Post-Salmonella reactive arthritis: late clinical sequelae in a point source cohort.
OBJECTIVE
To define the natural history of post-Salmonella-infection reactive arthritis (ReA) in a point source cohort concurrently exposed to the same microorganism, and to determine any relationship between anti-Salmonella humoral immune response to the organism and clinical outcome at 5 years.


METHODS
A cohort of 423 Ontario Provincial Police officers with a clinical diagnosis of Salmonella food poisoning were defined in 1984. Five years following the food poisoning, a mail and telephone survey was carried out to determine all those who developed ReA within 3 months of the onset of dysentery. Medical and physiotherapy charts from an earlier study on the same cohort were incorporated. All patients with a history compatible with reactive arthritis were interviewed and examined. Serum was taken to determine the presence of isotypic antibodies to the lipopolysaccharide of the causative Salmonella typhimurium.


RESULTS
Twenty-seven of the 423 individuals with dysentery were identified as developing acute ReA. In one third of them, the arthritis resolved within 4 months of onset. Two thirds continued to have subjective complaints, mostly of minor significance. However, symptoms were severe enough to force a change in work for 4 patients. Another 4 patients had objective damage to joints radiographically. Objective changes to joints were documented on physical examination in 37% of ReA patients 5 years following onset of disease. IgA antilipopolysaccharide antibodies correlated with the severity and duration of disease. Tests of cellular immune function did not correlate with clinical variables.


CONCLUSIONS
Chronic symptoms persist 5 years after the onset of ReA in the majority of patients. Joint damage by physical examination and radiographic assessment correlate with functional disability. Some early clinical features of disease, including prolonged diarrhea during the acute illness, may predict a worse outcome. IgA antilipopolysaccharides may serve as a disease marker for late post-Salmonella-infection ReA.
Thomson
G T
GT
Rheumatic Disease Unit, Toronto Hospital, University of Toronto, Ontario, Canada.
DeRubeis
D A
DA
Hodge
M A
MA
Rajanayagam
C
C
Inman
R D
RD
D000208:Acute Disease; D000328:Adult; D000704:Analysis of Variance; D000907:Antibodies, Bacterial / Q000097:blood*; D016918:Arthritis, Reactive / Q000276:immunology* / Q000382:microbiology; D016009:Chi-Square Distribution; D005260:Female; D005500:Follow-Up Studies; D005759:Gastroenteritis / Q000150:complications / Q000382:microbiology; D015235:HLA-B Antigens / Q000097:blood / Q000235:genetics*; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood*; D008070:Lipopolysaccharides / Q000276:immunology; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D000091402:Prohibitins; D012478:Salmonella Food Poisoning / Q000150:complications* / Q000382:microbiology; D012486:Salmonella typhimurium / Q000235:genetics / Q000276:immunology*
D000907:Antibodies, Bacterial; D015235:HLA-B Antigens; D007070:Immunoglobulin A; D008070:Lipopolysaccharides; C000717331:PHB2 protein, human; D000091402:Prohibitins