Jade and Kobi

August 2007

Yes, I'm 2 years behind with updating my web page... Beginning of August 2005 I took Jade and Kobi in. I took Jade in back in June '99 and she came with a hob kit. My neighbour fell in love with them and adopted them, she gave Jade her name and also named her son Zac. Zac died of a blockage in autumn 2002 and in 2003 she got Kobi who is Wesley's brother but from a second litter. Kobi's litter wasn't handled as much as Wesley's litter by the lady who had the kits so Kobi was a bit more timid from the start. Then my neighbour didn't spend quite enough time handling him so he got even more timid. Then my neighbour left home beginning of 2005 and left the ferrets with her parents who didn't feel confident handling Kobi and didn't really know what to do with them so I took them after visiting them in July and seeing that Jade had become quite frail.

I soon noticed that Jade had symptoms of low blood glucose so I tested her and she did indeed have a low BG so she was put on prednisolone. Around October 2005 she became quite ill and kept bringing her food back up and after having a blood test done, Michaela thought she had hepatitis and was likely to die. But then she got better and after another one or two mild bouts of bringing up her food, she was okay.

Kobi was very timid when he got here. He kept running away from me and hiding in tubes and it was awful trying to get him back into his cage. He also bit a lot and on one occasion he got his canine stuck inside my thumb and it was hooked right inside and he couldn't get it back out, it was rather painful and scary! With Jade being so old and sick, he didn't really have anybody to play with so I tried him with the new kits Jake and Phoebe and they all got on so well from the beginning so I started to let them out together. First Jade and Kobi would come out and once Jade was tired and went to bed, I would let Jake and Phoebe out with Kobi. And then when Kobi went back in, Jake and Phoebe had a run with their cage mate Ruby. Kobi soon realised the routine and would get very excited when I came to put Jade back in and then he would run to Jake and Phoebe's cage and put his paws against their door and then run to me and then back to the cage, just very excited like he was asking "Are Jake and Phoebe coming out now???" He just adores the two, especially Jake.

Kobi with Jake

And because Kobi spent time with Jake and Phoebe who were not frightened of me and would come to me, he soon copied their behaviour and became tame, too. After a few months he even cuddled with me. When I took Jade and Kobi out at night, I would cuddle them first and he enjoyed that a lot. And when he was out he stopped running away from me and soon even came when I called him. He is extremely intelligent and one of the few ferrets who know their names and actually come when called. :-)


Jade did quite well for 1 1/2 years. She eventually lost a lot of hair and had a sparse coat so it looked like she had adrenal disease on top of the insulinoma. But the insulinoma never got worse, in the beginning she started out on 1/4 mg of pred twice a day but then she was quite underweight and only 500g. As she put on weight, her pred dose was increased to 1/2 mg twice a day and she never needed more and never showed severe symptoms. She was active until the end and always ran around for about half an hour, exploring the upstairs first and then going downstairs to have a look through the lounge, kitchen and utility before going to her favourite bed in the lounge.

She developed an abscess at the front of her mouth/ on the jaw around November 2006 and I immediately gave her antibiotics. It wasn't a root abscess, it was just sort of at the front of her jaw. It didn't cause her much pain as she still ate well. She had also developed 2 skin tumours, I'm not sure whether they were mast cell tumours or sebaceous epitheliomas. They opened up and bled from time to time and in the end also abscessed. In February 2007 it so happened that she first developed one of her skin tumour abscesses and then the abscess on her jaw happened again. This time it got quite bad within a day so on 14th of February I took her to the vets. Jade still ate in the morning even though the abscess looked quite bad but watching her throughout the day I thought I had better take her to the vets for maybe some stronger antibiotics and painkiller. But Michaela had one look and said some tissue had already become necrotic (and 24 hours before she had *no* abscess) so suggested we let her go this time. I was in shock because I just hadn't expected this, especially since Jade had still eaten. But necrotic tissue sure doesn't sound good and her immune system was obviously in a bad shape so I went along with what Michaela said. She put her to sleep and because it was evening, she didn't have time to do the autopsy... She was also off the next day and from what she said I was afraid that there wouldn't be a vet the next day to do it either- so we did it the same night. I'd already asked the vets for some pots for the lab before Christmas 2006 because I thought what if a ferret dies by itself during the holidays, I wouldn't want to call a vet out to do the autopsy. Of course it would be a different matter if a ferret had to be put to sleep but I thought if one died then I wouldn't want to call a vet out but I would also want an autopsy done so I asked for some pots and a needle and suture material. So we now used it on Jade. Pete cut her open and then I took tissue samples. I didn't do well, didn't find the adrenal glands and I went for the most obvious change in the pancreas but it wasn't insulinomas so I missed those, too (unless the pancreatic hyperplasia can cause low blood sugars and she didn't have insulinoma after all which would explain why she never got worse and her BG was steady around 60 mg/dl). But it was a good learning experience. It looks so easy when Michaela does it but was quite hard to do with just the 2 of us.

