PULLMAN, Wash. — Campylobacter jejuni. Its name may not be familiar, but its effects are. It causes the cramping, diarrhea, fever and nausea usually associated with food-borne gastrointestinal illness. Campylobacter jejuni causes more of this illness in the United States than its more famous cousins Salmonella or Escherichia coli, somewhere between two and eight million cases of gastrointestinal upsets a year.
If it’s so common, why is Campylobacter so unknown? “It may be because Campylobacter rarely causes outbreaks, as do the other two, or because we haven’t been educated about it,” says WSU microbiologist Mike Konkel. Konkel’s research on Campylobacter is funded by the National Institutes of Health and the USDA.
Most people become acquainted with Campylobacter by eating undercooked chicken, especially when the barbecue season fires up in the spring. Healthy chickens carry this bacteria in their intestines, and their carcasses often become contaminated during slaughter. When chicken in supermarkets are tested, up to 90 percent of them are found to be contaminated with Campylobacter.
Campylobacter can also be transmitted directly from person to person, as can most gastrointestinal bacteria. It can also be transmitted in unchlorinated water and unpasteurized milk.
Konkel sees the Campylobacter he studies as a model system for bacteria-host interactions, particularly for bacterial species that cause gastrointestinal problems in humans. Most of these bacteria share mechanisms of infection. After being ingested and spending a half hour or so in the stomach, the bacteria move along the gastrointestinal tract to the small intestine, one part of which is the eight foot jejunum. During the hour or two the bacteria spend moving through this continually contracting section, they must attach to the cells that line it in order to infect.
There are several different proteins on the surface of bacteria that bind to the intestinal cells. Konkel’s lab recently identified the first of these “adhesins,” five years after recognizing the importance of an unexpectedly revealing electron micrograph. Konkel was standardizing assay procedures for working with Campylobacter. The micrograph of cells grown in cold temperatures showed that the cells were contracted into balls, leaving large amounts of fibronectin exposed.
Fibronectin is a glycoprotein with several functions in the body, one of which is to help hold cells of the gastrointestinal tract together. The exposed fibronectin shown in the micrograph was covered with Campylobacter. Knowing that the bacteria bound to fibronectin was an important initial step in the identification of the first adhesin.
Bacteria always display their adhesins on their surfaces, for there would not be enough time to make and display them after the bacteria are ingested and before they reach the jejunum. But the “invasins,” the proteins that mediate the next step in the infection process, are produced by the bacteria only after they bind to the intestinal cell. The invasins help the bacteria enter the intestinal cells.
Konkel is working on a number of candidate invasins. “I think invasion into the cell is a much more complicated process than binding to it,” says Konkel.
In the United States, Campylobacter causes up to 800 deaths per year. It is also implicated in the pathogenesis of Guillain-Barre syndrome(GBs), a sometimes fatal degenerative neurological disorder. Twenty-five to thirty percent of GBs cases were preceded within a few months by Campylobacter infection. GBs is thought to be an autoimmune disease. One of the molecules on the outside of a few of the Campylobacteri strains is similar to a molecule on normal nerve cells. Infection with these strains results in the production of antibodies that will bind to the nerve cells and cause damage to them.
Luckily, resistance to antibiotics is not a big problem with Campylobacter yet. The drug of choice for its treatment is erythromycin, and treatment usually reduces the length of illness from one or two weeks to one or two days.
Konkel’s immediate research goal is to better understand Campylobacter’s adhesins and invasins as well as other bacterial molecules that are responsible for its ability to cause illness. Understanding the infection process is a necessary first step to developing new treatments, should the bacteria develop antibiotic resistance on a wide scale. It’s also the first step in working to reduce the level of contamination of chicken or become better able to detect it when it occurs. Both of these are considered to be the most effective ways to deal with food borne illness.
Although Konkel’s focus is on the basic aspects of this goal, he collaborates with the USDA at College Station, Texas. They are trying to determine whether strains of bacteria that do not make the adhesin are less able to colonize chickens. They are also immunizing chickens against the adhesin to see if that helps reduce colonization.
What’s the best way to reduce your chances of a Campylobacter infection? Just follow Julia Child’s advice, even though her criteria is meant to protect us from dry, over-cooked chicken, not bacteria. She always emphasizes cooking chicken until its juices run clear. That should mean the chicken’s interior has reached 190 degrees, a temperature that should kill not only Campylobacter jejuni but most any other bacteria hitching a ride on your chicken.