“…5,[9][10][11]38,39,54 This reaction is unlike that seen in free-ranging cheetahs or other felid species (both domestic and zoo held) that usually only develop mild inflammatory lesions when infected with similar Helicobacter. 20,24,25,27,29,30,40,44,49,54,58 The lesions in cheetahs occur predominantly in the gastric fundus and are characterized by florid lymphocyte and plasma cell infiltrates, infiltration of glandular epithelium, parietal cell apoptosis and, in more chronic cases, may include gland hyperplasia, goblet cell metaplasia, fibrosis and/or atrophy. 5,10,38,39 Because no single strain of Helicobacter has been associated with gastritis in captive cheetahs 54 and the magnitude of the immune response differs considerably between captive and free-ranging cheetahs infected with similar bacteria, the pathogenesis of cheetah gastritis is suspected to be attributable to the nature of the immune response rather than bacterial factors alone.…”