So 2 days later I made an appointment with Mr Jones and gave him the pots and I'd also printed the autopsy photos out. He was amazed at the quality and what the pancreas had looked like and found it very interesting.

Jade's histopathology report:


Low blood glucose, alopecia. Samples from:- upper lip, left and right kidney, spleen and ? adrenal gland.


Lymphoma (Lymphosarcoma) and Glomerulonephritis


Not Applicable

Histopathology report

Haired-skin, kidney, spleen and pancreas are examined (2 slides, 6 sections).

In the skin, there is a diffuse inflammatory infiltrate, mainly neutrophilic, associated with deposits of basophilic debris and fewer plasma cells. PAS and Gram stains are negative for fungi and bacteria.

In the kidney, there is thickening of the basement membrane and mesangium of many glomeruli. Some tufts are completely collapsed and fibrotic (glomerular sclerosis). There is moderate increase in interstitial fibrous tissue. A focus of osseous metaplasia is present.

The pancreas has multifocal and marked exocrine nodular hyperplasia (Incidental finding).

The spleen has been effaced by nodular aggregates of intermediately differentiated lymphoid cells. The majority of these cells have rather small nuclei (approx 1x RBC diameter), moderately hyperchromatic, without prominent nucleoli, but with a rather open appearance featuring coarsely clumped chromatin; not the densely stained appearance of normal small lymphocyte nuclei. Mitoses are infrequent (generally <1 per high power field).


The spleen of this ferret had been effaced by a population consistent with a small-cell lymphoma, low or intermediate grade. Malignant lymphoma (lymphosarcoma) is the commonest malignancy of the domestic ferret. It most commonly arises spontaneously, although there is increasing evidence of a transmissible form. Several variants of the disease exist; a small-cell type is more commonly encountered in older animals (as here) whilst a lymphoblastic form is seen more frequently in younger (less than 2 years old) ferrets. The disease eventually spreads to multiple organs, causing multi-systemic disease.

There was also an incidental suppurative dermatitis and evidence of chronic membranoproliferative glomerulonephritis.

No adrenal gland was included.

So this was the end of Jade, and Kobi was now on his own, still having some time out with Jake and Phoebe though. By March I tried to integrate Kobi in with Jake, Phoebe and Ruby but he bullied Ruby. I put Bitter Apple on her and the bullying almost stopped- but then got worse again. All this coincided with me taking in another rescue called Honey, and Spike being taken out of his group and put with Honey so eventually Ruby was put with Spike and Honey and all 3 got on so well so Kobi is now with Jake and Phoebe. All very complicated, sigh... But Kobi is very happy with Jake and Phoebe and they are a lovely playful group. :-)

Jake, Kobi and Phoebe


On the 15th of December, Leo had his second Suprelorin implant and I took Kobi as well because he's showing a sexual interest in Jake plus he smells almost like a whole hob and has a thinning coat. Well, Kobi had the implant and when he came round from the gas, he started scratching the implant site immediately. Then it swelled up a little and got red, probably partly from the scratching. Then at night he had a seizure, it was the first time I'd seen one. I got him out of his cage and was like "Oh my God, oh my God" and thought he was dying on me, thought he had an anaphylactic shock. His eyes were wide open, he sounded like he was gasping for air, then his body relaxed again and I thought he'd died. It took a while before he came round and then he was so weak, he flat ferreted every few steps. I phoned the emergency vets and the vet didn't know what to do, whether to take the implant out or not. In the end we decided that I was to keep an eye on Kobi. He was okay after. I did measure his BG and it was 32 mg/dl first and then 38. So then I didn't know whether he had insulinoma and the BG suddenly dropped, causing the seizure, or whether the seizure caused the low BG. And then I thought to check the best before date on the strips and it was May '08! so now I don't know whether he had a low BG at all. The worst thing is I don't know whether Leo has insulinoma at all as I tested him Jan '09 with the out of date strips... I bought the AlphaTRAK from Abbott now as it's supposed to be very accurate with ferrets and will test both Leo and Kobi.

