Different types of Campylobacter have been linked with disease in humans, but by far the type most commonly associated with foodborne disease is Campylobacter jejuni. C. jejuni is now considered to be the most common bacterial cause of foodborne disease in the US, with approximately 2.5 million cases per year, based on recent estimates from the Centers for Disease Control. Yet, C. jejuni is a relative newcomer to the field of foodborne pathogens; it was first described in the mid-1970s and it took a while before it gained wide recognition as a significant cause of disease in humans. One contributing factor is that it is a difficult organism to culture and development of routine diagnostics tests was slow to come on line.

C. jejuni causes gastroenteritis that is often indistinguishable from the other classic foodborne bacterial pathogens such as Salmonella and Escherichia coli. However, in recent years it has become clear that this organism has a much more sinister side to it in the form of a major complication in some patients following the gastrointestinal infection. I refer, of course, to Guillian-Barré syndrome (GBS). We will discuss what is known about the link between C. jejuni and GBS in the second part of this article. First, however, we will look at the typical clinical presentation of an acute infection with C. jejuni.

Acute Infection with C. jejuni

C. jejuni bacteria are found in fowl and many wild and domestic animals, and most human infections probably result from contamination of milk and other animal food sources, especially poultry. The organisms can also be transmitted by direct contact with infected animals or contaminated water. Cross-contamination between infected poultry and other foods is probably one of the most frequent modes of transmission. Small numbers of organisms can cause disease; as few as 500 have been shown to cause infection in some volunteer studies. But the problem with these studies is that they are usually done in healthy young adults rather than a high-risk population. As with many other foodborne pathogens, C. jejuni infections are more common in the summer months.

The incubation period for C. jejuni infection varies, typically between one and seven days, with most cases occurring two to four days after exposure. Very short incubation periods of less than 12 hours have been reported. Illness typically begins with fever, headache, muscle aches and malaise for up to 24 hours before intestinal symptoms develop. The infection initially appears much like the beginnings of an attack of the flu then typically develops into a more classical gastroenteritis with nausea, abdominal pain, vomiting and diarrhea­more in line with the symptoms one experiences with Salmonella or E. coli. The fever can be high, up to 104°F, and the diarrhea can be copious. Blood is frequently present in the stool but varies in amount. The illness usually lasts less than a week, but patients untreated with antibiotics frequently continue to excrete the organisms for several weeks.

Not all C. jejuni infections require antibiotics, and antibiotic treatment should be reserved for the more severe cases. One of the recent worrying trends with C. jejuni is the increasing number of isolates that are resistant to the standard first-line antibiotics used to treat diarrheal disease. This is becoming a major problem, especially in infections that are acquired overseas. Person-to-person spread is not generally considered to be a major concern with Campylobacter, so treating to prevent this is not generally recommended, except in the case of food handlers. There can, however, be exceptions to this; for example, the reduction of spread in daycare settings.

C. jejuni are generally considered to be invasive bacteria, which means they have the capacity to get inside the cells lining the intestinal tract. This results in local inflammation and tissue damage, and this is one of the factors that is thought to be important in the development of bloody diarrhea in some patients. However, the bacteria usually remain confined to the cells of the intestinal tract and it is unusual for them to invade the blood stream.

The natural history of C. jejuni infection in most individuals is that it will settle spontaneously without the need for specific treatment. However, as with all diarrheal diseases, it is important to pay attention to adequate hydration. Occasionally the bacteria do get into the blood stream and can then infect other parts of the body, such as heart valves (endocarditis), the gall bladder (cholecystitis) and the pancreas (pancreatitis). As with other foodborne pathogens, such as Salmonella, Shigella and Yersina, another complication following Campylobacter infection is a condition known as reactive arthritis. This follows several weeks after the acute infection and is more common in certain groups of people who have a specific tissue type known as HLA-B27. Of course, one of the more feared complications following C. jejuni infection is the development of GBS.

Guillian-Barré syndrome is a disease that affects the peripheral nerves, which run from the spinal cord to individual muscles, as opposed to the brain, that control the arms, legs and body. Patients with GBS have flaccid paralysis, meaning their muscles and limbs become floppy and unusable. This is in contrast to spastic paralysis that typically follows a stroke when arms and legs become stiff and unusable through damage to the brain itself. Since the control of polio, GBS is the most common cause of acute flaccid paralysis.

Patients who develop GBS will experience a progressive weakness that usually begins in their feet and gradually extends up the body in a symmetrical pattern. This will evolve over a period of days and will lead to an inability to walk and loss of the use of arms. If it spreads far enough up the body, then it can result in paralysis of the respiratory muscles leading to an inability to breathe. Clearly this is a major complication that can result in patients requiring mechanical ventilation for a period of time.

