
1988;259:2737-2739
4
Leff Robert D, Akre Steven P. Late Stage Lyme Borreliosis in Children.
Southern Med Journal 1989;82(8):954-956
Lissman BA, et al. Spirochete-associated Lyme Arthritis in a Dog.
Amer Vet Assc 1984;185:219-20
J
MacDonald, Alan B. Gestational Lyme Borreliosis. Rheum Dis Clin North
America 1989;15(4(:657-672
MacDonald, 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):657-677
MacDonald AB, Benach JL, Burgdorfer W. Stillbirth Following Maternal
Lyme Disease. New York State Journal of Med 1987
MacDonald AB, Berger BW, Schwan TG. Clinical implications of delayed
growth of the Lyme disease spirochete, Borrelia burgdorferi. Acta
Tropica 1991;48:89-94
Massarotti EM, Luger SW, Rahn DW et al. Treatment of Early Lyme
Disease. American J Med 1992;92:396-403
Masters EJ, Donnell D, Fobbs M. Missouri Lyme disease: 1989-1992.
J Spiro and Tick-borne Dis 1994;1(1):12-17
Michigan 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):57-64
Moulton Chris. Lyme Disease: New facts only add to diagnostic
frustrations. Adv for Med Lab Professionals July 29, 1991:18-19
Mulberg AK, Linz C, et al. Identification of nonsteroidal drug induced
gastrodoudenal injury in children with juvenile rheumatoid arthritis.
Journal of Pediatrics 1993;122:647-649
Nadleman RB et al. The clinical spectrum of early Lyme borreliosis in
patients with culture-confirmed erythema migrans. Amer J Med, May
1996;100:502-508
NIH State of the Art Conference. Diagnosis and Treatment of Lyme
Disease. Cin Courier August, 1991;9:1-8
5
NIH Gears up to test a hotly disputed theory. Science, October
1995;270(13):228-229
Nields JA, Kveton JF. Tullio Phenomena and Seronegative Lyme Disease.
Lancet. 1991;338:128-129
Norcross Karen. Injustice Based on Misunderstanding. September 6,
1994 Masters Thesis Treatment
Ostrov BE, Athreya DJ. Lyme Disease-difficulties in diagnosis and
management. Pediatric Clinics of North America, June 1991;38(3):
535-553
Pfister HW, Einhapl K, Preac-Mursi V, Wilske B, Schierz G. The
spirochetal etiology of lymphocytic meningoradiculitis of Bannwarth’s
Syndrome. J Neurol 1984;231:141-144
Pfister HW, Wilske B, Weber K. Lyme Borreliosis: Basic science and
clinical aspects. Lancet, April 23, 1994;343(8904):1013-1016
Pfluger 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 1992
Pietrucha, 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, 07753
Pietrucha, D. IV Treatment and follow-up for children with neurologic
Lyme disease. Lyme Times-Lyme Disease Resource Center 1991;
2(2):30-31
Plotkin SA, Georges P. Treatment of Lyme Borreliosis in children.
Pediatrics July 1991; 88:176-79
Putkonen T, Salo OP, Mustakaillio KK. Febrile Jarisch-Herxheimer
reaction in different phases of primary and secondary syphilis. British
Journal of Venereal Diseases 1966; 42:181-184
Rahn DW. Lyme Disease: Clinical manifestations, diagnosis, and
treatment. Sem Arthritis and Rheum 1991;20(4):201-218
6
Rahn DW, Malawista SE. Lyme disease: Recommendations for diagnosis
and treatment. Annals of Internal Med 1991;114:472-482
Rahn DW. Lyme Disease: Where’s the bug? [Letter} New Engl J Med,
1994;330(4):282-3
Scrimenti RJ et al. Lyme disease redux: The legacy of Sven Hellerstrom.
Wis Med J January 1993;92(1):20-21
Scott JD. How to diagnose Lyme disease in children. [Letter] Canada
Med Assoc J, January 15, 1993;148(2)132
Shadick 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;121:560-567
Shrestha M, Grodzicki RL, Steere AC. Diagnosing Early Lyme Disease.
American J Med 1985;78:235-240
Sigal 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 08903-0019
Sigal LH. Lyme disease: don’t let disguises fool you. Intern Med, June
1992;13:24-33
Sigal LH. Lyme disease: Immunologic manifestations and possible
immunologic mechanisms. Seminars in Arthritis and Rheum
1989;18:151-67
Sigal LH, Lyme disease in New Jersey: A practical guide for clinicians.
Princeton NJ: Academy of Med New Jersey 1993
Sigal 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;1993
Sigal LH. Summary of the first 100 patients seen at a Lyme disease
referral center. American J Med 1990;88:577-581
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Sigal LH, Schutzer S. Possible autoimmune mechanisms in Lyme
disease. Molecular and Immunologic approaches to Lyme disease. Cold
Spring Harbor Press, Plainview, NY
Sigal Leonard H. MD. The Lyme Disease Ccontroversy. Arch Internal
Med, July 26,1996;156:1493-1500
Steere AC. Seronegative Lyme Disease JAMA 1993;270(11):1369
Steere AC, Levin RE, Molloy PJ et al. Treatment of Lyme Arthritis.
