Chronic secondary complications of foodborne illness occur in about 2 to 3 percent of patients. 22 The true incidence is probably higher because chronic sequelae may be difficult to link to the acute illness and may occur despite successful elimination of the primary organism. Frequently, the host and pathogen have common surface antigens. Host recognition of the foreign antigen initiates an autoimmune response. A low but consistent incidence (0.2 to 2.4 percent) of seronegative reactive arthritis has been noted following outbreaks of Salmonella typhimurium, Shigella flexneri, and Campylobacter jejuni.2 23 Superantigens—protein virulence factors that can elicit extreme immune responses in the host—have been isolated from several foodborne bacteria and are thought to be associated with several autoimmune disorders, such as rheumatoid arthritis, multiple sclerosis, Graves disease, and psoriasis. 22 A link between Campylobacter and Guillain-Barre syndrome has been suspected for over a decade. It is estimated that possibly 40 percent of Guillain-Barre cases are secondary to primary infection, with Campylobacter usually developing 7 to 21 days after resolution of gastrointestinal symptoms. 2223 Hemolytic-uremic syndrome (HUS), characterized by acute renal failure, thrombocytopenia, and microangiopathic hemolytic anemia, develops in some patients, particularly children, following acute colitis with E. coli O157:H7. HUS is caused by toxin-mediated damage to the glomerular epithelial cells and possibly the tubular epithelial cells and is the leading cause of acute renal failure in children. 2 23 Other organisms that have been linked to HUS include other strains of E. coli, Citrobacter, Campylobacter, Shigella, Salmonella, and Yersinia.223 Many of the acute symptoms of ciguatera poisoning can persist as a waxing and waning chronic symptom complex that is often misdiagnosed as chronic fatigue syndrome, brain tumor, or multiple sclerosis. 23
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