Update 11/02/14 Ferrets Peanut, Charlie and Franklin

Peanut, Charlie and Franklin

Peanut

Charlie

Franklin

I have another 3 ferrets. I know, I know, I wanted *less* ferrets, not more. End of August my friend Sheila from Bolton Ferret Welfare suddenly phoned. I hadn't spoken to her for 3 years... She was coming down to St. David's to do a show and was wondering if she could pop in on the way down and whether we were coming. So she came here on the 27th and the show was on Saturday and Sunday 30th and 31st. My dad was going home on the Saturday so we couldn't go that day but we went Sunday. I'd emailed Cris who adopted a ferret (Bubbles) from me 7 years ago. He only lives an hour away but we never met up again, only wrote. I told him about the show and Sheila and asked if he wanted to come and he came so it was Cris, Pete and I helping Sheila. And well Sheila had just taken in 3 ferrets, the “Wigan Three”. They were left in a hutch by a stream or river and eventually a man was fishing there and found them or, well, he found the hutch and decided to take it home, not knowing that ferrets were in it. At home he found the 3 surviving ferrets and a dead half eaten one... Again it is beyond me how a person can inflict so much suffering on ferrets/ animals. Why couldn't the person take the ferrets to an animal shelter or dump them where they could be found? So the ferrets were taken in by Sheila. 2 hobs and a tiny skinny jill who weighed 410 g when Sheila took her in. And they were at the show with Sheila. And I soon became very attached to them. The jill was waking up my maternal instinct and one of the hobs reminded me of Fox and Spike. When Pete and I left, we drove to St. David's beach (scroll down) because the show was very close to the beach and we discussed whether to ask Sheila if we could have the ferrets. Obviously we asked and obviously we have them now. The silver hob is now called Charlie, the polecat hob Franklin and the little jill Peanut. The boys were castrated on the 5th of September. I don't know why I wanted them, partly because I fell in love with them, partly their story, partly because I thought they would get on well with Honey and Snoopy because they were a similar age.

At the moment they're out twice a day for a total of 4 hours. They enjoy their freedom here and can run outside and they are so happy and so lovely. After a week or so I started letting Peanut, Charlie and Franklin out with Ruby, Honey and Snoopy and it was the easiest introduction ever. They've been living together since the middle of September. A few minor squabbles to sort out who's above whom but nothing bad. I had to take Nipper out of Honey's group though because he was too sick and old to deal with this. But he hadn't bonded with Ruby or Honey or Snoopy, he tolerated them for most of the time but didn't really enjoy their company unless they were all asleep together. So he's on his own now and looking much better and happier. And my group of 6 is so happy and playful. They run and war dance so much, it is lovely to see.

Maybe not the best pictures but they capture how much fun the boys have and how much I enjoy watching them.

Charlie, Franklin and Snoopy

Charlie and Snoopy

Charlie and Snoopy- only playing!

Snoopy, Charlie and Franklin

Best friends Charlie and Snoopy

Peanut is a little cuddly girl. :-)








Franklin update December 2011

Franklin started limping one day and at first I wanted to wait and see what happens but then I thought maybe it's something that requires anti-inflammatories and would get worse if not treated so I took him to the vets on 23.11.2011. My vet thought straight away that it was a torn cruciate ligament (in his right back leg/ knee) and an x-ray confirmed it. He didn't seem to be in pain at all, still eager to run and play, just that his leg would sort of collapse underneath him which gave the limping appearance. He was on Metacam for 2 1/2 weeks and off it now, I'm to see how he gets on to determine if he needs pain relief or not. Hopefully it will stabilise in time.

Franklin update May 2012

Franklin is pretty much completely fine now, he doesn't seem to be limping at all. His body is sort of strange, he never had as much muscle tone as the others so has always been running strangely. But he is very happy and runs and plays just like the others.

Charlie update 31/05/12

This month I had a lot of worries with Charlie.

I felt his abdomen early May after cleaning his teeth and it felt very tight and full. The spleen was massive but I wondered if there were other enlarged organs. Charlie was at that point still full of beans, very active and energetic, but he "flat ferreted" a lot. And I palpated his abdomen a few times and he looked in pain afterwards, a few times I put him back into the cage and he just lied there, another time he sat there with his back hunched which can be a sign of pain. Of course he didn't display this at the vets on the 8th of May so my vet said to just keep an eye on him and yes, the spleen was large (it was massive!) but she couldn't feel any lumps. So I got all the dentals out of the way (Poppy, Peanut, Squirt and Franklin all had to have dentals...) and then concentrated on Charlie. I took him back to the vets on the 22nd when Franklin had his dental and Charlie was definitely worse by then, he could not eat much anymore, the spleen was pushing against his stomach, Charlie lost weight, muscle mass, condition, was weak and more quiet, so my vet x-rayed him and did an in-house blood test:

Haematology:

WBC: 2.9 (5-11) low
RBC: 3.07 (5-10) low
HGB: 5.2 (8-17) low
HCT: 16.7 (27-47) low
PLT: 190 (180-430)
MCV: 54 (40-55)
MCH: 17.1 (13-17)
MCHC: 31.3 (31-36)
RDW: 13.5 (17-22) low
MPV: 20.3 (6.5-15) high

% LYM: 28.1
# LYM: 0.8 (1.0-4.0)
% MON:8.5
# MON: 0.2 (0-0.5)
% GRAN: 63.4
# GRAN: 1.9 (3-12)

Chemistry:

ALB: 27 (26-38) G/L low
ALP: 106 U/L
ALT: 134 U/L
AMY: 16 U/L
TBIL: 6 (1.71 max) UMOL/L (x)
BUN: 14.0 (16 max) MMOL/L
CA: 2.37 (2.95) MMOL/L
PHOS: 3.24 (2.94 max) MMOL/L high
CRE: 55 UMOL/L
GLU: 6.3 MMOL/L
NA+: 142 MMOL/L
K+: 5.7 MMOL/L
TP: 64 (51-74) G/L
GLOB: 37 G/L high

QC: OK
HEM: 0 LIP: 0 ICT: 0

My vets comments were "?Haemobartonella, blue coccoid inclusions in numerous neutrophils + monocytes, seen 1 eosinophile, ?better after Baytril inj, many reticulocytes seen".

Charlie was much sicker than he looked. So Wednesday 23rd he first had a blood transfusion and new boy Skippy was the blood donor... None of the other ferrets could have given as much blood as he could plus Skippy is the healthiest ferret so maybe if I had never got him, Charlie would have not made it... So anyway, Skippy gave blood and was perfectly fine after, the vet nurses looked on in amazement as Charlie was going pinker when he received the blood. And then my vet did a splenectomy on Charlie. I really thought we would either let him go under anaesthetic (because of him being riddled with cancer) or that he wouldn't survive the operation (because it's a big operation or because of blood loss during the operation). There were 2 vet nurses taking care of Charlie (thank you!!!) and keeping a close eye on his heart rate and breathing which made me feel very happy and at ease, knowing he was in safe hands. The spleen was so big it was silly. Unfortunately I didn't weigh Charlie after the operation to see just how much that spleen had weighed. Charlie looked bad after the operation- but by the next morning he was pratting around in his sick cage wanting out with the others! He did not at any point look like he was in pain or feeling bad in any way. The spleen must have caused him more pain and discomfort than the operation... As the days went by, Charlie was acting much better, eating big portions again, running around, war dancing. :-) I've kept him more quiet and confined than he appreciated and not let him run up the stairs or climb and jump upstairs, I've only let him have short runs in the garden. Hopefully he'll be okay now. :-)

Charlie update 01/06/12

Charlie had his stitches out today and his PCV/ HCT was checked again, it was 30%. :-) On the 22nd it was 16.7 %, normal range is 27-47. So it seems the spleen was responsible for the low blood count. Charlie also put on weight, when he had his first vet visit on the 8th of May, his weight was 1.26 kg. On the 22nd his weight was down to 1.16 kg. Unfortunately neither the vets nor I weighed Charlie after his operation but my vet thinks the spleen was at least 100g. To be honest Charlie weighed 1 kg after the op at the most. So today, 9 days after the operation, his weight was back up to 1.14 kg. :-) The histopathology report is back, it's not ruling out lymphoma but it's probably “just” splenic nodular hyperplasia and extramedullary haematopoiesis. ADV was ruled out as a cause, too. :-)


Charlie's histopathology report:

Diagnosis Splenic Nodular Hyperplasia and Extramedullary Haemopoiesis
Prognosis Probably good

Histopathology Result
Spleen: 1 sample received; 1 section evaluated.

The splenic parenchyma is markedly expanded by approximately 1.5 cm thick, but remains confined within a histologically normal capsule. There is marked nodular expansion of some lymphoid follicles and sheaths by a mixed population of small lymphocytes with fewer large lymphocytes, occasional histiocytes and the odd plasma cell. The intervening red pulp appears congested and includes substantial extramedullary haematopoiesis (EMH).

MORPHOLOGICAL DIAGNOSIS:
Spleen: Lymphoid Nodular Hyperplasia, Congestion and Extramedullary Haematopoiesis

PROGNOSIS:
Probably Good

COMMENTS:
Splenomegaly is common in the ferret, especially in middle-aged to older patients, but may be seen in young animals. It has been associated with several a variety of disease conditions, including lymphoma, other types of neoplasia, Aleutian Disease, bacterial infections, anaemia, generalized chronic illnesses, extramedullary haemopoiesis (EMH) and congestion. In this case, the pleomorphic nature of the white pulp proliferation is most consistent with benign nodular hyperplasia of the spleen, which in other species, is an incidental finding often associated with ageing. This lesion is not typical of lymphoma; however it should be noted that occasionally in the ferret, splenomegaly can be seen in cases of lymphoma without any neoplastic lymphocytes in the spleen itself, the splenomegaly caused only by EMH, so lymphoma could not be excluded with absolute certainty. There is no overt evidence of neoplasia of any other kind. There is no marked plasmacytic infiltration of the red pulp to suggest Aleutian disease and no increase in splenic granulocytes, so bacterial infection seems unlikely.

