From:
"fret.popper"
Date: 2009-06-14 09:48:06 UTC
Subject: [ferrethealth] Re: Sick ferrets in Australia
To: ferrethealth@yahoogroups.com
I have pasted ferret Reggie's blood test results and ferret Bella's PM and =
test results.
Please note: Ferrets Reggie and Thug became ill and died at the same time s=
uffering the same clinical signs. Blood tests were done on Reggie and PM on=
Thug.
Pasted also results and PM of ferret Bella. I have no medical history on fe=
rret Ringin other than that she died under similar circumstances as Reggie =
and Thug. Reggie, Thug, Ringin and Bella were 'black-eyed whites' or 'Roan'=
like in horses. Their white fur is interspersed, to varying degrees, with =
pigmented hair (our definition of BEW).
Latest news is that all the surviving ferrets, including Poco, are doing fi=
ne.
I ought to mention that the owners have been breeding and keeping ferrets f=
or many years. Their ferrets are amongst the best there are, prize winners =
and show champions. The owners are very fond of their ferrets and therefore=
it is so distressing to lose some of their best ferrets under the circumst=
ances, especially not knowing the cause.
-------------------------------------------------------------------
Ferret REGGIE 4 1/2 years
Date: 07/04/09
Red Cell Count 11.60 x 10 ^12 /L
Haemoglobin. 210 g/L
Hct 0.62 L/L
MCV 53 fL
MCH 18.0 pg
MCHC 340 g/L
White Cell Count 4.8 x 10 ^9 /L
Neutrophils 90% 4.3 X 10 ^9 /L
Band Forms 0% 0.0 x 10 ^9 /L
Lymphocytes 10% 0.5 X 10 ^9 /L
Monocytes 0% 0.0 x 10 ^9 /L
FILM MORPHOLOGY: RBC: Normal WBC: Morphology normal. Platelets aggregated a=
nd adequate
GENERAL BIOCHEMISTRY SPECIMEN : SERUM
sodium 155 mmol/L
Potassium 4.5 mmol/L
Chloride 103 mmol/L
Na/K 34.4
Urea 11.0 mmol/L
Creatinine 46 umol/L
Calcium 2.17 mmol/L
Phosphate 2.82 mmol/L
Protein 58 g/L
T. Bilirubin 2 umol/L
Alk Phos 33 U/L
ALT 80 U/L
GGT 1 U/L
AST 111 U/L
Cholesterol 5.0 mmol/L
SERUM INDICES (Clear/+/++/+++)
icterus index Clear
Lipaemia index Clear
Haemolysis index Clear
No significant abnormalities seen using ISIS referenc e range data. Your hi=
story of 2 ferrets with the same clin sx suggests access to toxins. If infe=
ctious, I would expect at least mild differences in the presentation clinic=
ally.
Some analytes unavailable due to insufficient sample.
Re: Reggie a 4 year old,
HISTORY:
23:27 Reggie presented on 6/04/2009 at 22:38 with the following problems:
> has been to vet during day with breathing difficulties and seizures, was=
taken home after and put in humidi=1Ecrib, ferrets breathing became a lot =
more laboured this evening..
Owner has 20 ferrets at home. All were normal this morning. Owner came home=
this afternoon to find two ferrets having respiratory distress. This ferre=
t had a seizure =1E treated with 0.1ml Diazepam SC. Chest xrays revealed NA=
D.
Other ferret improved with treatment given (?)
This ferret continued to decline. Had another seizure just prior to visitin=
g AVEC =1E treated by owner with another 0. 1 ml Diazepam SC
PHYSICAL EXAMINATION:
> Weight: 1.100 kg, 2.42 lb, 0.11 m2 Body Condition Score 4/9
> Temperature: 38.4; pulse: 200/good; respiration: tachypnoeic .
> Temperament: sedated.
>Skin: NAD.
>Skeletal: NAD. Cardiovascular: MM colour is slightly cyanotic.
>Respiratory: Deep laboured breathing with effort on inspiratory phase.
> Gastrointestinal: NAD.
> Genitourinary: NAD.
Neuromuscular: Ferret is in lateral recumbancy and heavily sedated.
Lymph Nodes: NAD
Eyes: NAD
Ears: NAD
Dental Score: 314: Gingivitis around teeth
INVESTIGATIONS:
The following investigations were performed:
None
PROCEDURES:
>Start on O2 therapy
SC fluids
ASSESSMENT:
Ferret responded well to O2 therapy and slowly become more responsive as di=
azepam wore off.
