Chlamydiae as etiologic agents in chronic undifferentiated spondylarthritis

Abstract

Objective. The majority of patients with Chlamydia-induced reactive arthritis do not present with the classic triad of arthritis, conjunctivitis/iritis, and urethritis. Moreover, acute chlamydial infections are often asymptomatic. The aim of the present study was to assess the prevalence of synovial Chlamydia trachomatis and Chlamydia pneumoniae infections in patients with chronic undifferentiated spondylarthritis (uSpA).Methods. Study patients met the European Spondylarthropathy Study Group criteria for SpA, without evidence of ankylosing spondylitis, psoriasis, inflammatory bowel disease, or preceding dysentery. Symptoms were present for >6 months. Each patient underwent a synovial biopsy; tissue and concomitantly obtained peripheral blood mononuclear cells (PBMCs) were analyzed by polymerase chain reaction (PCR) for C trachomatis and C pneumoniae DNA. Other data collected on the day of the biopsy included standard demographic information and medical history, including any known history of C trachomatis or C pneumoniae. Physical examination (including joint count, evaluation for dactylitis and/or enthesitis, and skin examination) and HLA-B27 typing were performed. Synovial tissue (ST) samples from 167 patients with osteoarthritis (OA) were used as controls.Results. Twenty-six patients met the entry criteria and underwent synovial biopsy (25 knee, 1 wrist). Sixteen of them (62%) were positive for C trachomatis and/or C pneumoniae DNA (10 for C trachomatis, 4 for C pneumoniae, and 2 for both). PCR analysis of ST revealed the presence of Chlamydia significantly more frequently in patients with uSpA than in OA controls (P < 0.0001). No specific clinical characteristics differentiated Chlamydia-positive from Chlamydia-negative patients. PBMCs from 4 of the 26 uSpA patients (15%) were positive for Chlamydia, and Chlamydia was found in ST from 2 of these 4 patients. No significant correlation between PCR positivity and HLA-B27 positivity was found.Conclusion. The frequency of Chlamydia-positive ST samples, as determined by PCR, was found to be significantly higher in patients with uSpA than in patients with OA. Our results suggest that in many patients with uSpA, chlamydial infection, which is often occult, may be the cause.

Aberrant expression of microRNAs in T cells from patients with ankylosing spondylitis contributes to the immunopathogenesis

“…These DAMPs could activate TLRs to elicit the inflammatory reaction and ectopic enchondral bone formation in AS spine [32]. Although bacterial infection such as Chlamydia could cause chronic arthritis [40], it is still premature to conclude that bacterial infection can cause AS [41]. Conversely, evidence suggests that AS disease activity became worse, following the different bacterial infections such as Salmonella, Yersinia, Campylobacter and Chlamydia [42][43][44][45][46].…”

Diagnosis of Chlamydia trachomatis in patients with reactive arthritis and undifferentiated spondyloarthropathy

“…Reports indicate that approximately 5% of those with a genital chlamydial infection will develop acute ReA, and about half of these will proceed to chronicity [30]. Further, published data indicate that 20%-40% of individuals with inflammatory arthritis but no documented prior genital infection with C. trachomatis who are given a diagnosis of uSpA, oligoor mono-arthritis are PCR positive in synovial tissue and/or fluid for C. trachomatis DNA [31,32]. A study published in 2009 reported that C. trachomatis DNA in ReA and uSpA patients is rather high (100% and 64%, respectively) [13], while other studies reported relatively low frequencies (25%) [11].…”

The Role of Chlamydia and Chlamydophila Infections in Reactive Arthritis

“…It should be suspected when there is a recent history of diarrhea, cystitis, conjunctivitis, unexplained genitourinary symptoms, prostatitis or chlamydial infection (17). Some studies have raised the possibility that C. pneumoniae, like C. trachomatis, may be a causative agent in ReA (18)(19)(20) and as both are often asymptomatic (21,22), the causative trigger is less clinically apparent in many cases (23). Genetic factors and infections have a very strong correlation with the development of ReA (24).…”