Lyme and Autoimmune Disease

[LymeEnigma]

Thyroid. 2004 Nov;14(11):964-6.

Homologies between proteins of Borrelia burgdorferi and thyroid autoantigens.

Benvenga S, Guarneri F, Vaccaro M, Santarpia L, Trimarchi F.

Sezione di Endocrinologia del Dipartimento Clinico Sperimentale di Medicina e Farmacologia, Università di Messina, Messina, Italy. [e-mail]

Subclinical exposure to microbic antigens that share amino acid sequence homology with self antigens might trigger autoimmune diseases in genetically predisposed individuals via molecular mimicry. Genetic predisposition to Graves' disease (GD) or Hashimoto's thyroiditis (HT) is conferred by HLA loci DR3 or DR5, respectively. Yersinia enterocolitica (YE) outer proteins (YOPs) are candidate triggers based on the high prevalence of serum antibodies (Ab) against YOPs in autoimmune thyroid diseases (AITD) and reactivity of these Ab with hTSH-R, suggesting homology between YOPs and hTSH-R. We have reported previously that the spirochete Borrelia burgdorferi (Bb) could be another trigger. We have explored further the homology of hTSH-R with YE and Bb. Using the Basic Local Alignment Search Tool (BLAST), we found four matches with YE and five matches with Bb . Residues 22-272, 186-330, 319-363 and 684-749 of hTSH-R matched YopM, Ysp, exopolygalacturonase and SpyA of YE (identity 23-31%, similarity 40-48%). Residues 112-205, 127-150, 141-260, 299-383 and 620-697 of hTSH-R matched outer surface protein A, flagellar motor rotation protein A, two hypothetical proteins (BBG02 and BBJ08) and DNA recombinase/ATP dependent helicase of Borrelia (identity 27-50%, similarity 40-75%). Interestingly, the above hTSH-R regions coincide with (or include) known human T-cell epitopes: aa 52-71, 140-176, 240-270, 340-380 and 441-661. Our data strengthen the hypothesis of Bb and YE as environmental triggers of AITD in genetically predisposed persons through molecular mimicry mechanisms.

PMID: 15671776 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/15671776?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

[LymeEnigma]

Association of Lichen Sclerosis and Autoimmune Thyroiditis: Possible role of Borrelia burgdorferi?

www.liebertonline.com/doi/abs/10.1089%2F105072502321085261

[LymeEnigma]

Women and Autoimmune Diseases

DeLisa Fairweather* and Noel R. Rose*
*Johns Hopkins University, Baltimore, Maryland, USA

Abstract:

Autoimmune diseases affect approximately 8% of the population, 78% of whom are women. The reasons for the high prevalence in women are unknown, but circumstantial evidence links autoimmune diseases with preceding infections. Animal models of autoimmune diseases have shown that infections can induce autoimmune disease. For example, coxsackievirus B3 (CB3) infection of susceptible mice results in inflammation of the heart (myocarditis) that resembles myocarditis in humans. The same disease can be induced by injecting mice with heart proteins mixed with adjuvant(s), which indicates that an active infection is not necessary for the development of autoimmune disease. We have found that CB3 triggers autoimmune disease in susceptible mice by stimulating elevated levels of proinflammatory cytokines from mast cells during the innate immune response. Sex hormones may further amplify this hyperimmune response to infection in susceptible persons, which leads to an increased prevalence of autoimmune diseases in women.

Full Article: www.cdc.gov/ncidod/EID/vol10no11/04-0367.htm

[LymeEnigma]

Pediatr Neurol. 1998 Mar;18(3):231-5.

Overstimulation of nerve growth factors in postinfectious and autoimmune diseases.

Riikonen RS, Söderström S, Korhonen LT, Lindholm DB.

Children's Hospital, University of Helsinki, Finland.

Nerve growth factor (NGF) in cerebrospinal fluid was measured by ELISA in ten children with postinfectious diseases and in five children with diseases suggested to be of autoimmune etiology. Three groups of patients were studied: (1) those with moderately elevated concentrations (50.67 +/- 17.02 pg/mL, mean and SEM), (2) those with high concentrations (mean 424.25 +/- 125.41 pg/mL, mean and SEM), and (3) those with enormously high concentrations (mean 2,745 +/- 1,819.46 pg/mL, mean and SEM). We suggest that CSF-NGF could be used as an immunologic marker of an ongoing CNS process. Uncontrolled signaling of NGF receptors may lead to long-term inflammatory and autoimmune responses, which in turn can lead to disease.

