Infection with candidatus "Helicobacter heilmannii" is associated with gastritis and mucosa-associated lymphoid tissue lymphoma in people. Infection with "H. heilmannii" type 1 predominates (80%) and is thought to be acquired from dogs, cats, or pigs. We further examined the zoonotic potential of dogs and cats by amplifying gastric DNA from cats (n ‫؍‬ 45) and dogs (n ‫؍‬ 10) with primers against "H. heilmannii" ureB and 16S rRNA genes and sequencing the products. Fluorescence in situ hybridization (FISH) with eubacterial and "H. heilmannii"-specific probes was employed to directly visualize "H. heilmannii" types and their intragastric distribution. ureB sequences of "H. heilmannii" amplicons clustered with human and feline isolates of "H. heilmannii" and were distinct from the "H. heilmannii"-like organisms (HHLO) H. felis, H. salomonis, and H. bizzozeronii. 16S ribosomal DNA sequences in 20 "H. heilmannii"-infected cats and dogs were distinct from "H. heilmannii" type 1 and "H. suis" and clustered with "H. heilmannii" types 2 and 4. FISH confirmed the presence of "H. heilmannii" types 2 and 4 in dogs but failed to definitively characterize the "H. heilmannii" types present in cats. In infected dogs, "H. heilmannii" inhabited the gastric mucus and glands, and in dogs coinfected with other HHLO it shared the same gastric niche. The results indicate that dogs and cats are predominantly colonized by "H. heilmannii" bacteria that are distinct from type 1 and from "H. suis." As "H. heilmannii" type 1 predominates in people, the zoonotic risk posed by dogs and cats is likely small.Helicobacter heilmannii is the name proposed for a 4-to 10-m-long, spiral-shaped, motile bacterium with three to eight coils, a wavelength of about 1 m, up to 14 uni-or bipolar flagella, and no periplasmic filaments (1, 24) that is found in the stomachs of 0.2 to 4% of patients with gastritis

The present study sought to quantitatively examine mucosal inflammatory and immune responses in dogs with gastritis and the relationship of these responses to infection with Helicobacter. Gastric biopsies from 30 dogs were evaluated for B- and T-lymphocytes, neutrophils, eosinophils, macrophages, and mast cells. Mucosal atrophy, fibrosis, cellularity, and severity of gastritis were graded qualitatively. Messenger-RNA (mRNA) for actin, interleukin-1beta (IL-1beta), IL-4, IL-8, and IL-10, transforming growth factor beta (TGF-beta), and interferon gamma (IFN-gamma) was quantified by polymerase chain reaction (PCR). The presence of Helicobacter spp. was determined by urease activity, histology, PCR, and enzyme-linked immunosorbent assay. mRNA for IL-1beta, IL-8, IL-10, TGF-beta, and IFN-gamma was detected in most dogs. IL-4 mRNA was detected in only 1 dog. Correlations were observed for IL-1beta versus IL-8 and IL-10; IL-8 versus IL-10, IFN-gamma, and TGF-beta; and IL-10 versus IFN-y. Mucosal pathology was related to cytokine mRNA expression (neutrophils to IL-8 and IFN-gamma, macrophages and lymphocytes to IFN-gamma, and fibrosis to IL-1beta). Gastritis was categorized as lymphoplasmacytic in all dogs, and its histologic severity correlated with atrophy, infiltration with lymphocytes and macrophages, and expression of IL-10 and IFN-gamma. Of the dogs examined, 76.7% were infected with Helicobacter spp. Infection was associated with increased expression of TGF-beta and fibrosis. Circulating anti-Helicobacter immunoglobulin G titers were higher in uninfected than infected dogs. We conclude that lymphoplasmacytic gastritis in dogs is characterized by concurrent activation of proinflammatory and immunomodulatory cytokines, with increased mRNA expression related to mucosal pathology. No significant associations between Helicobacter infection and proinflammatory cytokine expression, severity of gastritis, or differences in the pathogenicity of different Helicobacter spp. were found.

The present study sought to quantitatively examine mucosal inflammatory and immune responses in dogs with gastritis and the relationship of these responses to infection with Helicobacter. Gastric biopsies from 30 dogs were evaluated for B- and T-lymphocytes, neutrophils, eosinophils, macrophages, and mast cells. Mucosal atrophy, fibrosis, cellularity, and severity of gastritis were graded qualitatively. Messenger-RNA (mRNA) for actin, interleukin-1beta (IL-1beta), IL-4, IL-8, and IL-10, transforming growth factor beta (TGF-beta), and interferon gamma (IFN-gamma) was quantified by polymerase chain reaction (PCR). The presence of Helicobacter spp. was determined by urease activity, histology, PCR, and enzyme-linked immunosorbent assay. mRNA for IL-1beta, IL-8, IL-10, TGF-beta, and IFN-gamma was detected in most dogs. IL-4 mRNA was detected in only 1 dog. Correlations were observed for IL-1beta versus IL-8 and IL-10; IL-8 versus IL-10, IFN-gamma, and TGF-beta; and IL-10 versus IFN-y. Mucosal pathology was related to cytokine mRNA expression (neutrophils to IL-8 and IFN-gamma, macrophages and lymphocytes to IFN-gamma, and fibrosis to IL-1beta). Gastritis was categorized as lymphoplasmacytic in all dogs, and its histologic severity correlated with atrophy, infiltration with lymphocytes and macrophages, and expression of IL-10 and IFN-gamma. Of the dogs examined, 76.7% were infected with Helicobacter spp. Infection was associated with increased expression of TGF-beta and fibrosis. Circulating anti-Helicobacter immunoglobulin G titers were higher in uninfected than infected dogs. We conclude that lymphoplasmacytic gastritis in dogs is characterized by concurrent activation of proinflammatory and immunomodulatory cytokines, with increased mRNA expression related to mucosal pathology. No significant associations between Helicobacter infection and proinflammatory cytokine expression, severity of gastritis, or differences in the pathogenicity of different Helicobacter spp. were found.

The ultrasonographic findings in a one-and-a-half-year-old female basenji with immunoproliferative enteropathy are described. On ultrasonographic examination, generalised thickening of the small bowel wall was found, ranging between 4 and 6 mm. The normal layered appearance of the intestinal wall was replaced by three distinct layers; an innermost enlarged hyperechogenic layer; an enlarged poor echogenic layer, and an outer hyperechogenic layer. These findings are consistent with the histopathological appearance of this particular chronic inflammatory bowel disease, since the inner layer probably represents the infiltrated mucosa, the middle layer the infiltrated lamina propria and the outer layer the serosa. Thus, the ultrasonographic finding of generalised thickening of the intestinal wall in a basenji presenting with chronic diarrhoea, weight loss, anorexia or vomiting is strongly indicative of immunoproliferative enteropathy.

2016-12-23T18:52:10