Publication

[Toxic megacolon as a complication of Campylobacter jejuni enterocolitis]

Journal Paper/Review - Oct 10, 1998

Units
PubMed

Citation
Kummer A, Meyenberger C. [Toxic megacolon as a complication of Campylobacter jejuni enterocolitis]. Schweizerische medizinische Wochenschrift 1998; 128:1553-8.
Type
Journal Paper/Review (Deutsch)
Journal
Schweizerische medizinische Wochenschrift 1998; 128
Publication Date
Oct 10, 1998
Issn Print
0036-7672
Pages
1553-8
Brief description/objective

We report the case of a previously healthy 53-year-old white male who developed an extraordinary complication of acute Campylobacter jejuni colitis. Toxic megacolon occurred while the patient was treated with a fluoroquinolone antibiotic and glucocorticoids, which were given for endoscopically suspected Crohn's colitis. During the course of the disease no cause of colitis was found other than C. jejuni. Despite the extreme dilatation, the patient was treated conservatively with parenteral nutrition and repeated decompression colonoscopies and made a full, though slow, and uneventful recovery. Follow-up colonoscopies for up to 4 years showed persistent scarring of the transverse colon, probably due to the extreme dilatation, and mild unspecific inflammation of the terminal ileum without histological evidence of inflammatory bowel disease. A comparison with the 6 previously published cases leads to the following conclusions: in most cases the transverse colon is most severely affected. Treatment with either antimotility agents or systemic glucocorticoids does not seem to promote colonic dilatation. The complication has affected patients of both sexes (4 women, 3 men), in the age range of 21 to 83 years, most of them without an underlying disease. The interval between the start of diarrhea and development of the megacolon ranged widely from 3 to 33 days, as did recovery time (2 days to several months). Three of the 7 patients underwent colectomy for imminent or actual colonic perforation. The delayed recovery of our patient was partly attributed to colonic damage caused by extreme dilatation, leading to ischaemia and subsequent scarring of the mucosa, which persisted. Histologically no Crohn's disease or ulcerative colitis could be found at any stage. A rapid increase in resistance of C. species against fluoroquinolone antibodies has been observed in recent years, due to use of the antibiotics in farming. Our patient's severe illness may partly have resulted from delayed effective antibiotic treatment due to resistance. Antibiotic resistance to common enteropathogens should be considered in the case of unusually prolonged or severe enterocolitis. The level of suspicion for either infection or inflammatory bowel disease should remain high as it may be impossible to distinguish between them on the basis of clinical or endoscopic criteria alone.