Bb and Reactive Arthritis

[LymeEnigma]

Drugs. 2001;61(3):343-51.

Bacteria-Triggered reactive arthritis: implications for antibacterial treatment.

Toivanen A.

Department of Medicine, Turku University, Finland. [e-mail]

Reactive arthritis (ReA) is definitely caused by an infection. Several observations suggest that the triggering microbe may persist in the tissues of the patient for a prolonged time. The obvious conclusion is to consider antibacterial treatment. In two instances antibacterial agents are of definite value: in the primary and secondary prevention of rheumatic fever and for early eradication of Borrelia burgdorferi in order to prevent development of the arthritis associated with Lyme disease. Altogether, clinical and experimental data exist to indicate that if antibacterial treatment of ReA can be started very early during the pathogenetic process, the disease can be prevented or the prognosis improved. In fully developed ReA, the value of antibacterial agents is less certain. All available evidence indicates that short term antibacterial treatment has no effect on the prognosis and final outcome of ReA, and the results with long term administration of antibacterials are also overall poor. In some instances sulfasalazine appears useful, rather as a result of its antirheumatic effect or influence on an underlying inflammatory bowel disease than its action as an antibacterial agent. Tetracyclines have also been found to have an effect on ReA, but again, this is probably due to their anti-inflammatory action rather than any antibacterial effect.

PMID: 11293645 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/11293645

[LymeEnigma]

Chromosomal DNA from a variety of bacterial species is present in synovial tissue from patients with various forms of arthritis


*Correspondence to Alan P. Hudson, Department of Immunology and Microbiology, Wayne State University School of Medicine, Gordon H. Scott Hall, 540 East Canfield Avenue, Detroit, MI 48201


Abstract

Objective
We and others have reported the presence of Chlamydia and other bacterial species in joint specimens from patients with reactive arthritis (ReA). The present study was conducted to investigate whether bacteria other than those specified by diagnostic criteria for ReA could be identified in synovial fluid (SF) or tissue from patients with various arthritides, and whether the presence of such organisms corresponds to particular clinical characteristics in any patient set or subset.

Methods
DNA in synovial biopsy samples and SF obtained from 237 patients with various arthritides, including ReA, rheumatoid arthritis, and undifferentiated oligoarthritis, was assayed by polymerase chain reaction (PCR) using panbacterial primers; we chose only samples known to be PCR negative for Chlamydia, Borrelia, and Mycoplasma species. PCR products were cloned, and cloned amplicons from each sample were sequenced; DNA sequences were compared against all others in GenBank for identification of bacterial species involved.

Results
Ten percent of patient samples were PCR positive in panbacterial screening assays. Bacterial species identified belonged to the genera Neisseria, Acinetobacter, Moraxella, Salmonella, Pseudomonas, and others. Thirty-five percent of PCR-positive patients showed the presence of DNA from more than a single bacterial species in synovium; overall, however, we could identify no clear relationship between specific single or multiple bacterial species in the synovium and any general clinical characteristics of any individual or group of patients.

Conclusion
This analysis provides the first systematic attempt to relate bacterial nucleic acids in the synovium to clinical characteristics, joint findings, and outcomes. Many patients with arthritis have bacterial DNA in the joint, and, in some cases, DNA from more than a single species is present. However, except for 1 case of a control patient with staphylococcal septic arthritis, it is not clear from the present study whether the synovial presence of such organisms is related to disease pathogenesis or evolution in any or all cases.

www3.interscience.wiley.com/journal/84504284/abstract?CRETRY=1&SRETRY=0

*edited to fix link.

[LymeEnigma]

Arthritis Rheum. 2001 Nov;44(11):2679-85.Links

Comment in:
Arthritis Rheum. 2001 Nov;44(11):2463-6.
Arthritis Rheum. 2002 Aug;46(8):2259-60; author reply 2260.

Chlamydia and Borrelia DNA in synovial fluid of patients with early undifferentiated oligoarthritis: results of a prospective study.

Schnarr S, Putschky N, Jendro MC, Zeidler H, Hammer M, Kuipers JG, Wollenhaupt J.

Hannover Medical School, Division of Rheumatology, Germany. [e-mail]

OBJECTIVE: More than 50% of patients with synovitis involving 1-4 joints remain classified as having undifferentiated oligoarthritis (UOA) after 1 year of disease. The clinical presentation is often similar to that of reactive arthritis (ReA) and other spondylarthropathies or to Lyme arthritis. We therefore determined how often Chlamydia trachomatis (Ct) and Borrelia burgdorferi (Bb) can be identified in patients with UOA, by using an extensive laboratory approach. METHODS: We prospectively studied 52 patients with UOA who presented at an early synovitis clinic in a region highly endemic for Lyme disease. Patients were examined by standardized clinical and immunoserologic procedures. Synovial fluid was screened for the presence of Ct and Bb DNA by polymerase chain reaction (PCR). Urine was tested for Ct DNA by ligase chain reaction, and serum was tested for Ct antibodies by enzyme-linked immunosorbent assay and Bb antibodies by hemagglutination test and Western blotting. PCR results in the UOA patients were compared with the results in cohorts of patients with definite rheumatoid arthritis (RA), Lyme arthritis, and Chlamydia-induced arthritis (CIA). RESULTS: In the synovial fluid of 9 of 52 patients with UOA (17%), we found Ct DNA, and in 6 of the 52 patients (12%), Bb DNA was found. The frequency of bacteria-specific DNA was 50% (7 of 14) in CIA patients and 69% (11 of 16) in patients with Lyme arthritis. No Bb or Ct DNA was found in the synovial fluid of the 31 RA patients. CONCLUSION: With optimized PCR protocols, it is possible to detect considerable levels of Bb and Ct DNA in the synovial fluid of patients with UOA. Although the presence of bacterial DNA does not unequivocally prove its etiologic significance, we suggest that at least one-third of patients with UOA may have a form of ReA that involves asymptomatic primary infection.

