Gremlin's autopsy pictures
Chest cavity and lungs.
Heart and lungs.
Heart and lungs.
Heart and lungs.
Kidneys (with (empty) cysts).
Blood test 30/08/2006
Total Protein 71 g/l (51 - 74)
Albumin 35 g/l (26 - 41)
Globulin 36 g/l
Urea 25.3 mmol/l (1.9 - 7.49)
Creatinine 187 umol/l (< 75.0)
ALP 45 iu/l (34 - 66)
ALT 81 iu/l
Bile Acids 10 umol/l
Triglycerides 1.05 umol/l
Haemoglobin 17.6 g/dl (12.0 - 18.0)
Red Blood Cells 9.66 x10^12/l (6.7 - 12.1)
PCV 0.61 % (0.43 - 0.55)
MCHC 28.4 g/dl
MCH 18.2 pg
MCV 64.0 fl
Platelets 550 x10^9/l (297 - 910)
White Blood Cells 4.8 x10^9/l (3.5 – 7.0)
Neutrophils 67% 3.65 x10^9/l (1.5 – 5.9)
Neutrophils (Band) 0% 0.00 x10^9/l
Lymphocytes 16% 0.77 x10^9/l (1.7 – 2.9)
Monocytes 5% 0.24 x10^9/l (0 - 1.17)
Eosinophils 3% 0.14 x10^9/l (< 0.35)
Basophils 0% 0.00 x10^9/l (< 0.14)
Blood Film Examination
Blood smear prepared from EDTA sample was examined. Red cells appear normocytic and normochromic. A mild mature neutrophilia is seen with no evidence of toxic changes observed. A mild lymphopaenia is seen. Platelets appear normal in number and morphology with no evidence of platelet clumping or EDTA clots seen.
Gremlin's histopathology report:
Weakness, grey mucous membranes, still eating, muscle wastage, still plenty of visceral fat, Treated with Frusemide, Fortecor, recently Vetmedin. PM - clinically in heart failure, lungs dyspnoe with crackles. Liver engorged/enlarged, fatty and infrequent firm lumps. Spleen - 2 medium to large circular blood filled areas, soft to touch not encapsulated. Numerous brown/enlarged visceral ?NLL post prandial. Pancreas small nodule, clinically hypoglycaemia. 2 kidneys - multiple small to large fluid filled parenchymal cysts. Adrenals - left enlarged/calcified. Right - central ? necrosis.
Cardiomyopathy and Pathological changes in various tissues
Sections from necropsy samples of multiple tissues from a 7-year-old, female Ferret were examined microscopically.
LIVER: 2 samples received; 2 sections examined. Both sections reveal marked sinusoidal congestion, most obvious in the centrilobular zones, where the effect is compounded by atrophy of hepatocytes. There is also mild to moderate, patchy hepatocytc lipidosis; mild, multifocal extramedullary haemopoiesis; and, in one of the sections, a substantial focus of cystic biliary hyperplasia.
KIDNEYS: 2 samples received; 2 sections examined. Each of these sections contains a fairly substantial cyst, one in the cortex and the other at the corticomedullary junction and both associated with interstitial fibrosis. Occasional other small foci of interstitial fibrosis, accompanied by lymphocytic infiltration and tubular basophilia, are present and there is also widespread thickening of glomerular capillary basement membranes.
SPLEEN: 1 sample received; l section examined. The red pulp is severely congested and there is a large area of parenchymal haemorrhage. There is widespread extramedullary haemopoiesis. The white pulp is moderately hypercellular.
HEART: 1 sample received; l section examined. Grossly, the heart appeared unusually globular in shape and the left ventricle appeared diluted, with a thinner wall than normal. Microscopy reveals widespread myocyte degeneration accompanied by marked, patchy fibrosis, involving both ventricles end atria. There is only a scant associated inflammatory infiltrate, predominantly mononuclear.
LUNG: 2 samples received; 3 sections examined. These reveal moderate to marked congestion, with areas of atelectasis and increased numbers of alveolar macrophages, some containing pigment.
PANCREAS: 1 sample received; l section examined. This reveals a small focus of exocrine (acinar) nodular hyperplasia as well as two small, well-circumscribed islet cell tumours (insulinomas).
ADRENALS: 2 samples received; 2 sections examined. Both show marked proliferative change, involving multiple cell types. In neither case is there any marked nuclear atypia, but in one case mitoses are moderately frequent and, in combination with the pleomorphic cell population, this is probably enough to justify a diagnosis of carcinoma.
LYMPH NODES: Multiple samples received and examined. All are markedly enlarged, chiefly as a result of dilatation of the medullary (and to a lesser extent subcapsular) sinuses by a combination of oedema and haemorrhage. One also features multiple, substantial aggregates of macrophages containing abundant, faintly pigmented, needle-shaped, crystalline inclusions.
DIAGNOSIS: Dilative cardiomyopathy; Adrenal cortical carcinoma (bilateral); Pancreatic islet cell tumours (insulinoma); Glomerulonephritis; Renal cysts; Cystic biliary hyperplasia; Splenic congestion, haemorrhage and extramedullary haemopoiesis.
DISCUSSION: I believe the principal cause of this ferret's deteriorating condition was the dilative cardiomyopathy, which was causing congestive heart failure, evidence of which is present in the liver, lung, spleen and lymph nodes. Dilative cardiomyopathy is increasingly recognized as a cause of congestive heart failure in ferrets, but, as far as I am aware, a definite cause has not yet been identified. The possible role of taurine deficiency (as proposed in cats) has been considered. Adrenal cortical tumours and pancreatic islet cell tumours are the two commonest neoplasms in ferrets and it is not unusual to see both in the same patient. Cystic biliary hyperplasia is an uncommon, apparently spontaneous condition seen occasionally in most species. It is usually of minimal clinical importance, but in this case I wonder whether there may have been some bile leakage, which could account for the clusters of crystal-laden macrophages present in one of the lymph nodes in this submission. Renal cysts are moderately commonly seen in ferrets and are usually of no clinical significance. Chronic interstitial nephritis, present in this individual at a mild degree, is also common in aging ferrets. Glomerulonephritis is less common. The degree in this patient was moderate and it may have been sufficient to be causing biochemical changes associated with renal failure. No obvious cause was found for the glomerulopathy.