Chlamydia pneumoniae--a new causative agent of reactive arthritis and undifferentiated oligoarthritis.

OBJECTIVE--To examine whether reactive arthritis (ReA) known to occur after a urogenital infection with Chlamydia trachomatis can also follow an infection with Chlamydia pneumoniae, a recently described species of Chlamydiae that is a common cause of respiratory tract infections. METHODS--Specific antibodies (microimmunofluorescence test) and lymphocyte proliferation to C trachomatis and C pneumoniae in paired samples of peripheral blood and synovial fluid were investigated in 70 patients with either reactive arthritis (ReA) or undifferentiated oligoarthritis (UOA). RESULTS--Five patients with acute ReA after an infection with C pneumoniae are reported. Three had a symptomatic preceding upper respiratory tract infection and two had no such symptoms. In all patients a C pneumoniae-specific lymphocyte proliferation in synovial fluid and a high specific antibody titre suggesting an acute infection was found. CONCLUSION--C pneumoniae needs to be considered a new important cause of reactive arthritis.     

Use of a peptide based enzyme immunoassay in diagnosis of Chlamydia trachomatis triggered reactive arthritis.

OBJECTIVE: To assess the presence of circulating IgA and IgG antibodies to Chlamydia trachomatis in sera of patients with reactive arthritis (ReA) and other arthritides. METHODS: A peptide based enzyme immunoassay (EIA) was used to study 132 patients divided into 5 groups: C. trachomatis triggered ReA, uroarthritis, enteroarthritis, oligoarthritis, and rheumatoid arthritis (RA). Followup sera were available from 19 patients. RESULTS: An increased prevalence of C. trachomatis antibodies was observed in patients with ReA triggered by C. trachomatis; 18/23 (78%) had IgA and 19/23 (83%) had IgG antibodies. In patient groups with uroarthritis (n = 12), enteroarthritis (n = 56), oligoarthritis (n = 16), and RA (n = 25), C. trachomatis IgA/IgG antibodies were detected in 58%/75%, 27%/21%, 25%/31%, and 20%/32% of patients, respectively. Both the IgA and IgG antibodies were positive in 74%, 50%, 16%, 25%, and 12% of the patients with C. trachomatis triggered ReA, uroarthritis, enteroarthritis, oligoarthritis, and RA, respectively. Based on positivity of both isotypes the sensitivity of the assay was 74% and specificity 84%. In the followup sera, an association between circulating C. trachomatis-specific antibody concentrations and clinical disease outcome of the arthritis was seen in patients with culture-positive C. trachomatis triggered ReA. CONCLUSION: C. trachomatis species-specific peptide EIA correlates well with conventional diagnosis of primary C. trachomatis infection in patients with ReA. This assay may be a valuable contribution to the diagnosis of C. trachomatis triggered ReA.     

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

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.     

Potential triggering infections of reactive arthritis

OBJECTIVES: The aim of the study was to investigate possible triggering infections causing reactive arthritis (ReA) of urogenital origin. METHODS: One hundred and twenty ReA patients, 85 control group patients with other arthritides (61 with rheumatoid arthritis, 13 with osteoarthritis, and 11 with microcrystal arthritis), and 52 healthy persons were tested for urogenital tract inflammation and several infectious agents. Ligase chain reaction was used for detection of Chlamydia trachomatis (CT). Genital mycoplasmas Ureaplasma urealyticum (Uu) and Mycoplasma hominis (Mh) were tested using the Mycoplasma Duo Test (MDT). Only titres greater than 10(4) CCU/mL were accepted as pathogenecity threshold levels for Uu. RESULTS: Inflammation of the urogenital tract (most frequently urethritis in men and cervicitis in women) was found in 95% of patients with acute ReA. Possible causative pathogens were identified in 58% of ReA patients. CT was found in 29%, Uu in 21%, and Mh in 8% of patients with ReA. While CT and Uu were found more often in HLA-B27-positive than in HLA-B27-negative patients, this was statistically proved only for CT. In ReA males Uu was found four times more frequently than in men with other arthritides. CONCLUSIONS: In active ReA of urogenital origin, inflammation of the urogenital tract is found in the majority of patients. Although CT is the main microorganism associated with urethritis in men and cervicitis in women, mycoplasmas, especially Uu, may be possible aetiological factors for ReA.     

