Here's an excerpt from my contribution to the lecture notes from
the 8th Annual Small Mammal Conference put on by the American Ferret
Association in Baltimore, where I had the opportunity to
lecture to 120+ vets on GI diseases....
....This bacterium, first described in 1990, has rapidly become the
most important disease-causing agent of the pet ferret. H. mustelae has the
ability to cause two distinct forms of gastric disease - peptic ulcer
disease (presumptive) and chronic atrophic gastritis.
Helicobacter mustelae is extremely widespread in the pet ferret
population. Several studies using random source ferrets have shown that
almost every ferret carries this bacterium. As the bacterium is passed by a
fecal-oral route, kits generally are infected by the mother within the first
two weeks of life.
H. mustelae appears to be able to cause two distinct syndromes in the
stomach of affected ferrets - chronic atrophic gastritis and peptic ulcer
disease. Chronic atrophic gastritis is a common finding in ferrets over four
years of age. In these animals, the bacterium causes gastritis via two
mechanisms - a) the stimulation of a marked lymphoplasmacytic inflammatory
response, resulting in loss of glandular epithelium most prominently in the
pylorus, and b) the ability to increase the pH of the stomach. While
clinical signs and disease progression may vary markedly between
individuals, the progressive damage to the gastric mucosa most commonly
results in clinical signs in animals of four years or more.
Additionally, although a definitive cause-and-effect relationship has not
yet been conclusively proven between the presence of Helicobacter mustelae
and gastric ulcers, evidence connecting the two is beginning to mount.
Cytotoxins liberated by several species of Helicobacter have the ability to
directly injure gastric mucosal epithelial cells. Additionally, recent
evidence has shown that ferrets infected with H. mustelae have elevated
levels of plasma gastrin at 30 and 60 minutes following feeding. For these
reasons, any treatment of gastric ulcers in ferrets should be combined with
concomitant antimicrobial therapy for Helicobacter mustelae.
Treatment for gastric helicobacteriosis should
be strongly considered in any ferret with vague gastrointestinal signs
including inappetance, loose stools, or intermittent vomiting.
Gross lesions: Endoscopy or gross necropsy is generally unrewarding in
cases of chronic atrophic gastritis. Surgical biopsy of the pyloric region
of the stomach is highly recommended for definitive diagnosis of H. mustelae
infection. The gross aspects of gastric ulcers have been previously
described (above). H. mustelae infection is also the most common cause of
mesenteric lymph node enlargement in ferrets, due to the profound
inflammatory response which it initiates in the pyloric stomach.
Microscopic lesions: Silver stains are the stain of choice to demonstrate
the presence of the bacteria in the superficial mucus and in extracellular
locations within the gastric glands. The pyloric stomach is the preferred
biopsy site, although low numbers of bacilli may also be seen in the fundus
and duodenum in severely infected animals. In affected animals, varying
degrees of lymphoplasmacytic gastritis and loss of gastric glands may be
seen, with the most severe damage occurring in the pylorus.
There are numerous treatments for H. mustelae in ferrets, most of which
have been derived from the treatment of H. pylori, a common bacterium in
man, which has been definitively linked to the development of gastric ulcers
The most commonly accepted treatment is a combination of amoxicillin at
10-20 mg/kg twice daily, metronidazole (Flagyl) at 30 mg/kg once daily, and
Pepto-Bismol (1/15th of a tablet once daily). This "triple
therapy" has been shown to be effective in man, and to a large part
effective in ferrets, but must be continued for 4-6 weeks. Unfortunately,
ferrets CANT STAND the taste of both Flagyl and Pepto-Bismol, and client
compliance with therapy is often a problem.
A recently published protocol for treating ferrets is a combination of
Clarithromycin (Biaxin) at 50 mg/kg once daily, and amoxicillin at 35 mg/kg
once daily, or 20 mg/kg twice daily. This therapy is only continued for two
weeks, and supposedly has great efficacy and causes minimal resistance in
Other antibiotics, such as chloramphenicol, Baytril, gentamicin, or sulfa
drugs such as DiTrim are of no use in this condition.
Finally, it has been asked whether all ferrets in a household need to be
treated. Because Helicobacter is shed in the feces of infected animals, it
is very easy for cleared animals to become reinfected. In large facilities,
treating all animals, especially with Biaxin is cost prohibitive. In most
cases, temporary respite from the ravages of Helicobacter can result in
marked clinical improvement in most animals. While you may clear some
animals, the majority are often reinfected, or simply maintain the infection
at a low level. My recommendations would be to treat only the animals
showing clinical signs.
1. Fox JG, et al. Helicobacter mustelae-associated gastritis in ferrets.
An animal model of Helicobacter pylori gastritis in humans.
Gastroenterology 99:352-361, 1990.
2. Fox JG et al. Gastric colonization of the ferret with Helicobacter
species: Natural and experimental infections. Rev Infect Dis 13(suppl 8):
3. Fox JG et al. Role of gastric pH in isolation of Helicobacter
mustelae from the feces of ferrets. Gastroenterology 104:86-92, 1993.
4. Gottfried MR et al. Helicobacter pylori-like microorganisms and
chronic active gastritis in ferrets. Am J Gastroenterol 85:813-818, 1990.
5. Otto G et al. Eradication of Helicobacter mustelae from the ferret
stomach: an animal model of Helicobacter pylori chemotherapy. Antimicrob
Agents Chemother 34:1232-1236, 1990.
6. Perkins SE; Fox JG; Walsh JH. Helicobacter mustelae-associated
hypergastrinemia in ferrets (Mustela putorius furo). Am J Vet Res 1996