It is important to know the clinical picture, diagnostic findings, and pathogeneses
unique to these syndromes in order to correctly identify the cause of
gastroenteritis.
Eosinophilic gastroenteritis: Eosinophilic
gastroenteritis (EGE) is a relatively uncommon alimentary disease in ferrets
characterized by eosinophilic infiltrates in the gastrointestinal tract with
clinical signs of chronic gastroenteritis. Eosinophilic gastroenteritis has
been described in other species such as the horse, dog, cat and humans, and has
been associated with Hodgkin's-like lymphoma in the ferret. The cause of EGE
in ferrets is unknown.
Clinical signs of EGE include chronic weight loss, diarrhea, vomiting,
lethargy, and inappetance. Intestinal loops can be thickened with cystic,
dilated serosal lymphatics. One of the most suggestive diagnostic findings of EGE is a peripheral eosinophilia; however, cases have been
described in which no eosinophilia was observed throughout the course of the
clinical assessment. A definitive diagnosis is based on histopathology.
Histologic lesions of EGE are characterized by focal diffuse inflammatory infiltrates
in the stomach or intestinal mucosa with significant proportions of
eosinophils. Eosinophilic infiltrates are often present in other tissues
including the liver, pancreas, and lymph nodes. The Splendore-Hoeppli
phemomenon may also be seen in mesenteric lymph nodes. Treatment is based on
immunosuppression with corticosteroids which might be life-long.
Helicobacter mustelae-associated gastritis: Helicobacter mustelae iis
a gram negative comma-shaped (Campylobacter-like)
bacterium which has been associated with atrophic gastritis, peptic
ulcers, gastric adenocarcinomas and gastric mucosa-associated lymphoid
tissue (MALT) lymphoma in ferrets. Chronic atrophic gastritis caused by H. mustelae is associated
with bacterial stimulation of a lymphoplasmacytic inflammatory response and
increases in gastric pH. Peptic ulcers may be related to elevated blood
gastrin levels. Ferret colonies often have up to 100% prevalence of Helicobacter mustelae despite
clinical disease being quite uncommon. The inciting cause of the transition
from benign gastric inhabitant to relevant pathogen is unknown; however,
similarities between H. mustelae infections in ferrets and Helicobacter
pylori infections in humans has led to the use of H. mustelae as a model
for Helicobacter pylori-related
human gastric disease and neoplasia.
Clinical
signs of H. mustelae-associated
gastritis include lethargy, anorexia, vomiting, emaciation, dehydration and
anemia. Stress appears to be a factor in disease severity, and might be
related to inadequate diets or changes in feed. Gross lesions are infrequent
in mild forms of the disease; however, in severe cases, the gastric mucosa
contains small ulcers and is covered with digested blood.
Histopathology
is needed for a definitive diagnosis and the pylorus is the preferred biopsy
site. Histologic lesions consist of lymphoplasmacytic gastritis with loss
of glandular epithelium. Bacteria can be demonstrated with a Warthin-Starry silver
stain..Treatment involves anti-microbials and gastric protectants.
Epizootic Catarrhal Enteritis:
Epizootic catarrhal enteritis (ECE) is a high morbidity, low mortality,
self-limiting diarrheal disease in ferrets caused by a ferret coronavirus. Clinically,
ECE presents with the sudden onset of profuse bright green diarrhea in older
ferrets, which rapidly distributes throughout the ferret colony. The
incubation period is 48-72 hours and primarily clinical signs last
approximately 5-7 days. Affected ferrets may be lethargic, anorexic and
dehydrated. Mortality is low with few animals dying from dehydration or
concurrent illnesses. Treatment is aimed at correcting and preventing
dehydration and secondary infections.
The diagnosis of ECE is based on clinical signs, epidemiological
characteristics and histopathology. Biopsies acquired from the jejunum of
affected ferrets show vacuolar degeneration and necrosis of apical
enterocytes with significant villus atrophy and fusion, and lymphocytic
proprial infiltrates. Coronavirus particles can be seen in feces via electron
microscopy during the acute stages of the disease, although lack of viral
particles does not rule out coronaviral disease.
-by
Dr. Ryan Jennings, Michigan State Extern
-edited
by Dr. Robert Johnson, ADDL Graduate Student
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