through the bloodstream to multiple locations, including joints (Yu and Kuipers 2003). How Campylobacter and other ReA-causing bacteria survive persistently in joint cells remains unknown, as does the viability of Campylobacter organisms in those cells. Yu and Kuipers (2003) present a plausible hypothesis for the mechanism by which Campylobacter organisms induce joint-specific inflammation: that macrophages present antigenic peptides to CD8+ T lymphocytes through histocompatibility antigen HLA-B27. The T-cell receptor of CD8+ T lymphocytes is specific for both foreign and self peptides carried by HLA-B27. The process may activate CD8+ T lymphocytes and produce the initial inflammatory response. The mechanism of sustained inflammatory response is unknown.

Despite the ambiguous pathogenesis of postinfection ReA, the weight of epidemiologic evidence convincingly illustrates that a small percentage of people infected by Campylobacter spp. later develop ReA.

The committee concludes that there is sufficient evidence of an association between Campylobacter infection and reactive arthritis (ReA), if the ReA is manifested within 3 months of the infection. Most cases of ReA are manifested within a month of the infection.


Uveitis is an inflammation inside the eye that affects the uvea. Known causes of uveitis include autoimmune disorders, infection, and exposure to toxins (MedlinePlus Medical Encyclopedia 2006). In many cases, the cause is unknown.

Three case reports describe uveitis after C. jejuni infection (Hannu et al. 2004b; Howard et al. 1987; Lever et al. 1984). The first report involves one of 350 patients who contracted C. jejuni infection in an outbreak in Finland in August 2000 (Hannu et al. 2004b). The subject of the report, a 72-year-old woman who had gastritis, developed pain and mucopurulent exudation in her left eye without marked redness after the C. jejuni outbreak. Although C. jejuni infection was not confirmed with a stool culture, it was “epidemiologically highly probable” that her prior gastrointestinal symptoms were caused by C. jejuni (Hannu et al. 2004b). About 3 weeks after the acute illness, the woman sought medical attention for the eye symptoms, and mild acute anterior uveitis was diagnosed. An HLA-B27 antigen test was negative. She was treated with local corticosteroid drops and corticosteroid-antibiotic ointment. The condition resolved about 2 months after the acute illness. In a second case report, a previously healthy 39-year-old woman with a culture-confirmed C. jejuni infection developed redness and pain in her eyes about 4 weeks after the gastritis resolved (Howard et al. 1987). The eye condition was diagnosed as nonspecific anterior uveitis. The eye inflammation was treated and resolved over a period of 2 weeks. An HLA-B27 antigen test was negative. In the third case report, acute anterior uveitis was reported in a 34-year-old woman who had a culture-confirmed C. jejuni infection (Lever et al. 1984). She also had hypogammaglobulinemia and chronic diarrhea. No information was given on how the uveitis was treated, how long after onset of the infection the uveitis developed, or how long it took the condition to resolve.

The committee concludes that there is limited or suggestive evidence of an association between C. jejuni infection and uveitis, if the uveitis is manifested within a month of the infection.

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