Ferret began to show signs of pain on handling. Palpation of caudal abdomen=
revealed a very full,
rock hard and painful bladder which would not express. 1
Discussion with owner =1E agreed to attempt some diagnostic work to assess =
for possible urinary tract obstruction.
Obtained a small amount of blood of 6+ istat cart =1E only got a K+ and Na+=
reading (both normal) =1E other readings were not available.
Two minutes after getting blood sample ferret urinated spontaneously and th=
is appeared to be accompanied by significant amounts of discomfort. Ferret =
then displayed ongoing signs of pain with increased RR and vocalising on ab=
dominal palpation.
Abdominal xray taken (at no charge) =1E NAD =1E initially thought kidneys w=
ere enlarged but they are wnl. Similar with heart shadow =1E wnl.
Ferret responded to IM analgesia (initially given 0.1 mg methadone IM follo=
wed by 0.2 mg butorphanol IM)
Obtained 0.25 ml EDTA and 0.25 ml Heparin blood for possible limited analys=
is at lab In house blood glucose 21.lmmol/L
Ferret had another seizure for about 30 seconds. Blood glucose taken immedi=
ately after was 22.2mmol/L =1E this largely rules out insulinoma.
DDx: Primary neurological disease
Toxicity/Poison/Venom
Metabolic disease with secondary neurological signs
Ferret has slowly recovered from diazepam sedation but as he has done so ha=
s begun to show signs of increasing abdominal pain. On initial palpation hi=
s bladder was full and very hard. Pain on gentle abdominal palpation. Suspe=
cted urinary tract obstruction. Blood taken for 6+ cart in the hopes of get=
ting some results to confirm or r/o UTO
TREATMENT:
>Dexamethasone Injection 2mg.ml # 0.05 ml(s) Rx: Given SC
PLAN:
Maintain on O2 overnight and allow to wake up from sedation
Diagnostic Plan
Ferret is consistently showing signs of pain when sedation/analgesia wears =
off but cannot isolate cause at this stage =1E initially appeared to be abd=
ominal but this is not consistent. Responsive to opioid analgesia
Continue with analgesia and O2 therapy overnight. Blood taken for analysis =
at lab (removed relatively easily from cephalic veins =1E advise second sam=
ple in heparin to maximise results.
DDx: need to investigate underlying causes of seizuring =1E metabolic/toxic=
/neoplastic and require CBC/MBA for this analysis Insulinoma was high on li=
st of differentials until BG came back as high @ 21.1
Owner to collect ferret and take back to own vet with blood samples taken h=
ere
Administered another 15ml warm LRS @ 0500 to hopefully increase blood volum=
e and allow for further blood sampling.
Treat in light of blood results
----------------------------------------------------------------------
Ferret Thug 4 =BD years
All Tests Complete
GROSS PATHOLOGY REPORT.
HISTORY
Several of 20 ferret's showing signs of weakness, bloating, abdominal
pain, agonal gasping. ?Toxin, viral, other.
Gross Post Mortem.
GROSS PATHOLOGY
We are presented with a entire male white ferret in good body condition. Th=
ere are large amounts of subcutaneous fat and as well as intra-abdominal fa=
t in the carcass. The animal has a moderate periodontal disease, with sever=
al tooth being loose, and most teeth coated with thick calculous.
On opening the carcass the lungs are mildly mottled a pink dark red colour.=
The heart is round in shape, but no other abnormalities are noticed in the=
chest.
The abdominal cavity is opened and no abnormal findings are revealed.
The stomach contains a brown thin fluid, and the faecal material consists o=
fla thick toothpaste brown consistency. Both kidneys are mildly mottled how=
ever.
CONCLUSIONS
open diagnosis.
COMMENTS
A urine sample was taken and the urine specific gravity was 1.035. A number=
of samples were taken. All organ systems were sampled including the brain =
and placed in Formalin. As well fresh liver, kidney and lung have been refr=
igerated, and urine has also been collected.
There is nothing to reveal the cause of the clinical signs on gross post mo=
rtem. I would suggest the histopathology be undertaken to try and reveal an=
y organic disease. If you have specific toxins that you would like to test =
for, I have kept back a urine liver and kidney. Please let me know how you =
wish to proceed with this case.
=09=09
HISTOPATHOLOGY FROM NECROPSY
09/04/2009
CLINICAL HISTORY
See previous gross post mortem - several of a group of 20 ferrets
showing signs of weakness, bloating, abdominal pain and agonal gasping.
?viral toxic other.