PMID: 9568920 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/9568920?ordinalpos=73&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
_______________________________________________________

LE note: might this be one of the causative factors to Lyme-induced neuralgias?

[LymeEnigma]

Journal of Clinical Microbiology, December 1999, p. 3997-4004, Vol. 37, No. 12 0095-1137/99/$04.00+0

Copyright © 1999, American Society for Microbiology. All rights reserved.

Human Antibody Responses to VlsE Antigenic Variation Protein of Borrelia burgdorferi

M. B. Lawrenz,1 J. M. Hardham,1,dagger R. T. Owens,2 J. Nowakowski,3 A. C. Steere,4 G. P. Wormser,3 and S. J. Norris1,*

Departments of Pathology and Laboratory Medicine and Microbiology and Molecular Genetics, University of Texas Medical School at Houston,1 and Institute of Biosciences and Technology, Texas A & M University,2 Houston, Texas; Department of Medicine, Division of Infectious Disease, New York Medical College, Valhalla, New York3; and Division of Rheumatology/Immunology, Tufts University School of Medicine, New England Medical Center, Tupper Research Institute, Boston, Massachusetts4

Received 22 March 1999/Returned for modification 29 April 1999/Accepted 13 September 1999

Abstract:

VlsE is a 35-kDa surface-exposed lipoprotein of Borrelia burgdorferi that was shown previously to undergo antigenic variation through segmental recombination of silent vls cassettes with vlsE during experimental mouse infections. Previous data had indicated that sera from North American Lyme disease patients and experimentally infected animals contained antibodies reactive with VlsE. In this study, sera from patients with Lyme disease, syphilis, and autoimmune conditions as well as from healthy controls were examined for reactivity with VlsE by Western blotting and enzyme-linked immunosorbent assay (ELISA). Strong Western blot reactivity to a recombinant VlsE cassette region protein was obtained consistently with Lyme disease sera. Although sera from Lyme disease patients also reacted with a band corresponding to VlsE in B. burgdorferi B31-5A3, interpretation was complicated by low levels of VlsE expression in in vitro-cultured B. burgdorferi and by the presence of comigrating bands. An ELISA using recombinant VlsE was compared with an ELISA using sonically disrupted B. burgdorferi as the antigen. For a total of 93 Lyme disease patient sera examined, the VlsE ELISA yielded sensitivities of 63% for culture-confirmed erythema migrans cases and 92% for later stages, as compared to 61 and 98%, respectively, for the "whole-cell" ELISA. The specificities of the two assays with healthy blood donor sera were comparable, but the VlsE ELISA was 90% specific with sera from syphilis patients, compared to 20% specificity for the whole-cell ELISA with this group. Neither assay showed reactivity with a panel of sera from 20 non-Lyme disease arthritis patients or 20 systemic lupus erythematosus patients. Our results indicate that VlsE may be useful in the immunodiagnosis of Lyme disease and may offer greater specificity than ELISAs using whole B. burgdorferi as the antigen.

Full article: jcm.asm.org/cgi/content/full/37/12/3997?view=long&pmid=10565921

[LymeEnigma]

Nature Immunology 2, 797 - 801 (2001)
doi:10.1038/ni0901-797

Autoimmunity provoked by infection: how good is the case for T cell epitope mimicry?

Christophe Benoist & Diane Mathis

Section on Immunology and Immunogenetics, Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, One Joslin Place, Boston, MA, USA.
Correspondence should be addressed to Diane Mathis [e-mail]

Autoimmune diseases remain one of the mysteries that perplex immunologists. What makes the immune system, which has evolved to protect an organism from foreign invaders, turn on the organism itself? A popular answer to this question involves the lymphoid network's primordial function: autoimmunity is a by-product of the immune response to microbial infection. For decades there have been tantalizing associations between infectious agents and autoimmunity: beta-hemolytic streptococci and rheumatic fever; B3 Coxsackieviruses and myocarditis; Trypanosoma cruzi and Chagas' disease; diverse viruses and multiple sclerosis; Borrelia burgdorfii and Lyme arthritis; and B4 Coxsackievirus, cytomegalovirus or rubella and type 1 diabetes, to name the most frequently cited examples1. In addition, animal models have provided direct evidence that infection with a particular microbe can incite a particular autoimmune disease2. Nonetheless, many of the associations appear less than convincing and, even for those that seem to be on solid footing, there is no real understanding of the underlying mechanism(s).

www.nature.com/ni/journal/v2/n9/abs/ni0901-797.html

[LymeEnigma]

Epidemiol Mikrobiol Imunol. 2002 Apr;51(2):60-5.

