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    Gastritis in dogs and its relationship with helicobacter

    The main symptoms of gastritis in dogs are vomiting and abdominal pain. Acute gastritis is nearly always associated with the intake of harmful substances. If not treated correctly, the acute form can evolve into chronic gastritis, which causes long-term damage in the form of atrophy of the mucosa. Other causes of chronic gastritis in dogs are infections (bacterial, viral, etc.) cancer, kidney disorders, liver disease and food allergies.

    What is gastritis?

    The main clinical signs of gastritis in dogs are vomiting and abdominal pain. Acute gastritis is nearly always associated with the intake of harmful substances. If not treated correctly, the acute form can evolve into chronic gastritis, which causes long-term damage in the form of atrophy of the mucosa.  Other causes of chronic gastritis in dogs are infections (bacterial, viral, etc.) cancer, kidney disorders, liver disease and food allergies.

    The treatment of chronic atrophic gastritis is based on a specific, easy-to-digest diet and medical treatment. Pharmacological treatment should be based on a combination of mucosal protectors, prokinetic agents, antibiotics and corticosteroids.

    Relationship with Helicobacter spp.

    Based on the pathophysiology, Helicobacter spp. infections are known to be highly prevalent processes in dogs. Two studies have assessed the relationship between helicobacter infection and gastritis in dogs.

    The first was performed on dogs in Denmark (1) and examined the relationship between helicobacter infection and gastric mucosa inflammation and immune responses in dogs with spontaneous gastritis. Accordingly, they performed gastric biopsies primarily on dogs with gastrointestinal disorders, but also in some dogs that were unaffected by these problems. The biopsy was used to look at the presence and density of Helicobacter spp., cell infiltrates and the grade of gastritis, while the mRNA concentrations of some interleukins and interferon gamma were evaluated by PCR. Signs of infection were found in most biopsies, but there was no relationship between the presence/absence of Helicobacter spp. or the class of helicobacter and any differences in cytokine levels or the histological grade of gastritis. Gastritis is characterised by concurrent activation of pro-inflammatory and immunomodulatory cytokines.

    Therefore, the clinical significance of Helicobacter spp. lies in its high prevalence in dogs in Spain.

    The purpose of the second study (2) was to assess the prevalence of Helicobacter spp. infection in dogs with chronic digestive disease and the relationship between Helicobacter spp. infection and gastric inflammation.  To this end, the authors performed gastric biopsies on dogs with chronic vomiting or chronic diarrhoea and healthy dogs as a control group, grading the gastritis histologically as absent, mild, moderate or severe and using three techniques to identify Helicobacter spp. infection (urease test, WS staining and PCR testing). None of the dogs in the control group had histological signs of gastric inflammation but they were all positive for Helicobacter spp. in the three tests performed. In the group of sick animals, 10% had no signs of gastritis, 46% had mild gastritis, 23% moderate gastritis, 20% severe gastritis and 13% had gastric atrophy. Most dogs were Helicobacter spp. positive and only two were negative for at least 2 weeks. WS staining revealed the highest density of spiral bacteria in one control dog, one dog with vomiting and significant gastric atrophy, and three dogs with chronic diarrhoea. No relationship was observed between reticular lymphoid hyperplasia and the density of the spiral bacteria. In five dogs, the sequence of amplicons detected in PCR tests showed infection by at least two strains of Helicobacter spp. They concluded that there is no clear relationship between the clinical signs, gastric histology and Helicobacter spp. infection in dogs.