Anaemia is commonly associated with splenomegaly in ferrets. Such anaemia may simply be a consequence of increased phagocytic capacity associated with enlarged spleen, but other underlying causes may merit clinical investigation.

The underlying cause for the congestion and EMH could not be determined from the histological appearance (although the EMH could represent a response to the anaemia), so this is classified as idiopathic splenomegaly, as is usually the case in enlarged ferret spleens. Most patients do well, so the prognosis is probably good with continued clinical care. Remember that the splenectomized patient has a lifelong increased susceptibility to infections and also that when there is marked EMH in the spleen, it may be the main source of erythrocytes and it may take some time for the bone marrow to resume production at a satisfactory level, so marked anaemia may ensue after splenectomy.


The whole thing with Charlie happened very suddenly and unexpectedly. I felt his enlarged spleen by accident. I mean I handle and carry him every day and yet I never felt it. What I realised in hindsight, too, was that Charlie suddenly could not jump up any more. He used to chase the cats and jump over the "ferret gates" in order to follow them but then suddenly he could not lift off anymore. I'm sure his spleen did not start to enlarge much earlier than beginning of May. And at first there were only subtle hints that he was not quite okay. And then he went downhill quite rapidly. Right now he is still not fully back to normal but I suppose I can't expect miracles, his HCT/ PCV has gone up remarkably but is still at the low end of the normal range so I suppose it will still take some time for him to get back to normal and maybe he will never be 100% the same again. But still much better than dead. He is such a lively boy and enjoys life to the full. :-)

Charlie before the operation:




Snoopy and Charlie 5 days after the operation:

Franklin

Franklin and Peanut

Peanut

Charlie update 31/07/12

Charlie did incredibly well after the operation. He put on weight. I eventually stopped hand feeding him (after he had his stitches out) because he ate by himself but then a week or so later (approx. 7th - 10th of June) I thought he looked thin so weighed him and he'd lost quite a bit of weight. So I started hand feeding him again, huge portions. A week later he had not put on any weight and was becoming weaker. He also got an urinary infection on 16th of June, I took him and his group out of the cage at night and Charlie was not right at all, he was peeing small amounts every 5 minutes, appeared to be in pain and just very weak. I quickly took a video of him like this, I took it for my vet to see and then of course put Charlie back in his cage and started him on Baytril immediately. I'm adding the video here so people can see how ill ferrets can become literally within hours:

Of course it was a Saturday night, I was just grateful that I still had Baytril on hand. By Sunday he was already much better. Monday 18th to the vets, the left kidney was enlarged so my vet did a fine needle aspirate, she also did another blood test. Haematocrit had steadily gone up, at the time of his operation it was 16%, 10 days later 30% and on that Monday it was 38%. But BUN was high on that Monday and ALT very very high despite Charlie eating like a horse. The liver felt enlarged and after looking at the fine needle aspirate of the kidney, my vet thought lymphoma. On the slide she saw red blood cells, renal cells, quite a few lymphocytes and very few neutrophils.

Blood profile:

HCT 38%
ALP 379 U/L high
ALT 930 U/L high
BUN 22.7 MMOL/L high
CRE 44 UMOL/L
GLU 5.5 MMOL/L
TP 65 G/L
QC OK
HEM 0 LIP 3+ ICT 0 high

That Monday Charlie really didn't look well, he was as weak as he was when he was anaemic. In fact he looked so weak that my vet at one point suggested euthanasia. But then Charlie got a shot of dexamethasone and has been on prednisolone since, 1 mg twice a day. He is so much better! He is so active, before he was just slowly walking around the garden, now he runs and dances and even wrestles with the others, taken on 5th of July, what a difference to the previous video:

He has finally put on weight and has become stronger and is very active and has a good appetite. If his kidneys were failing, the pred would accelerate it and his appetite would be getting worse- none of which is happening. So I try not to worry too much, for the time being he is happy and that is all that counts. I keep shooting videos so if he deteriorates suddenly, I can show my vet how well he was! On the downside his external lymph nodes are getting bigger, the one by the right jaw was enlarged around the 7th of July and then the lymph node on his neck on the right enlarged by the 11th / 12th of July. I've never had a ferret with lymphoma that had external hard enlarged lymph nodes. Strange thing is though, now at the end of July, the enlarged lymph node by his jaw has gone down and is not enlarged any more. I have read about lymphoma that it can get better initially, the nodes can go down, but then one day it'll come back with a vengeance, the pred will stop working and then the lymphoma can suddenly get out of control and kill quickly. I rather not think about this but enjoy the moment. :-)

Charlie

Charlie and Peanut

Franklin update 31/07/12

Franklin has been passing bloody stools. It started Thursday 19th July and it took us a day to figure out who it was- until we finally saw Franklin pass stools. Sometimes it looked like he was passing a blood clot, other times it was stools and blood. He didn't have diarrhoea, his stools were well formed, he was not in pain in any way, he was as active as ever, and still ate fine. The blood was neither black nor bright red so the bleed could't be too far up or too low down. So I was keeping an eye on him. Hedgy had bloody stools for quite a while, she had faecals done which were all negative and then for a day or two she bled like crazy and then it just stopped. Must have been something in her intestine that healed. Maybe it was the same with Franklin as the bloody stools stopped after exactly 1 week.

