Fig.15.24A ),madeupofanadherentlayerofinflammatorycellsanddebrisatsitesofcolonicmucosalinjury.Thesurfaceepitheliumisdenuded,andthesuperficiallaminapropriacontainsadenseinfiltrateofneutrophilsandoccasionalfibrinthrombiwithincapillaries.Damagedcryptsaredistendedbyamucopurulentexudatethat“erupts”tothesurfaceinafashionreminiscentofavolcano(
Fig.15.24B
In addition to antibiotic exposure, risk factors for C. difficile– associated colitis include advanced age, hospitalization, and immunosuppression. The organism is particularly prevalent in hospitals; as many as 20% of hospitalized adults are colonized with C. difficile (a rate 10 times higher than in the general population), but most colonized patients are free of disease. Individuals with C. difficile–associated colitis usually present with watery diarrhea and abdominal cramping; dehydration, fever, and leukocytosis may be seen in more severe cases. Fecal leukocytes and occult blood may be present, but grossly bloody diarrhea is rare. Diagnosis of C. difficile–associated colitis usually is accomplished by detection of C. difficile toxin, rather than culture, and is supported by the characteristic histopathologic findings. Regimens of metronidazole or vancomycin are generally effective treatments, but antibiotic-resistant and hypervirulent C. difficile strains are increasingly common, and the infection may recur in at-risk patients. Recent reports suggest that, particularly in patients with recurrent disease, fecal microbial transplantation may restore a normal microbiota and lead to lasting cure.
Fig. 15.24 Clostridium difficile colitis.(A)Thecoloniscoatedbytanpseu-domembranescomposedofneutrophils,deadepithelialcells,andinflamma-torydebris(endoscopicview).(B)Typicalpatternofneutrophilsemanatingfromacryptisreminiscentofavolcaniceruption.
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Mycobacterial species, including M. tuberculosis, M. bovis, and M. avium species can involve the gastrointestinal tract primarily or be part of disseminated infection. Gastrointestinal tuberculosis is uncommon in Western countries, except in immunosuppressed individuals. In such cases,
M. avium infection is most common. In endemic areas, including India and Pakistan, intestinal M. tuberculosis generally presents in the third and fourth decades of life and typically afflicts those of lower socioeconomic status. In such settings, primary intestinal infection is more common than disseminated disease. As the incidence of Crohn disease increases in these areas, differentiation between
M. tuberculosis and Crohn disease has become more difficult.
M. avium tends to accumulate within the cytoplasm and distend lamina propria histiocytes. In some cases, this may result in a sheet-like expansion of histiocytes that fill the lamina propria and, in the small intestine, compress lympatic vessels leading to malabsorption. These cases can mimic Whipple disease clinically and morphologically. However, M. avium is positive by acid fast stain, while Tropheryma whippelii is not; both organisms are labelled by the periodic acid-Schiff (PAS) stain.
M. tuberculosis can present with granulomatous disease. In contrast to Crohn disease, these granulomas, which are generally multiple, often have caseous necrosis, but this can be difficult to determine on biopsies. Because the granulomas can be present in all layers of the bowel wall, trans-mural disease with fibrosis, perforation, and stenoses, or strictures, can be present. Patients may also have peritoneal dissemination with ascites.