Triggers Of Reactive Arthritis Research Articles

Yersinia enterocolitica biotype 1A: a possible new trigger of reactive arthritis.

Yersinia enterocolitica (YE) biotype 1A is generally considered non-pathogenic, and the role of it in causing reactive musculoskeletal complications is unclear. We evaluated the capability of YE biotype 1A to induce reactive arthritis (ReA) and other reactive musculoskeletal symptoms. Analysis of self-reported musculoskeletal symptoms was supplemented with a telephone interview (with a permission to acquire copies of patient files from a local physician or hospital) and/or clinical examination of subjects with recent musculoskeletal symptoms after a positive stool culture for YE. The diagnoses of ReA and reactive tendinitis and enthesitis (ReTe) were defined as "definite" when based on clinical examination and/or on interview by phone and "probable" when based solely on the questionnaire. Of 120 subjects, who reported musculoskeletal symptoms, 100 were included in the final analysis. Among these 100 patients, 68% had YE biotype 1A, 16% YE bio/serotype 4, and 1% biotype 2 infection; the remaining 15% had different YE-like strains or a non-biotypable strain. Of the 21 patients with ReA and of the 14 patients with ReTe, the diagnosis was definite in 9 and 7 patients and probable in 12 and 7 patients, respectively. The clinical picture of ReA caused by YE biotype 1A was similar with other bio/serotypes of YE. The definite ReA due to YE biotype 1A occurred in middle-aged adults (5 men, 4 women) with the most frequently affected joints being the knees and ankles. We suggest that YE biotype 1A should be taken into account as a new trigger of ReA.

Combination antibiotics as a treatment for chronic Chlamydia‐induced reactive arthritis: A double‐blind, placebo‐controlled, prospective trial

Chlamydia trachomatis and Chlamydophila (Chlamydia) pneumoniae are known triggers of reactive arthritis (ReA) and exist in a persistent metabolically active infection state in the synovium, suggesting that they may be susceptible to antimicrobial agents. The goal of this study was to investigate whether a 6-month course of combination antibiotics is an effective treatment for patients with chronic Chlamydia-induced ReA. This study was a 9-month, prospective, double-blind, triple-placebo trial assessing a 6-month course of combination antibiotics as a treatment for Chlamydia-induced ReA. Eligible patients had to be positive for C trachomatis or C pneumoniae by polymerase chain reaction (PCR). Groups received 1) doxycycline and rifampin plus placebo instead of azithromycin; 2) azithromycin and rifampin plus placebo instead of doxycycline; or 3) placebos instead of azithromycin, doxycycline, and rifampin. The primary end point was the number of patients who improved by 20% or more in at least 4 of 6 variables without worsening in any 1 variable in both combination antibiotic groups combined and in the placebo group at month 6 compared with baseline. The primary end point was achieved in 17 of 27 patients (63%) receiving combination antibiotics and in 3 of 15 patients (20%) receiving placebo. Secondary efficacy end points showed similar results. Six of 27 patients (22%) randomized to combination antibiotics believed that their disease went into complete remission during the trial, whereas no patient in the placebo arm achieved remission. Significantly more patients in the active treatment group became negative for C trachomatis or C pneumoniae by PCR at month 6. Adverse events were mild, with no significant differences between the groups. These data suggest that a 6-month course of combination antibiotics is an effective treatment for chronic Chlamydia-induced ReA.

HLA-B27 expression does not modulate intracellular Chlamydia trachomatis infection of cell lines.

Chlamydia trachomatis is an obligate intracellular pathogen. Infection of susceptible individuals with this bacterium can trigger the development of reactive arthritis, an acute inflammation that is associated with the expression of the class I major histocompatibility antigen, HLA-B27. Other facultative intracellular pathogens, such as Yersinia and Salmonella spp., are also known triggers of reactive arthritis. Previous studies report conflicting results concerning whether the presence of HLA-B27 modulates the infection of cells with these enteric pathogens. In the present study, we have examined whether the expression of HLA-B27 can influence the infection of cell lines with C. trachomatis and also whether the replication of these bacteria is altered in HLA-B27-expressing cell lines. To do this, we have used a sensitive flow cytometric approach. We fixed and permeabilized cells and used fluorescein isothiocyanate-conjugated monoclonal antibody specific for chlamydia lipopolysaccharide to detect intracellular bacteria. The staining pattern obtained closely resembled the intracellular life cycle of chlamydia, with the appearance of brightly staining cells correlating to the microscopic detection of mature inclusion bodies. Moreover, since the percentage of cells that stained with the antibody was proportional to the infectious inoculum used, we were able to use the technique to quantitate the number of infectious organisms recoverable from infected cell lines. An important component of our study was the use of heparin to prevent reinfection of cells and thus enable the infection to be followed from a discrete time point. Our results suggest that HLA-B27 influences neither the infection nor replication of C. trachomatis serovar L2 within cell lines. Consequently, the role of HLA-B27 in the pathogenesis of reactive arthritis may lie downstream of the invasion and replication stages of the triggering pathogenic infection.

