What Is Lyme Disease?

Lyme Disease is a controversial subject in Australia, the Federal Government doesn’t officially recognise its existence in this country. However the Australian Government is “monitoring Lyme disease, in consultation with the states and territories, through the Communicable Diseases Network Australia“. The Department of Health does have an “interest in an Australian Lyme disease-like syndrome”.

There is a research group at The University of Sydney, the Tick Borne Diseases Unit that was until recently pursuing Lyme disease in Australia. There are a number of medical experts in Australia who believe Lyme disease or at least a Lyme-like disease is present in this country (Mayne, 2015). Research is continuing into native spirochetes and ticks that may be the culprits (Mayne et al. 2014, Gofton et al., 2015, Gofton et al., 2015). To date (Sep 2016), the Lyme disease causing species of Borrelia burgdorferi (the bacteria responsible for Lyme disease) from overseas have not been found in Australia, nor have native species of Borrelia been found to cause a Lyme-like disease. Read here for an article by the Australian Medical Association (AMA).

A recent episode (July 5 2016) of the ABC’s Catalyst program featured a story on the possible presence of a Lyme-like disease in Australia from several viewpoints. Find the story here.

Much of what suspected sufferers in this country refer to as Lyme disease is actually what is referred to in the US as Post-Lyme Disease Syndrome (PLDS) or, Post-Treatment Lyme Disease Syndrome (PTLDS). PLDS or PTLDS is still not fully understood but is the subject of research by the scientific community (Chandra, A., et al., 2011, Schutzer et al., 2011, Kanjwal et al., 2011, Strle et al., 2014). Most medical experts believe that the lingering symptoms are the result of residual damage to tissues and the immune system that occurred during the infection.

Post-Treatment Lyme Disease Syndrome, and other unrelated illnesses, are also referred to by some physicians, patients and patient advocates as chronic Lyme disease (CLD), which they believe is due to a persistent, active Borrelia (vide infra) infection (Stricker, R. B., 2007). The current scientific consensus of the Infectious Diseases Society of America and the CDC is that there is no evidence that diagnosed chronic Lyme disease is due to a persistent Borrelia infection (Halperin, 2015).  Recent animal studies have given rise to questions that warrant further research (Barbour, 2012, Bockenstedt et al., 2012, Embers et al., 2012). Diagnosis of chronic Lyme disease remains controversial (Halperin, 2016Lantos, 2015, Aguero-Rosenfeld and Wormser, 2015Feder, et al., 2007, Johnson and Feder, 2010, Stricker, 2007, Stricker and Johnson, 2011, Feder, 2010). ME/CFS has been known to be triggered by many infections and may also occur following Lyme disease (Halperin, 2015). The terms Lyme disease and chronic Lyme disease are sometimes used interchangeably by some of these advocates. In what follows below, Lyme disease and chronic Lyme disease are not to be confused with each other, and will be not used as synonyms.

Technically speaking, the name Lyme disease refers to an infection caused by a spirochete-type (pronounced ‘spirokeet’) of bacterium called Borrelia burgdorferi, common on the East Coast of USA. The name derives from the small town of Lyme, Connecticut where in 1975, when following an outbreak of apparent juvenile arthritis, mothers noticed their children’s illness had been preceded by a rash. Before this time illnesses which would now be called Lyme were reported in Europe as early as 1883 but it wasn’t until 1975 that they were recognized as a single infection.

It’s full name, Borrelia burgdorferi sensu lato consists of three pathogenic genospecies: in the United States, Lyme Disease is caused by B. burgdorferi sensu stricto; in Europe and Asia, Lyme borreliosis is due to infection with B. gariniiB. afzelii, and B. burgdorferi sensu stricto.

The previously unidentified spirochetal bacterium B. burgdorferi (see Figure 1) was first recovered from ticks and infected patients in 1982 and 1983 (Burgdorfer et al., 1982Steere, et al., 1983).

Borrelia burgdorferi spirochetes (magnified)

Figure 1. Borrelia burgdorferi spirochetes – the cause of Lyme Disease (magnified).