Kobi's skin reaction after implant


At the moment I'm trying to figure out whether I want Leo and Kobi to have an operation for the insulinoma. I'm just really worried, Leo will be 6 and Kobi will be 7 this summer. Last Saturday Kobi had another funny spell very suddenly, he stood in the cage, near midnight, and his head was swaying from left to right, up and down. I measured his BG with the new AlphaTRAK meter and it was 41.81 mg/dl. Then I measured his BG on Sunday when he hadn't eaten for 3 or 4 hours and it was 69.09 mg/dl. He didn't show any symptoms of a low BG then. It wasn't very low but low. So he gets very low BG out of the blue... :-( So now I'm wondering what to do, whether to operate or not and whether to do both Leo and Kobi or what... I just really do not like the thought of operating... Actually I do not know what to do about Kobi at all. He's not even on pred, yet. He doesn't show symptoms of low BG, only very occasionally (well, twice so far, like once a month). I do feed him meat every morning now (and they get meat at night anyway and have dry food available at all times) so that hopefully his BG will be stable...

Kobi on the 25th of January, new hair regrowth after implant


Kobi suddenly started coughing and had bad coughing fits. When he was coughing badly, I gave Kobi Furosemide and apart from the two times he's coughed, he's been perfectly fine. He plays, eats, cuddles, no problems at all. If he has another coughing episode, I will take him in for x-ray. Obviously it's awful seeing him cough like this and strange at the same time that he coughs like this and then all is fine again.


Kobi is doing okay considering all the things that are wrong with him. Most of the time his BG isn't too low and then he doesn't show symptoms at all but it will plummet suddenly out of the blue and then he just falls over and needs a sweet paste immediately.

I took him to the vet because of his coughing and Michaela could actually feel a heart murmur by putting her hand on his chest. He was x-rayed on the 23rd of February and his heart is quite big and pushes his windpipe up. He was put on Furosemide which took care of the coughing and we did a heart ultrasound on 23rd of March to make sure it wasn't hypertrophic cardiomyopathy (which it wasn't) so now he's on Vetmedin for his heart as well. He's not treated for the insulinoma at all as the prednisolone made his heart and coughing worse. If his insulinoma gets worse, I'll have to figure out what to do. Right now he's so happy and acting so normal that you wouldn't think he was sick at all, he's actually still more active and playful than his friends Jake and Phoebe although they are 2 years younger than Kobi.

Kobi still best friends with Jake


Kobi has more and more low sugars. I was away from the 30th of April to June the 8th and in my abscence Pete gave him, after speaking to me, 0.5 mg pred bid which didn't make a difference so he took Kobi back off it. But when I got back, Kobi had so many low sugars that I started him on 0.75 mg pred bid which seems to be working. He has not had any more bad low blood sugars. Obviously Michaela okayed the pred, too, ages ago actually. But Kobi has been so stable so far that I felt he didn't need pred, yet.


Kobi is slwoing down and has problems with low BG again. I've started him and also Leo on diazoxide finally, will update when I know whether it's working...


The diazoxide is definitely working! Kobi has been really quiet, slow, and wobbly this month but is not showing any more symptoms of a low BG. On the downside, the diazoxide has made his cardiomyopathy worse. Kobi was coughing a lot with fluid in his lungs and the coughing would exhaust him and cause him a low BG. Kobi has so far been on 2 mg/kg furosemide in the morning only but now I added another dose at night. He's also been on Vetmedin, 1/4 of a 1.25 mg tablet, morning and night, and now I started him on Fortekor, half a 2.5 mg tablet once a day, in addition to the Vetmedin. I just want to do everything I can medically for him and at the moment it's working really well, no more coughing and Kobi is more active again, although not as active as he was before September.



