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A further case of reactive arthritis following Campylobacter jejuni enteritis is reported. The interim results of a small prospective study are discussed. It may be desirable to do serological studies for campylobacter infection in the investigation of mono- or polyarthritis of acute onset.
Among a group of children hospitalized for "joint pain", four of the cases of reactive arthritis were due to Yersinia infection. These four cases are described. Some patients had suggestive clinical symptoms but serologic studies were needed to establish the diagnosis. Tissue group studies showed that two children were HLA B27 and one was HLA B7. Reactive arthritis due to Yersinia in a form of "enteral arthritis". The prevalence of Yersinia arthritis has not been documented. Serologic tests are essential to outrule the main differential diagnosis, i.e. chronic juvenile arthritis (juvenile rheumatoid arthritis). Short-term resolution of symptoms is seen in every case. The long-term outcome is less well documented, especially with regard to the risk of recurrence and to relationships with peripheral joint disease and spondylarthropathies of early adulthood. HLA B27 positivity may be a risk factor. The pathogenesis of Yersinia-induced reactive arthritis is unclear; current studies are focusing on immunologic factors. The uncertainties concerning long-term outcome justifies renewed interest in childhood reactive arthritis.
Certain microbes like yersinia, salmonella, shigella, campylobacter, chlamydia, and possibly gonococcus can trigger reactive arthritis especially in patients of the HLA-B27 type. In the present study we have used serological and culture methods to identify the probable triggering infection in 50 consecutive HLA-B27 positive patients diagnosed as having reactive arthritis. The two most common triggering agents thus identified were Yersinia enterocolitica (12 patients) and Chlamydia trachomatis (11 patients). In addition six patients had high antistreptolysin O titres and two high teichoic acid antibody titres suggesting group A streptococci and Staphylococcus aureus as triggering agents. In 13 patients no preceding infection could be identified. The identity of the infective agent seems to have very little effect on the clinical picture of the reactive arthritis - the only difference between the various aetiological groups in the present material was absence of fever in the patients with a preceding C. trachomatis infection, of whom only one out of 11 had a temperature greater than or equal to 38 degrees C, whereas 13 of 16 patients with a preceding enterobacterial, and five of the eight patients with a streptococcal or staphylococcal infection had raised temperatures.
Synovial fluid (SF) mononuclear cells from patients with reactive arthritis (ReA) proliferate in vitro when challenged with ReA-associated bacteria, the maximal response being for the organism causing the triggering infection. We report the results of a study of the antigenic specificity of synovial T lymphocytes from an HLA-B27 positive ReA patient whose SF mononuclear cells responded preferentially to Yersinia antigens. This is the first report of the isolation of Yersinia-specific T cell clones from synovial membrane (obtained by closed-needle synovial biopsy). We present a detailed analysis of these clones, together with others obtained from the SF.
We describe two patients with acute reactive arthritis (ReA) caused by Yersinia enterocolitica who were treated with infliximab with a good response in the acute phase. In a patient with prior ankylosing spondylitis (AS) and subsequent ReA the peripheral joint disease responded well to three infliximab infusions, but later he needed retreatment with infliximab to control the spinal symptoms of AS. The other previously healthy patient with acute ReA also responded well to one infliximab infusion although he did not fully recover and needed further treatment with disease modifying antirheumatic drugs. The influence of new drugs on the short and long term prognosis of the patients with ReA remains to be evaluated.
Reiter's syndrome [also called reactive arthritis (ReA)] is the triad of arthritis, urethritis, and conjunctivitis. Two cases of Reiter's syndrome triggered by travelers' diarrhea are presented. Health care providers should suspect ReA in travelers with joint symptoms and antecedent diarrheal disease.
