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Chapter 15 : as a Cause of Antibiotic-Associated Colitis

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as a Cause of Antibiotic-Associated Colitis, Page 1 of 2

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Abstract:

Antibiotic-associated diarrhea (AAD) is a frequent adverse effect observed during or shortly after antibiotic therapy. The frequency of AAD differs with the antibiotic given, with 5 to 25% of patients who receive antibiotic therapy developing the disorder. The majority of patients developing AAD report mild, self-limiting diarrhea. A special form of antibiotic-associated colitis is antibiotic-associated hemorrhagic colitis (AAHC; synonyms include segmental antibiotic-associated hemorrhagic colitis, penicillin-associated hemorrhagic colitis, and right-sided antibiotic-associated hemorrhagic colitis). An in vivo animal model for AAHC and , as exists for induced colitis, was only recently established. In addition to endoscopy, microbiological tests are most crucial for the differential diagnosis of -associated AAHC. The cytotoxic effect can be assessed by microscopy and is based on cell rounding and cell death. In the context of clinical presentation, results of microbiological testing, and endoscopy, these two entities can be easily differentiated. There is evidence that patients with AAHC differ in their demographic characteristics from patients with -associated disease (CDAD). The causative role of has only been proven for AAHC.

Citation: Högenauer C, Hinterleitner T. 2008. as a Cause of Antibiotic-Associated Colitis, p 293-311. In Scheld W, Hammer S, Hughes J (ed), Emerging Infections 8. ASM Press, Washington, DC. doi: 10.1128/9781555815592.ch15
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Figures

Image of Figure 1.
Figure 1.

Histological specimen from the colon of a patient with AAHC (hematoxylin and eosin stain). The typical histopathological findings of AAHC are present: alteration of the surface epithelium with loss of goblet cells, anisonucleosis, an increased rate of mitosis and apoptosis, mucosal hemorrhage, and a mild inflammatory infiltrate of neutrophils in the lamina propria. (Courtesy of Cord Langner, Institute of Pathology, Medical University of Graz.)

Citation: Högenauer C, Hinterleitner T. 2008. as a Cause of Antibiotic-Associated Colitis, p 293-311. In Scheld W, Hammer S, Hughes J (ed), Emerging Infections 8. ASM Press, Washington, DC. doi: 10.1128/9781555815592.ch15
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Image of Figure 2.
Figure 2.

Histological specimens of rat cecum. (a) Colitis induced by a clinical isolate from a patient who had developed AAHC. The bacterium was administered in combination with an antibiotic and an NSAID (experimental group 4). (b) Normal cecum from a control animal that received antibiotics and an NSAID (experimental group 5).

Citation: Högenauer C, Hinterleitner T. 2008. as a Cause of Antibiotic-Associated Colitis, p 293-311. In Scheld W, Hammer S, Hughes J (ed), Emerging Infections 8. ASM Press, Washington, DC. doi: 10.1128/9781555815592.ch15
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Image of Figure 3.
Figure 3.

Cytotoxic effect of the supernatant from on monolayers of HEp-2 cells. (a) Cell rounding and cell death after 48-h incubation of an HEp-2 monolayer with a supernatant of a clinical isolate from a patient with AAHC. (b) For comparison, HEp-2 cells that were incubated with the supernatant from a laboratory control strain (ATCC 13182), showing no cytotoxic effect.

Citation: Högenauer C, Hinterleitner T. 2008. as a Cause of Antibiotic-Associated Colitis, p 293-311. In Scheld W, Hammer S, Hughes J (ed), Emerging Infections 8. ASM Press, Washington, DC. doi: 10.1128/9781555815592.ch15
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Image of Figure 4.
Figure 4.

Endoscopic aspect of -associated AAHC compared to associated pseudomembranous colitis. On endoscopy, the colonic mucosa shows severe edema and mucosal hemorrhage (a); colitis is typically segmental and predominantly involves the right colon (b). Pseudomembranous colitis has the characteristic yellowish plaques consisting of fibrin, inflammatory cells, and debris (c). The latter is usually continuous in the left colon and rectum, with or without involvement of the whole colon (d).

Citation: Högenauer C, Hinterleitner T. 2008. as a Cause of Antibiotic-Associated Colitis, p 293-311. In Scheld W, Hammer S, Hughes J (ed), Emerging Infections 8. ASM Press, Washington, DC. doi: 10.1128/9781555815592.ch15
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Image of Figure 5.
Figure 5.

Ultrasonography of AAHC. Colonic wall thickening to a diameter of 13 mm of the ascending colon was apparent on ultrasound examination of a 37-year-old patient with AAHC after 3 days of treatment for tonsillitis with amoxicillin-clavulanate.

Citation: Högenauer C, Hinterleitner T. 2008. as a Cause of Antibiotic-Associated Colitis, p 293-311. In Scheld W, Hammer S, Hughes J (ed), Emerging Infections 8. ASM Press, Washington, DC. doi: 10.1128/9781555815592.ch15
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Tables

Generic image for table
Table 1.

Demographic, clinical, and laboratory characteristics of 19 patients with AAHC treated at the Department of Internal Medicine, Medical University of Graz

Citation: Högenauer C, Hinterleitner T. 2008. as a Cause of Antibiotic-Associated Colitis, p 293-311. In Scheld W, Hammer S, Hughes J (ed), Emerging Infections 8. ASM Press, Washington, DC. doi: 10.1128/9781555815592.ch15
Generic image for table
Table 2.

Endoscopic features in AAHC patients

Citation: Högenauer C, Hinterleitner T. 2008. as a Cause of Antibiotic-Associated Colitis, p 293-311. In Scheld W, Hammer S, Hughes J (ed), Emerging Infections 8. ASM Press, Washington, DC. doi: 10.1128/9781555815592.ch15
Generic image for table
Table 3.

Experimental design and results of experiments in rats

Citation: Högenauer C, Hinterleitner T. 2008. as a Cause of Antibiotic-Associated Colitis, p 293-311. In Scheld W, Hammer S, Hughes J (ed), Emerging Infections 8. ASM Press, Washington, DC. doi: 10.1128/9781555815592.ch15
Generic image for table
Table 4.

Clinical characteristics of patients with -or -associated colitis treated at the Department of Internal Medicine, Medical University of Graz

Citation: Högenauer C, Hinterleitner T. 2008. as a Cause of Antibiotic-Associated Colitis, p 293-311. In Scheld W, Hammer S, Hughes J (ed), Emerging Infections 8. ASM Press, Washington, DC. doi: 10.1128/9781555815592.ch15
Generic image for table
Table 5.

Differences between -associated colitis and -associated colitis

Citation: Högenauer C, Hinterleitner T. 2008. as a Cause of Antibiotic-Associated Colitis, p 293-311. In Scheld W, Hammer S, Hughes J (ed), Emerging Infections 8. ASM Press, Washington, DC. doi: 10.1128/9781555815592.ch15

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