Experimental infection in cats with a cagA+ human isolate of Helicobacter pylori.

Abstract

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. Four H. pylori-negative cats treated with cimetidine were orally dosed 3 times at 2-day intervals with 3 ml (1.5 x 108 CFU/ml) of H. pylori. 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. 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.