The diagnosis of reactive arthritis (ReA) is easy in typical cases with a history of an infection within 3 weeks in combination with an asymmetric mono or oligoarthritis with or without extra-articular manifestations. Subclinical microbial infections, a possible co-existing inflammatory bowel disease and the fact that in 25% of the cases the microbial agent remains unidentified, make the diagnosis more troublesome. The course of disease is usually self-remittent within 6 months but a less good long-term prognosis is pre-determined by two factors-namely, the presence of HLA-1327 and the recurrence of triggering infections. The finding of microbial fragments in the joint cavity have led to new treatment strategies especially in Chlamydia-triggered ReA. It must, however, be remembered that the antibiotics mostly used (namely, tetracyclines) also possess immunoregulatory and anticollagenolytic potential. In chronic destructive cases, antirheumatic treatment, similar to that used in rheumatoid arthritis, is recommended.
We investigated a patient with Salmonella infantis triggered reactive arthritis (ReA) for a possible occurrence of S. infantis-specific antigens and DNA in the synovial fluid (SF) cells. S. infantis-specific antigens were abundantly observed by immunofluorescence in SF cells of the patient during acute joint inflammation. Salmonella-specific DNA was detected by Southern blotting of the amplified polymerase chain reaction product once, but the result could not be repeated. It seems that if bacterial DNA exists in inflamed joints in Salmonella triggered ReA, its amount is extremely low. This is the first report of intraarticular S. infantis antigens and potentially of Salmonella DNA in Salmonella triggered ReA.
Giardia lamblia infection is rarely associated with adult reactive arthritis. We report the first North American case and review the pediatric and adult literature to date. Antimicrobial treatment is essential to eradicate the parasite and control the arthritis.
Results are submitted of bdellotomy in patients with reactive arthritis. Shown in the above patients were palliative and and anti-inflammatory effects of bdellometers. Bdellotomy has proved to be efficient treatment option in a major proportion of patients. Bdellotomy will, we believe, come to be a valuable adjunct in the physician's therapeutic arsenal, that can be used not only in the treatment of patients with rheumatic disorders but by family doctors as well and in other general practice settings.
The association between reactive arthritis and Giardia lamblia infestation, although it has been previously described, is not very common. We present a 32 year-old woman who had oligo-arthritis and erythema nodosum after Giardia lamblia infestation. We think that a Giardiasis should be more frequently considered in patients with arthritis after an episode of diarrhea.
The treatment of reactive arthritis and Reiter's syndrome depends on the joints affected, on extra-articular symptoms, and the infection responsible for the disease. Purely symptomatic measures are inadequate in the treatment of therapy-resistant or chronic arthritis. The choice of a suitable "remission-inducing agent" is also frequently determined by the involvement of the skin, intestines or eyes which may dominate. Antibiotics are necessary if the infectious process does not clear up completely. The survey systematically discusses the different methods of treatment and presents them in tabular form.
Poststreptococcal reactive arthritis (PSRe A) is a sterile synovitis associated to the evidence of previous streptococcal infection. PSRe A has different clinical features from those observed in rheumatic fever. Regarding systemic complications, PSRe has in general a good prognosis. A new case is described and the literature is reviewed in this article.
The aim of this study was to search infections that trigger reactive arthritis. Eighty-six patients with seronegative arthritis (SNA) were studied; 32 had reactive arthritis, 21 ankylosing spondylitis, 7 psoriatic arthritis and 26 undifferentiated seronegative oligoarthritis. As controls, 70 patients with connective tissue diseases (CTD) and 55 healthy volunteers (HV) were studied. Serological evidence for infection with Chlamydia trachomatis was studied with micro immunofluorescence, looking for L2 and BED serotypes and serological evidence for Yersinia infection, using a commercial kit. Stool cultures were done in seven patients with recent diarrhea, and endourethral or endocervical cultures in 35 individuals. Serotypes L2 or BED were positive in 23 of 83 patients with SNA, 3 of 39 patients with CTD and 4 of 55 HV (p < 0.03). IgG class antibodies against L2 were detected in 17% of SNA patients, 2.6% of CTD patients and 5.4% of HV (p < 0.05). IgM class antibodies were detected in 6 SNA patients, 0 CTD patients and 2 HV (NS). Twelve of 35 cultures were positive for Chlamydia. As a whole 30% of SNA patients has serological or bacteriological evidence for Chlamydia infection. Serology for Yersinia was positive in 39 of 81 SNA patients, 1 of 54 CTD patients and 3 of 51 HV (p < 0.01). Rates of infections were similar among male, female, HLA B27 positive and HLA negative subjects. It is concluded that SNA patients have a high prevalence of infections by Chlamydia trachomatis or Yersinia enterocolitica.