Franklin 02.05.13

Charlie update 17/08/12

Charlie is coughing a lot which makes me think "lung cancer" and it reminds me of my mum who died of lung cancer of course and that reminds me of all the family problems and every time I hear Charlie cough, I have a meltdown. He's been back to the vets yesterday and considering all the external lymph nodes are up, my vet thinks the thymus or lymph node in the chest cavity is enlarged and pushing up against the wind pipe, making him cough. The lungs sounded clear. She is now wondering about a cough suppressant and I was asked to find out if ferrets can have codeine. My mum took that...

Charlie update 17/09/12

Today I had Charlie put to sleep. Charlie didn't give the impression that he was suffering, like in pain. But he had gone downhill rapidly. In July he was so active, in August he slowed down but still fairly okay. But in September he had no energy any more and developed breathing problems. I let him out in the morning with his group, he liked going out to lick water off the grass. But after 5 minutes he was back in bed. After his breakfast I let him out again and he ran around a tiny bit longer, went upstairs and went to bed. Same at night, I let him out for a short while with his group and again at night after dinner. He ate extremely well, like me eating 8 kg of food a day! Yet he didn't put on (much) weight. Then the last one or two weeks of his life I kept watching him and thinking there is not extreme suffering but neither quality of life. Then on the 17th of September I filmed him, the way he walked around in the garden, came in, went up the stairs, he had to have a break after every few steps up the stairs and would lie there breathing heavily, I opened up the doors to the forbidden rooms which he was not interested in, he went straight to bed. So I took him to the vets to be put to sleep. Very peaceful again. We did a post mortem and it was shocking the amount of damage the lymphoma had done and so quickly. When we took the spleen out end of May, the spleen and all organs looked healthy apart from the spleen being grossly enlarged. Now the chest cavity was full of tumours, the lungs, the heart was infiltrated by something, and the liver was looking awful, full of cancer. It is amazing he still ate and produced normal stools. I mean seeing the extent of the damage the cancer had done I felt I did the right thing and at the right time. I thought why wait until he suffers. At the rate he had gone downhill, that would have soon happened. And the way he breathed I thought I do not want to risk him suffocating. So I felt I did the right thing.

Charlie on his last day



Charlie's histopathology report

Diagnosis Lymphoma (Lymphosarcoma)
Prognosis Not Applicable

Histopathology Result

Sections from necropsy samples of various tissues from a 5.5-year-old, male, Ferret were examined microscopically.

LIVER; 1 sample received; 1 section examined. Microscopy reveals large, often coalescing nodules composed of solid sheets of intermediately differentiated lymphocytes, often, but not invariably, centred upon blood vessels; all together these comprise some 30-40% of the total area of this section of liver. The cells have a moderate amount of pale-staining cytoplasm and somewhat variably-sized, round to irregular nuclei with a rather variable chromatin pattern (finely stippled to coarsely clumped) and some with a small but distinct nucleolus. Mitoses are frequent (up to 10 per single high power field). The intervening hepatic parenchyma is markedly congested.

KIDNEY; 1 sample received; 1 section examined. Apart from several tiny foci of interstitial infiltration with normal-looking lymphocytes and one or two dilated tubules, both findings considered to be of negligible pathological significance, this is histologically largely unremarkable.

LUNG; 1 sample received; 1 section examined. This is mildly congested. There is a substantial focus of so-called phospholipidosis - alveoli filled with foamy macrophages - immediately beneath the pleura and associated with two small nodules of bone (osseous metaplasia). This is a fairly common incidental finding of negligible significance. There are also several smallish foci of lymphocytic infiltration, but with normal-looking rather than overtly neoplastic lymphocytes and again of little significance.

HEART; 1 sample received; 1 section examined. The myocardium is largely normal in appearance, but residual blood in the lumen contains a few atypical lymphocytes.

LYMPH NODES; 2 received; 2 sections examined. One of these was submitted as possible pancreas and has a small portion of that organ attached, but is mostly lymph node. The other is identified on the submission form as prescapular lymph node. Both nodes have similar changes, their normal architecture being completely effaced by solid sheets of intermediately differentiated lymphocytes identical to those seen and described in the liver (qv). The attached portion of pancreas is histologically unremarkable.

DIAGNOSIS: Lymphoma.

DISCUSSION: 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 while the lymphoblastic form is seen more frequently in younger (less than 2 years old) ferrets. In this particular case, the lymphocytes are somewhat intermediate in morphology.


