Franklin's autopsy pictures

Franklin after being pts, shows how much muscle loss there was

Muscle loss, very thin around shoulders

Heart

Chest cavity & lungs

Lung

Abdomen with strange nodule

Liver cysts

Liver cyst

Kidney cyst

"Pocket hernia"

Liver tumour

Cystic liver, nodules along bile duct

Nodules along bile duct

Cystic kidney

Cystic kidney



Franklin's histopathlogy report

Post-Mortem Tissues from a Polecat Ferret, per history. 12 samples received; 13 sections evaluated on 7 slides.

Heart (2 sections, slides 1 and 2). The cardiac myocytes generally appear broad. Nuclei vary mildly in size. In a few foci, especially at the papillary muscles, there is mild interstitial fibrosis accompanied by a light infiltrate of small mononuclear leucocytes. Myocytes in these foci sometimes show vacuolated sarcoplasm and are occasionally multinucleate. There are no other remarkable findings.

Large Intestine (slide 6). Architecture and cellularity appear normal. The lumen contains many apparently non-adherent and non-invasive bacterial rods (probably post-mortem bacterial overgrowth). There are no other remarkable findings.

Pancreas (2 sections, slides 6 and 7). The sections are fundamentally similar. The pancreas is multinodular. Many of the nodules, including the largest nodule approximately 15 mm in greatest diameter, are composed of orderly arrangements of well-differentiated but enlarged acinar cells with no atypia (nodular hyperplasia). Multiple other nodules, ranging up to approximately 7 mm in diameter, comprise moderately well-differentiated, predominantly cuboidal or columnar cells arranged chiefly as nests, islands, trabeculae and cords -- nuclei show mild anisokaryosis, and there is the odd mitotic figure (approximately 1 per 10 high-power 400x fields). Several of these latter nodules have irregular margins and multifocally appear to invade the pancreatic stroma, separate pancreatic acini, and slightly infiltrate the abdominal adipose tissue. Small numbers of plasma cells are scattered within and just outside the pancreatic capsule. There are no other remarkable findings.

Gall Bladder to Bile Ducts and fragment of Pancreas (fragmented section, slide 7). The biliary epithelium is sometimes eroded and in some other foci appears mildly proliferative, associated with proliferation of bland-appearing mucosal glands. The stroma around proliferative glands shows a dense, multinodular infiltrate of neutrophils with fewer macrophages. Neutrophils are sometimes present in glandular lumens. Clusters of neutrophils multifocally breach the bile duct walls and slightly penetrate adjacent adipose tissue. The small fragment of pancreas shows no lesions. There are no other remarkable findings.

Adipose Tissue (2 sections, slides 6 and 7). Two oval sections of adipose tissue show central hypereosinophilia with loss of detail (fat necrosis). In one of the sections (slide 7), affected adipocytes are sometimes infiltrated by cellular debris and are occasionally bounded by attenuated macrophages and fibroplasia. There are no other remarkable findings.

Liver (2 sections, slides 3 and 4). The hepatic parenchyma is multifocally to extensively displaced and replaced by an often well-demarcated but sometimes minimally infiltrative, polycystic mass. The cysts are blind-ended to anastomosing. They are lined by uniform cuboidal to attenuated epithelium, which closely resembles the epithelium of bile ductules, and are supported by collagenous trabeculae. In one cyst, the epithelium lines anastomosing glandular to cribriform to papillary structures that project into the lumen. The epithelium shows moderate anisokaryosis but mitotic figures are scarce. The adjacent parenchyma appears mildly compressed and adjacent sinusoids appear congested. Multifocally and apparently randomly, several tiny foci of hepatocytes appear lost and replaced by clusters of neutrophils. Portal tracts sometimes contain a moderate infiltrate of plasma cells. There are no other remarkable findings.

Kidney (slide 5). The renal parenchyma is extensively displaced and compressed by an expansile cyst lined by attenuated epithelium. There is no atypia nor invasiveness. Elsewhere, the odd glomerulus appears sclerotic, but generally no lesions are visible.

Adrenal Gland (2 sections, slides 6 and 7). Multifocally in a smaller section (slide 6) and extensively in a larger section (slide 7), the cortex is expanded by unencapsulated but well demarcated nodular proliferations of cells that closely resemble those of the adjacent cortex but with slightly expanded to vacuolated cytoplasm. Nuclei are bland and uniform. There are no mitotic figures. A few proliferative similar cells extend multifocally beyond the capsule, just into adjacent adipose tissue. There are no other remarkable findings.

