Well, my mail is all screwed up, so I haven't gotten the FML in three days.
If you have asked a question during that time, I apologize.
I did have a call from Meg Cowan asking to talk about Helicobacter
infections in ferrets, so I'll do that for the moment.
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Here's an excerpt from my recent contribution to the lecture notes from the
8th Annual Small Mammal Conference put on by the American Ferret Association
in Baltimore this past weekend, 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.
Additional references:
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):
S671-680, 1991.
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
Feb;57(2):147-50"
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 in
man.
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
chlorythromycin (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
the organisms.
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. Becuase Helciobacter 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.
A bit of exciting news - I am currently working with a company who is
developing a blood test for Helicobacter mustelae and plans to make it both
commercially available and economical. Shortly, you will be able to
diagnose Helicobacter infection from a blood sample rather than an invasive
biopsy of the stomach. We are hoping to have it available within a few
months. More later on this....
Bruce Williams, DVM, DACVP Chief Pathologist, AccuPath
Dept. of Veterinary Pathology [log in to unmask]
Armed Forces Institute of Pathology
[log in to unmask]
[Posted in FML issue 1678]
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