The crucial question is whether an autoimmune disease runs an independent course after the initial bacterial trigger or whether it requires chronic interaction. Unfortunately, good studies have not been conducted on the effect of healing of gut lesions in Crohn's disease or in AS. One interesting study suggests that treatment with antibiotics can prevent development of AS or related conditions. Patients with an acute enteral ReA treated for 3 months with ciprofloxacin did not benefit during the first 12 months of follow-up . However, 11 out of 27 (45%) patients from the placebo group had developed chronic rheumatic diseases when re-evaluated after 4-7 years, compared to only 2 out of 26 (7.7%) of the patients who originally received antibiotic treatment . Furthermore, all rheumatic manifestations in the former but not the latter group manifested AS-type features and occurred in HLA-B27-positive individuals. At last we have data indicating that uncontrolled bacterial infection can cause AS manifestations and that an initial infection controlled by antibiotics cannot do so; nevertheless, this must occur in the context of HLA-B27.
This interpretation is supported by additional indirect evidence. In the 1940s and 1950s, arthritis associated with urogenital infections was associated with development of ankylosing spondylitis in Sweden in a higher percentage than 20-30 years later . Long-term antibiotic treatment was the main difference between the management of these groups. Similarly, AS and related diseases were more severe in lower social classes with poorer hygiene (without a refrigerator) in North Africa . AS starts at an earlier age and runs a more severe course in countries such as Mexico , China , and North Africa  as compared with Western Europe. Furthermore, the first generation of immigrants from North Africa to France suffered more severe
AS than does the second (B. Amor, unpublished observations). All these data indicate that persistent or repeated infection, mostly probably gut-derived, makes an important contribution to the pathogenesis and severity of AS. The mechanisms that lead from infection to autoimmunity in AS have not yet been defined.
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