MORPHOLOGICAL DIAGNOSES:

1. Heart: Cardiomyopathy -- hypertrophic, chronic
2. Pancreas: Islet Cell Carcinoma (Insulinoma, presumptive) -- multiple
3. Pancreas: Pancreatic Nodular Hyperplasia -- multifocal to widespread
4. Gall Bladder and Bile Ducts: Cholecystitis and Choledochitis -- suppurative,
multifocally extensive, subacute or chronic-active, marked, with mild associated peritonitis
5. Liver: Hepatitis -- suppurative, multifocal and random, acute, mild
6. Liver: Biliary Cystadenocarcinoma, well-differentiated
7. Adipose Tissue: Fat Necrosis with Steatitis -- multifocal
8. Kidney: Renal Cyst
9. Adrenal Glands: Adrenal Cortical Nodular Hyperplasia -- bilateral

COMMENTS:

This ferret had a large number of different lesions that might have contributed to serious illness. As you had suspected, the heart shows myocardial hypertrophy. The lesion is associated with some fibrosis and mild inflammation, common acute and chronic changes associated with cardiomyopathy in this species. Cardiomyopathy is a fairly common finding in ferrets, especially those aged 5 to 7 years, as here. More often, the cardiomyopathy is of the dilatative form, but all forms of cardiomyopathy can occur. The cause is unknown -- genetic factors have been postulated in some lines, but are not proven to my knowledge. At least in the sections provided, there is no evidence of congestive heart failure (a section of lung, listed on the submission form, was not received). Nevertheless, hypertrophic cardiomyopathy can cause respiratory distress and/or syncope or sudden death associated with rhythm disturbances.

The largest of the pancreatic nodules and several of the smaller ones are simply nodular hyperplasia, a benign age-associated change of no known importance; however, several of the pancreatic nodules are islet cell tumours. According to most sources, pancreatic islet cell tumours are the commonest neoplasms of ferrets. They arise mostly from the beta cells and secrete insulin, hence their popular name of "insulinoma". Clinical signs of insulinomas are referable to hypoglycaemia. Peak prevalence of these tumours is between 4 and 7 years old and there is no sex predilection, although there is a suggestion that neutered animals are more frequently affected than intact ones. Pancreatic islet cell tumours in ferrets can be either benign (adenoma) or malignant (carcinoma). Adenomas are generally small, well circumscribed and may be cured by excision, but carcinomas tend to be infiltrative, sometimes multiple and eventually metastasize to the draining lymph nodes, liver and sometimes other abdominal viscera. At least one of the islet cell tumours here shows invasiveness, indicative of malignancy, but no metastasis is found in the other submitted organs. It is likely that this ferret had clinically significant metabolic disease associated with these tumours.

The ferret had suppurative inflammation of the bile ducts and gall bladder, accounting for the nodular appearance of the duct, and also had a few suppurative foci in the liver, probably representing dissemination of the same process. The inflammation is very likely to reflect ascending bacterial infection of the biliary tree from the anterior intestine.

The multiple masses in this ferret's liver are a cystic biliary neoplasm. In ferrets, biliary cystic neoplasms are often very well-differentiated, as is the case here. Even so, there are reports that such tumours in ferrets behave in a slowly progressive manner, and that they may eventually replace the hepatic lobe and transfer to other liver lobes. Hence, such tumours are usually classified as malignancies (cystadenocarcinomas). The potential for metastasis is not reported but appears likely to be low -- no metastasis is seen in the other submitted tissues.

The two nodular mesenteric lesions are areas of fat necrosis with minor secondary inflammation and reactive fibrovascular proliferation. The histopathology is consistent with nodular steatitis. Steatitis in intra-abdominal fat is reasonably common in all species and has several potential causes including ischaemia, trauma, pancreatic disease (possible here) and possibly nutritional disorders. In addition, it may occur in association with some systemic infections or peritonitis (also possible here), usually as a consequence of intestinal perforation, but perforation of the biliary tree could be another possible cause. In themselves, these two masses would have had little clinical importance.

The ferret also had a renal cyst, an incidental finding, seen in approximately 33 % of ferrets on post-mortem examination. In this species, such cysts are generally of no clinical importance.

Finally, both adrenal glands show adrenal cortical nodular hyperplasia. This benign lesion is commonly found in the adrenal glands of ferrets. Hyperplasia can be bilateral (as here) or unilateral, with the left adrenal gland more commonly affected than the right. Cortical nodular hyperplasia is the underlying cause of adrenal-associated endocrinopathy in just under half of affected ferrets (the remainder are associated with adrenal cortical adenomas or carcinomas).