Large spiral shaped helicobacters, different from the human adapted Helicobacter pylori, have been associated with gastritis, peptic ulcers and gastric Mucosa Associated Lymphoid Tissue (MALT) lymphoma in human patients. H. suis is the most prevalent gastric non-H. pylori Helicobacter species (NHPH) in humans and is often present in the stomach of pigs. Other NHPH colonizing the human stomach are H. felis, H. salomonis, H. bizzozeronii and H. heilmannii sensu stricto (s.s.). These microorganisms are often detected in the stomach of dogs and cats. H. suis causes gastritis and decreased daily weight gain in experimentally infected pigs. It also appears to be one of the factors involved in gastric ulcer disease in pigs. The pathogenic significance of gastric NHPH for dogs and cats remains enigmatic and is probably Helicobacter species- and strain-dependent. NHPH are most likely transmitted from animals to humans through direct contact. H. suis can be present and survive in pork meat, suggesting that this might also act as a source of infection for humans. Recently, the genome of several gastric NHPH has been sequenced, revealing the presence of several genes involved in pathogenicity and adaptation to the hostile gastric environment. Gerbils experimentally infected with H. suis developed histopathological changes in their stomach similar to those described in infected humans and characterized by a marked lymphocytic infiltration in the antrum and development of MALT lymphoma-like lesions. In part, this pathology might be explained by the mainly T helper (Th)17/Th2 polarized immune response. Both in experimentally infected mice and gerbils, H. suis induces gastric epithelial cell death which has been associated with production of γ-glutamyl transpeptidase. This enzyme also inhibits proliferation of lymphocytes and is present in all gastric helicobacters. Its pathologic effect is at least partly related to cleavage of extracellular glutathione into pro-oxidants.