Pathogenetic role of Chlamydia, Yersinia and Borrelia in undifferentiated oligoarthritis.

We studied the cellular and humoral immune response to Chlamydia trachomatis, Yersinia enterocolitica and Borrelia burgdorferi in paired samples of peripheral blood and synovial fluid (SF) in undifferentiated oligoarthritis, reactive arthritis (ReA) and rheumatoid arthritis. Antigen specific lymphocyte proliferation was found in SF of 43% of patients with ReA and 34% of patients with undifferentiated oligoarthritis. C. trachomatis was the most frequent single agent. HLA-B27 was positive in 83% of patients with ReA and in 62% of patients with undifferentiated oligoarthritis with antigen specific lymphocyte proliferation. Antigen specific lymphocyte proliferation correlated poorly with the specific antibody response. Only chlamydial antigen was detected in SF cells using monoclonal antibodies. We conclude that some patients with undifferentiated oligoarthritis may have a forme fruste of ReA. This finding is important in view of recent evidence supporting the efficacy of antibiotic therapy in ReA.     

The role of diagnostic tests in the identification of Chlamydia trachomatis infection in reactive arthritis

Reactive arthritis (ReA) is a sterile inflammation of the synovial membrane of one or more joints developing after urogenital or gastro-intestinal infection. The syndrome most frequently follows infection with Chlamydia trachomatis. Useful for the diagnosis can be the serological tests. At present there is the possibility to identify the specific antibodies (IgG, IgA, IgM) to Chlamydia trachomatis. The subject of the study was the group of 87 patients in age 19-78; 58 women and 29 men from whom urogenital smear and serum were tested. The control group were 30 people age 25-70 without rheumatological disorders. Chlamydia trachomatis was found in urogenital smear in 42 (48%), in 56 (64%) patients immunoglobulin IgG were positive, and immunoglobulin IgA in 16 (18%). The laboratory tests and clinical symptoms allow to make a diagnosis of ReA in 38 (43%) and possible ReA in 5 (5.7%) of patients. CONCLUSIONS: 1. There is no gold standard for the diagnosis of ReA. 2. None of the tests or the clinical symptoms alone are strong enough to make a definite diagnosis of ReA. 3. Tests to identify Chlamydia trachomatis, with respect of typical clinical symptoms are useful the diagnosis of ReA. 4. The diagnosis of ReA is most probable if we have typical clinical symptoms, clinical evidence of a preceding infection plus a positive result of serology or PCR plus positivity for HLA-B27.     

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

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.

     

The 19 kDa protein of Yersinia enterocolitica O:3 is recognized on the cellular and humoral level by patients with Yersinia induced reactive arthritis.

OBJECTIVE: Gastrointestinal infections with Yersinia enterocolitica O:3 (YE O:3) can trigger reactive arthritis (ReA). The cellular immune response seems to be of pathogenic importance in ReA, since synovial fluid mononuclear cells (SFMC) of patients with ReA have been shown to recognize YE O:3 antigens. One of these, a 19 kDa protein identified as the beta-urease subunit of YE, has been identified as a target of SFMC. We investigated the humoral immune response to this antigen. METHODS: Sera of 32 patients with SFMC proliferation to YE O:3 diagnosed as having ReA (n = 16) and undifferentiated oligoarthritis (UOA, n = 16), and of patients with other rheumatic diseases (n = 32) and healthy persons (n = 12) were investigated for the humoral response to the biochemically purified 19 kDa protein of YE. Anti-19 kDa antibodies (ab) were identified by immunoblotting; ab to the Yersinia outer membrane protein (YOP) antigen were detected by ELISA. Proliferation of SFMC to 19 kDa and other YE O:3 antigens was tested in 12 patients in parallel. RESULTS: SFMC of all 32 patients with ReA and UOA showed the highest proliferation to YE O:3 (13.7+/-7.5), and 10/12 of these patients had the highest stimulation index to the 19 kDa (14.9+/-6.4). Anti-19 kDa IgG ab were detected in 93% and 55% and anti-19 kDa IgA ab in 56% and 36% of the ReA and UOA patients, respectively, compared to 26% (p = 0.002) and 8% (p = 0.001) in controls. IgG ab to the 19 kDa were sensitive (93%) and IgA ab specific (92%) to detect patients with a synovial cellular response to YE. IgG ab to YOP were found in 62% and IgA ab in 46% of the ReA patients and in 32% (p = 0.002) and 13% (p = 0.004) of the controls. CONCLUSION: This study provides evidence of a cellular and a significant humoral immune response to the 19 kDa protein in Yersinia triggered arthritis. Detection of IgG antibodies to the 19 kDa correlates with a synovial cellular immune response in YE induced arthritis. These antibodies can be used as a screening system for research and possibly also for clinical purposes, since absence of such antibodies seems to negatively predict YE O:3 directed immune reactivity.     

