There are numerous medical complications associated with Campylobacter infection, many of which have a worse prognosis than the acute infection itself. Campylobacter infections can cause extraintestinal diseases involving the neurologic, pulmonary, immunologic and cardiac systems. The main recognized sequelae are Guillain-Barré Syndrome (GBS), reactive arthritis (REA), and post-infectious irritable bowel syndrome (P-IBS). The Miller Fisher Syndrome, a variant of GBS, can also be associated with a previous Campylobacter infection. Evidence suggests a possible association with Inflammatory Bowel Disease (IBD), and there is evidence that other functional gastrointestinal disorders may be related to gastroenteritis in general (not specifically caused by Campylobacter).
Guillain-Barré Syndrome (GBS)
The exact cause of Guillain-Barré syndrome (GBS) is unknown. Researchers do not know why it strikes some people and not others. It is not contagious or inherited, despite the fact that it can be triggered by an infection. The most common preceding infection involves the bacterium Campylobacter jejuni. Guillain-Barré syndrome is not itself contagious. However, according to the CDC, outbreaks of associated pathogenic viruses and bacteria, including Campylobacter, can lead to clusters of people with Guillain-Barré syndrome. About one in every 1,000 reported Campylobacter illnesses leads to the disorder. As many as 40% of cases in the United States are thought to be triggered by Campylobacter infection.
The role of Campylobacter has now been extensively studied in triggering an autoimmune response that leads to damage of the peripheral nervous system and the development of GBS. The Campylobacter-induced GBS is now considered a real disease related to the phenomenon of molecular mimicry. Specifically, “the C. jejuni lipopolysaccharide resembles GMi ganglioside on peripheral nerve myelin. Infection can lead to the development of cross-reacting antibodies that cause nerve damage. The Miller Fisher variant of GBS is thought to be caused by antibodies that cross react with Campylobacter lipopolysaccharide and ganglioside GQib in cranial nerve myelin.”
There may be factors other than molecular mimicry that also play a role in the development of Campylobacter-associated GBS. Additional host factors seem to be important, since not all patients who develop antibodies to GMi ganglioside develop neurologic symptoms. Some researchers postulate that there may be an association between HLA types and the development of Campylobacter-associated GBS.
Reactive arthritis after Campylobacter enteritis can occur 3 to 40 days (mean: 11 days) after the onset of diarrhea. It is usually oligoarticular and asymmetrical (one joint, one side of body), and it predominantly affects the knees. It is more common and possibly more severe in patients with HLA-B27 phenotype. The development of arthritis does not seem to be related to the severity of the initial Campylobacter illness. Symptoms generally last for up to 21 days, and most patients have spontaneous recovery within 6 months without long-term sequelae. The arthritis is reactive, not infectious; synovial fluid is sterile. Arthritis (joint inflammation) occurs in up to 7% of patients, but as many as 20% of patients report joint pain.
Irritable Bowel Syndrome (IBS)
Infectious gastroenteritis is one of the major predisposing factors for the development of irritable bowel syndrome (IBS). Some studies have reported that up to 36% of individuals with acute campylobacteriosis develop IBS within 1-2 years. There seems to be a close correlation between risk of developing IBS and the severity of the acute illness. Following an outbreak of infection with Campylobacter and Enterohemorrhagic E. coli (EHEC) caused by contaminated water, some studies have reported an increased risk of IBS among those who had had a greater length of diarrhea, dysentery, and abdominal cramps during the acute phase of the disease.
Other functional gastrointestinal disorders related to Campylobacter
Recent studies have shown evidence linking infectious diarrheal syndromes with other functional gastrointestinal disorders such as functional dyspepsia (indigestion), including Campylobacter. There is also some evidence that there is a relationship between the presence of Campylobacter and other functional gastrointestinal disorders, such as diarrhea, functional constipation, and gastroesophageal reflux disease (GERD).
Inflammatory bowel disease (IBD)
In recent years, some studies have strengthened a hypothesis of an association between IBD and acute diarrheal infection caused by Campylobacter. The first studies that described such a possible association between acute infection and inflammatory bowel disease date back to the ‘90s. Campylobacter was isolated from 10% of cases of relapsing IBD. Recent cohort studies have shown a higher risk of developing IBD following an acute infection with Campylobacter.