Gastric colonization can illicit a strong immune response, which may develop into pathologies like gastritis, gastric ulceration and precancerous lesions. The lifelong colonization of the gastric mucosa suggests that these Helicobacter species are well adapted to this harsh environment and are able to combat the diverse antimicrobial activities employed by the host within the gastric mucosa, such as iron restriction and acidity
An association between Helicobacter spp and gastrointestinal lymphoma has been established, as well as Helicobacter spp migration from the duodenal papilla into the hepatobiliary tree with hepatitis and hepatobiliary neoplasia.
Species which are pathogenic to ferrets include:
- Helicobacter mustelae
H. mustelae remains the only helicobacter other than H. pylori that causes gastric ulceration and cancer in its natural host. This species of Helicobacter appears to be ferret specific and survives in the gastric mucosa by expressing a blood group-like antigen as a method of immune evasion by mimicry of gastric epithelial cells.
Clinical signs in affected ferrets include lethargy, anorexia, hypersalivation, tooth-grinding, halitosis and melena.
Diagnosis is difficult with ferrets and may require barium series, endoscopy or exploratory surgery.
Treatment is usually aimed at multi-drug therapy including:
- Amoxycillin/clavulanate (20 mg/kg q 12 hours) and metronidazole (20 mg/kg q 12 hours) combined with an antacid such as omeprazole
- Clarithromycin (12.5 mg/kg orally twice daily) and ranitidine bismuth citrate(24 mg/kg orally twice daily)
Most ferrets respond to this conservative regimen, providing underlying neoplasia is not present.
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