I’ve got a 7 1/2 year old hob, Kobi, with multiple health problems. He started showing symptoms of adrenal disease a year ago and got a Suprelorin implant. Insulinoma developed at almost the same time as the adrenal disease. He’s on prednisolone and diazoxide. On top of that he has got cardiomyopathy, he's on Fortekor, Vetmedin, and furosemide. The problems are all amazingly controlled with all his medications. But beginning of December he started developing problems urinating. I had booked him in for the 10th December to have his second Suprelorin implant but on the night of the 6th he could barely urinate. He went to the toilet every 10 minutes to do tiny pees and would moan. This was the first night he emptied his bladder during his sleep. So first thing on the 7th he went to the vets, prostate was enlarged, some blood in urine, he immediately got his Suprelorin and was put on Clavamox for 10 days. It seemed like he was able to urinate better/ okay, but after the antibiotics were finished, he started urinating in his sleep. Does that indicate that his (enlarged) prostate is giving him problems? Or the infection still? He urinates when I put him on the toilet, it just seems like he either thinks he can't pee or doesn't feel the urge to go although his bladder is so full that he's leaking. I searched the archives but could not find anything on ferrets emptying their bladder in their sleep so was wondering if others have seen this problem in their adrenal ferrets. Also I found one post in the archives that said that ferrets with prostate problems/ infection should be on antibiotics for 6-8 weeks? Thoughts on that? Finasteride is already on order.



I've just been to the vets with Kobi again because he is still peeing in his sleep although he has no problems peeing when he is awake. For example if I feed him and put him back into the cage, he will go to sleep and pee in his sleep. If I feed him and let him have a run, he will go the the toilet within a few minutes and empty his bladder without any problems. My vet palpated his bladder and it feels normal and does not cause Kobi pain. She expressed some urine and tested it and it had blood and protein in it and the pH was 5. Last time the pH was 5.5 and I'm wondering whether the pH does fluctuate or whether it's likely that his urine is too acidic. If so, how bad is a pH of 5? I have read the normal pH is 6 so is 5 still okay or is it "dangerously" acidic?

Kobi has just been on Synulox/ Clavamox for about 4 weeks and at first the urine cleared up. Usually when he peed on his bed, you could see brown(ish) urine stains which I thought were from the blood in the urine. On Clavamox this didn't happen anymore but the effect didn't last long and the blood came back as the urine test showed. Kobi is now being started on Baytril. He does have adrenal disease and had a Suprelorin implant in December and has been on Finasteride for about a month.



Is it possible to relieve nausea associated with renal failure?

Kobi, almost 8 years old, neutered male, has adrenal disease (with prostatic disease/ infections), insulinoma and cardiomyopathy. He's recently not been keen on eating, he is hungry and part of him wantsto eat, but he feels nauseous and will sometimes gag after eating though not throw up. He's only eating about half his usual portion, I'm surprised he's still fairly active and not showing signs of low BG. Bloods today showed the renal failure. I just want him to feel more comfortable and maybe get some of his appetite back because he's too good to be put to sleep.

Any help appreciated.

Blood test 16.05.2011

PLT Flags: MIC
WBC: 4.3 10^3/mm^3 (2.5 - 5.5)
RBC: 5.21 10^6/mm^3 (6.50 - 12.0) LOW
HGB: 10.8 g/dl (15.0 - 18.0) LOW
HCT: 34.2 % (40.0 - 60.0) LOW
PLT: 350 10^3/mm^3 (300 - 900)
MCV: 66 µm^3 (45 - 65) HIGH
MCH: 20.8 pg (15.0 - 20.0) HIGH
MCHC: 31.6 g/dl (30.0 - 34.0)
RDW: 12.3 % (14.0 - 17.0) LOW
MPV: 8.2 µm^3 (6.7 - 11.1)

%LYM: 12.4 % (12.0 - 50.0) #LYM: 0.5 10^3/mm^3 (0.3 - 1.3)
%MON: 9.6 % (0.0 - 6.0) HIGH #MON: 0.4 10^3/mm^3 (0.0 - 0.2) HIGH
%GRA: 78.0 % (15.0 - 80.0) #GRA: 3.4 10^3/mm^3 (0.4 - 2.0) HIGH