Loosing Charlie this meant I could put 2 groups together. I had 3 groups then, old Jake on his own, then the group of five Honey, Snoopy, Peanut, Charlie, Franklin and last not least a group of three Squirt, Skippy, Tigger. They all got on except for Charlie. While Charlie was sick, I let the 2 groups out together when Charlie went to bed and I put him back in the cage, and now with Charlie gone I could put both groups together, they get on well, they're all very peaceful ferrets.

Franklin update April 2013

Just before or just after Charlie was gone, sometime during September 2012 anyway, Franklin showed symptoms of low blood glucose. The standard treatment for insulinoma is prednisolone to raise the blood glucose, another treatment is diazoxide which decreases the release of insulin. Since pred causes muscle loss and weight gain, I said to my vet if at all I want to give a low dose of pred only and start on diazoxide straight away. So she suggested doing diazoxide only. It does not work for all ferrets but has improved Franklin, he had a very low blood glucose before diazoxide but it was much higher after starting treatment. We still need to get the dose right but he is already better. Fast forward half a year and Franklin is doing really well. I think I started pred end of 2012 or beginning of 2013 and it has made a huge difference although the dose of pred is ridiculously small, around 1/4 mg per kg twice a day.

Franklin update 01/08/13

Franklin got a Suprelorin implant today as he was showing symptoms of adrenal disease, hair loss and some urine marking.

Franklin update 21/01/14

I keep having nightmares about Franklin, he is poorly and 6 1/2 year old, he has insulinoma and adrenal disease and his cruciate ligaments are torn so he has weak back legs. He also poops (frank) blood on and off, like he has a bleeding polyp in his intestine. It doesn't seem to affect him so I am not having him cut open. He has an implant for adrenal disease but his coat has not got better. He looks awful but he's a trooper and runs around and plays as good as he can. But I keep having nightmares that he goes downhill dramatically and needs to be put to sleep. One dream was, after he had a dental and a canine removed, I dreamt that he was running around and all of a sudden his head flipped back because my vet had almost cut his head off and it was only connected at the back of his neck and I could look into his chest cavity as his head was flipped back. I freaked and screamed “he needs to be put to sleep”, I could not imagine the suffering he must be going through, I thought how is he still alive, I hate for the animals to suffer. :( I can't remember the other dream I had but a few nights ago I dreamt I was feeding him and he choked, he could not swallow or breathe... I have never had nightmares about sick animals before, I did have 2 about Snoopy and the second nightmare I had a day before he was put to sleep but apart from Snoopy and Franklin I have never had such dreams before. Franklin had a bout of coughing and it sounded like he had fluid in his lungs, luckily I had furosemide so gave him some and he was fine and it didn't happen again.

Franklin update 11/02/14

Franklin and Honey have been coughing occasionally. While Franklin's cough was loud and sounding like he had fluid in his lungs from possibly heart disease, Honey's cough was just very quiet and didn't seem bad. So last Thursday 6th February I finally took both to the vets, they had chest x-rays and Franklin was sent home with heart tablets, Honey with antibiotics. My vet didn't have time to talk to me, she was operating, so Honey and Franklin have a follow-up appointment this Thursday 13th so my vet can tell me what's wrong.

Franklin update 17/02/14

Franklin had x-rays along with Honey on the 6th and his heart is massive so he is on Vetmedin now. He is not really doing well, the implant for the adrenal disease is not working so he has muscle loss from the adrenal disease and from the pred although his pred dose (for insulinoma) is very low (he is on 0.5 mg bid and weighs over 1 kg). Then the heart disease is making him weaker, too. But for now he can still get up the stairs but looks so frail. :( Still pooping blood occasionally, more often recently. I feel sad that Honey and Franklin are nearing the end of their life. :(

Franklin 17.02.14

Franklin update 04/03/14

Honey is looking so good while Franklin looks awful. I'm amazed he is still around. Hate seeing him frail though and he looks even worse compared to the other 3 big healthy boys.

Franklin update 07/03/14

Franklin had a check-up at the vets today and my vet started him on Cardalis and Furosemide.

Franklin update 10/03/14

Franklin is actually doing better today! I've been giving him Furosemide 3 times a day and he is not coughing if I space it correctly and don't forget a dose... This morning he went upstairs, too!!! When I looked for ferrets to put them back in the cage, Franklin wasn't in his bed in the kitchen, of course I thought he collapsed somewhere. But he had actually gone upstairs. This afternoon he's been up a few times and wanted out so I just let him out and again he went upstairs. :) I can't believe he has the strength. :) I haven't closed doors upstairs so it sounds like he has a good time going into all the “forbidden” rooms. I do this with the very sick ferrets because it gives them a boost.