Infections preceding early arthritis in southern Sweden: a prospective population-based study

OBJECTIVE: To detect evidence of infections preceding early arthritis in Southern Sweden and to compare the clinical outcome of remission during a 6-month followup for patients with and without signs of prior infection. METHODS: Adult patients with arthritis of less than 3 months' duration were referred from primary health care centers to rheumatologists. All patients were systematically screened for infections caused by Salmonella typhimurium and Salmonella enteritidis, Yersinia enterocolitica, Campylobacter jejuni, Borrelia burgdorferi, Chlamydia trachomatis, Chlamydia pneumoniae, and parvovirus B19. RESULTS: Seventy-one patients were included in this study. Twenty-seven (38%) patients had reactive arthritis (ReA), 17 (24%) undifferentiated arthritis, 15 (21%) rheumatoid arthritis (RA), 4 (6%) psoriatic arthritis, and the rest (11%) other diagnoses. Of all the patients, 45% had evidence of a recent infection preceding the arthritis, as indicated by laboratory tests and/or disease history. C. jejuni dominated the ReA group. The occurrence of recent C. trachomatis, B. burgdorferi, C. pneumoniae, and parvovirus B19 infections was low. Overall, 58% of the patients went into remission during the 6-month followup. Of the patients with a preceding infection, 69% went into remission as compared to 38% of the patients without a preceding infection (p = 0.011). Thirty-three percent of the patients with RA were in remission after 6 months. CONCLUSION: In this population-based cohort, 45% of the patients presenting with a new-onset arthritis had had a prior infection. Campylobacter ReA dominated the ReA group. There were only a few cases preceded by infections by C. trachomatis, B. burgdorferi, C. pneumoniae, and parvovirus B19 infections. Remission during the first 6 months was especially frequent in the group of patients with a prior infection, but the remission rate was relatively high even for arthritis without prior infection.     

THE POSSIBLE ROLE OF SHIGELLA IN SPORADIC ENTERIC REACTIVE ARTHRITIS

Reactive arthritis (ReA) occurs after a urogenital infectionusually with Chlamydia trachomatis or an enteritis due to Yer-sinia,Salmonella, Campylobacter or Shigella, Shigella, except duringepidemics, is not considered to be a frequent cause of entericreactive arthritis. However this might be due to the lack ofa reliable antibody test, which makes diagnosis difficult. Wecompared synovial and peripheral blood lymphocyte proliferationto various bacterial antigens in 19 consecutive patients withReA or undifferentiated oligoarthritis. In five patients Shigellawas identified as the causative microbe by a specific synoviallymphocyte proliferation. All five patients had a history ofsymptomatic diarrhoea and had negative stool cultures by thetime arthritis developed. Four of the five were HLA B 27 positive.We conclude that Shigella may be underestimated as a cause ofnon-epidemic ReA. KEY WORDS: Reactive arthritis, Shigella, Antigen specific lymphocytes, Synovial fluid     

Evaluation of amplicor chlamydia PCR and LCX chlamydia LCR to detect Chlamydia trachomatis in synovial fluid