MACROSCOPY
Various organs taken at gross post mortem. by [Veterinarian's name removed =
as per FHL rules]. These are placed into sections A2, kidney and liver. B5,=
obex, middle cerebella, peduncle, spleen and thyroid. C2 duodenum and rost=
ral colliculus. D1 thalamus. E2, lung. F4, heart, -tongue and small intesti=
ne. G3 small intestine and skeletal muscle. ak
MICROSCOPY
Kidney: Diffusely, glomeruli exhibit varying degrees of one or more of the =
following changes: thickening of capillary basement membranes and mesangium=
with eosinophilic hyaline to fibrillar material with occasional reduction =
in glomerular tuft cellularity; thickening of Bowman' s capsule with sparse=
mineralisation; mild hyperplasia of parietal epithelium; synechiae; or occ=
asional replacement by hypocellular collagen with shrinkage and obsolescenc=
e of the glomerular tuft (glomerulosclerosis). Multifocally, cortical tubul=
es exhibit mild vacuolar swelling and degeneration of epithelial cells, wit=
h very occasional individual cell necrosis. Tubular cells sometimes contain=
granular to globular golden-brown cytoplasmic pigment (haemosiderin and/or=
bilirubin). occasional tubules are ectatic, lined by attenuated epithelium=
and filled with homogenous eosinophilic proteinaceous fluid. Rare tubules =
contain small amounts of mineral and/or oxalate crystals. Multifocally, the=
interstitium contains small numbers of lymphocytes and rare plasma cells.
Liver: Lobular architecture is intact. Diffusely, hepatocytes exhibit
mild vacuolar change with pale feathery cytoplasm. Few hepatocytes
contain discrete round clear cytoplasmic vacuoles (lipid vacuolation).
Multifocally, portal tracts contain small numbers of lymphocytes and few
RBC precursors (extramedullary haematopoiesis). Multifocally,
haemosiderin-laden macrophages form small clusters within sinusoids
(pigment granulomas), or are scattered within portal connective tissue. Dif=
fusely, there is moderate congestion.
Spleen: The red pulp is diffusely congested. There is moderate extramedulla=
ry haematopoies-is with prominent megakaryocytes and megakaryoblasts. Lymph=
oblasts and macrophages outline sinusoids and trabeculae. White pulp is int=
act and appears generally unremarkable.
Thyroid gland: Diffusely, there is mild to moderate vascular congestion; no=
other significant findings.
Brain (cerebellum, obex, rostral colliculus, thalamus, cerebral cortex):
occasional spongiotic vacuoles are present in white matter tracts, mostly w=
ithin the cerebellar folia. occasional neuronal cell bodies contain discret=
e perinuclear aggregates of pale golden pigment (lipofuscin). Rarely within=
the leptomeninges, there are small psammoma-like bodies, composed of conce=
ntric lamellae of pale basophilic mineralised material, surrounded by conce=
ntric collagen fibres, and occasional macrophages. Rarely, small clusters o=
f lymphocytes are also present. Within the thalamus, there are rare shrunke=
n and hypereosinophilic neurons with pyknotic nuclei (degeneration/necrosis=
).
Small intestine/pancreas: There is autolytic sloughing of the superficial m=
ucosa. Multifocally, the lamina propria is mildly expanded by increased amo=
unts of hyalinised collagen that occasionally separates adjacent crypts (fi=
brosis). The lamina propria contains low numbers of lymphocytes, plasma cel=
ls and scattered eosinophils. occasional crypts appear mildly hyperplastic,=
and in one section, rare crypts are ectatic and contain sparse eosinophili=
c flocculent material and few degenerate cell nuclei.
Lung: Diffusely, there is moderate to marked congestion. Multifocally, alve=
olar airspaces are collapsed with increased proximity of septa (atelectasis=
), often accompanied by mild flooding of alveoli with pale eosinophilic oed=
ema fluid. These changes are most prominent within the subpleural stroma. M=
ultifocally, bronchiolar lumina contain amorphous particulate globules of p=
ale basophilic to amphophilic proteinaceous material, aspirated medication?=
?). Bronchioles also contain scant oedema and few small eosinophilic protei=
n globules. Multifocally, there is mild perivascular anthracosis.
Skeletal muscle: NO significant findings.
Heart: No significant findings.
DIAGNOSES
1. Kidney: Glomerulonephritis, membranous, segmental to global,
diffuse, chronic, moderate, with mild tubular degeneration/ectasia
and minimal lymphocytic interstitial nephritis.
2. Lung: Congestion, diffuse, moderate to marked, with oedema and
mild atelectasis.
3. Small intestine: Mucosal fibrosis, diffuse, chronic, mild, with
minimal to mild lymphocytic and eosinophilic enteritis.