Infectious Agents as Triggers of Reactive Arthritis

Reactive arthritis was originally defined as a sterile joint inflammation after infection elsewhere in the body, but this view has been challenged in the past decade since different antigens and DNA and RNA of various triggering microbes have been shown to exist at the sites of inflammation in the joints. It has been suggested that microbial antigens, or intact pathogens, are important for the pathogenesis of reactive arthritis, at least in the early phase of the disease, but the exact mechanism of how the pathogens contribute to the development of this usually self-limiting polyarthritis has not been discovered. This article reviews the theories on the role of infectious agents as triggers of reactive arthritis.

Infectious agents as triggers of reactive arthritis.

Reactive arthritis was originally defined as a sterile joint inflammation after infection elsewhere in the body, but this view has been challenged in the past decade since different antigens and DNA and RNA of various triggering microbes have been shown to exist at the sites of inflammation in the joints. It has been suggested that microbial antigens, or intact pathogens, are important for the pathogenesis of reactive arthritis, at least in the early phase of the disease, but the exact mechanism of how the pathogens contribute to the development of this usually self-limiting polyarthritis has not been discovered. This article reviews the theories on the role of infectious agents as triggers of reactive arthritis.

Reactive arthritis.

The complex interactions between the triggering microbe and the defense mechanisms of the host in reactive arthritis have been studied in several laboratories around the world, and interesting observations have been made. Research has also focused on the mediators in the inflammatory process in joints, and these results are helping to slowly build a comprehensive picture about the pathogenetic process in reactive arthritis. For the practicing clinician, some important new findings have emerged. It is known that asymptomatic urogenital infections are quite common as a trigger of reactive arthritis. More aggressive treatment, including disease-modifying drugs as used in the therapy of rheumatoid arthritis, is becoming accepted. The value of antibiotic treatment is being studied, but final conclusions will not be made for perhaps a few years.

Current perspectives in reactive arthritis

Reactive arthritis (ReA) is an inflammatory arthritis triggered by infection, usually urethritis or gastroenteritis, and is strongly associated with the MHC class I antigen HLA-B27. Two recent observations have excited interest: first, antigen and DNA from the triggering bacteria have been identified in the joint and, second, ReA synovial T cells have been found to respond specifically to the bacterium that caused the initiating infection. Because the trigger of ReA, its onset and the MHC association are all clearly defined, we can investigate hypotheses that are impossible to study in other forms of human arthritis. Here, Gabrielle Kingsley and Jochen Sieper review the topic in the light of a recent workshop.

Über den Nachweis von Tuberkelbazillen und Muchschen Granula bei Lupus vulgaris, Lupus erythematodes, Erythema induratum Bazin, Lupus pernio und papulo-nekrotischem Tuberkulid

The diagnosis of reactive arthritis relies mainly on the presence of clinical symptoms caused by the initiating infection in the urogenital or enteral tract. An oligoarthritis mainly of the lower limbs occurs 1-6 weeks later. Chlamydia trachomatis and Yersinia enterocolitica are the most frequent triggers of reactive arthritis. Since the infections caused by these microbes are clinically often asymptomatic diagnostic evaluation can be difficult; serology is often nonspecific and cultures are mostly negative. The microscopic detection of bacterial antigens in the joint and the determination of a bacteria specific lymphocyte proliferation in the synovial fluid have changed the pathogenetic concept of reactive arthritis. However, these methods are technically difficult and not suitable for daily routine. There is no indication for short-term antibiotic treatment, as is often prescribed, except in the case of Chlamydia-induced urethritis, which should be treated in any case to prevent the onset or a relapse of reactive arthritis; the sexual partner must also be treated. Long-term therapy with various antibiotic regimens is now being tested in clinical trials. The symptomatic therapy of arthritis comprises physical methods and the use of nonsteroidal anti-inflammatory drugs; intra-articular administration of corticosteroids is of benefit in some cases. If the arthritis takes a chronic course disease modifying drugs such as sulfasalazine are partly successful; in refractory cases arthroscopic synovectomy may become necessary.