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The Relationship Between Campylobacter and GBS

For those persons who suffer a Campylobacter infection that does not resolve on its own, the complications (or sequelae) can be many. The complications can include septicemia (bacterial pathogens in the blood, also known as bacteremia), meningitis, inflammation of the gall bladder (cholecystitis), urinary tract infections, and appendicitis.

“Each year, there are an estimated 2,628 to 9,575 people who develop GBS in the United States.” A sizeable percentage of persons who suffer Campylobacter infections develop GBS. Since the vaccination programs have eliminated polio in the United States, GBS is the leading cause of acute neuromuscular paralysis. Over time, the paralysis is to some extent typically reversible; nonetheless, approximately 20% of patients with GBS are left disabled, and approximately 5% die.

An estimated one case of GBS occurs for every 1,000 Campylobacter infections. Along these same lines, researchers estimate that between 20% and 40% of all GBS cases are caused by Campylobacter infections. Indeed, up to 40% of GBS patients have evidence of recent Campylobacter infection. “Assuming that 20 to 40 percent of all patients with GBS have prior Campylobacter infections, there are an estimated 526 to 3, 830 new patients diagnosed with Campylobacter-associated GBS each year in the United States.”

GBS occurs when an infected person’s immune system makes antibodies against components of Campylobacter, and these antibodies attack components of the body’s nerve cells because they are chemically like bacterial components. Miller Fisher Syndrome is another, related neurological syndrome that can follow campylobacteriosis, and is also caused by a triggered immune response. Overall, there is no one factor that appears to cause a greater percentage of GBS cases other than Campylobacter infections.

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