The progression is usually rapid and may take only a matter of days to progress from the first signs of difficulty in walking to a need for a breathing machine. The weakness usually reaches a peak within two to three weeks of the beginning of the disease and then typically there is a gradual recovery that may take weeks or even months. The chances that GBS will progress to requiring mechanical ventilation is around 20% and although the majority of people will make a full recovery, 15% to 20% of patients have some residual physical problems. Modern medical intensive-care support has reduced the mortality rate from GBS, but even now 2% to 3% of patients with GBS will die from the disease, often due to complications that arise during the acute part of the disease when patients are paralyzed and require intensive medical support.

The link between C. jejuni and GBS was first described in 1982 in a 45-year-old man. In recent years the link has become stronger and it is now clear that 30% to 40% of GBS cases are related to a prior infection with C. jejuni. Still, the risk of developing GBS following infection with C. jejuni is quite low and current estimates are that one person will develop GBS for each 1,000 people infected with C. jejuni. There are, in fact, approximately 100 different serotypes of C. jejuni, not all of which are equally likely to lead to GBS. Strain O:19 is one that is frequently associated with GBS but at least 11 other serotypes also have been linked to the disease.

In order to address the question of how GBS and C. jejuni infection in the intestine are linked, I first want to say a little about what causes the initial nerve damage. Peripheral nerves that run to and from the spinal cord to muscles are composed of a mixture of motor nerves and sensory nerves. Each nerve is covered in an insulating material called myelin that is important to enabling the electrical impulses to move along the nerves at speeds approaching 2,500 feet per second. The principal problem in GBS is that the patient's immune system begins to attack the myelin surrounding the nerves, which dramatically affects the nerve's ability to function.

The myelin is composed of various molecules. One of the major constituents is polysaccharides, which are made up of a string of different types of sugar molecules. The C. jejuni bacterium has the same string of sugars on its outer coat, as illustrated in the figure on the facing page. Thus, when a person is infected with C. jejuni, the body regards this bacterium as foreign and begins to generate an immune response to the invader. Unfortunately, these same antibodies that are made to bind to the sugars on the outer coat of the organism also bind to the sugars on the myelin. This process is known as molecular mimicry.

After antibodies have bound to the myelin coating, a series of events is initiated that includes the arrival of new immune cells that begin to attack the myelin. This interferes with the nerve function and, as a result, leads to the clinical manifestations of GBS.

In some patients GBS follows very rapidly­often in less than a week­after the gastrointestinal infection. This is probably because the patient already had some antibodies present from a previous exposure to C. jejuni but not at a high enough level to cause problems. Then following a second infection the exposure to C. jejuni acts like a booster to the immune response, leading to the rapid development of GBS as the antibody levels quickly rise to a point where they can bind to the myelin and begin to interfere with nerve function. This concept is important in view of current attempts to make vaccines against Campylobacter: clearly one does not want to make a Campylobacter vaccine that can lead to the production of antibodies that increase the likelihood of getting GBS following a natural C. jejuni infection.

This evolving story of how a bacterium that was thought to cause a straightforward gastroenteritis but is now found to be responsible for major systemic disease is an interesting illustration of the hidden dangers of foodborne infections. Clearly, it is important for clinicians, epidemiologists and food scientists to be aware of both the immediate and long-term consequences of foodborne infections. There are many other examples of how different foodborne pathogens can lead to both an immediate upset, usually in the form of gastroenteritis, and then reappear in some format in a much more dangerous or even life-threatening way. Future articles will address some of the other food-borne pathogens that can cause such unexpected complications.

Other Changes To Make

• drink 6-8 glasses of steam distilled or filtered water a day

• eat 50% raw fruits and vegetables (organic is best)

• nuts, seeds, and whole grains are good

• juice is good (make your own with a juice machine)

• do not worry as much about calories as eating the right foods

• carrot and celery sticks are good to use as a snack

• a colon cleansing can be very helpful - (do several times each year)

• do not drink coffee, alcohol, soda pop, other junk food drinks

• do not eat processed foods white sugar, white flour, etc...

• use stress relief like going for walks in the park (or the 10/90 rule - see Stress)

• brown rice is good to eat

• avoid red meat and animal fats

• reduce dairy products cheese, milk, and others

• fast a few days a month

• get at least 8 hours of sleep 

• exercise light to moderate amounts

• avoid artificial sweeteners like Aspartame and NutraSweet

• do not smoke and avoid second hand smoke

• do not skip meals - just eat better and not as much at each meal

• do not chew gum - it can cause you to feel hungry

• do not watch too much TV try reading a book or something else