Gastroesophageal ulceration is an important disease entity in swine.1,2 Erosions, ulcers and accompanying gastritis develop in the glandular and nonglandular gastric mucosa in affected pigs with a prevalence ranging from 5% to 100%.1 Death losses attributable to GEU may exceed 3%.1 Although presently poorly documented, subclinical hemorrhage and associated anemia, anorexia, and weight loss result in additional economic losses to the producer.1
Unlike humans or other carnivores, the corpus (body) of the porcine stomach contains an extension of the esophageal mucosa into what is termed the pars esophagea or pars. This region of the stomach of pigs is lined by nonglandular stratified squamous epithelium.3 Not only is it devoid of mucus-secreting cells, it also lacks both an extracellular mucus layer and a local bicarbonate production buffering mechanism thought necessary to neutralize gastric acidity.3–5 Ulcerative lesions in the nonglandular pars esophageal region are similar to those of so-called acid reflux gastritis in humans.6 Gastric acid-mediated ulceration of the pars is believed to be potentiated by the physical and nutrient content of the diet, and diet is thought to be the major contributory factor to development of GEU.1,4,5
Helicobacter pylori is a gram-negative, motile, microaerophilic, gastric bacterium that colonizes a highly specialized microecological niche in humans comprising the gastric epithelial surfaces and the overlying gastric mucus layer.7 This bacterium is estimated to infect more than half the human population worldwide, with higher infection rates in developing countries, where 80% of middle-aged adults are infected, compared with rates of only 20% to 50% in developed countries.7 Overwhelming evidence now causally links H pylori with peptic ulcers in humans.8 As well, H pylori is recognized as a contributor to other illnesses ranging from childhood malnutrition and type B gastritis to gastric cancer. Infection with this agent also increases susceptibility to infection with other food and waterborne pathogens.7 Since the first reports of H pylori and its association with disease in humans, related Helicobacter organisms have been detected in other species ranging from cats and dogs9,10 to cheetahs.11
AHelicobacter sp morphologically distinct from human H pylori, Helicobacter heilmannii (formerly Gastrospirillum suis), is a common gastric commensal organism in swine.12–14 Infection with H heilmannii has been associated with GEU in swine,15,16 although attempts to reproduce GEU with H heilmannii have not been successful.17 Presently, the role, if any, of H heilmannii in GEU is not known. Recently, isolation of an HPLO from swine18 and experimental reproduction of GEU with the HPLO were reported.19 Although the isolate was both pathogenic and ulcerogenic in gnotobiotic swine, the prevalence of gastric infection with the organism and resultant gastritis in commercial swine populations is unknown. As an initial step toward understanding the epidemiologic features of porcine HPLO infection, the study reported here was performed to determine the prevalence of antibodies against a swine-origin HPLO in conventionally reared swine. The same sera were tested in an ELISA by use of H pylori as the antigen to determine whether differences in antibody responses represent antigenic differences between 2 closely related organisms18 that are recognized by the porcine immunologic system.
Helicobacter pylori–like organism
Phosphate-buffered saline solution with Tween 20
Novocastra Laboratories Ltd, Newcastle upon Tyne, UK.
Zymed Laboratories Inc, San Francisco, Calif.
KPL Inc, Gaithersburg, Md.
Microplate Manager III software, BioRad Laboratories Canada Ltd, Mississauga, ON, Canada.
SPSS for Windows, version 12.0, SPSS Inc, Chicago, Ill.
PROC MIXED, SAS, version 8.2, SAS Institute Inc, Cary, NC.
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