the relationship between the two diseases and have published more than 200 reports in peer-reviewed journals. By the year 2000, those investigations had established that infection by C. jejuni causes about 30% of all cases of GBS (Allos 1997; Dingle et al. 2001; McCarthy and Giesecke 2001; Nachamkin 2002; Nachamkin et al. 1998; Nachamkin et al. 2001; Sinha et al. 2004; Tam et al. 2003). A number of other infectious diseases are also associated with GBS.

GBS is a severe acute neurologic disease characterized by ascending paralysis with involvement of motor neurons and sometimes sensory neurons (Rhodes and Tattersfield 1982). Developing over a period of days, the symptoms of GBS may lead to paralysis of the respiratory muscles and death; however, with rapid supportive care, the fatality rate has been reduced from more than 10% to less than 5%. Between 10 and 20% of affected persons have permanent neurologic deficits, such as persistent muscle weakness and contractures. Most patients with GBS require hospitalization, and more than 20% require ventilatory support at some time during their illness. Recommended treatment should be started immediately and may include plasmapheresis and intravenous administration of immunoglobulins.

Approximately 0.01-0.03% of US patients who suffer acute gastrointestinal disease due to C. jejuni will develop GBS (Allos 1997; Tauxe and Blake 1992). The risk of developing GBS during the 2 months after a symptomatic episode of C. jejuni infection is about 100 times greater than the risk in the general population (McCarthy and Giesecke 2001). The symptoms of GBS usually are manifested 7-28 days after the onset of gastrointestinal symptoms (Allos 1997; McCarthy and Giesecke 2001). There is no association between the severity of C. jejuni-induced gastrointestinal illness and the risk of developing GBS (Allos 2001).

Rigorous serologic and culture studies have found and validated evidence of recent infection by C. jejuni in high percentages of patients with GBS. Several studies, including at least two case-control studies, showed that GBS patients were more likely than controls to have increased titers of antibodies to C. jejuni (Liu et al. 2003; Mishu et al. 1993). They demonstrated important trends and associations in populations but are neither standardized nor sufficiently accurate to be used for conclusive diagnosis in an individual patient. In another line of inquiry, seven independent studies found that 8-50% (mean, 30%) of stool specimens obtained from patients with GBS at the onset of symptoms were culture-positive for C. jejuni (Enders et al. 1993; Gruenewald et al. 1991; Hariharan et al. 1996; Kuroki et al. 1993; Rees et al. 1995; Ropper 1988; Speed et al. 1984). A positive culture is sufficient for diagnosis of Campylobacter-induced GBS but may be falsely negative, depending on the accuracy of the cultural procedures used, timing after symptom onset, clinical status, and antibiotic use.

There are several types of GBS, including acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and Miller-Fisher syndrome (MFS). Antecedent Campylobacter infections have been linked with AMAN and MFS (Dingle et al. 2001; Kuwabara et al. 2004; Nachamkin et al. 1998); their association with AIDP is controversial (Kuwabara et al. 2004; Nachamkin et al. 1998).

Molecular mimicry is believed to play a role in the nerve damage that occurs in Campylobacter-associated GBS (Nachamkin et al. 1998). Although the mechanism is unknown, some molecular structures on the surface of particular strains of Campylobacter appear to mimic either the glycolipids of peripheral nerves or specific proteins found in myelin (Allos 2001).

The committee concludes that there is sufficient evidence of an association between Campylobacter jejuni infection and GBS, if the GBS is manifested within 2 months of the infection.

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