4. Spleen: Congestion, moderate, with extramedullary haematopoiesis
COMMENTS
Pulmonary congestion and oedema are common nonspecific 'agonal' changes; si=
milarly, splenic congestion occurs with splanchnic pooling associated with =
terminal vasodilation/loss of vascular Lone and failing cardiac output. The=
glomerulonephritis is a reasonably significant histopathological finding, =
but most likely to be incidental and not directly related to illness/death =
within these animals. Chronic glomerulonephritis often develops secondary -=
to diseases associated with prolonged antigenaemia e.g. chronic infection, =
endoparasitism, or immune-mediated disease. However, glomerulosclerosis and=
chronic interstitial fibrosis are common age-related changes observed in f=
errets, often as incidental and subclinical lesions. Early changes are typi=
cally present from 2 years onward, and marked changes can lead to renal fai=
lure by 4-5 years. The finding of hypersthenuria suggests intact renal tubu=
lar concentrating ability advanced primary glomerular disease is more likel=
y to be associated with proteinuria/nephrotic syndrome. There is evidence o=
f mild intestinal mucosal fibrosis, possibly reflecting a previous insult, =
or, more likely to be the product of chronic enteritis e.g. inflammatory bo=
wel disease, also a common finding in middle-aged to older ferrets. I think=
it unlikely that this change would be associated with the abdominal pain/b=
loating you describe, and the degree of inflammatory cell infiltration into=
the mucosa was only mild. Overall, there are no histopathological features=
to indicate a specific disease process or obvious cause of death in this a=
nimal. There is no evidence to suggest viral infection e.g. distemper, or o=
ther systemic infectious agents. As per the gross necropsy report fresh tis=
sue has been retained should further investigation be required e.g. toxicol=
ogy.
--------------------------------------------------------------------
Patient: ferret BELLA=09
Referred: 26/05/2009
Collected: 26/05/2009
Tested: 26/05/2009 13:23
Age: 7 months Reported: 26/05/2009 14:18
Test: PBC =1E VET HEALTH SCREEN CBC
GENERAL HAEMATOLOGY
Red Cell Count 7.19 X 10 ^12 /L
Haemoglobin 126 g/L
Hct 0.37 L/L
Mcv 51 fL
MCH 18 pg
MCHC 341 g/L
White Cell Count 9.4 x 10 ^9 /L
Neutrophils 62% 5.8 x 10 ^9 /L
Band Forms 27% 2.5 x 10 ^9 /L
Lymphocytes 9% 0.9 x 10 ^9 /L
monocytes 1% 0.1 x 10 ^9 /L
Eosinophils 1% 0.1 X 10 ^9 /L
Test: PBM =1E VET HEALTH SCREEN MASTER
GENERAL BIOCHEMISTRY SPECIMEN : SERUM
Sodium 147 mmol/L Protein 47 g/L
Potassium 3.8 mmol/L Albumin 21 g/L
Globulin 26 g/L
Na/K 38.7 Alk Phos 28 U/L=09
Urea 6.0 Mmol/L ALT 288 U/L
Creat. 39 umol/L
Calcium 1.83 mmol/L AST 170 U/L
SERUM INDICES (Clear/+/++/+++)
Icterus index Clear
Lipaemia index Clear
Haemolysis index Clear
Test: GP =1E GROSS PATHOLOGY
GROSS PATHOLOGY REPORT
REF: 2009/5314310/lo 28/05/2009
CLINICAL HISTORY Third ferret that had died in two weeks from same owner (s=
ee previous autopsy report from Thug). Lethargy, pyrexia, tachypneic three =
days,
then died. (bloods were normal, done 26/5/09). On antibiotics. 15hrs
on 27/05/09.
NECROPSY FINDINGS
=1E Received carcass ferret, female 0.7 kg, white.
=1E The carcass was in good condition.
=1E post mortem changes mild.
=1E The right lung lobes were hepatised, red and sunk in fomalin. In the
cranial lobe there was a discrete dull white rounded nodule
7mm in diameter. In the intermediate lobe there were several 1=1E2mm whit=
e foci.
In the mid region of the caudal lobe, which was non=1Ehepatised, there
was a focus of fibrosis subpleural l0 mm, diameter with surrounding=09=09
alveolar emphysema and collapse. The left lung lobes were multifocally
emphysematous, congested and oedematous. There was copious mucopurulent
exudate at the tracheal bifurcation and extending into the bronchi deep
into the lung tissue in both lungs.
=1E The tracheobronchial and mediastinal lymph nodes were prominent,
enlarged and hyperaemic. The R mediastinal tissue was extremely
reddened and velvety in appearance.