Franklin update 22/03/14

Franklin is up and down, some days his heart is worse and better other days. When he gets fluid in his lungs and coughs, that upsets me so much. He is on 2 diuretics and normally they work well but some days I need to give him extra Furosemide. He is so frail, lost his muscle mass, has cataracts, I just feel so helpless and sorry that he is so bad. It's like when ferret Leo was so ill, he “only” had insulinoma and adrenal disease but also lost all muscle mass and had bad cataracts. But Leo was a trooper. But I still hate it when they get so sick. :(

Franklin update 06/04/14

Franklin is getting harder to feed, sort of the last 2 weeks. He has always been eager to eat and now it is becoming a struggle. He is now at a point where he's between having quality of life and having none. He did enjoy being out in the garden when it was warm and seems content but if he gets any worse I will have him pts. I just cannot stand seeing them suffer. I would not let him get to the point where he is barely hanging on and I have to fight to get him to eat. If they have one or more illnesses and get to the point where they don't want to eat then that is usually the point where I take them to the vets because usually they are not having a good time at all then.

Franklin update 08/04/14

Franklin was very nauseated after I fed him this morning and it was horrible, he was violently pawing at his mouth and gagging- for ages. :( If he is the same tonight and tomorrow morning I will have him put to sleep tomorrow. There is just sooo much wrong with him it could be nausea from the heart disease, pancreas troubles, some other cancer we don't know about... It was just distressing watching him. :(

Franklin 11.04.14


Franklin update 28/04/14

Franklin and Honey are so stable. Franklin had a few rough days last week where he had this horrible nausea 3 times in a row after feeding. I thought we'll try some stomach medicine (Carafate/ Sucralfate) to see if that helps or else he will be put to sleep. And then no more nausea and he's been really good. Honey actually wants to go out into the garden every morning now and Franklin usually does, too. They can't use the cat flap anymore because of their hind leg weakness so I have to open the door for them. At night I always put them out into the garden to make them walk to strengthen their legs.

Franklin update 28/05/14

I had Franklin put to sleep Tuesday 27th May. It was a somewhat hard decision because he was not obviously suffering as such. I find it easier to put them to sleep when they are definitely suffering. But with him there was just no quality of life left, he was so weak from his bad cruciate ligaments and muscle loss in his hind legs, when he did have a little run in the garden, he would then lie down tired, then walk a few steps, then lie down again. He was not interested in exploring anymore and it became increasingly difficult to feed him, he was fighting it bad at times and a lot of the time he would turn away from his food in disgust. His portion was 55 g not long ago and then it went down to 40 g and then I was lucky to get 35 g into him.

So last weekend (24th/25th May) I made the decision to have him put to sleep and I have a real problem with the premeditated aspect of it. Monday I prepared and portioned meat for the old and sick ferrets and I changed the portions to Honey and Peanut only and not including Franklin anymore. Monday night he had the last quarter of his heart tablet, Tuesday morning he had the last portion of his ground up diazoxide tablet. It was like everything was coming to an end simultaneously. So I took Franklin to the vets and talked with my vet and asked her is it just me, am I weak and selfish because I can't stand watching Franklin anymore? Or do I feel that way because he is really not well anymore? He was definitely in pain but not the sort of pain I can see in their eyes that requires opioid meds. I mean there were moments when he looked in a lot of pain but not all the time. But the last week he just had no interest in anything, not even checking out the “forbidden” rooms that the old and ill ferrets have access to. It was like he was just existing (and in some pain) but not living anymore. And I hated seeing him that way. I feel like a weight has been lifted off my shoulders now because I do not have to worry about how ill he really feels. When we first arrived at the vets, Franklin was alert, head held high and he did not at all look like an animal that needed to be put to sleep. But once the excitement died down, his head went down and he closed his eyes and was shivering which showed that he was in pain and not well.

We knew he had heart disease, insulinoma and adrenal disease but his liver was very cystic and one cyst or tumour was almost black. One kidney had a huge cyst on one end. He had growths lining his bile duct. He had been passing frank blood at times during the last almost 2 years but my vet did not find an apparent reason for this. He had strange little growths that were loosely attached to organs, really strange.

Franklin 11.04.14



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).


Reading the histopathology report, I am glad I had him put to sleep and definitely did the right thing... Poor Franklin with all those problems. :(

Peanut and Honey 11.04.14


Peanut update 21/07/14

I've had lots more animal problems and the worst has been Peanut... Peanut had been coughing a little, very occasionally, since about February 2014. Then she started to cough a little more, and towards the middle/ end of June it was becoming more frequent so I thought I take her to the vets for an x-ray (Monday 23 June). She was totally *fine* in herself, pretty active for a 7 year old, running around and eating fine. Then the x-ray showed a very bad looking chest, heart very probably enlarged and the lungs were all congested, apparently they were supposed to be dark and they were just hazy meaning not much air or oxygen in the lungs. So my vet put her on Fortekor and Furosemide and an antibiotic in case it was a fungal infection that ferrets can get (Pneumocystis carinii ). So she got this injectable Trimethoprim /Sulfamethoxazole antibiotic and slowly stopped eating. I started the drug Wednesday 25 June in the evening and by Saturday night she would not eat so I stopped giving it.