[Lyme borreliosis--incidence of serum anti-myelin antibodies]
[Article in Czech]

Rysková O, Vyslouzil L, Honegr K, Lesná J, Horácek J, Skrabková Z.

Ustav klinické mikrobiologie, UK Praha, LF Hradec Králové. [e-mail]

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 did not differ 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 - indexed for MEDLINE]

www.ncbi.nlm.nih.gov/pubmed/11987581?ordinalpos=42&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

[LymeEnigma]

Neuropathy and cognitive impairment following vaccination with the OspA protein of Borrelia burgdorferi

* Norman Latov11Department of Neurology and Neurosciences, Weill Medical College of Cornell University, New York, NY, USA**Norman Latov, MD, PhD, The Peripheral Neuropathy Center, Weill Medical College of Cornell University, New York, NY 10022, USA. Tel: [phone]; Fax: [phone]; E‐mail: [e-mail],
* Anita T. Wu11Department of Neurology and Neurosciences, Weill Medical College of Cornell University, New York, NY, USA,
* Russell L. Chin11Department of Neurology and Neurosciences, Weill Medical College of Cornell University, New York, NY, USA,
* Howard W. Sander11Department of Neurology and Neurosciences, Weill Medical College of Cornell University, New York, NY, USA,
* Armin Alaedini11Department of Neurology and Neurosciences, Weill Medical College of Cornell University, New York, NY, USA, and
* Thomas H. Brannagan, III11Department of Neurology and Neurosciences, Weill Medical College of Cornell University, New York, NY, USA

*
1Department of Neurology and Neurosciences, Weill Medical College of Cornell University, New York, NY, USA

*Norman Latov, MD, PhD, The Peripheral Neuropathy Center, Weill Medical College of Cornell University, New York, NY 10022, USA. Tel: [phone]; Fax: [phone]; E‐mail: [e-mail]

Abstract

Neurological syndromes that follow vaccination or infection are often attributed to autoimmune mechanisms. We report six patients who developed neuropathy or cognitive impairment, within several days to 2 months, following vaccination with the OspA antigen of Borrelia burgdorferi. Two of the patients developed cognitive impairment, one chronic inflammatory demyelinating polyneuropathy (CIDP), one multifocal motor neuropathy, one both cognitive impairment and CIDP, and one cognitive impairment and sensory axonal neuropathy. The patients with cognitive impairment had T2 hyperintense white matter lesions on magnetic resonance imaging. The similarity between the neurological sequelae observed in the OspA-vaccinated patients and those with chronic Lyme disease suggests a possible role for immune mechanisms in some of the manifestations of chronic Lyme disease that are resistant to antibiotic treatment.

www.blackwell-synergy.com/doi/abs/10.1111/j.1085-9489.2004.09306.x

[LymeEnigma]

Lyme borreliosis and multiple sclerosis are associated with primary effusion lymphoma

Tanja Batinaca, Duska Petranovicb, Gordana Zamoloc, Corresponding Author Contact Information, E-mail The Corresponding Author, Davor Petranovicd and Alen Ruzice

aDepartment of Dermatovenerology, Rijeka University Hospital, Kresimirova 42, 51000 Rijeka, Croatia

bDepartment of Haematology, Rijeka University Hospital, Kresimirova 42, 51000 Rijeka, Croatia

cDepartment of Pathology, Rijeka University School of Medicine, Brace Branchetta 20, 51000 Rijeka, Croatia

dDepartment of Radiology, Rijeka University Hospital, Kresimirova 42, 51000 Rijeka, Croatia

eDepartment of Internal medicine, Thalassotherapy Hospital, M. Tita 188, 51410 Opatija, Croatia

Received 6 November 2006;
accepted 7 November 2006.
Available online 2 January 2007.

Summary

Multiple sclerosis (MS) is a chronic disease of the central nervous system characterized by chronic inflammation and demyelination. Studies suggested that the viral, especially Epstein-Barr virus infection, and bacterial infections, especially Borrelia burgodorferi infection, play a role in etiology of MS. MS prevalence parallels the distribution of the Lyme disease pathogen B. burgdorferi.