Arthritis and Rheum 1994;37(6):878-888
Steere AC, Bartenhagen NH, Craft JE et al. The Early Clinical
Manifestations of Lyme Disease. Ann Intern Med 1983;99:76-82
Steere AC, Grodzicki RL, Kornblatt AN et al. The spirochetal etiology of
Lyme disease. New Eng J Med 1983;308:733-744
Steere AC. Distinguishing Lyme Disease from Its Look-A likes.
Emergency Medicine, August 1992;15:28-44
Steere AC, Malawista AC. Cases of Lyme Disease in the United States:
locations correlated to the distribution of Ixodes dammini. Ann Internal
Med 1979;91:730-733
Steere 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):1812-1816
Sullivan, 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 1989
Ziska MH, Donta ST, Demarest FC. Physician Preferences in the
Diagnosis and Treatment of Lyme Disease in the United States.
Infection, 1996;24(2):182-186
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Lyme/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 3:537-543
Bakken LL, Case KL, Callister SM et al. Performance of 45 Laboratories
participating in a proficiency testing program for Lyme disease serology.
JAMA 1992;268:891-895
Barbour AG. Laboratory Aspects of Lyme borreliosis. Clin Microbiol Rev
1988;1:399-414
Cameron DJ. False Positive. [Letter/Commentary on Arch Internal Med
1991;151(9):1837-40] Arch Internal Med 1992;152(6):1331
Coyle 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;28:6:739-744
Coyle PK, Deng Z, Schutzer SE, Belman AL, Benach J, Krupp LB, Luft B.
Detection of Borrelia burgdorferi antigens in the cerebrospinal fluid.
Neurology 1993;43:1093-1097
Craft JE, Grodzicki RL, Steere AC. Antibody response in Lyme Disease:
an evaluation of diagnostic tests. J Infect Dis 1988 158:754-60
Craft JE, Fisher DK, et al. Antigens of Borrelia burgdorferi recognized
during Lyme disease, Appearance of a new immunoglobulin M response
9
and expansion of the IgG response late in the illness. J Clin Invest
1986;78:934-939
Dattwyler RJ, Volkman DJ et al. Seronegative Lyme Disease. New Eng J
of Med 1988;319:1441-1446
Fawcett 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):705-708
Fawcett 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):3213-3221
Golightly MG. Laboratory considerations in the diagnosis and
management of Lyme Borreliosis. [Review Article with 51 references]
Amer J Clin Pathol 1993;99(2):168-74
Hansen K, Hinderson P, Pederson NS. Measurement of antibodies to
Borrelia burgdorferi flagellum improves serodiagnosis in Lyme disease. J
Clin Microbiol 1988;26:338-346
Karch 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):2312-2314
Hansen, Klaus. Serodiagnosis of erythema Migrans and Acrodermatitis
Chronica Atrophicans by Borrelia burgdorferi flagellum ELISA. J Clin
Microbiol, March 1989;27(3):545-551
Harris, 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)
10
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 1992
Hedberg CW, Osterholm MT, MacDonald KL, White KE. An interlaboratory study of antibody to Borrelia burgdorferi. J Infect Dis
1987;155:1325-27
Johnson 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;174:346-53
Kaiser R, Lucking CH. Intrathecal Synthesis of Specific Antibodies in
Neuroborreliosis. J Neurological Sciences, 1993;118:64-72
Lane RS, Lennette ET, Madigan JE. Interlaboratory and Intralaboratory
Comparisons of Indirect Immunofluorescence Assays for Serodiagnosis
of Lyme Disease. J Clin Microbiol 1990;28(8):1774-1779
Magnarelli LA. Quality of Lyme disease tests. JAMA 1989;262:
3464-3465
Magnarelli 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)818-825
Magnarelli 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):1154-1158
Magnarelli LA. Serologic Diagnosis of Lyme Disease. Annals New York
Academy of Sciences, 1988;539:154-161
Magnarelli LA, Anderson JF, Johnson RC. Cross Reactivity in Serological
Tests for Lyme Disease and other Spirochetal Infections. J Infectious
Diseases, July 1987;156(1):133-138
Magnarelli LA, Meegan JM, Anderson JF, Chappell JF et al. Comparison of
indirect fluorescent antibody test with an ELISA for serological studies of
Lyme disease. *
11
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):1958-1962
Russell H, Sampson JS, Schmid GP, Wilkonson HW, Plikaytis B.
Enzyme-linked immunosorbent assay for Lyme disease. J Infect Dis
1984;149:465-470
Schwartz BS, Goldstein MD, Rebeiro JMC, Schulze TL. Antibody testing in
Lyme disease: A comparison of results in four different laboratories.
