Ferret Scotty's autopsy report

One morning at the start of February this year I went to put my ferrets out in the run. On approaching the cub my hob ferret Scotty was in the hutch laying flat out. He was struggling to breath and appeared to be in a state of shock; his body had shut down and his mouth was tightly closed. I picked him up and rang the vets who saw him straight away. She checked his reactions by pinching his paw, he responded. Scotty's temperature was high and when the vet repeated the reaction test there was little response.

The vet suggested an x-ray to see if there was a blockage but the results did not show up anything although there appeared to be fluid on his lungs. The vet suggested that this is particularly normal when a ferret is suffering from severe shock.

I left the ferret with the vet and later received a call from her to say the chances of a recovery were not very good. She was not sure what was wrong with him and as we were speaking he passed away. As the hob died suddenly and I had lost 2 other ferrets within the last 9 months the vet and I agreed that a further investigation should be carried out. The results of a postmortem revealed that there was inflammation in the lungs, congestion of the spleen and kidneys and puss near the lung cavity. The cause of this is uncertain and may have been a viral infection or a foreign body. I'm keeping a close eye on my other ferrets, which appear fine so maybe it was a mysterious illness that had just affected the hob.

The hob was 3½ years old and up until his sudden collapse he appeared healthy and full of life.

His sister had to be put down in May last year and it was thought she had kidney disease. The mother was 5 years old and died last October and it was thought she had problems with her kidney's/adrenal. She had to be re-jabbed in the May as she had come back into season but started to lose weight dramatically. She became very thin, her coat in late summer had broken and looked like she had had a crew cut. She had been given treatment, which may have prolonged her life. The night before she died, her gums appeared very pale and she did not look well at all. I had a feeling by the morning she would have died and come morning she had.

A male ferret (ID Scotty 3 ½ years old) weighing 1680g was presented for post mortem examination following sudden collapse and death.

The animal was found to be very obese. Examination of the skin, hair, eyes, nostrils, mouth, ears, anus and feet found these all to be macroscopically unremarkable. No evidence of trauma or parasitism was noted.

The general carcase condition was good though grossly overweight with large amounts of fat present.

The trachea and thyroids were examined and found grossly unremarkable. Examination of the heart revealed pericarditis. The lungs were solid and congested upon examination (pyothorax).

The liver was bronze in colour with rounded edges ? secondary hepatitis. The gall bladder was small but relatively normal. The spleen was enlarged and revealed the presence of white foic throughout. The kidneys were macroscopically unremarkable. The bladder was empty. The stomach, small & large intestines, rectum, reproductive tract (male) and musculoskeletal system were all examined and found to be macroscopically unremarkable.

Right lung swab: Culture
Lung: Histology
SI/LI/Pancreas/Stomach: Histology
Liver/Spleen/Pericardium: Histology

Routine aerobic cultures from this sample have proved unrewarding with no bacteria being isolated despite prolonged incubation.

Urinary bladder, pancreas, stomach, small intestine (x 2), large intestine: Unremarkable.

Spleen: Diffuse pulp expansion by macrophages, fewer neutrophils, and clumps of haematopoietic cells including prominent megakaryocytes. Scant granular haemosiderin deposits.

Liver: Moderate diffuse microvesicular steatosis of hepatocytes, which is pronounced around the central veins across the majority of the section. There is sinusoidal and vascular congestion.

Kidneys (x 2): There is marked venous congestion, particularly at the corticomedullary zone. Many epithelial cells contain granular orange brown pigment deposits (lipofuscin).

Lungs (x 2): There is diffuse collapse of the sections examined, with few patent alveoli, generalised congestion, and wrinkled pleura. There is subpleural haemorrhage into alveoli in some areas. Minimal anthrasilicosis around bronchioles, which otherwise contain small quantities of mucus. The pleural surfaces have deposits of amphophilic debris, comprising a mixture of amorphous basophilic material, red blood cells and small numbers of degenerate leukocytes.

Mediastinal tissues: Adipose tissue, lymphoid tissue (thymic remnants?) and serosal membranes displaying haemorrhage, mild mesothelial hyperplasia, infiltrations of mixed inflammatory cells, capillary hyperplasia and superficial debris similar to that seen on the pleural surfaces.

Comment:
The histological changes in the lungs are consistent with the pyothorax reported grossly, although the leukocytic component of the exudates is sparse. This would tend to exclude the pyogranulomatous forms of the disease caused by agents such as Nocardia and Actinomyces (common causes in the dog and cat), and to suggest a relatively acute onset. There is no specific evidence of an aetiological agent, and definitive identification of an agent would require microbiological culture. Bite wounds and penetrating foreign bodies are both reasonably common causes of pyothorax. The remaining changes are of incidental interest. The liver changes are likely to reflect hypoxia and perhaps disruption of venous return in the latter stages.

Splenomegaly and extramedullary haematopoiesis are extremely common in ferrets, occur in animals as young as 6 months old, and often remain idiopathic. Occult inflammatory stimuli are generally presumed to play a role.