Lyme diseases or more strictly Lyme borreliosis, exists in the forested areas of Asia, north-western, central and eastern Europe, and the USA (WHO). The bacteria of Lyme disease are spread by infected nymphal Ixodes ticks: I. scapularis in the northeastern, north midwestern, and middle Atlantic states of the United States and I. pacificus along the northern Pacific coast; I. ricinus in Europe; and I. persulcatus in Asia. Note that not all ticks in an endemic region are infected and infection rates among ticks can vary greatly from state to state and local region to local region, so being bitten by a tick is not a guarantee of acquiring Lyme Disease.

Climate change modelling (Brownstein, et al., 2003, Ostfeld and Brunner, 2015) has predicted a greater distribution of ticks in the US and worldwide in the future.

The spirochete can be transmitted to the host (be it human or animal) when the tick bites, through the saliva of the tick. If left untreated the bacteria can spread from the initial bite site, via the bloodstream and establish themselves in various tissues of the body and can cause a wide range of symptoms, some of which can be severe.

Back To Lyme Disease Home :: Next To The Stages And Symptoms of Lyme Disease

Websites And Links

Centers for Disease Control and Prevention (CDC) page on Lyme Disease

American Lyme Disease Foundation

Infectious Diseases Society of America

University of Sydney’s Tick Borne Diseases Unit

US National Institute of Health

US National Institute of Allergy and Infectious Diseases (Lyme Disease Page)


Institute of Medicine (US) Committee on Lyme Disease and Other Tick-Borne Diseases: The State of the Science. Critical Needs and Gaps in Understanding Prevention, Amelioration, and Resolution of Lyme and Other Tick-Borne Diseases: The Short-Term and Long-Term Outcomes: Workshop Report. Washington (DC): National Academies Press (US); 2011. Available from: http://www.ncbi.nlm.nih.gov/books/NBK57020/

Lyme Disease: the Great Controversy Halperin, J.J., Baker, P., and Wormser, G.P. In, “Lyme Disease: An Evidence-based Approach”(American Lyme Disease Foundation) (Link to Chapter 17 pdf)

Wang, G. (2015). Chapter 104 – Borrelia burgdorferi and other Borrelia species, Molecular Medical Microbiology (Second Edition), Pages 1867–1909, Elsevier Ltd.

Radolf, J. D., et al. (2010). Lyme disease in humans, Caister Academic Press.

Journal Articles

Halperin, J. J. “Nervous system Lyme disease, chronic Lyme disease, and none of the above.” Acta Neurol Belg, 2016, 116(1): 1-6.

Lantos, P. M. “Chronic Lyme disease.” Infect Dis Clin North Am, 2015, 29(2): 325-340.

Aucott, J. N. “Posttreatment Lyme disease syndrome.” Infect Dis Clin North Am, 2015, 29(2): 309-323.

Mayne, P. J. “Clinical determinants of Lyme borreliosis, babesiosis, bartonellosis, anaplasmosis, and ehrlichiosis in an Australian cohort.” Int J Gen Med, 2015, 8: 15-26.

Gofton, A. W., et al. “Inhibition of the endosymbiont “Candidatus Midichloria mitochondrii” during 16S rRNA gene profiling reveals potential pathogens in Ixodes ticks from Australia.” Parasit Vectors, 2015, 8: 345.

Gofton, A. W., et al. “Bacterial profiling reveals novel “Ca. Neoehrlichia”, Ehrlichia, and Anaplasma species in Australian human-biting ticks.” PLoS One, 2015, 10(12): e0145449/0145441-e0145449/0145416.

Patrick, D. M., et al. “Lyme Disease Diagnosed by Alternative Methods: A Phenotype Similar to That of Chronic Fatigue Syndrome.” Clin Infect Dis, 2015.

Ostfeld, R. S. and J. L. Brunner. “Climate change and Ixodes tick-borne diseases of humans.” Philos Trans R Soc Lond B Biol Sci, 2015, 370(1665).

