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Reactive Joint Symptoms Following an Outbreak of Salmonella typhimurium Phage Type 135a
ANITA T.Y. LEE, ROBERT G. HALL, and KEVIN D. PILE
ABSTRACT. Objective. To quantify the incidence and clinical features of reactive arthritis (ReA) developing in a cohort exposed to an outbreak of Salmonella typhimurium phage type 135a, and factors affecting host susceptibility to ReA. Methods. A screening questionnaire was mailed to 493 patients with confirmed Salmonella infection. Musculoskeletal symptoms and extraarticular manifestations of ReA were quantified. Positive responders with joint pain were invited to participate further, with a detailed history, examination, and investigations including HLA-B27 status. Results. A total of 261/461 (57%) subjects responded to the questionnaire, with 23/54 adults (43%) and 41/207 children (20%) reporting joint symptoms. Although joint pains were less common in children compared with adults, those children affected usually had eye (34%) or mucocutaneous (37%) symptoms. The incidence of ReA was 14.6%, with adults more frequently affected (24%) than children (12%). This may be an underestimate given the large proportion of children involved. Associated clinical features were similar to previous studies, with the distribution of arthritis affecting the lower limbs predominantly in an oligoarticular pattern, as were the extraarticular manifestations and enthesopathy. We found 17% of subjects were HLA-B27 positive, and 55% were still symptomatic after 6 months. Conclusion. In an Australian cohort study of a S. typhimurium phage type 135a outbreak, joint symptoms were common, affecting 25% of subjects. The incidence of ReA of 14.6% and the clinical features were comparable to previous studies. There was a small effect of HLA-B27 status on the development of ReA. (J Rheumatol 2005;32:524-7) Key Indexing Terms:
REACTIVE ARTHRITIS
From the Department of Rheumatology, The Queen Elizabeth Hospital, Adelaide; Department of Human Services, Melbourne; and Department of Medicine, James Cook University, Townsville, Australia. A.T.Y. Lee, MBBS, FRACP, Department of Rheumatology, Queen Elizabeth Hospital; R.G. Hall, MBBS, MPH DipRACOG, FRACMA, FAFPHM, Department of Human Services, Melbourne; K.D. Pile, MBChB, MD, FRACP, Department of Medicine, James Cook University. Address reprint requests to Dr. A. Lee, Department of Rheumatology, Level 4, Eleanor Harrald Building, Royal Adelaide Hospital, North Terrace, Adelaide SA 5000, Australia. E-mail: alee@mail.rah.sa.gov.au Submitted October 7, 2003; revision accepted November 15, 2004. |