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Pathologic Changes in the Small Bowel in Nine Patients with Diarrhea Associated with a Coccidia-like Body

Bradley A. Connor, MD; David R. Shlim, MD; John V. Scholes, MD; Joseph L. Rayburn, MD; Jason Reidy, MA; and Ramachandran Rajah, ASMLT
[+] Article and Author Information

From the Canadian International Water and Energy Consultants Clinic, Kathmandu, Nepal; the New York Hospital-Cornell University Medical College, New York University School of Medicine; Beth Israel Medical Center and Mount Sinai School of Medicine, New York, New York. Requests for Reprints: Bradley A. Connor, MD, 50 East 69th Street, New York, NY 10021. Acknowledgments: The authors thank Peter Echeverria, MD, for his help in performing the bacteriologic and virologic studies.


Copyright 2004 by the American College of Physicians


Ann Intern Med. 1993;119(5):377-382. doi:10.7326/0003-4819-119-5-199309010-00005
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Objective: To confirm a suspected small-bowel injury in patients with a syndrome of protracted diarrhea associated with a coccidia-like body (CLB).

Design: Investigation of an epidemic including a casecontrol study.

Setting: Outpatient clinic in Kathmandu serving primarily the tourist and expatriate community in Nepal.

Patients: Nine patients with diarrhea with at least one stool specimen that was positive for the presence of a CLB and seven noninfected volunteer controls.

Measurements: Clinical data, microscopic examination of stool, bacteriologic and viral studies on submitted stool specimens, upper gastrointestinal endoscopy including duodenal aspiration and microscopy, small-bowel biopsy with subsequent light and electron microscopy.

Results: Endoscopic evidence of inflammation of the distal duodenum was present in five of nine patients with CLB and in none of the seven controls. All nine patients with CLB were noted to have histologic evidence of small-bowel injury, which included acute and chronic inflammation, surface epithelial disarray, and varying degrees of villous atrophy and crypt hyperplasia. One of the seven controls had similar pathologic findings and developed CLB-related diarrhea 5 days later. The other controls had normal distal duodenal histologic results. The organism was found in two of nine duodenal aspirates but was not present in the preserved biopsy specimens as determined by light or electron microscopy.

Conclusions: The pathologic basis of CLB-associated diarrhea appears to be small-bowel injury whose cause remains to be elucidated.

Figures

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Figure 1.
The number of new cases infected with coccidia-like bodies per week, defined as the date of the first positive stool specimen for each patient.

Recording of these bodies in the stool began only on 19 June 1989, apparently missing the first part of that year's outbreak. These bodies were not noted in stool examinations during the rest of the year.

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Figure 2.
Oil immersion photograph of smear of concentrated stool specimen of patient with chronic diarrhea.

Three coccidia-like bodies (red) with central morula containing refractile globules (pale pink to clear) and outer membrane are shown. Organisms measure 9 to 10µmin width. (Acid-fast stain. Original magnification, 4000.).

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Figure 3.
Oil immersion photograph of smear from duodenal aspirate stained with modified acid-fast stain.

Three coccidia-like bodies are shown (center). Organisms stain strongly positive (red-pink) but are imperfectly preserved. Acid-fast bacilli are present in the background. (Modified acid-fast stain. Original magnification, 2500.).

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Figure 4.
Photograph of section of endoscopic duodenal biopsy showing partial atrophy of villi.

Elongated hypertrophic crypts (with a villous-to-crypt ratio of 1:1) and chronic inflammation of lamina propria with increased mononuclear cells are shown. (Hematoxylin and eosin. Original magnification, 250.).

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Figure 5.
Medium-power photograph of section of duodenal biopsy obtained by endoscopy from a patient with coccidia-like bodies in the stool.

Partial villous atrophy, crypt hyperplasia with increased crypt length and mitoses (villous-to-crypt ratio, 1:1), and chronic inflammation with increased mononuclear cells in the lamina propria are evident. (Hematoxylin and eosin. Original magnification, 500.).

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