From:
FHbytheSea@aol.com
Date: 2002-08-20 23:16:58 UTC
Subject: Attn Dr. Williams/Vets
To: ferrethealth@smartgroups.com
Message-ID: <fc.1ca7db1f.2a9427ea@aol.com>
I just got the pathology results back from Peanut, the little one that passed
last Sunday..they are very puzzling and the case is being forwarded to you,
Dr. Williams from the lab..
This is the text of the path:
Nine specimens were submitted in the container labeled with the patients
name. Three specimens are unopened lengths of intestine measuring from 3.5 to
3 to 2.5cm in length; two of the specimens demonstrate a dark red-brown
serosal and mucosal surfaces while the other demonstrates a pale tan serosal
and mucosal surface. Representative cross sections are submitted in cassette
(1). There is also a pale yellow brown, wedge of hepatic parenchyma measuring
2.5cm in greatest length. Two wedges of pale red-brown pulmonary parenchyma,
two fragments of pale tan, soft tissue measuring 1cm in greatest dimension
and a portion of the stomach at the pyloris measuring 1cm in greatest
dimension. Representative sections of all tissues are submitted on a total of
three cassettes.
Diagnosis: Stomach, small intestine and large intestine: markedly severe,
diffuse, chronic gastroenteropathy/enteritis characterized by prominent
proprial deposition of collagen( presumed, see comment) associated with
overall mild to moderate proprial imflammatory infiltrates,
compression/atrophy of gastric, intestinal, and colonic glands resulting in
glandular ectasia and crypt abscesses, and focal mucosal erosion.
Note: Congo red staining is negative in multiple specimens.
Liver: Markedly severe, diffuse, hepatocellular hepatic degeneration
(macrovesicular) unassociated with significant imflammation, necrosis or
fibrosis.
Spleen: Moderate extramedullary hematopoiseis and diffuse lymphoid atrophy.
Lung, adrenal gland and pancreas: No significant Microscopic lesions.
Note: The pancreas does demonstrate significant autolysis.
Comments: Clinical history indicates suspected Inflammatory bowel disease
that initially responded to steriod therapy, though progressed to acute
lethargy and watery green diarrhea preceding death. Clinical pathology
included hypoalbuminemia, electrolyte abnormalities and hyperphosphatatemia.
Within the gastrointestinal tract, the histological lesions are striking and
dominated by deposition of pale eosinophilic, generally amorphous to slightly
fibrillar, extracellular matrix that prompted the primary differential of
amyloid. However, this material is not located in the typical places amyloid
is identified, such as surrounding vessles and withint hte muscular tunics;
this material is limited to the lamina propria. Furthermore the material
failed to stain with congo red, though occasionally, other special stains for
and electron microscopy are necessary to demonstrate amyloid. For those
reasons consideration should also be given to the material representing
collagen as part of the fribrosis/sclerosis. Under this category, it is
possible that firbrosis/sclerosis count potentially accompany severe
gastrointestinal inflammations, though the degree of deposition is quite
marked and uniformly diffuse. The young age of the patient prompts the
question of possible congenital "sclerosing disease" of limited
distribution. Further complicating the clinical scenario in this patient is
sever hepatic lipidosis.
Any analysis is appreciated. Dr. Williams, please forward the results of your
analysis/diagnosis to me when you are finished and thank you all in advance.
Lisa Leidig, Head Ferret
The Ferret Haven "By-the-Sea"
www.ferrethaven.org
End of ferrethealth Digest
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