Experimental Infection in Cats with a cagA+ Human Isolate of Helicobacter pylori

Background. Helicobacter pylori has been cultured from the inflamed gastric mucosa of naturally and experimentally‐infected cats. The lesions in the H. pylori‐infected cat stomach mimic many of the features seen in human stomachs infected with H. pylori. This study sought to determine whether H. pylori‐negative, specific pathogen‐free cats with normal gastric mucosa were susceptible to colonization with a human cagA+ strain of H. pylori, and whether gastritis developed after infections. Methods. Four H. pylori‐negative cats treated with cimetidine were orally dosed 3 times at 2‐day intervals with 3 ml (1.5 × 108 CFU/ml) of H. pylori . Results. All experimentally‐infected cats became persistently colonized as determined by H. pylori isolation from gastric tissue by culture at 12 weeks, and all 4 cats were found positive by PCR during serial gastric biopsies and necropsy at 15 weeks postinoculation. The 2 control cats did not have H. pylori isolated, nor was gastric tissue positive by PCR. The H. pylori isolated from the 4 experimentally‐infected cats had RFLP patterns specific for the flaA gene identical to those of the inoculating strain. All 4 H. pylori‐infected cats had multifocal gastritis, consisting of lymphoid aggregates plus multiple large lymphoid nodules. In the control cats, one cat had a few focal lymphocytic aggregates in the body submucosa, whereas the second cat had normal gastric mucosa. Conclusion. Human cagA+H. pylori readily colonized the cat stomach and produced a persistent gastritis. The findings demonstrate the utility of the cat to study H. pylori induced pathogenesis.