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 stom achs infected with H. pylori. This study sought to determine whether H. pyl ori-negative, specific pathogen-free cats with normal gastric mucosa were s usceptible to colonization with a human cagA(+) strain of H. pylori, and wh ether gastritis developed after infections. Methods. Four H. pylori-negativ e cats treated with cimetidine were orally dosed 3 times at 2-day intervals with 3 mi (1.5 x 10(8) CFU/ml) of H. pylori. Results. All experimentally-i nfected cats became persistently colonized as determined by H. pylori isola tion 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 pos tinoculation. The 2 control cats did not have H. pylori isolated, nor was g astric tissue positive by PCR. The H. pylori isolated from the 4 experiment ally-infected cats had RFLP patterns specific for the flaA gene identical t o those of the inoculating strain. All 4 H. pylori-infected cats had multif ocal gastritis, consisting of lymphoid aggregates plus multiple large lymph oid nodules. In the control cats, one cat had a few focal lymphocytic aggre gates in the body submucosa, whereas the second cat had normal gastric muco sa. Conclusion. Human CagA(+) H. pylori readily colonized the cat stomach a nd produced a persistent gastritis. The findings demonstrate the utility of the cat to study H. pylori induced pathogenesis.