Esophagogastric Ulcers in Swine Infected with <i>Ascaris suum</i> (1979)

Esophagogastric ulcers were induced in swine by sequential inoculation with ova or larvae of Ascaris suum [ 1, 61. In one study large ulcers developed in the stomachs of 15 swine given an oral inoculation of embryonated ova. Two weeks later they were given either a second oral inoculation of ova or an injection of ascarid larvae via a mesenteric vein. Five control swine did not develop lesions. In another study, 25 pigs that were inoculated when 8 weeks old with embryonated ascarid ova were given a second inoculum of ova 15 days later. At autopsy, 4 to 10 days after the second inoculation, epithelial thickening, erosions and ulcers in the pars esophugea of the stomach were found. Three pigs given a single inoculum and two controls were free of lesions. The development of esophagogastric ulcers also has been related to a spontaneous second invasion by ascarid larvae when a group of 3-month-old pigs was moved to a new location. These pigs also had lesions of ascaridiasis of the liver and lung. Pigs left in their original location remained healthy [5]. Based upon these observations [ I , 5, 61, the development of gastric ulcers in swine has been attributed to an immune mechanism such as occurs with a second invasion by ascarids, or when production of histamine is increased by trauma to liver and lungs during migration of ascarid larvae. If this relationship were an important factor in the development of gastric ulcers in swine under field conditions. it should be substantiated by autopsy records. Autopsy records from the Institute of Animal Pathology, University of Berne, from 197 I to 1976 were reviewed. During this period 11,784 swine were examined. These pigs were mainly from farms of the Swiss pig health service, and most were less than 3 months old. The methods of study have been described [2]. The chief and secondary diagnoses of each pig according to the “standard nomenclature of veterinary diseases and operations” [7] were transferred to veterinary case abstract forms of the World Health Organization (WHO). These data were recorded at the WHO Center in Geneva, Switzerland, and analysed by the Chi-square test. Lesions of the esophageal region included hyperkeratosis, parakeratosis, erosions, acute and chronic ulcers, and scars that sometimes had obliterated the esophageal opening. If adult worms were found in the gut or if there were evidence of interstitial hepatitis (milk spots) a diagnosis of ascaridiasis was made. Lung lesions were not recorded. Of the 11,784 reviewed, 654 had lesions of the pars esophagea and 1.216 were infested by ascarids. Lesions of the stomach were combined with ascaridiasis in 121 pigs (P < 0.001). This result is a statistical pitfall because the two diseases d o not occur with a constant probability in each pig. An earlier study [3] had shown that the greatest frequency of gastric lesions and of ascaridiasis was in swine 3 to 6 months old. The 5,405 autopsies during 1971 to 1973 were further analysed by age groups. In pigs 0 to 4 weeks old (1,778 autopsies) few lesions were seen; in pigs 4 to 8 weeks old (2,503 autopsies) 86 had gastric lesions and 271 had ascaridiasis, but the two were combined in only 15 pigs, a weakly significant association (P < 0.05). In 757 pigs 8 to 12 weeks old, gastric lesions were found in 74 and ascaridiasis in 233, with the two combined in only 21, which was not significant statistically. In 292 pigs 3 to 6 months old, 79 had gastric lesions and 115 had ascaridiasis, but the two were combined in only 24, which was not significant statistically. The small group of pigs (75) over 6 months old was not analysed.