Aguero-Rosenfeld, M. E. and G. P. Wormser. “Lyme disease: diagnostic issues and controversies.” Expert Rev. Mol. Diagn., 2015, 15(1): 1-4.

Halperin, J. J. “Chronic Lyme disease: misconceptions and challenges for patient management.” Infect Drug Resist, 2015, 8: 119-128.

Borchers, A. T., et al. “Lyme disease: a rigorous review of diagnostic criteria and treatment.” J Autoimmun, 2015, 57: 82-115.

Mayne, P., et al. “Evidence for Ixodes holocyclus (Acarina: Ixodidae) as a Vector for Human Lyme Borreliosis Infection in Australia.” J Insect Sci, 2014, 14(1).

Lantos, P. M. and G. P. Wormser. “Chronic coinfections in patients diagnosed with chronic lyme disease: a systematic review.” Am J Med, 2014, 127(11): 1105-1110.

DeBiasi, R. L. “A concise critical analysis of serologic testing for the diagnosis of lyme disease.” Curr Infect Dis Rep, 2014, 16(12): 450.

Brissette, C. A. and R. A. Gaultney. “That’s my story, and I’m sticking to it–an update on B. burgdorferi adhesins.” Front Cell Infect Microbiol, 2014, 4: 41.

Groshong, A. M. and J. S. Blevins. “Insights into the biology of Borrelia burgdorferi gained through the application of molecular genetics.” Adv. Appl. Microbiol., 2014, 86: 41-143.

Lantos, P. M., et al. “A systematic review of Borrelia burgdorferi morphologic variants does not support a role in chronic Lyme disease.” Clin Infect Dis, 2014, 58(5): 663-671.

Pavia, C. S. and G. P. Wormser. “Culture of the entire mouse to determine whether cultivable Borrelia burgdorferi persists in infected mice treated with a five-day course of ceftriaxone.” Antimicrob. Agents Chemother., 2014, 58(11): 6701-6703, 6704 pp.

O’Day, D. H. and A. Catalano. “A lack of correlation between the incidence of lyme disease and deaths due to Alzheimer’s disease.” J Alzheimers Dis, 2014, 42(1): 115-118.

Strle, K., et al. “Elevated Levels of IL-23 in a Subset of Patients With Post-Lyme Disease Symptoms Following Erythema Migrans.” Clin. Infect. Dis., 2014, 58(3): 372-380.

Halperin, J. J., et al. “Common misconceptions about Lyme disease.” Am J Med, 2013, 126(3): 264.e261-267.

Klempner, M. S., et al. “Treatment trials for post-Lyme disease symptoms revisited.” Am J Med, 2013, 126(8): 665-669.

Kobayashi, Y., et al. “A novel macrolide solithromycin exerts superior anti-inflammatory effect via NF-κB inhibition.” J Pharmacol Exp Ther, 2013, 345(1): 76-84.

Ajamian, M., et al. “Serologic markers of lyme disease in children with autism.” JAMA, J. Am. Med. Assoc., 2013, 309(17): 1771-1772.

Burbelo, P. D., et al. “Lack of serum antibodies against Borrelia burgdorferi in children with autism.” Clin. Vaccine Immunol., 2013, 20(7): 1092-1093.

Krut, J. J., et al. “Cerebrospinal fluid Alzheimer’s biomarker profiles in CNS infections.” J. Neurol., 2013, 260(2): 620-626.

Barbour, A. “Remains of infection.J. Clin. Invest., 2012, 122(7): 2344-2346.

Bockenstedt, L. K., et al. “Spirochete antigens persist near cartilage after murine Lyme borreliosis therapy.J. Clin. Invest., 2012, 122(7): 2652-2660.

Embers, M. E., et al. “Persistence of Borrelia burgdorferi in rhesus macaques following antibiotic treatment of disseminated infection.PLoS One, 2012, 7(1): e29914.

Huyshe-Shires, S. “Lyme disease antiscience.” Lancet Infect Dis, 2012, 12(5): 361; author reply 362-363.

