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Epidemiologic Notes and Reports Investigation of a Cluster of Appendicitis Cases - Texas

Although appendectomy for acute appendicitis is the most commonly performed emergency abdominal surgery in the United States (1 ), epidemiologic investigations to determine risk factors for and causes of this condition are limited. A 1984 investigation of a cluster of cases of appendicitis in Texas illustrates how the epidemiologic approach may be used to address this problem.

In April 1984, the Texas Department of Health learned of an apparent cluster of appendicitis cases in a town of 8,000 inhabitants. In the resulting investigation, 13 patients with histologically confirmed appendicitis during the period February - April 1984 were identified. During the same time period in the previous year, there had been two cases. Eleven of the 13 patients with appendicitis (85%) were males; in 1983, three of seven patients (43%) were males. The median age of patients in 1984 was 13 years, compared with 20 years in 1983. Eight of the 13 patients experienced their first episode of severe abdominal pain during a 15-day period in February (Poisson distribution, p <0.01).

Initially, five physicians examined the various patients and diagnosed their illnesses. A surgeon from a neighboring community performed 12 of the 13 appendectomies. Seven patients (54%) had fecaliths, and four (31%) had perforated appendices at the time of surgery. Salmonella was isolated from one patient's appendix. Cultures for Campylobacter and Yersinia and viral studies were not performed.

Eleven of the patients attended the town's five schools. The absentee rate for their respective grades peaked during a 1-week period in late January (Figure 1). The school nurse reported that both acute upper respiratory tract and gastrointestinal illnesses occurred simultaneously in January and February. The cluster of appendicitis occurred 2 to 3 weeks after the majority of illnesses in the schools.

A case-control study was conducted for the school-aged patients. Two controls per patient were chosen at random from each patient's grade roster. Ninety-one percent of the patients, and 77% of the controls were absent at least 1 day between January 15 and February 12, 1984. Similar percentages of patients and controls had experienced antecedent symptoms of upper respiratory tract illness (36% compared with 27%), while 36% of patients and only 9% of controls reported antecedent symptoms of gastrointestinal illness.

A survey including questions on exposure to 41 food items was conducted. Statistical associations were detected between appendicitis and some food exposures. However, studies demonstrating a specific causal role for these foods have not been conducted.

Abstracted with permission from: Martin DL, Gustafson TL. A cluster of true appendicitis cases, Am J Surg 1985; 150:554-7. Reported by: D Martin, C Alexander, MD, State Epidemiologist Texas Dept of Health. Enteric Diseases Br, Div of Bacterial Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Symptoms that mimic appendicitis can be caused by several enteric pathogens, including Yersinia enterocolitica (2), Yersinia pseudotuberculosis (3), and Campylobacter jejuni (4). Although specific cultures were not performed to exclude these agents in the Texas cluster, the absence of mesenteric adenitis and concurrent gastroenteritis suggests that these agents were not the cause of the cluster. The criteria for the pathologic diagnosis of early appendicitis are somewhat subjective (5), and the particular criteria used were not specified in this report. However, the high perforation rate combined with the pathologic diagnoses strongly suggest that the cases in this cluster were true appendicitis.

Appendicitis has long been presumed to be related to mechanical obstruction of the appendix (6). However, appendiceal obstruction can be difficult to demonstrate (7), and increasing evidence points to external causes. Since appendicitis appears to be rare in industrially undeveloped countries, Burkitt advanced the hypothesis that diets high in fiber protect against appendicitis (8). In two case-control studies, controls had slightly higher fiber intake than patients, although the possible protective effect of a high-fiber diet is not consistent with long-term trends in the United Kingdom (9-11).

In a recent case-control study, siblings (but not parents) of children with appendicitis were 10 times more likely than siblings of control children to have had appendicitis themselves. This difference suggests that illness may have been attributable to a common environmental risk factor (12). The cluster reported here supports the hypothesis that environmental factors may contribute to appendicitis. The etiology may be related to exposures to specific foods, infectious agents, or toxins, alone or in combination with general dietary factors (13). It is also possible that the associations reported in this cluster occurred by chance because of the large number of comparisons in the study. However, they provide useful and testable hypotheses, and the potential roles of antecedent illness and certain foods should be examined further.

Clusters of appendicitis offer a unique opportunity to identify possible risk factors and to search for precipitating infectious agents. In the event of such clusters, clinicians should perform cultures for pathogens causing the pseudoappendiceal syndrome and should confirm the diagnosis using explicit pathologic case definitions. State health departments are encouraged to report such clusters to the Enteric Diseases Branch, Center for Infectious Diseases, CDC, which could advise or assist in investigations.

References

  1. Cooperman M. Complications of appendectomy. Surg Clin North Am 1983;63:1233-47.

  2. Jepsen OB , Korner B, Lauritsen KB, et al. Yersinia enterocolitica infection in patients with acute surgical abdominal disease: a prospective study. Scand J Infect Dis 1976:8:189-94.

  3. Tertti R, Granfors K, Lehtonen OP, et al. An outbreak of Yersinia pseudotuberculosis infection. J Infect Dis 1984;149:245-50.

  4. Blaser NJ, Berkowitz ID, LaForce FM, Cravens J, Reller LB, Wang WL. Campylobacter entertis: clinical and epidemiologic features. Ann Intern Med 1979:91:179-85.

  5. Klein HZ, Coulson WF. The appendix. In: Coulson WF, ed. Surgical pathology. Philadelphia: Lippincott, 1978:160-3.

  6. Wangensteen OH, Dennis C. Experimental proof of obstructive origin of appendicitis in man. Ann Surg 1939:110:629-47.

  7. Arnbjornsson E, Bengmark S. Role of obstruction in the pathogenesis of acute appendicitis. Am J Surg 1984;147:390-2.

  8. Burkitt DP. The aetiology of appendicitis. Br J Surg 1971:58:695-9.

  9. Arnbjornsson E. Acute appendicitis and dietary fiber. Arch Surg 1983;118:868-70.

  10. Brender JD, Weiss NS, Koepsell TD, Marcuse EK. Fiber intake and childhood appendicitis. Am J Public Health 1985;75:399-400.

  11. Barker DJP. Acute appendicitis and dietary fibre: an alternative hypothesis. Br Med J 1985;280:1125-7.

  12. Brender JD, Marcuse EK, Weiss S, Koepsell TD. Is childhood appendicitis familial? Am J Dis Child 1985:139:338-40.

  13. Environmental Epidemiology Unit, Medical Research Council. The aetiology of acute appendicitis (scientific report no. 7): proceedings of a meeting held on May 22, 1986. Southampton, England: Medical Research Council, 1986.



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