A family of five (with children aged 3, 4, and 5) decide to stop at their favorite fast-food restaurant for lunch. Everyone orders a chicken sandwich, with French fries and a large soft drink. The mother notices that the chicken filet in her sandwich is a tad pink in the middle and is tempted to take the sandwiches back to the counter. However, the children are quite hungry and were beginning to fuss in the car before the family stopped, so they are likely to throw a major tantrum if there is another delay. The mother wants to avoid this. Besides, her sandwich tastes OK, so she decides that she's just worrying about nothing.

The next day, the mother and two of the children begin to experience fever, headaches, myalgias, and general malaise. They do not seek medical attention because the symptoms are not all that severe. However, the symptoms persist for another day, when all three victims start to experience watery diarrhea, abdominal cramps, and continued fever. By the next morning they have each had about 10 bowel movements and it is apparent that additional movements are on the way, so they immediately go to their family physician. On examination, their vital signs are normal, except for fevers ranging from 38-38.5ºC. The physical examination is generally unremarkable, except that the two children are showing signs of mild dehydration. Smears of stool specimens are examined microscopically and found to contain fresh blood and PMNs (especially obvious in the specimens from the two children). There are no signs of protozoan cysts or ova. The mother relates her concerns about the chicken sandwiches but also dismisses them because only three family members are ill.

Question 6.1: What is your preliminary diagnosis?

The combination of fever and fecal leukocytes and erythrocytes is indicative of an inflammatory diarrhea. The differential diagnosis includes infections by Salmonella, Shigella, Campylobacter jejuni, Yersinia enterocolitica, and other GI pathogens. It is impossible to accurately distinguish among these illnesses on the basis of their symptoms alone because they are too similar. Definitive diagnosis must be based on culturing and laboratory identification of the causative agent.

Question 6.2: What tests should be performed?

Stool samples should be examined for the presence of possible causative agents. Stool cultures should also be ordered, and the lab should be told of the range of possibilities suspected, so that they can use the appropriate media.

Test Results

Gram stains of the stool samples reveal the presence of curved, Gram-negative bacilli in each of the samples. Isolates are obtained from each of the stool samples and identified as Campylobacter jejuni.

Figure 6.2 - Electron micrograph of isolated C. jejuni

Question 6.3: How does the lab detect and identify this causative agent?

When Campylobacter enteritis is suspected on the basis of findings indicating inflammatory diarrhea (fever, fecal leukocytes), clinicians can ask the lab to attempt visualization of bacteria with characteristic vibrioid morphology by direct microscopic examination of stools with Gram staining or to use phase-contrast or dark-field microscopy to observe Campylobacter's characteristic "darting motility." Confirmation of the diagnosis requires identification of bacterial isolates cultured from stool, blood, or other sites. Campylobacter-specific media must be used for isolation of these organisms. Detection of the organism in a stool sample almost always implies infection.

Question 6.4: How does this causative agent produce diarrhea?

The pathogenesis of infection is uncertain. Both the motility of C. jejuni and its ability to adhere to host tissues appear to favor disease, but classic enterotoxins and cytotoxins (which have been described) do not appear to play any substantial role in tissue injury or disease production. The organisms have been visualized in the epithelium, albeit in low numbers. The documentation of a significance tissue response and occasional C. jejuni bacteremia further suggests that invasion of tissues is clinically significant. Regardless of the actual mechanism involved, the sites of tissue injury include the jejunum, ileum, and colon. Biopsies show an acute nonspecific inflammatory reaction, with neutrophils, monocytes, and eosinophils in the lamina propria. There is also damage to the epithelium, including loss of mucus, glandular degeneration, and crypt abscesses.

Question 6.5: What is the epidemiology of this disease?

C. jejuni is a common resident of the digestive systems of various animals and birds, so most infections of humans are zoonotic. Humans acquire infections after consumption of contaminated water, food, or milk. Contaminated poultry products (including eggs) are responsible for more than half of the C. jejuni infections seen in developed countries, especially when such foods are not cooked thoroughly (obviously a factor in this case). Infections are also acquired from undercooked meats, dairy products, and exposure to infected pets. C. jejuni is the most frequent cause of bacterial gastroenteritis in the U.S. The actual number of cases is unknown (because this disease is not reported to public health officials), but it is estimated that > 2.5 million cases occur each year (making it more common than Salmonella and Shigella infections combined).

Question 6.6: Why did only there of the family members become ill?

Most likely, the sandwiches consumed by the father and the child that did not become ill were cooked thoroughly enough to kill the C. jejuni contaminants in the chicken. Only three of the sandwiches undercooked.

Question 6.7: How should these cases be treated?

The disease usually resolves within 7 days, but relapses are possible. Moderate or severe Campylobacter diarrhea may benefit from treatment with erythromycin (500 mg PO qid for 5 days) or ciprofloxacin (500 mg PO bid for 5 days).