ALB 42 G/L
ALP 218 U/L
ALT 151 U/L
AMY 25 U/L
CA 2.45 MMOL/L
NA+ 153 MMOL/L
K+ 4.9 MMOL/L
TP 65 G/L

HEM 0 LIP 3+ ICT 0

Urine analysis 16.05.2011

Dip Stick:
GLU= Neg
BIL= Neg
KET= Neg
S.G= 1.015 S/G 1.014
BLD= +++
pH= 6.5
PRO= +++
UBG= Norm
NIT= Neg
LEU= Neg


I've still got sick ferret Kobi. He is one trooper... About 3 1/2 weeks ago I took him to the vets again as he was eating less and less, acting nauseous, and I thought he may have renal failure on top of his adrenal disease, insulinoma and cardiomyopathy. Blood test confirmed this. He was started on Antepsin (sucralfate) to help with his nausea but it didn't work. Or it did work but did not increase his appetite. I still gave it though so that his meds would not upset his tummy when he was hardly eating and not getting meds on a full tummy. He quickly got to the point where he was only eating 1/4 of his normal portion and I didn't think he'd last much longer. Well, he's still here. He supplements his 1/4 portion of mince with some kibble and he does get sweet high calorie paste with his meds (and strangely it does not affect his BG negatively in any way, if anything it keeps it stable...) but has lost a lot of weight but nevertheless he still runs around and is nowhere near the point where he needs to be put to sleep. But I hate watching him every day, wondering how he will be the next day.


I think I'll have Kobi put to sleep tomorrow. He's hardly been eating for the last 4 weeks, only about a quarter of his usual portion but he's been eating some kibble. The worst thing is that he has been way too good to be put to sleep, despite the anorexia. He's up a few times a day, wanting out, he runs around, has no problems with the stairs... But he can't pee properly, he's hardly been using the toilet the last few months and instead just empties his bladder in his sleep. In the past a course of antibiotics usually helped but not since April. And now he has problems peeing at all. Yesterday his bladder was so full and he leaked as he was walking along so I expressed his bladder. This morning the bedding was dry which means he didn't pee at all last night so I expressed him again this morning and will continue to do so until tomorrow (Monday). He is still running around though and apart from looking a bit on the thin side, he does not look unwell or like he's suffering (a lot). So it's difficult to reach a decision.


I thought I'd have Kobi put to sleep today, but last night he was so active again, that is why I have decided against putting him to sleep today, I have no idea how he keeps his strength up while loosing weight and being so ill. He is just one amazing guy.


Kobi is still with me, I actually took Kobi to the vets twice to possibly be put to sleep but then at the vets he was so active that by looking at him you would never have guessed that he was sick at all! The first time I took him Michaela wasn't there so I asked the other vet whether he could have pain medication- just in case. Every now and again he lies down in a way that makes me think he's in pain, eyes half closed, shivering. So she gave me buprenorphine which I gave for about 5 days, then I got more and haven't needed it since.

As I mentioned before, Kobi was barely eating, then I realised that he was preferring chunks of meat to his mince so he's been getting chicken breast, meat of chicken drumsticks, and turkey breast for the last week and he's now eating about half of his usual portion so that is excellent. I'm feeding him 4 to 5 times per day. But he's not been wanting his medications. He's been getting his tablets ground with some sweet paste but he's been fighting his meds so badly that for a few days he hardly got any. But then his blood glucose went low so I forced him to have at least his prednisolone and diazoxide. Sometimes he sort of takes it okay, other times it's a struggle to get him to take it. He's not been getting his vetmedin and benazepril for his heart but seems okay, though more sleepy than usual, but no coughing. He is still taking his furosemide though.

And two weeks ago I had to start expressing his bladder and have been doing it ever since, about 6-8 times a day. We don't know what is wrong, whether the prostate is enlarged or infected or he has developed prostatic cysts. It's working okay, sometimes he even helps me by straining to pee so it flows more easily. He's just got an amazing drive to live like I've never seen in a ferret. He also adores his friends Jake and Phoebe, Jake especially. I've also never seen such a strong bond in ferrets before. I mean Kobi fell in love with Jake the moment he set eyes on him, grin. When I was thinking of having Kobi put to sleep, what hurt me most was that by doing this I was separating him from Jake. But for now Kobi is comfortable, even putting on some weight again, so who knows how long he's going to live. He is such an amazing ferret and if he wants to live, who am I to stand in the way. I'll do anything possible to make him enjoy whatever time he's got left.