JAMA. 1989;262:3431-3434
Sczepanski 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;171:1368-1370
Weiss 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:
1057-1064
Williams 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;3:345-353
Zoschke DC. Is it Lyme disease? How to interpret results of laboratory
testing. Postgrad Med, 1992;91(7):46-55
12
(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):934-939
Dattwyler RJ, Luft BJ. Immunodiagnosis of Lyme Borreliosis. Rheumatic
Disease Clinics of North America, November 1989;15(4):727-734
Dressler F, Whalen JA, Reinhardt BN. Western Blotting in the
Serodiagnosis of Lyme Disease. J Infect Dis. February 1993;167:
392-400
Dressler F. Lyme Borreliosis in European Children and Adolescents.
Clinical and Experimental Rheumatology. September-October
1994;12(supplement 10):S49-S54
Engstrom 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 3:774-776
Jain 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):2033-35
Karlsson M. Western Immunoblot and Flagellum Enzyme-Linked
Immunosorbent Assay for Serodiagnosis of Lyme Borreliosis. J Clin
Micro, Sept 1990;28(9):2148-2150
Ma 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):370-376
Norman 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):1732-1738
13
Simpson, 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):1329-1331
Technical 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 # 1254
Western 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
New NIH Criteria
Old W. Blot Criteria
100 % positive
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.•
14
(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):378-383
Coyle 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):1093-8
Dattwyler 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;319:1441-1446
Dressler F, Yoshinari NH, Steere AC. The T-cell proliferation assay in the
diagnosis of Lyme disease. Ann Intern Med. 1991;115:533-539
Dorward 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):11621170
Dressler F, Yoshinari NH, Steere AC. The T-cell proliferation assay in the
diagnosis of Lyme disease. Ann Intern Med. 1991;115:533-539
Klempner 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):1011-1017
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questions answered. 1-617-860-0705,
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Abstract
A 36-year-old Japanese woman presented with progressive cerebellar
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Her serum antibody to spirochete Borrelia burgdorferi was significantly
54
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
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The internal capsule was partially vacuolated and the spinal cord,
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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
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The dentate nucleus and inferior olivary nucleus showed the most
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Occlusive vascular change was relatively mild, and fibrous thickening of
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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
55
characteristic pathological features in the present case.
The cerebellar ataxia and subsequent mental deterioration are
unusual clinical features of Lyme neuroborreliosis.
Spirochete B. burgdorferi can cause focal inflammatory
parenchymal change in the central nervous tissues and the
present case may be an encephalitic form of Lyme
neuroborreliosis.
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Pregnancy and Lyme
TITLE:
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):99-101
TITLE:
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:
89
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:
90
Paediatr Perinat Epidemiol 1995 Jul;9(3):320-30
TITLE:
[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):150-2
TITLE:
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.
91
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):669-90
TITLE:
[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
92
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):425-8
TITLE:
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,
93
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):267-8
TITLE:
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,
94
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):657-77
TITLE:
[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.
95
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 maternalfetal 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, 655-6
TITLE:
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,
96
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):426-7
TITLE:
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):279-81
97
TITLE:
[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;
98
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):765-75
TITLE:
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
99
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):3394-6
Additional References pertaining to Multiple Sclerosis
and Neurological invasion by Borrelia
1. MRI Reveals Pathology in Neuro Lyme Disease. "Diagnostic ImagingMRI Insights".
2. "Biopsy-confirmed CNS Lyme Disease: MR Appearance at l.5T"
American Journal of Neuroradiology-11:482-484.
100
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,
143-145
5. 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: Casecontrolled 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.
101
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
102
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):765775. [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,
103
ataxic or spastic gait disorder,
bladder disturbances,
cranial nerve sydrunction including
optic atrophy and
hypoacusia,
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
with
pelocytosis,
abnormal EEG and
evoked 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 cause
acute 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
104
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.
_____________________, Nervenar
zt. 1990 Apr;61(4):248-9. German.
Further Reading on Neuroborreliosis/MS
Lawrence C, Lipton RB, Lowy FD, Coyle PK, Seronegative chronic
relapsing 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., 1993
Antimyelin 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.
[email protected]
The method of enzyme immunoassay (ELISA) was used for detection of
105
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 Disease
Raymond 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,
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M.D., Donald Oswald, Louise Cockey, and Dionigi Maladorno, M.D.
N Engl J Med 1997; 337:289-295, July 31, 1997
Abstract
Article
References
Citing Articles (24)
BACKGROUND
Localized 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...
METHODS
We 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...
RESULTS
Of 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
107
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...
CONCLUSIONS
In 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 INFORMATION
From 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.
108
Lecture DVD Available
A 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 55812
Checks payable to MIBDEC for tax deductible contribution.
Bulk quantities, please e-mail [email protected]
109