Perronne, C. “Lyme disease antiscience.” Lancet Infect Dis, 2012, 12(5): 361-362; author reply 362-363.

Tuttle, C. “Lyme disease antiscience.” Lancet Infect Dis, 2012, 12(5): 362; author reply 362-363.

Auwaerter, P. G., et al. “Lyme disease antiscience – Authors’ reply.” Lancet Infect Dis, 2012, 12(5): 362-363.

Bastos, L. F. S., et al. “Tetracyclines and pain.” Naunyn-Schmiedeberg’s Arch. Pharmacol., 2012, 385(3): 225-241.

Auwaerter, P. G., et al. “Antiscience and ethical concerns associated with advocacy of Lyme disease.” Lancet Infect Dis, 2011, 11(9): 713-719.

Chandra, A., et al. “Anti-Borrelia burgdorferi antibody profile in post-Lyme disease syndrome.” Clin. Vaccine Immunol., 2011, 18(5): 767-771.

Stricker, R. B. and L. Johnson. ““Lyme literacy” and physicians in Connecticut.” J Pediatr, 2011, 158(3): 518-519; author reply 519-520.

Lantos, P. M. “Chronic Lyme disease: the controversies and the science.” Expert Rev Anti Infect Ther, 2011, 9(7): 787-797.

Halperin, J. J. “Nervous system lyme disease: is there a controversy?” Semin Neurol, 2011, 31(3): 317-324.

Schutzer, S. E., et al. “Distinct cerebrospinal fluid proteomes differentiate Post-Treatment Lyme disease from Chronic Fatigue syndrome.” PLoS One, 2011, 6(2): e17287.

Kanjwal, K., et al. “Postural orthostatic tachycardia syndrome following Lyme disease.” Cardiol J, 2011, 18(1): 63-66.

Alvarez, J. I., et al. “Disruption of central nervous system barriers in multiple sclerosis.” Biochim. Biophys. Acta, Mol. Basis Dis., 2011, 1812(2): 252-264.

Johnson, M. and H. M. Feder, Jr. “Chronic Lyme disease: a survey of Connecticut primary care physicians.” J Pediatr, 2010, 157(6): 1025-1029.e1021-1022.

Holzbauer, S. M., et al. “Death due to community-associated Clostridium difficile in a woman receiving prolonged antibiotic therapy for suspected lyme disease.” Clin Infect Dis, 2010, 51(3): 369-370.

Feder, H. M., Jr. “Reply.” J Pediatr, 2010, 158(3): 519-520.

Berende, A., et al. “Activation of innate host defense mechanisms by Borrelia.” Eur. Cytokine Network, 2010, 21(1): 7-18.

Nau, R., et al. “Lyme disease–current state of knowledge.” Dtsch Arztebl Int, 2009, 106(5): 72-81.

Wormser, G. P. and E. D. Shapiro. “Implications of gender in chronic Lyme disease.” J Womens Health (Larchmt), 2009, 18(6): 831-834.

Wahlberg, P. and D. Nyman. “Chronic Lyme borreliosis–fact or fiction?” Duodecim, 2009, 125(12): 1269-1276.

Qureshi, M., et al. “Lyme disease serology in amyotrophic lateral sclerosis.” Muscle Nerve, 2009, 40(4): 626-628.

ALSUntangled update 1: investigating a bug (Lyme Disease) and a drug (Iplex) on behalf of people with ALS.” Amyotrophic Lateral Sclerosis, 2009, 10: 248-250.

Allan, E. J., et al. “Bacterial L-forms.” Adv. Appl. Microbiol., 2009, 68: 1-39.

Wormser, G. P. and I. Schwartz. “Antibiotic treatment of animals infected with Borrelia burgdorferi.” Clin. Microbiol. Rev., 2009, 22(3): 387-395.