Kobi is doing remarkably well! He went through this spell 1 1/2 - 2 months ago where he hardly ate for a few weeks. Usually he would eat 40 g of mince morning and night and suddenly he went off his food and only ate 10 g, sometimes only 8 g! He was not weak at any point though. He was diagnosed with renal failure and then one day he snatched a chunk of meat off one of the skunks' plates so I started offering him chunks of meat, cut small. At first he still ate little- but he ate and I didn't have to force him. Eventually he would eat 10 g of chunks about 4 times a day again, then he started eating bigger portions so I cut him back to 2 meals a day again, and now he's eating like a little pig, sometimes over 40 g of chunks! He likes chicken drumsticks and thighs. I admit I upped his pred from 1/2 mg twice a day to 1 mg twice a day in the hope it would improve his appetite, even if it meant his kidneys would deteriorate quicker. 7 years ago I had Baby with renal failure, because of all her big lymph nodes my vet thought she had lymphoma so prescribed pred. Baby hardly ate for quite some time and I maintained her on goats milk. Then as the pred started to work, she started eating again and had some quality of life again. That is more important to me than the length. Mind you Kobi doesn't act like he has renal failure at all, he is not deteriorating at all but just getting better all the time. I've been expressing his bladder for over a month now and he has also been on painkillers since, Buprenorphine 0.05 ml three times a day. And since we started Buprenorphine he is a lot better again. He even sometimes pees a little, last night he emptied his bladder although with *a lot* of straining and sometimes he at least empties some by himself.


I've had to have Kobi put to sleep Tuesday 16th. He'd had so many problems, insulinoma and cardiomyopathy were well under control but he had adrenal disease and I think the problems urinating were associated with that. Since the end of last year he's been unable to pee properly and usually emptied his bladder in his sleep although he had phases where he also peed on the toilet. But 2 months ago he stopped peeing, the bedding was dry one day and his bladder very big so I started expressing his bladder and he did not pee in his sleep at all any more. It caused him some discomfort but he was happy for me to do it. But the pain became worse over the last few weeks despite being on Buprenorphine the whole time I expressed his bladder. It was killing me, on the one hand he was in pain and I was causing him pain by expressing his bladder but on the other he enjoyed life so much and loved his companions Phoebe and Jake. Only in the last 2 weeks did he become quieter but still ran around a bit. I was hoping he would slowly get to the point (without too much suffering) where I could say that the quality of life wasn't there any more and that he ought to be put to sleep, but then Tuesday morning he was in such a bad way... In a lot of pain and he could barely walk, he must have had very bad pain in his lower abdomen, like “down below”, I don't know how to describe it but it was like he was straining to urinate while walking, his legs were not straight when walking but crooked (bent). I took him to the vets and Michaela saw us before seeing any other clients. I couldn't watch him being put to sleep (by intra peritoneal injection) but his eyes were wide open when he was dead, it kills me wondering in how much agony he was, it's haunting me... On the way back home I was crying so hard, why did he have to suffer so much?! Why is there so much suffering in the world, why could Kobi not just deteriorate slowly, why the sudden severe deterioration? The night before he was so easy to express, what happened in the night? He was just so stable and then this. I find it hard to watch all this suffering...