The authors studied microbiocenosis of the intestine and its influence on the course of postenterocolitic reactive arthritis in 43 patients. The data obtained confirm the participation of intestinal dysbacteriosis in the development of a chronic form of reactive arthritis. The favourable effect of sour milk bifidumbacterin on articular manifestations in postenterocolitic reactive arthritis has been noted.
Undifferentiated oligoarthritis (UOA) resembles clinically reactive arthritis (ReA), but does not fulfill the diagnostic criteria. In 46 patients with UOA, in 16 with ReA, and in 15 with rheumatoid arthritis (RA) the humoral and cellular immune response to the ReA-associated bacteria Chlamydia trachomatis, Yersinia enterocolitica, Shigella flexneri, Salmonella enteritidis, Campylobacter jejuni and Borrelia burgdorferi was investigated in paired samples of synovial fluid and peripheral blood. An antigen-specific lymphocyte proliferation in SF was found in 75% of the ReA and in 39% of UOA patients, but in none with RA. Shigella and Chlamydia in ReA and Yersinia and Chlamydia in UOA were the most frequent stimulating antigens. There was a poor correlation between antigen specific lymphocyte proliferation and specific antibodies. We conclude that these bacteria might have a pathogenetic role, not only in ReA, but also in UOA.
OBJECTIVE: To find out whether a 10-14 days' course of antibiotics early in the course of reactive arthritis associated with enteric infections could reduce the severity and duration of the disease and whether the antibody response in patients with reactive arthritis associated with yersinia infection differed between those treated and those not treated with the antibiotics. DESIGN: Prospective multicentre trial in which patients were randomised to treatment or no treatment with antibiotics. Patients were seen at three and six weeks and three, six, nine, 12, and 18 months after their first visit. SETTING: Departments of infectious diseases in three hospitals in Linköping, Malmö, and Stockholm, Sweden. PATIENTS: 40 Consecutive patients who had had symptoms of reactive arthritis associated with enteric infection for less than four weeks. INTERVENTIONS: 20 Patients were allocated to treatment with antibiotics and 20 patients did not receive antibiotics. All patients received non-steroidal anti-inflammatory drugs, and four also received intra-articular steroid injections after at least six weeks' observation. MAIN OUTCOME MEASURES: Arthritic symptoms assessed clinically and by using Ritchies' index; blood measurements reflecting inflammatory activity; serum IgG, IgM, and IgA antibody titres; HLA tissue type. RESULTS: No difference was observed concerning duration of arthritis, grade of inflammation, and number of joints affected between patients treated and those not treated with antibiotics. Furthermore, there was no significant difference between the two groups in erythrocyte sedimentation rate and haptoglobin, IgG, and IgA concentrations. All values had returned to normal within three months. No patient developed chronic arthritis, but sustained slight arthralgia occurred in three patients. The HLA-B27 antigen was found in 23 (58%) of the patients, and its presence did not affect clinical outcome. The IgG, IgM, and IgA antibody responses were similar in patients treated with antibiotics and those not treated. CONCLUSION: Short term antibiotic treatment has no beneficial effect on the clinical outcome of reactive arthritis associated with enteric infection.
It is now clear that the deposition and persistence of bacterial antigens in the joint are significant features of reactive arthritis. It is possible that in some instances this represents persistence of live bacteria, and several studies point to the potential value of antimicrobial therapy. Searches for bacterial DNA and RNA have yielded conflicting data, however, so further developments in this area will be of great importance. It is likely that bacterial antigens interact in some way with class I major histocompatibility complex (MHC) antigens in the pathogenesis of reactive arthritis. However, with the increasing understanding of the structure and function of HLA molecules, some evidence of a classic antigen-class I MHC-CD8 T-lymphocyte interaction is now emerging. Thus far, the mechanisms that link HLA-B27 and bacterial antigens with reactive arthritis remain unclear.