Wormser, G. P., et al. “Impact of clinical variables on Borrelia burgdorferi-specific antibody seropositivity in acute-phase sera from patients in North America with culture-confirmed early lyme disease.” Clin. Vaccine Immunol., 2008, 15(10): 1519-1522.

Marques, A. “Chronic Lyme disease: a review.” Infect Dis Clin North Am, 2008, 22(2): 341-360, vii-viii.

Dandache, P. and R. B. Nadelman. “Erythema migrans.” Infect Dis Clin North Am, 2008, 22(2): 235-260, vi.

Steere, A. C., et al. “Prospective study of serologic tests for lyme disease.” Clin Infect Dis, 2008, 47(2): 188-195.

Fallon, B. A., et al. “A randomized, placebo-controlled trial of repeated IV antibiotic therapy for Lyme encephalopathy.” Neurology, 2008, 70(13, Pt. 1): 992-1003.

Hodzic, E., et al. “Persistence of Borrelia burgdorferi following antibiotic treatment in mice.” Antimicrob. Agents Chemother., 2008, 52(5): 1728-1736.

Wilske, B., et al. “Microbiological and serological diagnosis of Lyme borreliosis.” FEMS Immunol. Med. Microbiol., 2007, 49(1): 13-21.

Feder, H. M., Jr., et al. “A critical appraisal of “chronic Lyme disease”.” N. Engl. J. Med., 2007, 357(14): 1422-1430.

Auwaerter, P. G. “Point: antibiotic therapy is not the answer for patients with persisting symptoms attributable to lyme disease.” Clin. Infect. Dis., 2007, 45(2): 143-148.

Stricker, R. B. “Counterpoint: long-term antibiotic therapy improves persistent symptoms associated with lyme disease.” Clin. Infect. Dis., 2007, 45(2): 149-157.

Wormser, G. P. “Clinical practice. Early Lyme disease.” N Engl J Med, 2006, 354(26): 2794-2801.

Wormser, G. P., et al. “The clinical assessment, treatment, and prevention of lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America.” Clin Infect Dis, 2006, 43(9): 1089-1134.

Steere, A. C. and S. M. Angelis. “Therapy for Lyme arthritis.” Arthritis Rheum., 2006, 54(10): 3079-3086.

Ivetic Tkalcevic, V., et al. “Anti-inflammatory activity of azithromycin attenuates the effects of lipopolysaccharide administration in mice.” Eur. J. Pharmacol., 2006, 539(1-2): 131-138.

Aguero-Rosenfeld, M. E., et al. “Diagnosis of Lyme borreliosis.” Clin. Microbiol. Rev., 2005, 18(3): 484-509.

Bratton, R. L. and R. Corey. “Tick-borne disease.” Am Fam Physician, 2005, 71(12): 2323-2330.

Rothstein, J. D., et al. “β-Lactam antibiotics offer neuroprotection by increasing glutamate transporter expression.” Nature, 2005, 433(7021): 73-77.

Sanz, M.-J., et al. “Erythromycin exerts in vivo anti-inflammatory activity downregulating cell adhesion molecule expression.” Br J Pharmacol, 2005, 144(2): 190-201.

Cameron, D., et al. “Evidence-based guidelines for the management of Lyme disease.” Expert Rev Anti Infect Ther, 2004, 2(1 Suppl): S1-13.

Steere, A. C., et al. “The emergence of Lyme disease.” J. Clin. Invest., 2004, 113(8): 1093-1101.

Auwaerter, P. G., et al. “Lyme borreliosis (Lyme disease): molecular and cellular pathobiology and prospects for prevention, diagnosis and treatment.” Expert Rev Mol Med, 2004, 6(2): 1-22.

Domercq, M. and C. Matute. “Neuroprotection by tetracyclines.” Trends Pharmacol. Sci., 2004, 25(12): 609-612.

Tamaoki, J., et al. “Clinical implications of the immunomodulatory effects of macrolides.” Am. J. Med., 2004, 117(Suppl. 9A): 5S-11S.