On top of everything Michaela didn't have time to do the post mortem, I phoned another vet, he would have done it but didn't want me to take pictures. I found that sad, especially since we know this vet. So we did it ourselves, second time. It's bad because there was so much wrong with Kobi and now I feel we probably missed most. I don't think I found his adrenal glands but I made the mistake and got the kidneys out before even thinking about adrenal glands. I don't know if we saw his bladder, it had either ruptured or it was very thickened. If the thick hollow “structure” wasn't his bladder then I don't know what it was. I didn't find any insulinomas, I did find something but think it was just hyperplasia. Kidneys were looking bad, his heart was very hard, I'm wondering if he had hypertrophic cardiomyopathy as I thought the heart looks and feels different (squashy) in dilative cardiomyopathy. But he did have a heart scan to rule out hypertrophic cardiomyopathy and he was on Vetmedin which should not be given with hypertrophic cardiomyopathy. But thinking now he could barely use his hind legs that morning so maybe he threw a blood clot/ saddle thrombus. That would explain the severe pain. Pete is telling me I'm speculating, hope the histopathology will answer some questions... I just need to know what went wrong so I can get closure. And the most obvious thing, apart from the heart and kidneys and bladder or whatever it was, was the liver. I don't know if he had cysts on it or cancer. Looking at old necropsy pictures it looked similar to Jasmine's hepatic haemangiosarcoma. Kobi's abdomen was filled with bloody fluid (with possibly puss) but not as bloody or anywhere near as bad as Jasmine's. I'd been wondering if he'd had fluid and took him to the vets Thursday 11th because his abdomen was getting bigger rather quickly but she didn't say anything and Kobi was pretty bright and looked good. But I was right with the abdominal fluid... I just hope I will get answers...

But one thing I want to mention: the diazoxide is brilliant! Kobi has not had any problems with his blood glucose since I started him on diazoxide. It took me a while to realise but when he had his blood test in May, his BG was 8 mmol/l which is 145 mg/dl so if anything his BG was a bit high. At the same time I maintained him on 0.5 mg pred bid and the only reason I increased the pred to 1 mg bid was to help increase his appetite which worked. I may even try giving the next insulinomic ferret diazoxide from the start and not give pred at all or just a very small dose.


Kobi's histopathology report:

Post-Mortem Tissues from a Ferret: 11 samples received; 11 sections evaluated on 3 slides.

Heart (slide 2). Myocytes are equivocally broad and show mild to moderate anisokaryosis. Multifocally, especially in the ventricular subendocardium and in the centre of the ventricular muscle, there are irregular wedges of fibrosis associated with loss of myocytes and attenuation of residual myocytes.

Lung (slide 1). Generally, the lung appears well-aerated; however, a minority of alveoli and bronchioles contain luminal proteinaceous fluid, and some affected alveoli also contain low numbers of macrophages with brown granular pigment (haemosiderophages, "heart failure cells''). In several foci, in alveolar lumens beneath the pleura, there are clusters of foamy macrophages (endogenous lipid pneumonia; Insignificant). A tiny focus of parenchymal osseous metaplasia is also present.

Pancreas (2 sections, slide 3) with Duodenum and Lymph Node. The larger section of pancreas is focally multinodular and expanded to approximately 8 - 10 mm in diameter. The expansile

Liver and/or Adrenal Gland (3 sections, slides 1, 2 and 3). In one section with portal tracts and bile ducts (definitive liver) and two other sections that resemble liver, normal hepatic acinar architecture is difficult to discern. The samples consist instead of nodular aggregates, cords and sometimes islands formed from simple to bilayered polygonal cells with a strong resemblance to hepatocytes (but also resembling cells in the adrenal cortical masses, described below). Supporting stroma is delicate and vascularized, resembling irregular sinusoids. Some sinusoids show cavernous dilatation and congestion. The presumed hepatocytes have variable amounts of eosinophilic cytoplasm and somewhat variably sized, oval, nuclei. Nucleoli are sometimes seen. Mitotic figures are rare at approximately 1 per 10 high-power (400x) fields. The cells sometimes appear to interlace with possibly normal hepatocytes near one margin, but no definitive normal borders are visible.

Kidney (slide 1). Multiple radiating wedges of fibrosis extend from the medulla to the cortex, and all enclosed glomeruli and tubules appear sclerotic or attenuated. There is a scattered infiltrate of small mononuclear leucocytes. In adjacent areas, some tubules contain proteinaceous fluid. The inner medullary interstitium (renal crest) appears expanded by fibrosis, and ducts in this area sometimes lack epithelium.

Presumed Urinary Bladder (slide 2). This section is histologically compatible with urinary bladder, although dilated anterior urethra cannot be ruled out. The mucosa appears normal. The smooth muscle tunics appear thick, with wide myocytes that show hyaline to fibrillar sarcoplasm (hypertrophy).