Criteria used for diagnosis of MS can also be fulfilled in other conditions such as Lyme disease, a multisystem disorder resulting from infection by the tick-borne spirochete, B. burgdorferi. In the late period of Lyme disease demyelinating involvement of central nervous system can develop and MS can be erroneously diagnosed. A Lyme borreliosis can mimick central nervous system lymphoma. Also, B. burgdorferi has been implicated not only in etiology of MS, but also in etiology of lymphoma.

Studies suggested that there is an increased risk of non-Hodgkin lymphoma in patients, who had a history of autoimmune diseases such as MS and that both non-Hodgkin’s lymphomas and Hodgkin’s disease were associated with Epstein-Barr virus infection.

A small group of lymphomas called primary effusion lymphomas (PEL) is a recently individualized form of non-Hodgkin’s lymphoma (WHO classification) that exhibit exclusive or dominant involvement of serous cavities, without a detectable solid tumor mass. These lymphomas have also been linked to Epstein-Barr virus and human herpes virus type 8 infections but virus negative cases have been described.

Therefore, we propose that MS and neuroborreliosis are linked to central nervous system primary effusion lymphomas.

As a first step in confirming or refuting our hypotheses, we suggest a thorough study of CSF in the patients suspected for the diagnosis of MS and Lyme borreliosis.

www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WN2-4MR1KCP-6&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=644b11c5c65a7f3087b5eace2de89f5e

[LymeEnigma]

The Journal of Immunology, 2006, 177: 2486-2494.
Copyright © 2006 by The American Association of Immunologists

Autoantibodies from Synovial Lesions in Chronic, Antibiotic Treatment-Resistant Lyme Arthritis Bind Cytokeratin-101

Srimoyee Ghosh*, Robert Seward{ddagger}, Catherine E. Costello{ddagger}, B. David Stollar{dagger} and Brigitte T. Huber2,*

* Department of Pathology, Tufts University School of Medicine, Boston, MA 02111; {dagger} Department of Biochemistry, Tufts University School of Medicine, Boston, MA 02111; and {ddagger} Mass Spectrometry Resource, Boston University School of Medicine, Boston, MA 02118

Abstract:

Although the causative agent of Lyme disease is definitively known to be the tick-borne spirochete, Borrelia burgdorferi, the etiology of chronic joint inflammation that ensues in a subset of patients remains less well understood. Persistence of arthritis after apparent eradication of the spirochete suggests an autoimmune reaction downstream of the original bacterial infection. We have generated recombinant Ab probes from synovial lesions within affected arthritic joints in an attempt to recapitulate disease-relevant Ag-binding specificities at the site of injury. Using this panel of intra-articular probes, as well as Ab fragments derived from patient peripheral blood, we have identified cytokeratin 10, present in synovial microvascular endothelium, as a target ligand and a putative autoantigen in chronic, antibiotic treatment-resistant Lyme arthritis. Furthermore, there is cross-reactivity between cytokeratin 10 and a prominent B. burgdorferi Ag, outer surface protein A. Release of the self protein in the context of inflammation-induced tissue injury and the resulting in situ response to it could set in motion a feed-forward loop, which amplifies the inflammatory process, thereby rendering it chronic and self-perpetuating, even in the absence of the inciting pathogen.

Full article: www.jimmunol.org/cgi/content/full/177/4/2486

[LymeEnigma]

Serum Reactivity against Borrelia burgdorferi OspA in Patients with Rheumatoid Arthritis

Yu-Fan Hsieh,1 Han-Wen Liu,1 Tsai-Ching Hsu,1 James C.-C. Wei,2 Chien-Ming Shih,3 Peter J. Krause,4 and Gregory J. Tsay1,2*

Institute of Immunology,1 Department of Medicine, Chung Shan Medical University, Taichung, Taiwan,2 Department of Parasitology and Tropical Medicine, National Defense Medical Center, Taipei, Taiwan,3 Department of Pediatrics, University of Connecticut School of Medicine, Farmington, Connecticut4

Received 10 April 2007/ Returned for modification 5 July 2007/ Accepted 6 September 2007

Abstract:

Lyme arthritis and rheumatoid arthritis share common clinical features and synovial histology. It is unclear whether they also share similar pathogenesis. Previous studies have shown that the severity and duration of Lyme arthritis correlate directly with serum concentrations of antibody against outer surface protein A (OspA) of the causative pathogen Borrelia burgdorferi. We tested the sera of 68 subjects with rheumatoid arthritis, 147 subjects with other autoimmune diseases, and 44 healthy subjects who had never had Lyme disease, as well as sera of 16 patients who had Lyme disease, for reactivity against the B. burgdorferi OspA protein. The sera of about a quarter of the rheumatoid arthritis patients and a 10th of the autoimmune disease and Lyme disease patients reacted against OspA antigen. Of 50 rheumatoid arthritis patients who could be evaluated for disease severity, a 28-joint count disease activity score of >2.6 was noted for 11 of 15 (73%) patients whose sera reacted against OspA antigen and 13 of 35 (37%; P < 0.05) whose sera were nonreactive. Serum reactivity against OspA antigen is associated with the pathogenesis of rheumatoid arthritis.

Full article: cvi.asm.org/cgi/content/full/14/11/1437?view=long&pmid=17881508

[LymeEnigma]

Journal of Clinical Microbiology, February 2005, p. 850-856, Vol. 43, No. 2 0095-1137/05/$08.00+0 doi:10.1128/JCM.43.2.850-856.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Evidence of Borrelia Autoimmunity-Induced Component of Lyme Carditis and Arthritis

Elizabeth S. Raveche,1 Steven E. Schutzer,1* Helen Fernandes,1 Helen Bateman,1 Brian A. McCarthy,1 Steven P. Nickell,2 and Madeleine W. Cunningham3

Departments of Pathology and Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey,1 Department of Molecular Genetics and Microbiology, University of New Mexico, Albuquerque, New Mexico,2 University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma3

Received 2 January 2004/ Returned for modification 29 March 2004/ Accepted 5 September 2004

Abstract:

We investigated the possibility that manifestations of Lyme disease in certain hosts, such as arthritis and carditis, may be autoimmunity mediated due to molecular mimicry between the bacterium Borrelia burgdorferi and self-components. We first compared amino acid sequences of Streptococcus pyogenes M protein, a known inducer of antibodies that are cross-reactive with myosin, and B. burgdorferi and found significant homologies with OspA protein. We found that S. pyogenes M5-specific antibodies and sera from B. burgdorferi-infected mice reacted with both myosin and B. burgdorferi proteins by Western blots and enzyme-linked immunosorbent assay. To investigate the relationship between self-reactivity and the response to B. burgdorferi, NZB mice, models of autoimmunity, were infected. NZB mice infected with B. burgdorferi developed higher degrees of joint swelling and higher anti-B. burgdorferi immunoglobulin M cross-reactive responses than other strains with identical major histocompatibility complex (DBA/2 and BALB/c). These studies reveal immunological cross-reactivity and suggest that B. burgdorferi may share common epitopes which mimic self-proteins. These implications could be important for certain autoimmunity-susceptible individuals or animals who become infected with B. burgdorferi.

jcm.asm.org/cgi/content/abstract/43/2/850

[LymeEnigma]

Pathogen Specificity and Autoimmunity Are Distinct Features of Antigen-Driven Immune Responses in Neuroborreliosis{triangledown}
Sandra Kuenzle,1,{dagger} Hans-Christian von Büdingen,1,{dagger} Mirjam Meier,1 Melanie D. Harrer,1 Eduard Urich,2 Burkhard Becher,2 and Norbert Goebels1*

Clinical Neuroimmunology Unit,1 Experimental Neuroimmunology Unit, Department of Neurology, University Hospital Zürich, Frauenklinikstrasse 26, CH-8091 Zürich, Switzerland2

Received 16 February 2007/ Returned for modification 6 April 2007/ Accepted 7 May 2007