Peanut 11.04.14




Over the next few days her appetite gradually got a little better, she also saw my vet Monday 30 June. And then the appetite got worse until she stopped eating (again) Wednesday 02 July. She felt nauseous and looked *really ill* Wednesday evening. If I had to guess I would have said the kidneys packed in. So back to the vets Thursday 03 July. I said Peanut was acting absolutely FINE before the antibiotic and now she was on death's door. She was shivering and had her eyes closed and really looked like she needed to be put to sleep. I was distraught thinking an antibiotic killed her, I could just have cried... My vet said something about immune mediated reaction or something, like a reaction to the antibiotic that was reversible, and she gave Peanut dexamethasone and B12 and I was to start Peanut on 1 mg prednisolone bid on Friday.

That night she ate a little but Friday morning next to nothing. She even bit my finger when I tried to force feed her. But she looked much better after the steroid shot, so I didn't feel comfortable phoning the vets again.

Peanut 07.06.14

Anyway, Peanut improved a little, at least her appetite did. After about a week on pred she started eating almost normal portions of meat and even ate the odd kibble. But her activity was nowhere near as good as before, in fact it was non-existent. She really only ever got up to drink and pee. I still thought her kidneys were destroyed, she was drinking and drinking. But if the pred gives her quality of life then I don't care if it'll destroy her kidneys even quicker.

Peanut and Poley 22.07.14


Peanut update 25/07/14

This afternoon I am taking Honey and Peanut to the vets to possibly have both put to sleep... I am going crazy and can't stand looking at them anymore. :( And I figure if I feel so distraught at seeing them then surely they can't be feeling great.

This morning Peanut was scrabbling along on the floor like Honey. Her back legs had become too weak for her to walk on laminate or tile flooring so she pushed herself along with her back legs and pulled herself with her front legs. I couldn't make sense of it and thought how long has this been going on for??? My brain just couldn't process it. Then I thought a few days ago I took videos of her as she was *walking* on the tile floor. I took the videos because she was swaying while walking. I took a video on the 22nd and 23rd and she was walking and I assume she was walking yesterday so this morning she couldn't anymore? I've uploaded 3 short videos of her. All she did was eat and sleep, drinking and peeing loads. No running around *at all*. Since the antibiotic she has been a very sick ferret.

I have never done this, 2 ferrets put to sleep on the same day. But I am reaching the point where I think what is the point. Yes, they could go on for a few more days and weeks like ferrets do but in the end they will die and they don't have quality of life and maybe hopefully I can spare them some suffering.

Later at night...

Both Honey and Peanut were put to sleep. I got to the vets and Peanut was her usual self, no interest in anything whatsoever. She just curled up and slept, no energy. And Honey was having her usual breathing problems and because of the heat they were worse. When I put her on the examination table, she just laid there flat and did not move. The vet took one look and knew that Peanut was feeling like crap and Honey was not good at all, either. Both girls went so quickly once they got the euthanasia solution (by intraperitoneal injection- which they didn't notice while licking their sweet paste).

The vets did not have time to do a post mortem so we did one, I did all the cutting and even got over my squeamishness and cut the chests open... As usual I can only hope I found what was wrong.

With Peanut she had an angry looking nodule (lymph node?) in the middle of her mesentery, her liver was cystic, I hope it turns out her kidneys were damaged, they seemed very small and looked different to Honey's. Her heart seemed to be dilated and inside the chambers were big so I guess she did have dilative cardiomyopathy. I just hope we get to the bottom of what was so wrong with her after she got the antibiotic.

Peanut and Honey 23.07.14





Peanut's histopathlogy report

Post-mortem Tissues from a Ferret: 13 samples received; 13 sections evaluated on 4 slides.

Heart (slide 1). In this sagittal section of the myocardium with a great vessel, myocytes appear uniformly broad and show moderately frequent branching. A large subendocardial wedge of fibrosis, infiltrated by a few plasma cells, partly replaces the ventricular myocardium -- this area of the myocardium also contains several similar but much smaller wedges. There are no other remarkable findings.

Lung (3 sections, slide 3). There is mild, patchy congestion. There are patchy areas of atelectasis alternating with areas of apparently normal alveolar inflation. Rarely, clusters of macrophages laden with black pigment (pneumoconiosis, probably anthracosis) lie adjacent to bronchi. There are no other remarkable findings.

Liver (3 sections, slides 1 and 4). One of the sections (slide 4) shows local replacement of the parenchyma at the apex of the lobe by a mass approximately 8 x 7 mm in cross-section after processing. The mass consists of anastomosing, blood-filled vascular channels, supported by thin-walled collagenous trabeculae that are lined by endothelium. The endothelial cells are usually attenuated but are sometimes plump and very rarely are piled up. Nuclei are round to oval and show moderate anisokaryosis. Mitotic figures are uncommon, approximately 1 per 10 high-power (400x) fields. The mass is generally discrete but shows several foci of peripheral invasiveness into adjacent sinusoids. Throughout the remainder of this section and in the other two sections (slide 1), the hepatocytes have mildly lacy to vacuolated epithelium (lipid, possibly with glycogen, very mildly increased above normal levels) but appear slightly small. Plasma cells sometimes cluster in portal tracts, which rarely show proliferative bile ducts. There are no other remarkable findings.

