title: Chlamydophila psittaci subclinical infection in chronic polyarthritis.
abstract: OBJECTIVE
  Recent evidence indicates that Chlamydophila psittaci (Cp) may establish chronic infections, which may promote autoimmunity and/or B cell lymphoproliferation.
  
  
  METHODS
  The presence of a subclinical Cp infection was investigated in 293 patients with chronic inflammatory polyarthritis, including 175 patients with rheumatoid factor (RF)-positive and/or anti-CCP-positive rheumatoid arthritis (RA) and 118 with seronegative polyarthritis (46 RF-negative/anti-CCP-negative RA, 36 psoriatic arthritis and 36 undifferentiated spondyloarthritis). One hundred and eighty-five healthy controls were also investigated. The presence of Cp infection was assessed in peripheral blood mononuclear cells using several PCR protocols targeting different regions of the Cp genome (16S-23S spacer rRNA, OMP-A, and Gro-EL). The DNA of other Chlamydia species (C. Pneumoniae and C. Trachomatis) was also investigated. Amplicons were sequenced to confirm the specificity of PCR products.
  
  
  RESULTS
  The presence of a subclinical chronic Cp infection was observed in a significantly higher percentage of patients with chronic polyarthritis (38/293; 13%) compared to healthy controls (1/185, 0.5%; OR=27.4, 95%CI:3.73-201.6, p<0.0001). Furthermore, the prevalence of Cp was higher in seronegative polyarthritis (23/118; 19.5%) than in seropositive RA patients (15/175; 7.4%; OR=2.58, 95%CI: 1.28-5.19, p=0.0078). The highest prevalence of Cp infection was found in RF/anti-CCP double-negative RA patients (13/46, 28.3%), followed by patients with psoriatic arthritis (6/36; 16.7%). No differences in age, sex, disease duration and undergoing therapies were noticed between Cp-positive and Cp-negative patients; nor between seropositive and seronegative patients.
  
  
  CONCLUSIONS
  Cp may be an infectious trigger possibly involved in the pathogenesis of a fraction of inflammatory polyarthritis, particularly in seronegative patients.
authors.affiliation: Institute of Clinical Pathology, Azienda Ospedaliero-Universitaria of Udine, Udine, Italy. fabris.martina@aoud.sanita.fvg.it
authors.forename: Martina
authors.initials: M
authors.lastname: Fabris
authors.forename: Salvatore
authors.initials: S
authors.lastname: De Vita
authors.forename: Elisa
authors.initials: E
authors.lastname: Pasini
authors.forename: Luca
authors.initials: L
authors.lastname: Quartuccio
authors.forename: Elena
authors.initials: E
authors.lastname: Pontarini
authors.forename: Sandra
authors.initials: S
authors.lastname: Lombardi
authors.forename: Cinzia
authors.initials: C
authors.lastname: Fabro
authors.forename: Piercarlo
authors.initials: P
authors.lastname: Sarzi-Puttini
authors.forename: Raffaele
authors.initials: R
authors.lastname: Pellerito
authors.forename: Maurizio
authors.initials: M
authors.lastname: Benucci
authors.forename: Pia
authors.initials: P
authors.lastname: Morassi
authors.forename: Domenico
authors.initials: D
authors.lastname: Biasi
authors.forename: Francesco
authors.initials: F
authors.lastname: Curcio
authors.forename: Riccardo
authors.initials: R
authors.lastname: Dolcetti
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001168:Arthritis / Q000175:diagnosis / Q000453:epidemiology* / Q000382:microbiology; D015551:Autoimmunity; D002691:Chlamydophila psittaci / Q000235:genetics / Q000302:isolation & purification*; D002908:Chronic Disease; D015897:Comorbidity; D004269:DNA, Bacterial / Q000235:genetics; D005260:Female; D016680:Genome, Bacterial; D006801:Humans; D007558:Italy / Q000453:epidemiology; D007963:Leukocytes, Mononuclear / Q000382:microbiology; D008297:Male; D008875:Middle Aged; D009956:Psittacosis / Q000150:complications / Q000175:diagnosis / Q000453:epidemiology*; D016036:Seroepidemiologic Studies; D055815:Young Adult
chemical_list: D004269:DNA, Bacterial