Brownstein, J. S., et al. “A climate-based model predicts the spatial distribution of the Lyme disease vector Ixodes scapularis in the United States.” Environ Health Perspect, 2003, 111(9): 1152-1157

Krupp, L. B., et al. “Study and treatment of post Lyme disease (STOP-LD): a randomized double masked clinical trial.” Neurology, 2003, 60(12): 1923-1930.

Kaplan, R. F., et al. “Cognitive function in post-treatment Lyme disease. Do additional antibiotics help?” Neurology, 2003, 60(12): 1916-1922.

Sood, S. K. “Effective retrieval of Lyme disease information on the Web.” Clin Infect Dis, 2002, 35(4): 451-464.

Donta, S. T. “Late and chronic Lyme disease.” Med Clin North Am, 2002, 86(2): 341-349, vii.

Collignon, P. J. “11 Antibiotic resistance.” Med J Aust, 2002, 177(6): 325-329.

Alexopoulou, L., et al. “Hyporesponsiveness to vaccination with Borrelia burgdorferi OspA in humans and in TLR1- and TLR2-deficient mice.” Nat. Med., 2002, 8(8): 878-884.

Bockenstedt, L. K., et al. “Detection of attenuated, noninfectious spirochetes in Borrelia burgdorferi-infected mice after antibiotic treatment.” J Infect Dis, 2002, 186(10): 1430-1437.

Schmutzhard, E. “Multiple sclerosis and Lyme borreliosis.” Wien. Klin. Wochenschr., 2002, 114(13-14): 539-543.

Klempner, M. S., et al. “Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease.” N. Engl. J. Med., 2001, 345(2): 85-92.

Wooten, R. M. and J. J. Weis. “Host-pathogen interactions promoting inflammatory Lyme arthritis: Use of mouse models for dissection of disease processes.” Curr. Opin. Microbiol., 2001, 4(3): 274-279.

Steere, A. C. “Lyme disease.” N Engl J Med, 2001, 345(2): 115-125.

Lindgren, E. and R. Gustafson. “Tick-borne encephalitis in Sweden and climate change.” The Lancet, 2001, 358(9275): 16-18.

Gayle, A. and E. Ringdahl. “Tick-borne diseases.” Am Fam Physician, 2001, 64(3): 461-466.

Patel, R., et al. “Death from Inappropriate Therapy for Lyme Disease.” Clin. Infect. Dis., 2000, 31(4): 1107-1109.

Ozinsky, A., et al. “The repertoire for pattern recognition of pathogens by the innate immune system is defined by cooperation between toll-like receptors.” Proc Natl Acad Sci U S A, 2000, 97(25): 13766-13771.

Marques, A. R., et al. “Lack of evidence of Borrelia involvement in Alzheimer’s disease.” J Infect Dis, 2000, 182(3): 1006-1007.

Hirschfeld, M., et al. “Cutting edge: Inflammatory signaling by Borrelia burgdorferi lipoproteins is mediated by toll-like receptor 2.” J. Immunol., 1999, 163(5): 2382-2386.

Lien, E., et al. “Toll-like receptor 2 functions as a pattern recognition receptor for diverse bacterial products.” J. Biol. Chem., 1999, 274(47): 33419-33425.

Aliprantis, A. O., et al. “Cell activation and apoptosis by bacterial lipoproteins through toll-like receptor-2.” Science, 1999, 285(5428): 736-739.

Brightbill, H. D., et al. “Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors.” Science, 1999, 285(5428): 732-736.

Woodrum, J. E. and J. H. Oliver, Jr. “Investigation of venereal, transplacental, and contact transmission of the Lyme disease spirochete, Borrelia burgdorferi, in Syrian hamsters.” J Parasitol, 1999, 85(3): 426-430.

Brorson, O. and S.-H. Brorson. “An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to metronidazole.” APMIS, 1999, 107(6): 566-576.

Gutacker, M., et al. “Arguments against the involvement of Borrelia burgdorferi sensu lato in Alzheimer’s disease.” Res Microbiol, 1998, 149(1): 31-37.

