The role of infectious agents in the development of porcine gastric ulceration

Ulceration of the non-glandular part of the stomach is a common disease entity of pigs worldwide, with prevalences of up to 93%. It may result in decreased daily weight gain, decreased feed intake and sudden death, thus leading to significant economic losses, as well as animal welfare issues. The aetiology is multifactorial. Diet particle size, management and infectious agents have been hypothesised to be involved. The exact mechanism behind porcine gastric ulceration is, however, not completely clear. The aim of this article is to provide an overview of the role of infectious agents in the development of porcine gastric ulceration. Results of recent studies indicate that Helicobacter suis infection plays an important role in gastric ulceration, probably by affecting gastric acid secretion through alteration of the number and/or function of parietal, D and G cells. In a gastric environment altered by H. suis, higher numbers of Fusobacterium gastrosuis are present and this novel pathogen has a potential role in the development of porcine gastric ulceration. Inoculation of pigs with Lactobacillus sp., Bacillus sp. or Helicobacter pylori-like bacteria in combination with a carbohydrate-rich diet may induce gastric lesions. It has been hypothesised that production of short chain fatty acids by some of these bacteria might be involved in the pathogenesis of porcine gastric ulceration, but the lack of taxonomic characterisation hampers the interpretation of these studies. Severe infectious diseases have also been associated with gastric lesions, probably due to interruption in feed intake and/or histamine release. Other agents, including fungi and parasites such as Hyostrongylus rubidus and Ascaris suum, have occasionally been associated with gastric lesions in pigs.