Rheumatology International

, Volume 31, Issue 2, pp 215–220 | Cite as

Do infections trigger juvenile idiopathic arthritis?

  • Mustafa Aslan
  • Ozgur Kasapcopur
  • Hatice Yasar
  • Erdal Polat
  • Suat Saribas
  • Huseyin Cakan
  • Ahmet Dirican
  • Müzeyyen Mamal Torun
  • Nil Arısoy
  • Bekir Kocazeybek
Original Article

Abstract

Juvenile idiopathic arthritis (JIA) is a disease that was prominent with increased inflammation response in immune system, appeared mostly with peripheral arthritis and endogenous and exogenous antigens play a role in the pathogenesis of disease. Two major reasons were thinking to be considerably important. First of them is immunological predisposition and the second one is environmental factors. Infections are considered to be the most important between environmental factors but also stress and trauma are also important in the etiology of the disease. However, the relation between JIA and infections is not clearly defined but the relation between adult chronic arthritis and infections was well-defined. A total of 70 patients, 26 with primer JIA, 20 with recurrent JIA, 24 healthy control were included in this study. Mycoplasma pneumoniae, Chlamydophila pneumoniae and C. Jejuni were detected in 4, 1 and 1 of 10 (38.46%) patients with primer JIA, respectively. Salmonella enteritidis, EBV, M. pneumoniae, C. jejuni and Borrelia burgdorferi were detected in 1, 2, 2, 2, and 1 of the 8(40%) patients with recurrent JIA, respectively. S. enteritidis were isolated in feces culture and also identified by agglutination method. Infection was detected in total 18 (39.13%) of patient groups. C. pneumoniae and C. jejuni were detected in 1 and 1 of 2(8.33) healthy control groups, respectively. Throat culture positivity was not detected in any of the patient and healthy control groups. In conclusion, etiopathogenesis of JIA is not clearly understood and suggested that various factors can trigger the disease and it is the most common rheumatoid disease of childhood. However, there are some studies focusing especially on one infectious agent but this is the first study including such a big range of infectious agents in the literature for the microorganisms that can be suggested to have a role in the etiopathogenesis of JIA. We have a conclusion in the light of our results and suggest that some microorganisms can trigger and increase the intensity of clinical situation according to the case. When we evaluate the primer and recurrent JIA groups; M. pneumoniae and C. jejuni come forward and seen common in JIA cases. We also suggest that the pre-diagnosis of microorganisms, which can play a role as primarily or by intervening in the etiopathogenesis of JIA and adding specific antimicrobial therapy to the standard JIA therapy, it is possible to perform new, extended, especially molecular based serial case studies.

Keywords

Juvenile idiopathic arthritis Chlamydophila pneumoniae Mycoplasma pneumoniae 

References

  1. 1.
    Schneider R, Passo MH (2002) Juvenile rheumatoid arthritis. Rheum Dis Clin N Am 28:503–530CrossRefGoogle Scholar
  2. 2.
    Weiss JE, Ilowite NT (2005) Juvenile idiopathic arthritis. Pediatr Clin North Am 52:413–442CrossRefPubMedGoogle Scholar
  3. 3.
    Carty SM, Snowean N, Silman AJ (2003) Should infection still be considered as the most likely triggering factor for RA? J Rheumatol 30:425–429PubMedGoogle Scholar
  4. 4.
    Petty RE, Southwood T, Baum J et al (1998) Revision of the proposal classification criteria for Juvenile idiopathic arthritis. J Rheumatol 25:1991–1994PubMedGoogle Scholar
  5. 5.
    Petty RE, Cassidy JT (2005) Chronic arthritis. In: Cassidy JT, Petty RE (eds) Textbook of pediatric rheumatology, 5th edn. Elsevier, Philadelphia, pp 206–341Google Scholar
  6. 6.
    Hannu T, Puolakkainen M, Leirisalo-Repo M (1999) Chlamydia pneumoniae as a triggering infection in reactive arthritis. Rheumatology 38:411–414CrossRefPubMedGoogle Scholar
  7. 7.
    Brunner HI, Lovell DJ, Finck BK, Giannini EH (2002) Preliminary definition of disease flare in juvenile rheumatoid arthritis. J Rheumatol 29(5):1058–1064PubMedGoogle Scholar
  8. 8.
    Brunner HI, Ivaskova E, Haas JP, Andreas A, Keller E, Hoza J, Havelka S, Scholz S, Sierp G, Albert ED (1993) Class I associations and frequencies of class II HLA-DRB alleles by RFLP analysis in children with rheumatoid-factor-negative juvenile chronic arthritis. Rheumatol Int 13:83–88CrossRefPubMedGoogle Scholar
  9. 9.
    Haas JP, Kimura A, Truckenbrodt H, Suschke J, Sasazuki T, Volgger A, Albert ED (1995) Early-onset pauciarticular juvenile chronic arthritis is associated with a mutation in the Y-box of the HLA-DQA1 promoter. Tissue Antigens 45(5):317–321CrossRefPubMedGoogle Scholar
  10. 10.
    Albert LJ (2000) Infection and rheumatoid arthritis: guilty by association? J Rheumatol 27:564–566PubMedGoogle Scholar
  11. 11.
    Johnson RM, Brown EJ (2000) Cell-mediated immunity in host defense against infectious diseases. In: Mandell GL, Bennet JE, Dolin R (eds) Principles and practice of infectious diseases, 5th edn. Churchill Livingstone, Philadelphia, p 113Google Scholar
  12. 12.
    Benedek TG (2006) The history of bacteriologic concepts of rheumatic fever and rheumatoid arthritis. Semin Arthritis Rheum 36(2):109–123 (epub 13 July 2006)CrossRefPubMedGoogle Scholar
  13. 13.
    Hannu T, Inman R, Granfors K, Leirisalo-Repo M (2006) Reactive arthritis or post-infectious arthritis? Best Pract Res Clin Rheumatol 20(3):419–433CrossRefPubMedGoogle Scholar
  14. 14.
    Yang J, Hooper WC, Phillips DJ, Talkington DF (2004) Cytokine growth. Factor Rev 15(2-3):157–168CrossRefGoogle Scholar
  15. 15.
    Mardh A (2004) Mycoplasma and ureaplasma. In: Cohen J, Powderly W (eds) Infectious disease, 2nd edn. Elsevier, Philadelphia, p 2309Google Scholar
  16. 16.
    Sibilia J, Limbach F-X (2002) Reactive arthritis or chronic infectious arthritis? Ann Rheum Dis 61:580–587CrossRefPubMedGoogle Scholar
  17. 17.
    Villareal C, Whittum-Hudson JA, Hudson AP (2002) Persistent Chlamydiae and chronic arthritis. Arthritis Res 4:5–9CrossRefPubMedGoogle Scholar
  18. 18.
    Taylor-Robinson D, Rooney M (1998) Association of Chlamydia pneumoniae with chronic juvenile arthritis. Eur J Clin Microbiol Infect Dis 17:211–216PubMedGoogle Scholar
  19. 19.
    Altun S, Kasapçopur O, Aslan M, Karaarslan S, Koksal V, Saribaş S, Ergin S, Arisoy N, Kocazeybek B (2004) Is there any relationship between Chlamydophila pneumoniae infection and juvenile idiopathic arthritis? J Med Microbiol 53:787CrossRefPubMedGoogle Scholar
  20. 20.
    Montgomery RR, Malawista SE, Feen KJM, Bockenstedt LK (1996) Direct demonstration of antigenic substitution of Borrelia burgdorferi ex vivo: exploration of the paradox of the early immune response to outer surface proteins A and C in Lyme disease. J Exp Med 183:261–269CrossRefPubMedGoogle Scholar
  21. 21.
    Gross DM, Forsthuber T, Tary-Lehmann M, Etling C, Ito K, Nagy ZA et al (1998) Identification of LFA-1 as a candidate autoantigen in treatment-resistant Lyme arthritis. Science 281:703–706CrossRefPubMedGoogle Scholar
  22. 22.
    Gear AJ, Venables PJW, Edwards JMB, Maini RN (1986) Rheumatoid arthritis, juvenile arthritis, iridocyclitis and the Epstein-Barr virus. Ann Rheum Dis 45:6–8CrossRefPubMedGoogle Scholar
  23. 23.
    Saarinen M, Ekman P, Ikeda M, Virtala M, Grönberg A, Yu DTY, Arvilommi H, Granfors K (2002) Invasion of Salmonella into human intestinal epithelial cells is modulated by HLA-B27. Rheumatology 41:651–657CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag 2009

Authors and Affiliations

  • Mustafa Aslan
    • 1
  • Ozgur Kasapcopur
    • 3
  • Hatice Yasar
    • 1
  • Erdal Polat
    • 1
  • Suat Saribas
    • 1
  • Huseyin Cakan
    • 2
  • Ahmet Dirican
    • 4
  • Müzeyyen Mamal Torun
    • 1
  • Nil Arısoy
    • 1
    • 3
  • Bekir Kocazeybek
    • 1
  1. 1.Microbiology and Clinical Microbiology Department, Cerrahpasa Medical FacultyIstanbul UniversityIstanbulTurkey
  2. 2.Medical Sciences Department, Forensic Sciences InstituteIstanbul UniversityIstanbulTurkey
  3. 3.Pediatric Department, Cerrahpasa Medical FacultyIstanbul UniversityIstanbulTurkey
  4. 4.Department of Biostatistics, Cerrahpasa Medical FacultyIstanbul UniversityIstanbulTurkey

Personalised recommendations