An "experimental" epidemic of Reiter's syndrome revisited. Follow-up evidence on genetic and environmental factors.

The relation between a specific infective event (shigellosis), a specific disease entity (Reiter's syndrome), and a specific histocompatibility antigen (HL-A B27) is documented by follow-up study of an epidemic of post-Shigella Reiter's syndrome. Five of the original 10 patients have been traced, HL-A typed, and clinically assessed 13 years after the initial episode. One of the 5 has minimal disease, remains symptom-free, and is HL-A B27-negative. The remaining 4 have followed a chronic course, have persistent active disease, and are HL-A B27-positive. It is estimated that after this single episode of shigellosis, from one sixth to one third of the persons who were HL-A B27-positive developed Reiter's syndrome. The prognosis for postdysenteric Reiter's syndrome must be guarded, especially in the subject who is B27-positive.