=1E The spleen was greatly enlarged and had a dull pink colour. On=09=09
section red pulp bulged and had a meaty appearance.
=1E Gastro=1Eintestinal tract.
Stomach contained a small amount of semi=1Edigested ingesta and some mucus.
Small intestine=1E patchy gaseous dilation (probably post mortal) and patch=
y mucosal hyperaemia.
SAMPLES COLLECTED AND TESTS REQUESTED.
=1E A range of tissues were collected into 10% buffered formalin for histop=
athological examination. =1E samples of lung, liver, spleen and small intes=
tine have been collected into separate sterile pots. The lung will be cultu=
red for aerobic bacteria as discussed telephonically.
DIAGNOSIS
PNEUMONIA, diffuse right lungs, subacute.
CONMEMS Gross pathology has indicated pneumonia which can explain the clini=
cal signs.
Test: VSW =1E CULTURE
MICROBIOLOGY SPECIMEN: Lung
ANIMAL ID:BELLA.
MICROSCOPY
No bacteria seen.
CULTURE
1. Light growth of mixed coliforms
2. Light growth of mixed coagulase negative Staphylococci
COMMENT: Anaerobes NOT isolated.
Salmonella NOT isolated.
--------------------------------------------------------------------
[Moderator's Note:
This is the third or fourth time a vet report has suggested that
a toxin is likely and part of today's transcriptions note that the
person thinks that may be more likely that disease.
I also noticed that periodontal disease got mentioned again. If
our own experience is typical then periodontal disease is pretty
rare in ferrets so I am wondering what would eat up calcium.=20
A lot of dietary phosphorous can but that is such a common food
component that I doubt that would be the cause. This may be
coincidence or it may be an indicator that might point to cause
so see how the other's alveolar bones are.
Here is the summary on these ferrets worked from past posts:
Post 10700
[Moderator's note:
poster put her answers in capital letters
after each summary section to which she
is replying.]
Answers to your questions.
>
> These seem to be the symptoms in temporal order
>
> lack of desire to eat
YES
> disorientation
OBSERVED IN ONE FERRET, REGGIE
> lethargy, crying, "swollen under rib cage area"
YES
>(Do you refer to a large spleen
NO
>or to a swollen GI tract, both, or neither?)
SWOLLEN GI TRACT AND/OR ACCUMULATION OF FLUID
> seizures and trouble breathing at this point in some of the individuals
>
> Pamlin and Oxygen given
> (Question, were their lungs imaged at this point?)
YES X-RAYS TAKEN - SHOWED NOTHING
> more seizures and difficulty breathing
>
> diarrhea in some (survived)
YES
> furball prep given to some (survived)
YES
> some cold to the touch (Were any fevering and were anal
> temps taken? What were temps?)
TEMPERATURES NORMAL EXCEPT FOR POCO WHO WAS HYPOTHERMIC,
SHE SURVIVED.
BELLA HAD FEVER, ABOVE 41C, SHE DIED. SEE EMAILS 26 AND 28 MAY.
> Vet report notes 20 ferrets with weakness, bloating, abdominal pain,
> agonal gasping
NOT ALL OF THEM WERE AFFECTED TO THE SAME DEGREE, SOME OF
THEM JUST WENT OFF THEIR FOOD FOR 2-3 DAYS AND RECOVERED
> One of the ferrets (others?) in necropsy showed pronounced oral gum
> disease. (Was this definitely chronic or might it have been from a
> recent and extreme cause? Were there mouth sores?)
NOT SURE, BUT PROBABLY CRONIC
> Diet raw whole prey with kibble offered (Did I get that right?)
NO. VARIOUS FRESH RAW MINCED MEATS, CHICKEN WINGS AND NECKS,
NO DRY FOOD, THEY DON'T LIKE IT
> Lungs and kidneys slightly mottled
YES
> Detailed necropsy report and more in some posts in
> http://pets.groups.yahoo.com/group/ferrethealth/message/10657=20
-------
Does the ASPCA run a toxicology hot line there?=20
Could toxicology work reports be transcribed?
The US ASPCA runs two animal poisoning hotlines but at this
point they don't have a route for buying email international
consultations. I just asked them. They will be considering
that with executives now because they had not thought about
it before. If I get a call back with a way for your vets to access
their work I will let you know but usually the type of poison
is found first and then treatment given so they can help best
if the cause of the poisoning is found. Would it be possible
to move the entire ferret colony into quarantine elsewhere
to see what happens then and go over everything at that
home and/or yard with a fine tooth comb? Is the yard locked
from intruders?]
------------------------------------
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