Fraser, C. M., et al. “Genomic sequence of a Lyme disease spirochaete, Borrelia burgdorferi.” Nature, 1997, 390(6660): 580-586.

Weis, J. J., et al. “Pathological manifestations in murine Lyme disease: association with tissue invasion and spirochete persistence.” Clin Infect Dis, 1997, 25 Suppl 1: S18-24.

Halperin, J. J. “Neuroborreliosis: central nervous system involvement.” Semin Neurol, 1997, 17(1): 19-24.

Aguero-Rosenfeld, M. E., et al. “Evolution of the serologic response to Borrelia burgdorferi in treated patients with culture-confirmed erythema migrans.” J Clin Microbiol, 1996, 34(1): 1-9.

Kienle, G. S. and H. Kiene. “Placebo effect and placebo concept: a critical methodological and conceptual analysis of reports on the magnitude of the placebo effect.” Altern Ther Health Med, 1996, 2(6): 39-54.

Silver, R. M., et al. “Fetal outcome in murine Lyme disease.” Infect Immun, 1995, 63(1): 66-72.

Miklossy, J., et al. “Further ultrastructural evidence that spirochaetes may play a role in the aetiology of Alzheimer’s disease.” NeuroReport, 1994, 5(10): 1201-1204.

Aguero-Rosenfeld, M. E., et al. “Serodiagnosis in early Lyme disease.” J Clin Microbiol, 1993, 31(12): 3090-3095.

Dressler, F., et al. “Western blotting in the serodiagnosis of Lyme disease.” J Infect Dis, 1993, 167(2): 392-400.

Miklossy, J. “Alzheimer’s disease. A spirochetosis?” NeuroReport, 1993, 4(7): 841-848.

Ma, B., et al. “Serodiagnosis of Lyme borreliosis by western immunoblot: reactivity of various significant antibodies against Borrelia burgdorferi.” J Clin Microbiol, 1992, 30(2): 370-376.

Barthold, S. W. “Infectivity of Borrelia burgdorferi relative to route of inoculation and genotype in laboratory mice.” J Infect Dis, 1991, 163(2): 419-420.

Moody, K. D. and S. W. Barthold. “Relative infectivity of Borrelia burgdorferi in Lewis rats by various routes of inoculation.” Am J Trop Med Hyg, 1991, 44(2): 135-139.

Halperin, J. J., et al. “Lyme borreliosis-associated encephalopathy.” Neurology, 1990, 40(9): 1340-1343.

Halperin, J. J., et al. “Lyme neuroborreliosis: central nervous system manifestations.” Neurology, 1989, 39(6): 753-759.

Pappolla, M. A., et al. “Concurrent neuroborreliosis and Alzheimer’s disease: analysis of the evidence.” Hum Pathol, 1989, 20(8): 753-757.

Magnarelli, L. A. and J. F. Anderson. “Ticks and biting insects infected with the etiologic agent of Lyme disease, Borrelia burgdorferi.” J Clin Microbiol, 1988, 26(8): 1482-1486.

Steere, A. C., et al. “The clinical evolution of Lyme arthritis.” Ann Intern Med, 1987, 107(5): 725-731.

Takayama, K., et al. “Absence of lipopolysaccharide in the Lyme disease spirochete, Borrelia burgdorferi.” Infect. Immun., 1987, 55(9): 2311-2313.

MacDonald, A. B. and J. M. Miranda. “Concurrent neocortical borreliosis and Alzheimer’s disease.” Hum Pathol, 1987, 18(7): 759-761.

Beck, G., et al. “Chemical and biologic characterization of a lipopolysaccharide extracted from the Lyme disease spirochete (Borrelia burgdorferi).” J. Infect. Dis., 1985, 152(1): 108-117.

Steere, A. C., et al. “The spirochetal etiology of Lyme disease.” N Engl J Med, 1983, 308(13): 733-740.

Burgdorfer, W., et al. “Lyme disease-a tick-borne spirochetosis?” Science, 1982, 216(4522): 1317-1319.