Adrenal Gland (2 sections, slices 2 and 3). Two definite sections of adrenal gland are similar on histology. Cortical architecture is locally disrupted by zones of haemorrhage with cellular debris (necrosis). Partly replacing the cortex are irregular cords, trabeculae and solid sheets of polygonal to spindled cells with eosinophilic cytoplasm and variably sized but usually medium-large, oval nuclei with prominent nuclei. Mitotic figures are 1 per 10 high-power (400x) fields. The lesion is associated with light proliferation of a background of spindle cells (presumably smooth muscle cells). Some polygonal cells breach the capsule and extend into adjacent adipose tissue and others penetrate the medulla. At the junction of the cortex and medulla in one section, there is a local deposit of amorphous eosinophilic material (presumptive amyloid). This gland also shows a few small, discrete cortical nodules of vacuolated cells (probably cortical nodular hyperplasia) and a few cortical clusters of plasma cells and lymphocytes.


1. Heart: Cardiomyopathy -- hypertrophic, moderate, with multifocal fibrosis
2. Lung: Oedema -- multifocal, mild, with haemosiderophages ("heart failure cells")
2b. Lung: Endogenous Lipid Pneumonia
3. Pancreas: Islet Cell Carcinoma
3b. Pancreas: Pancreatic Nodular Hyperplasia
4. Liver: Hepatocellular Tumour (suggested well-differentiated Hepatocellular Carcinoma; ddx: metastatic adrenal cortical carcinoma)
5. Kidney: Nephritis -- interstitial, chronic, marked, with renal crest necrosis
6. Urinary Bladder: Muscular Hypertrophy -- diffuse, moderate
7. Adrenal Gland: Adrenal Cortical Carcinoma(s)
7b. Adrenal Gland: Amyloidosis, presumptive, with focal adrenalitis


This ferret died with serious lesions in virtually all of the submitted tissues, any of which might have contributed to clinical illness.

The heart shows hypertrophic cardiomyopathy with focal fibrosis, resembling resolved infarcts. Cardiomyopathy is common in middle-aged and older ferrets. The pulmonary oedema with haemosiderophages strongly suggests right-sided congestive heart failure.

The lung also shows endogenous lipid pneumonia, a common and clinically insignificant finding in mustelids, but which might have caused an abnormal, spotted appearance to the lungs at necropsy.

As you correctly suspected, the pancreas contains an islet cell carcinoma. 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". They can be benign or malignant, but as this example is invasive, it is clearly a malignancy. 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.

The pancreas also shows marked nodular hyperplasia; a benign change that is common in the pancreas of middle-aged and older carnivores, including ferrets. This harmless lesion is an incidental finding.

This ferrets liver contains a tumour that most closely resembles a primary hepatocellular malignancy (hepatocellular carcinoma). The cells in the adrenal cortical carcinoma also have a hepatoid appearance, and it is difficult to distinguish them on histology -- the possibility that some of the liver nodules might be metastases from the adrenal tumour(s) is not completely ruled out. Hepatocellular tumours are rarely reported in ferrets and other mustelids, although we have seen occasional cases. They have potential for metastasis and also for rupture, leading to abdominal haemorrhage.

Interstitial nephritis is a very common lesion in middle-aged to older ferrets. If the sample submitted is representative of both kidneys, then this ferret was probably in or approaching renal failure. As with most chronic lesions, the initiating cause is no longer visible.

Hypertrophy of the muscle of the urinary bladder might reflect partial outflow obstruction by the reportedly enlarged prostate.

The two sections of adrenal gland both contain an adrenal cortical carcinoma. These are common tumours in ferrets, and in spite of their designation as malignancies based on cytology and local invasiveness, the vast majority apparently do not metastasize or else metastasize late in the course of disease. As mentioned above, I cannot completely exclude metastasis to the liver in this case, based on very similar appearance of the adrenal tumour cells to liver cells, but in my opinion, the liver tumour is likely to be a separate entity. In ferrets, adrenal cortical carcinomas generally produce sex hormones (primarily oestrogens) rather than cortisol. Associated clinical syndromes include prostatic squamous metaplasia (possibly relevant here) and endocrine dermatopathy.

Thank you for the additional verbal history for this case. I apologize for the slightly delayed report.

Kobi when I first got him:

Index page
My ferrets & ferret health and information pages
Miscellaneous pages