OBJECTIVES: PCR has been successfully used in research for the detection of C. trachomatis DNA in synovial samples. However, each research laboratory has developed its own PCR, making inter-laboratory comparisons difficult. To allow for standardization we evaluated two commercially available amplification systems originally designed for the examination of urogenital samples (Roche Amplicor Chlamydia PCR and Abbott LCX Chlamydia LCR), using them to analyse spiked and clinical synovial fluid (SF) samples from reactive arthritis (ReA), undifferentiated arthritis (UA), and rheumatoid arthritis (RA) patients. We compared their sensitivity in assays of clinical SF samples with our in-house developed C. trachomatis specific nested PCR. METHODS: SF was spiked with purified C. trachomatis elementary bodies (EB) and analyzed by the commercial assays. Clinical SF samplesfrom ReA (n=21), UA (n=79) and RA (n=50) patients were examined by the two commercial assays and our in-house PCR. RESULTS: Using SF samples spiked with defined numbers of C. trachomatis EB, the sensitivity of the commercial tests was high and similar to published PCR sensitivity. In clinical SF specimens the commercial assays was also able to detect CT; however, the in-house PCR was more sensitive. Out of 10 PCR-positive SF samples Amplicor tested positive in only 4/10 and LCX in only 3/10. The in-house PCR detected chlamydial DNA in synovialfluidfrom 5/21 ReA (24%), 5/79 UA (6%) and in none of the 50 RA patients. CONCLUSION: Commercial amplification assays allow the detection of C. trachomatis in clinical specimens, although with a lower sensitivity than optimized PCR. Potential explanations are discussed.     

Reactive arthritis: newer developments

Reactive arthritis (ReA) is characterized by an aseptic inflammatory articular involvement occurring in a genetically predisposed individual secondary to an infectious process localized outside the joint. ReA usually refers to an acute or insidious oligoarthritis process after enteric (enteroarthritis) or urogenital (uroarthritis) infection. Conventional antirheumatic therapeutic modalities based on nonsteroid anti-inflammatory drugs, sulfasalazine, and steroids are effective in the majority of patients. In more refractory cases, the use of second-line agents including methotrexate and more recently biological agents such as etanercept and infliximab has been found highly effective. The role of antibiotics remains not well established, although they appear to be effective in acute ReA of urogenital origin.     

Chlamydia pneumoniae as a triggering infection in reactive arthritis.

OBJECTIVE: To determine the role of Chlamydia pneumoniae as a triggering infection in reactive arthritis (ReA). METHODS: Sixty patients with acute arthritis were screened for the evidence of triggering infections. In all patients, bacterial stool cultures, culture of Chlamydia trachomatis in urethra/cervix, and/or bacterial serology were studied. Chlamydia pneumoniae antibodies were measured by specific microimmunofluorescence test. RESULTS: Thirty-five of 60 patients fulfilled the diagnostic criteria for ReA. Thirty-one patients had microbial/serological evidence of preceding infection due to Salmonella, Yersinia, Campylobacter or Chlamydia trachomatis, or they had enteritis or urethritis prior to arthritis. Four additional patients had high antibody titre for C. pneumoniae. Three of these four patients had preceding lower respiratory symptoms, and were positive for HLA-B27. The clinical picture of C. pneumoniae-positive ReA patients was similar to that of ReA patients with other definite aetiology. CONCLUSION: Chlamydia pneumoniae is a triggering factor in approximately 10% of patients with acute ReA.     

Reactive arthritis

Reactive arthritis (ReA) can be defined as the development of sterile inflammatory arthritis as a sequel to remote infection, often in the gastrointestinal or urogenital tract. Although no generally agreed-upon diagnostic criteria exist, the diagnosis is mainly clinical, and based on acute oligoarticular arthritis of larger joints developing within 2-4 weeks of the preceding infection. According to population-based studies, the annual incidence of ReA is 0.6-27/100,000. In addition to the typical clinical picture, the diagnosis of ReA relies on the diagnosis of the triggering infection. Human leucocyte antigen (HLA)-B27 should not be used as a diagnostic tool for a diagnosis of acute ReA. In the case of established ReA, prolonged treatment of Chlamydia-induced ReA may be of benefit, not only in the case of acute ReA but also in those with chronic ReA or spondylarthropathy with evidence of persisting chlamydia antigens in the body. In other forms of ReA, there is no confirmed evidence in favour of antibiotic therapy to shorten the duration of acute arthritis. The outcome and prognosis of ReA are best known for enteric ReA, whereas studies dealing with the long-term outcome of ReA attributable to Chlamydia trachomatis are lacking.     