Adipose Tissue (slide 4). There are no remarkable findings.

Lymph Node (slide 4). The nodal parenchyma is displaced peripherally, and the centre of the node is replaced by a zone of haemorrhage with fibrinous thrombi, some macrophages, some necrotic debris, and a few thin collagenous trabeculae lined by endothelium similar to that described in the liver. There are no other remarkable findings.

Spleen (slide 2). The red pulp shows numerous dense aggregates of mixed haematopoietic precursor cells. There are no other remarkable findings.

Kidney (2 sections, slide 2). The sections are similar. There are multiple radiating wedges of fibrosis that extend from the medulla to the capsular surface of the cortex. These wedges contain moderate numbers of lymphocytes and plasma cell. Entrapped parenchymal elements are generally attenuated, but a few cysts (glomerular or tubular cysts) up to 3 mm in diameter are present in affected areas. Throughout the remaining cortex, approximately 10 % of glomeruli are sclerotic and many other glomeruli show thick and partly collapsed capillary loops. Tubules are often slightly dilated but only occasionally contain proteinaceous fluid. The medullary stroma is multifocally expanded by fibrosis. There are no other remarkable findings.

Haired Skin (slide 4). A well-demarcated, polycystic mass, approximately 5 mm in greatest diameter after processing, expands the subcutis and deep dermis. The mass is lined by bilayered to rarely pseudostratified cuboidal to columnar epithelium, with moderate amounts of eosinophilic to vacuolated cytoplasm that sometimes shows apical blebbing. Nuclei are bland, oval and central. Mitotic figures are extremely rare. There are lesion-free margins in all directions. There are no other remarkable findings. excised this cystadenoma completely, which should be curative.

MORPHOLOGICAL DIAGNOSES:

1. Liver and Lymph Node: Haemangiosarcoma -- presumed metastatic
2. Heart: Myocardial Hypertrophy-- diffuse, moderate, associated with multiple chronic infarcts
3. Lung: Atelectasis -- multifocally extensive
4. Spleen: Extramedullary Haematopoietic Hyperplasia -- marked
5. Kidney: Nephritis -- glomerular and interstitial, chronic, extensive, moderate to marked, with multiple renal cysts
6. Liver: Pericholangitis -- multifocal, chronic, mild to moderate
7. Haired Skin: Apocrine Cystadenoma

COMMENTS:

This ferret had a number of potentially serious lesions. In the liver and in one lymph node, there is haemangiosarcoma: a malignant neoplasm of vascular endothelium. Presumably, the nodal lesion represents a metastasis, possibly from the liver, though it is also possible that both lesions represent metastasis from some unidentified primary site. Primary hepatic haemangiosarcoma has been reported uncommonly in ferrets, and based on the limited available data, exhibits similar behaviour as in other mammals -- that is, the tumour metastasizes widely and aggressively. This tumour would have carried a poor prognosis.

This ferret also had myocardial hypertrophy associated with several old infarcts. Whether the hypertrophy is a compensatory lesion after loss of the myocardium to the infarcts, or whether it is part of a true cardiomyopathy, is undetermined. Hypertrophic cardiomyopathy is less common than dilatative cardiomyopathy in mature ferrets; however, hypertrophy can be seen as part of the end-stage of both lesions. In the sections of lung and liver provided, there is no evidence for passive congestion (congestive heart failure).

The lung shows extensive areas of atelectasis, but no pneumonia, no infectious agents, and no neoplasia are visible in the sections provided. Possible aetiologies for atelectasis include pneumothorax or compressive coelomic effusion of any cause, trauma, upper airway obstruction, and less commonly for a chronic condition in a mature pet animal, inhaled gases, viral or other infections (not noted) and surfactant defects.

Splenomegaly with extramedullary haematopoiesis is commonly seen in middle-aged to older ferrets, but has been found in ferrets as young as six months of age. The cause is not known, but it has been speculated that the lesions represent one manifestation of a response to chronic inflammatory disease. In this case, potential haemorrhage associated with the haemangiosarcomas, or conceivably, hypoxaemia associated with the cardiac lesion or the pulmonary atelectasis, might have been contributory. Many but not all affected ferrets are anaemic.

This ferret also had chronic interstitial and glomerular nephritis, the latter affecting a significant minority of the glomeruli. Some small cysts in these kidneys most probably represent acquired cysts in foci of renal scarring. The lesions here are sufficiently advanced that there might have been some impairment of renal function.

The liver shows mild pericholangitis, probably a reflection of ascending antigenic stimulation from the anterior intestine. This appears to be a chronic rather than an active lesion. Its significance is questionable.

Finally, the skin contains an apocrine cystadenoma, a benign neoplasm of paratrichial sweat gland origin. Apocrine cystadenomas are quite common in both male and female ferrets. They occur most often around the head, neck and genitalia, where scent glands are prominent, but can arise in any location in the skin. This lesion would have had no clinical importance.

Honey and Peanut 10.05.14



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