title: Gastric injury and invasion of parietal cells by spiral bacteria in rhesus monkeys. Are gastritis and hyperchlorhydria infectious diseases?
abstract: The possibility of using the rhesus monkey as a model for studying gastric function in the presence of infection with spiral bacteria was studied. Endoscopic evaluation of the gastric mucosa was performed under general anesthesia in 29 colony-bred rhesus monkeys, and gastric pinch biopsy specimens were obtained from each animal. On a separate day, gastric emptying and acid output were determined using a 99mTc dilution technique. Biopsy samples were fixed for light microscopy (H&E, Gram, and Warthin-Starry stains) and for transmission electron microscopy. The presence of spiral bacteria and gastritis was assessed and rated on coded slides. In 8 of 29 monkeys, Helicobacter pylori-like organisms were observed in close proximity to the mucosal epithelial cells or in the lumen of the gastric pits. In 14 other monkeys, "Gastrospirillum hominis"-like organisms were observed in the mucus covering the surface of epithelial cells, in the lumina of the gastric glands, and overlying parietal cells. Gastritis was present in 8 of 8 animals positive for H. pylori-like organisms, in 2 of 14 animals positive for "G. hominis"-like organisms, and in none of the uninfected monkeys, and the mean gastritis index was significantly greater in animals positive for H. pylori-like organisms. Moreover, acid output was significantly higher in monkeys positive for "G. hominis"-like organisms than in controls or animals positive for H. pylori-like organisms. Gastric emptying was not significantly different in the three groups. In conclusion, (a) H. pylori-like, but not "G. hominis"-like, organisms cause gastritis while not modifying acid output; (b) "G. hominis"-like, but not H. pylori-like organisms, invade and on occasion damage parietal cells while apparently causing hyperchlorhydria; and (c) the rhesus monkey appears to be a good model for the study of gastric infection with spiral bacteria.
authors.affiliation: Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland.
authors.forename: A
authors.initials: A
authors.lastname: Dubois
authors.forename: A
authors.initials: A
authors.lastname: Tarnawski
authors.forename: D G
authors.initials: DG
authors.lastname: Newell
authors.forename: N
authors.initials: N
authors.lastname: Fiala
authors.forename: W
authors.initials: W
authors.lastname: Dabros
authors.forename: J
authors.initials: J
authors.lastname: Stachura
authors.forename: H
authors.initials: H
authors.lastname: Krivan
authors.forename: L M
authors.initials: LM
authors.lastname: Heman-Ackah
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001419:Bacteria / Q000302:isolation & purification*; D001706:Biopsy; D006224:Cricetinae; D004195:Disease Models, Animal; D005744:Gastric Acid / Q000378:metabolism; D005746:Gastric Emptying / Q000502:physiology; D005753:Gastric Mucosa / Q000382:microbiology* / Q000473:pathology; D005756:Gastritis / Q000382:microbiology*; D016480:Helicobacter pylori / Q000302:isolation & purification; D006801:Humans; D007231:Infant, Newborn; D008253:Macaca mulatta; D008297:Male; D010295:Parietal Cells, Gastric / Q000382:microbiology*