Lower prevalence of Chlamydia pneumoniae DNA compared with Chlamydia trachomatis DNA in synovial tissue of arthritis patients.

OBJECTIVE: To assess the presence of Chlamydia pneumoniae DNA in the joints of patients with reactive arthritis (ReA) and other arthritides. METHODS: DNA was prepared from synovial tissue (ST) and several synovial fluid (SF) samples from 188 patients with either ReA, undifferentiated oligoarthritis, or other forms of arthritis, and from 24 normal (non-arthritis) individuals. Preparations were screened using polymerase chain reaction (PCR) assays that independently targeted the C. pneumoniae 16S ribosomal RNA and major outer membrane protein genes. RESULTS: Twenty-seven of 212 ST samples (12.7%) were PCR positive for C. pneumoniae DNA; 10 SF samples from these 27 patients were similarly positive. Among the PCR-positive patients, 3 had ReA, 2 had Reiter's syndrome, 7 had undifferentiated oligoarthritis, 4 had undifferentiated monarthritis, 6 had rheumatoid arthritis, and 5 had other forms of arthritis. No samples from normal control individuals were PCR positive. CONCLUSION: DNA of C pneumoniae is present in synovial specimens from some arthritis patients. The prevalence of this organism in the joints was lower than that of C trachomatis, and synovial presence of the organism was not associated with any distinct clinical syndrome. Widely disseminated nucleic acids such as those of C. pneumoniae might have some role in the pathogenesis of several arthritides, since the organism was not found in the ST from normal control individuals.     

Ligase chain reaction in detection of Chlamydia DNA in synovial fluid cells

Synovial fluid cells from 12 patients with reactive arthritis (ReA) triggered by Chlamydia trachomatis were studied for the presence of Chlamydia DNA using the ligase chain reaction (LCR) LCx (Abbott) and the polymerase chain reaction (PCR) Amplicor (Roche). In addition, peripheral blood leucocytes from 11 of these patients were analysed by LCR. As controls, seven patients with newly diagnosed rheumatoid arthritis (RA) were included. Chlamydia trachomatis DNA was detectable by LCR in samples of synovial fluid cells from 4/12 patients with C. trachomatis-triggered ReA, and in none by PCR. Chlamydia trachomatis DNA was not detectable in the synovial fluid cells of the seven RA patients by either method, neither was C. trachomatis DNA detectable in the peripheral blood leucocytes of the ReA patients (0/11) or controls (0/6) by LCR. The LCR technique may be useful in the demonstration of Chlamydia DNA in synovial fluid cells.      

Campylobacter-triggered reactive arthritis: a population-based study

OBJECTIVE: To study the incidence and clinical picture of Campylobacter-associated reactive arthritis (ReA) and other reactive musculoskeletal symptoms in the population. METHODS: A questionnaire on enteric and extraintestinal, including specifically musculoskeletal, symptoms was sent to 870 consecutive patients with Campylobacter-positive stool culture and 1440 matched controls. Analysis of self-reported musculoskeletal symptoms with clinical examination was performed. RESULTS: Forty-five of the patients (7%) had ReA and eight (1%) had reactive tendinitis, enthesopathy or bursitis. No child had ReA. The arthritis was oligo- or polyarticular, and, in most cases, mild. HLA-B27 was positive in 14% of ReA patients. Of the 45 ReA patients, 37 had C. jejuni and 8 had C. coli infection. No controls had ReA. CONCLUSION: ReA is common following Campylobacter infection, with an annual incidence of 4.3 per 100000. At the population level, acute ReA is mild, more frequent in adults, and not associated with HLA-B27. Besides C. jejuni, C. coli can trigger ReA.     

