Helicobacter spp

From Ferret
Melena, the first signs of gastritis associated with Helicobacter infection

Helicobacter spp are a common commensal bacterial disease of the mustelid stomach and the leading cause of gastritis in ferrets.

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[1]

An association between Helicobacter spp and gastrointestinal lymphoma has been established[2], as well as Helicobacter spp migration from the duodenal papilla into the hepatobiliary tree with hepatitis and hepatobiliary neoplasia[3].

Species which are pathogenic to ferrets include:

  • Helicobacter mustelae[4]

H. mustelae remains the only helicobacter other than H. pylori that causes gastric ulceration and cancer in its natural host[5]. This species of Helicobacter appears to be ferret specific[6] 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[7].

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.

A differential diagnosis would include inflammatory bowel disease, proliferative colitis and infections with Eimeria spp, Giardia spp, Rotavirus and parvovirus.

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)[8]

Most ferrets respond to this conservative regimen[9], providing underlying neoplasia is not present.


  1. Stoof J et al (2010) An ABC transporter and a TonB ortholog contribute to Helicobacter mustelae nickel and cobalt acquisition. Infect Immun 78(10):4261-4267
  2. Erdman SE et al (1997) Helicobacter mustelae-associated gastric MALT lymphoma in ferrets. Am J Pathol 151(1):273-280
  3. García A et al (2002) Hepatobiliary inflammation, neoplasia, and argyrophilic bacteria in a ferret colony. Vet Pathol 39(2):173-179
  4. O'Rourke, JL & Lee, A (2003) Animal models of Helicobacter pylori infection and disease. Microbes Infect 5(8):741-748
  5. O'Toole PW et al (2010) Comparative genomics and proteomics of Helicobacter mustelae, an ulcerogenic and carcinogenic gastric pathogen. BMC Genomics 11:164
  6. Patterson MM et al (2003) Failure of surface ring mutant strains of Helicobacter mustelae to persistently infect the ferret stomach. Infect Immun 71(5):2350-2355
  7. Cróinín TO et al (1998) Molecular mimicry of ferret gastric epithelial blood group antigen A by Helicobacter mustelae. Gastroenterology 114(4):690-696
  8. Marini RP et al (1999) Ranitidine bismuth citrate and clarithromycin, alone or in combination, for eradication of Helicobacter mustelae infection in ferrets. Am J Vet Res 60(10):1280-1286
  9. Forester NT et al (2000) Isolation of Helicobacter mustelae from ferrets in New Zealand. N Z Vet J 48(3):65-69