Abstract: Neuroborreliosis (NB) is a chronic infectious disease of the central nervous system (CNS) caused by a tick-borne spirochete, Borrelia burgdorferi. In addition to direct effects of the causative infectious agent, additional immunity-mediated mechanisms are thought to play a role in the CNS pathology of NB. In order to further understand the involvement of humoral immune mechanisms in NB, we dissected the intrathecal antibody responses down to the single-plasma-cell level. Starting with single-cell reverse transcription-PCR of fluorescence-activated cell sorter-sorted cerebrospinal fluid plasma cells from an NB patient, we identified expanded clones and resurrected the antigen specificity of their secreted antibodies through recombinant expression of the correctly paired immunoglobulin heavy- and light-chain genes as monoclonal antibodies (MAbs). As expected, we found specificity for the causative infectious agent, B. burgdorferi, among the clonally expanded plasma cell (cePC)-derived MAbs. However, from an independent cePC of the same patient, we could derive MAbs specific for human CNS myelin, without detectable cross-reactivity with B. burgdorferi antigens. While reactivity against B. burgdorferi is a known feature of humoral immune responses in NB, we show (i) that immune responses specific for self antigens may be a distinct feature of CNS infections independent of pathogen reactivity and (ii) that humoral autoimmunity in NB (since found in cePC) is the result of a truly antigen-driven immune response. Our findings indicate that in NB mechanisms may be at play that induce distinct immune responses specific for pathogen and self antigens independent from "molecular mimicry."

Full article: iai.asm.org/cgi/content/full/75/8/3842?view=long&pmid=17517881

[LymeEnigma]

J Vet Intern Med. 2005 Sep-Oct;19(5):654-62.

Suppurative, nonseptic polyarthropathy in dogs.

Rondeau MP, Walton RM, Bissett S, Drobatz KJ, Washabau RJ.

Department of Clinical Studies, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104, USA. [e-mail]

The goals of this study were to determine the historical, physical examination, and clinicopathologic findings in dogs with suppurative, nonseptic polyarthropathy and to identify concurrent disorders associated with this syndrome. Medical records of 52 dogs with cytologic evidence of suppurative inflammation in two or more joints were examined retrospectively. Age of dogs was 4.8 years (median, range: 0.5-12 years). There was no clear breed or sex predilection, but most were large-breed dogs (body weight > or = 20 kg [44.4 lbs] in 40/52). Body temperature was 103.0 degrees F (39.4 degrees C) (median, range: 100.0-105.9 degrees F), with 29 of 52 dogs having a body temperature > or = 103 degrees F (39.4 degrees C). Lameness was identified in 42 of 52 dogs. Erosive changes were found in only 1 of 37 dogs that had radiography performed. A clear underlying disease process was not identified in 34 of 52 dogs. Seven dogs had evidence of infectious or inflammatory processes at extra-articular sites; 4 dogs were diagnosed with systemic lupus erythematosus (SLE); 2 dogs had gastrointestinal disease; 2 dogs had been vaccinated within 1 month before onset of polyarthritis; 1 dog had cancer; 1 dog had polyarthritis and meningitis; and 1 dog had erosive polyarthritis. Of the 44 dogs tested, 25 had antibodies to Borrelia burgdorferi, detected by an ELISA assay, which was significantly greater than the general hospital population (P = .007). Antibodies against Rickettsia rickettsiae and Ehrlichia canis were not definitively identified in the sera of any dog tested in this study (45 and 44 dogs, respectively). We conclude that an underlying disease process is not identified in most cases of suppurative polyarthropathy in dogs and that intestinal disease, neoplasia, and SLE are uncommon causes of polyarthritis. While seropositivity against the causative agent of Lyme disease was common and possibly a cause of polyarthritis in some dogs of our study, evidence of other vector-borne infection was not identified.

PMID: 16231709 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/16231709?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

[LymeEnigma]

Med Microbiol Immunol. 2000 Nov;189(2):85-90.

Genes outside the major histocompatibility complex control resistance and susceptibility to experimental Lyme arthritis.

Brown CR, Reiner SL.

Gwen Knapp Center for Lupus and Immunology Research, University of Chicago, IL 60637, USA.

The mechanism controlling the development of experimental Lyme arthritis remains poorly understood. Mice with the H-2k haplotype have generally been thought to be more susceptible to Lyme arthritis development than those with the H-2d haplotype. In the present study the role of genes within the major histocompatibility complex (MHC) in determining resistance or susceptibility to the development of experimental Lyme arthritis was investigated. We found that C3H congenic mice were equally susceptible, and DBA congenic mice equally resistant, to arthritis development regardless of their H-2 haplotype (H-2k or H-2d). These results indicate that genes outside the murine MHC are the major determinants of both resistance and susceptibility to the development of experimental Lyme arthritis.

PMID: 11138641 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/11138641?ordinalpos=11&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum