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.
D000328:Adult; D016918:Arthritis, Reactive / Q000209:etiology / Q000235:genetics / Q000276:immunology*; D004196:Disease Outbreaks; D004405:Dysentery, Bacillary / Q000150:complications* / Q000276:immunology; D005500:Follow-Up Studies; D006680:HLA Antigens / Q000032:analysis*; D006649:Histocompatibility Antigens / Q000032:analysis*; D006801:Humans; D008297:Male
D006680:HLA Antigens; D006649:Histocompatibility Antigens