Intra-articular co-infection by Borrelia burgdorferi and Chlamydia trachomatis

OBJECTIVE: Chlamydia trachomatis and Borrelia burgdorferi infections are frequently the cause of unexplained oligoarthritis, as shown by identification of bacteria specific DNA in joint material from patients with reactive arthritis, Lyme arthritis, and undifferentiated oligoarthritis. The aim of this study was to determine whether the two organisms occur simultaneously in joint material from patients with arthritis. METHODS: Seventy six patients with unexplained arthritis were prospectively studied. Synovial fluid was obtained from all patients and examined for DNA from C trachomatis and B burgdorferi using specific polymerase chain reaction (PCR) protocols. Data concerning prior genitourinary infection or a history of tick bite were recorded and serum antibodies to C trachomatis and B burgdorferi were determined. RESULTS: Six patients (8%) had DNA from both C trachomatis and B burgdorferi in the same synovial fluid specimen (mean leucocyte count 11.925/mm(3), 65% granulocytes). These patients (four men, two women; mean age 33.7 years) all had oligoarthritis of the knee, ankle, or both (mean disease duration 11.3 months). From the history and serological examination, four patients had some evidence of actual or previous infection with one or other of the bacteria, while the other two patients had a positive serological test for Chlamydia only. CONCLUSIONS: DNA from two different microorganisms which are known to be triggering agents for arthritis may be present simultaneously in joint material from patients with unexplained oligoarthritis. This finding raises the question as to whether, in such cases, one or both bacteria contribute to the pathogenesis of the disease or whether they are only innocent bystanders.     

Immunoblot analysis of antibody response to Chlamydia trachomatis in patients with reactive arthritis and ankylosing spondylitis

Antibodies to Chlamydia trachomatis were found in 60% of patients with reactive arthritis (ReA) and 33% of patients with ankylosing spondylitis (AS), compared with 19% of healthy blood donors. The IgG, IgA and IgM immune responses in patients with ReA and AS were further analysed by immunoblotting. Most patients had IgG antibodies to a large number of C. trachomatis antigens. IgA (and especially IgM) antibodies were less prevalent. Differences in the antibody response to individual antigens were seen between the two groups of patients, with respect to both IgG and IgA. Especially evident was the high prevalence of IgA antibodies to a 60 kD antigen among patients with ReA (67%) compared with patients with AS (20%).     

Frequency of recent parvovirus infection in patients examined for acute reactive arthritis. A study with combinatorial parvovirus serodiagnostics

OBJECTIVE: To determine the causative role of human parvovirus B19 as a preceding infection in patients examined for acute reactive arthritis (ReA). METHODS: Sixty adult patients with acute arthritis were screened for evidence of triggering infections. In all patients, cultures of stool specimens and of Chlamydia trachomatis in urethra/cervix, and/or bacterial serology were studied. The timing of primary infection of human parvovirus B19 was determined by measurement in serum of VP2-IgM, VP2-IgG, epitope-type specifity of VP2-IgG, and avidity of VP1-IgG. RESULTS: Median time from onset of joint symptoms to the rheumatological consultation was five weeks (range 1-62). Of the 60 patients, 35 fulfilled the diagnostic criteria for ReA; in the remaining, the diagnosis was unspecified arthritis (UA). Thirty-six patients had antibodies for the B19 virus. Occurrence of these antibodies did not differ significantly between ReA and UA groups (P = 0.61). Of these 36 patients, 34 had a pre-existing immunity to the B19 virus. Of the two other patients, one had rash and self-limiting polyarthritis with serological evidence of B19 primary infection, and the other had arthritis of the lower extremities with serological evidence of a convalescence period after the B19 primary infection. The latter patient also had antibodies to Yersinia, with a clinical picture typical for ReA. CONCLUSION: In patients examined for acute ReA, the frequency of recent B19 virus infection was 3.3% (2 out of 60). The diagnostic utility of the presented methodology, by using a single serum sample, was evident.