PMID: 11710723 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/11710723

[LymeEnigma]

Clin Exp Rheumatol. 2008 Jan-Feb;26(1 Suppl 48):S12-7.

Bacterial triggers and autoimmune rheumatic diseases.

Girschick HJ, Guilherme L, Inman RD, Latsch K, Rihl M, Sherer Y, Shoenfeld Y, Zeidler H, Arienti S, Doria A.

Pediatric Rheumatology, Immunology, Infectious Diseases, Children's Hospital, University of Wuerzburg, Germany.

Autoimmune rheumatic diseases are generally considered as a multifactorial aetiology, mainly genetic susceptibility combined with environmental triggers of which bacteria are considered one of the most prominent. Among the rheumatic diseases where bacterial agents are more clearly involved as triggers are: reactive arthritis (ReA), rheumatic fever (RF) and Lyme disease. The role of bacterial infections in inducing other seronegative spondyloarthritis and antiphospholipid antibody syndrome has been hypothesized but is still not proven. The classic form of ReA is associated with the presence of HLA-B27 and is triggered by the urethritis or enteritis causing pathogens Chlamydia trachomatis and the enterobacteria Salmonella, Shigella, and Yersinia, respectively. But several other pathogens such as Brucella, Leptospira, Mycobacteria, Neisseria, Staphylococcus and Streptococcus have also been reported to cause ReA. RF is due to an autoimmune reaction triggered by an untreated throat infection by Streptococcus pyogenes in susceptible individuals. Carditis is the most serious manifestation of RF and HLA-DR7 is predominantly observed in the development of valvular lesions. Lyme disease is a tick-transmitted disease caused by the spirochete Borrelia burgdorferi. Knowledge is limited about how this spirochete interacts with human tissues and cells. Some data report that Borrelia burgdorferi can manipulate resident cells towards a pro- but also anti-inflammatory reaction and persist over a long period of time inside the human body or even inside human cells.

PMID: 18570749 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/18570749

[LymeEnigma]

Clin Exp Rheumatol. 2003 Mar-Apr;21(2):213-6.Links
Prevalence of Sindbis-related (Pogosta) virus infections in patients with arthritis.
Laine M, Vainionpää R, Uksila J, Oksi J, Nissilä M, Kaarela K, Luukkainen R, Toivanen A.

Department of Medicine, Medical Microbiology, Turku University, Turku, Finland.

OBJECTIVE: To determine the role of Pogosta virus as a triggering infection in non-specific arthritis. METHODS: Serum samples of 142 patients with acute arthritis were screened for the evidence of Pogosta virus infection. Serological tests for Chlamydia trachomatis, salmonella, parvovirus B19, and Borrelia burgdorferi were also carried out. As verified later, 78 of the patients had rheumatoid arthritis and 63 seronegative poly- or oligoarthritis, while one had systemic lupus erythematosus. RESULTS: In the early stage of the joint symptoms 4 patients with rheumatoid arthritis, 1 with seronegative polyarthritis and 1 with systemic lupus erythematosus had recent Pogosta virus infection. Four of them had probably had Pogosta disease at the time of the onset of arthritis. In 11 patients with a diagnosis of seronegative arthritis, serological evidence of preceding infection due to salmonella or Chlamydia trachomatis was found, strongly suggesting classical reactive arthritis in these cases. CONCLUSIONS: Our study suggests that also a Sindbis virus infection may be associated both to an acute joint inflammation as a part of Pogosta disease or chronic arthritis. At present, this possibility still needs further research.

PMID: 12747277 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/12747277?

[LymeEnigma]

Clin Microbiol Infect. 2008 Sep;14(9):873-5.

Cross-reaction between Yersinia outer membrane proteins and anti-Borrelia antibodies in sera of patients with Lyme disease.

Golkocheva-Markova E, Christova I, Stoilov R, Najdenski H.

Department of Pathogenic Bacteria, The Stephan Angeloff Institute of Microbiology, Bulgarian Academy of Sciences, Sofia, Bulgaria. [e-mail]

Diagnosis of Yersinia infections accompanied by reactive arthritis could be complicated by cross-reaction with other arthritogenic bacteria. The possible cross-reaction between Yersinia antigens and anti-Borrelia antibodies in blood sera of patients with Lyme disease was studied. The occurrence of specific IgA, IgG and IgM antibodies was analyzed in serum samples from 30 patients with Yersinia-triggered reactive arthritis, 30 patients with Lyme disease and five samples from healthy blood donors. For anti-Borrelia IgG antibodies, cross-reaction was detected with YopH, YopB, V-ag, YopD, YopN, YopP and YopE, and for IgA with YopD. For IgM, no cross-reaction was detected. Owing to cross-reactivity with Borrelia, the diagnosis of Yersinia-triggered reactive arthritis should be based on a combination of serological and clinical findings.

PMID: 18844689 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/18844689