Is there any relationship between toxoplasma infection and reactive arthritis?

SERT M., OZBEK S., Paydas S., YAMAN A.

JOURNAL OF POSTGRADUATE MEDICINE, vol.53, no.1, pp.14-16, 2007 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 53 Issue: 1
  • Publication Date: 2007
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.14-16
  • Çukurova University Affiliated: Yes


Background: The diagnosis of reactive arthritis is a challenging clinical problem in daily practice. Although there are many triggering infectious agents for reactive arthritis, Toxoplasmosis, a worldwide parasitic infection has not been reported. Aim: We investigated the serologic evidence of Toxoplasma gondii (T gondii) infection in patients with newly diagnosed reactive arthritis after six weeks of the onset of the first symptom but no demonstrable triggering agent for reactive arthritis. Setting and Design: Clinical controlled study. Materials and Methods: We screened serologically the serum toxoplasma IgM and IgG antibody (Ab) titers which revealed toxoplasma infection in 50 patients with reactive arthritis (40 female, 10 men) and no demonstrable triggering agent and control subjects (32 female, 8 male). Statistical Analysis: SPSS 10.0 software package program was used. Results: The mean age of the patients and controls was similar (41.3 +/- 12.0 vs. 39.6 +/- 11.8 years) respectively. The prevalence of IgG Ab titers of T. gondii in patients and controls were found to be 52% and 47.5%, respectively. Mean serum Toxoplasma IgG Ab levels were found to be 16.5 +/- 14.5 IU/ml, and 16.9 +/- 13.8 IU/ml in patients and control subjects respectively (P>0.05). We did not find any Toxoplasma IgM Ab titer demonstrating the acute or sub-acute infection in the serum of patients or controls. Conclusion: Although past Toxoplasma infection was prevalent in both groups, we did not find any subject with acute Toxoplasma infection in patients with newly diagnosed reactive arthritis and healthy controls. Despite the fact that our study group was small, we suggest that T gondii does not seem to be a triggering agent for reactive arthritis and past infection may be a coincidental finding.