A 26-year old male was referred to our unit because of severe epigastric pain¸ nausea, and vomiting lasting for about couple of days. Since the age of 22, he was diagnosed as having ileo - caecal   Crohn ,  s disease ( CD ). He experienced several relapses which were treated with metronidazole and prednisolone, but two years later surgery was performed. The histopathological report on resected ileo- caecal segment cofirmed the diagnosis of CD of penetretating type with multiple fistulous tracts. Postoperative course was uneventful for more than a year, when symptoms of coltitis reappered. Colonoscopic examination revealed segmental stenosis in sigmoid region with cobblestone appearance of the mucosa and biopsy showed focal chronic inflammation with granulomas. Figure 1. Since symptoms referred to gastric involvement of CD were present, gastroduodenoscopy was performed, revealing substantial mucosal changes as follow: distal stomach mucosal nodularity with multiple erosions, occasional  small ulcerations, and thickened antral mucosal folds. In addition, x - ray examination demonstrated antral luminal narrowing, rigidity, and intramural thickening. The histology of mucosal biopsies  showed an obvious inflammation of non - homogenous distribution, moderate increase of inflammatory cells in the lamina propria, and erosive defects. However, there were prominent viral inclusions, both nuclear and cytoplasmatic  in foveolar epithelium and mucous neck cells, and rarely in endothelial and mesenchymal stromal cells suggesting diagnosis of cytomegalovirus ( CMV ) gastritis. Figure 2. There was no evidence of underlying risk factors or medical conditions predisposing to CMV infection such as immunosupressive administration, transplantation, HIV positivity  etc.

Comment  An unusual presentation of CD and CMV infection recapitulates contraversies on etiopathogenesis of inflammatory bowel disease ( IBD ) ( 1 ). There are no pertinent facts of causative role of microbial agents, but many candidates appear to be involved in the pathogenesis of IBD. Besides experimental and clinical data supporting potential role of Mycobacterium paratuberculosis and  Listeria monocytogenes, the " granulomatous vasculitis " concept of CD became more attractive after measles virus, its mRNA, and  paramyxovirus - like structures  visualisation within endothelium and granulomas ( 2 - 4 ). This may  suggest possibility of persistent viral infection in the etiopathogenesis of IBD.  Howevere, this phenomenon was demonstrated only in subset of  patients with CD. Further on, there was no singificance in antibody titers for  measles virus , CMV, adenovirus, and  herpes simplex virus in patients with CD and controls ( 5 ).

All in all, there is no strong evidence for etiological role of virusis in IBD, including  measles virus and CMV ( 13 - 15 ). Reports of gastrointestinal CMV infections in patients with IBD indicating viral infection as an aggraviating factor only are few. On the contrary, it may be assumed that CMV gastrointestinal infection causing vasculitis of small mucosal vessels may be an introductory penomenon leading to further pathogenetic changes ( 6 - 12 ). Ananalogy could be made with CMV and  some other stomach infections, including Helicobacter pylori  and possible gastric involvement of CD ( 11,12 ). In addition, both conditions ( CMV  and Crohn's gastritis ) might have the same presentation with focal transmural  inflammation, deep mucosal ulcerations, and possible penetration or stricturing without distinctive features such as viral inclusions and granulomas ( 16 - 21 ). ********************************************************************************

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