HELICOBACTER PYLORI-INDUCED GASTRITIS IN THE DOMESTIC CAT

Helicobacter pylori has been cultured from the inflamed gastric mucosa e of naturally infected cats; the lesions in H. pylori-infected cat st omachs mimic many of the features seen in H. pylori-infected human sto machs. To determine whether H. pylori-negative specific-pathogen-free cats with normal gastric mucosae were susceptible to colonization by t his bacterium and whether gastritis developed after infections, four H . pylori-negative cats treated with cimetidine were orally dosed three times with 3 ml (1.5 x 10(8) CFU/ml) of H. pylori every 4 days. All f our cats became persistently colonized as determined by gastric cultur es and PCRs from serial gastric biopsy samples and necropsy samples at 7 months postinfection. H. pylori was not isolated from the two contr ol cats, nor were their gastric tissues positive by PCR; one of the tw o cats had a few focal lymphocytic aggregates in the body submucosa, w hereas the second cat had a normal gastric mucosa. All four H. pylori- infected cats had multifocal gastritis consisting of lymphoid aggregat es plus multiple large lymphoid nodules, which were most noticeable in the antral mucosa. In addition, one H. pylori-infected cat had a mode rate diffuse infiltration of polymorphonuclear leukocytes in the subgl andular region of the antrum. H. pylori-like organisms were focally di stributed in glandular crypts of the antrum. Two of the H. pylori-infe cted cats had significant (eightfold) increases over baseline in level s of immunoglobulin G H. pylori serum antibody. The H. pylori isolates from the four experimentally infected cats had restriction fragment l ength polymorphism patterns specific for the flaA gene that were ident ical to those of the inoculating strain. H. pylori readily colonizes t he cat stomach and produces persistent gastritis.