Joint observations with lessons for rheumatologists and gastroenterologists

To the Editor:

In 1962 the USS Little Rock, a navy ship with 1200 men on board, pulled into a Caribbean port to celebrate the ship's birthday. The cook contaminated the food line and 600 men became infected with shigella dysentery and 10 promptly developed inflammatory spondyloarthritis.1 Ten years later the 5 who could be found still had it.2

We recently described a woman who suffered blunt trauma to the abdomen and was admitted to the hospital for concern of a splenic rupture.3 She developed an Enterococcus faecalis bladder infection that was suspected to be related to translocation of bacteria from the bowel to the bladder. Psoriasis and psoriatic arthritis then blossomed. Bacterial immune activation in the bladder with a patent urachus could explain the strange occurrence of psoriasis in the umbilicus.

In rheumatology circles the clinical similarities among patients with spondyloarthropathies (ankylosing spondylitis, the arthritis of inflammatory bowel disease, reactive arthritis, and psoriatic arthritis) have suggested a common pathogenesis.4 The lesson suggests the common pathogenesis is immune perturbation to bacteria. Shigella, Salmonella, Yersinia, Campylobacter, and Chlamydia may be the culprits in reactive arthritis, while there is evidence that Group A streptococci contributes to psoriatic arthritis. Enteric bacterial flora is the obvious suspect in ankylosing spondylitis and arthritis of inflammatory bowel disease (IBD).

The spondyloarthropathies and IBD likely involve a poorly understood interaction of genetic and environmental factors. Common features include a genetic predisposition, a triggering antigen, and an abnormal immune response. In Crohn's disease (CD) multiple genetic defects have been described, while the antigen is thought to be derived from enteric bacterial flora. Studies of identical twins reveal a 60% concordance rate in CD.5 Interestingly, similar concordance rates apply to ankylosing spondylitis and psoriatic arthritis. There seems to be an increased prevalence of these rheumatologic disorders in patients with IBD. There have also been multiple recent case reports of patients with CD who were treated with anti-TNF agents who developed pustular psoriasis.6 A pathogenic link between skin, joint, and gut disease has been suggested in patients with psoriatic arthritis, demonstrated by subclinical, microscopic inflammatory changes of the colon in these patients.7 These observations suggest that these diseases may be a spectrum of a very complex and highly regulated process.

The bacterial answer to CD and ulcerative colitis (UC) could be revealed in the difference in the colonic flora between identical twins discordant for the disease. The twin data also suggest the organism needs to be present in 80% of people (60 +60 +40 = 80% of 200 individuals in 100 sets of identical twins). Antibodies to Enterococcus faecalis and E. coli have been found with increased frequency in affected bowel mucosa of patients with CD.8 The ubiquitous presence of E. coli in the stool would not fit the discordant twin data; however, the 80% prevalence of enterococcus would.

In view of these observations we feel further evaluation of the immune handling of enterococcus is important in understanding the pathogenesis of IBD.

Joseph McKinley MD*, Frank Vasey MD*, Angela McMillen MD*, John Carter MD*, Patrick Brady MD*, * Health Science Center, University of South Florida, Tampa, Florida.